Glossary of cardiopathology

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Created by kwithers

Name the 2 primary mechanisms of vascular pathology that result in disease.
1. Narrowing or complete obstruction of a vessel
2. progressive weakening of vessel walls
-leads to dilation and/or rupture

Why are arteries thicker than veins at the same branch point?
-b/c arteries have to accomodate:
1. pulsatile flow
2. higher blood pressures

True or false: veins have both an internal and external elastic laminas
-false; arteries
internal elastic lamina= between intima and media
-external elastic lamina= between media and adventitia

True or false: the biggest arteries in the body are muscular arteries
-the big ones are elastic arteries b/c have to withstand lots of pressure
-smaller arteries are muscular (coronary, renal arteries)

All of the following are elastic arteries EXCEPT:
1. aorta
2. pulmonary
3. iliac
4. renal

-renal artery (muscular)
What is the physiological significance of arterioles?
=principal control points for regulation of physiologic resistance to flow
-pressure and velocity of flow both decrease --> pulsatile flow replaced by steady flow
True or false: histamine acts on arterioles during inflammation to increase vascular permeability.
-increased vascular permeability due to HM acting on post-capillary VENULES
-HM acting on arterioles causes VASODILATION

Name some functions of vascular endothelial cells
1. maintain anti-thrombogenic surface when intact
2. modulate vascular resistance
3. metabolize hormones
4. regulate inflammatin
5. affect growth of other cell types through GFs and GIs
-SM cells
6. Maintenance of permeability barrier

True or false: vascular SM cells are able to synthesize ECM components
-can also make some GFs and cytokines
Name 3 properties of endothelial cells when injured.
1. leaky
2. SM thickening (healing response)
3. clotting
-b/c disruption of normal anti-thrombogenic surface of endothelium

True or false: intimal wall thickening is a stereotyped response to any vessel injury
-SM cells migrate into injured intima -> SM cells proliferate and make ECM
-this response is typical of injury due to ANY kind of insult
-recruitment of SM cells into intimal involves signals from cells and from mediators from complement and coagulation
-excessive thickening in intima -> luminal stenosis

Define arteriosclerosis.
=hardening of the arteries
-generic term reflecting arterial wall thickening and loss of elasticity
-3 patterns
1. Arteriolosclerosis
2. Monckeberg medial calcifical sclerosis
3. Atherosclerosis

Define Atherosclerosis
=one of the 3 types of arteriosclerosis (hardening of the arteries)
=chronic inflammatory response of the arterial wall to endothelial injury
-characterized by:
1. fatty streaks
2. atheromas (lesions in the intimal that protrude into vascular lumina)
-ubiquitous in developed nations

Define Atheroma
=raised intimal lesion that protrudes into the lumen of an artery
-characteristic lesion of atherosclerosis
-Composed of:
1. necrotic center
-lipids, cell debris, foam cells, Ca
2.fibrous cap
-SM cells, macrophages, foam cells, lymphocytes, ECM components

Name 2 major diseases associated with atherosclerosis
1. Ischemic heart disease
2. stroke
Name 3 major constitutional risk factors for ischemic heart disease
=non-modifiable risk factors
1. age
2. gender
-premenopausal women protected
-HRT increases risk
3. genetics

Name 4 major modifiable risk factors for ischemic heart disease

1. Hyperlipidemia
-esp high XOL
2. HTN
3. Cigarette smoking
4. DM

1. inflammation
2. hyperhomocystinemia
3. increased lipoprotein a
4. factors affecting hemosasis
? personality, obesity

How do inflammation increase your risk of ischemic heart disease
-b/c inflammation is present during all stages of plaque formation
-C reactive protein is a marker of inflammation that can strongly and independently predict risk of AMI, stroke, PVD
Define C reactive protein
-acute-phase reactant made by the liver
-marker of inflammation
-CRP levels strongly and independently predicts risk of AMI, stroke, PVD
-CRP levels can be decreased by:
1. exercise
2. smoking cessation
3. wt loss

Name the 7 major components in the pathogenesis of atherosclerosis.
1. chronic endothelial injury
2. accumulation of lipids
3. monocyte adhesion to endothelium
4. platelet adhesion
5. factor release
-from activate plts, macrophages, vascular wall cells -> SM recruitment
6. SM proliferation and ECM production
7. lipid accumulation
-extracellular and within cells

Name 2 important causes of endothelial injury and dysfxn in atherosclerosis
1. turbulent blood flow
-esp at branchpoints
2. Lipids
-increased prod of oxygen radicals -> oxidize LDL
-oxidized LDL is toxic to endothelial cells
=> both mechanisms result in intact but dysfxnal endothelial cells (leukocyte adhesion, altered gene expression)

Describe the stages of inflammation in formation of atherosclerotic plaques
1. injured endothelial cells recruit inflammatory cells
2. monocytes engulf oxidized LDL
3. T lymphocytes recruited into intima
-make cytokines and have mutual appreciation society with macrophages
4. chronic inflammation induces SM prolif. and ECM deposition

What is the role of endothelial SM proliferation in formation of atherosclerotic plaques?
-SM prolif. and ECM deposition convert fatty streak into full-blown atheroma
-neo-SM cells not contractile
-SM prolif. and ECM deposition actually stabilizes plaques

How do atherosclerotic plaques become unstable?
-activated inflammatory cells in atheromas can cause apoptosis of SM cells and increased ECM catabolism -> produce unstable plaques
Name 4 cell types that contribute chemical mediators that influence atherogenesis.
1. dysfunctional endothelial cells
2. recruited and proliferating SM cells
3. macrophages
4. T cells

Define fatty streaks
=early lesions in atherosclerosis
-composed of lipid-filled foam cells
-do not cause disturb blood flow
-capable of evolving into atherosclerotic lesions but NOT always

Describe the gross features of an atheroma
1. impinges on lumen
2. eccentric
3. yellow
4. soft -> crunchy texture (b/c calcified)
-atheromas induce flow abnormalities that can promote further plaque formation

Name 5 most common arteries where atheromas form.
1. Abdominal aorta
2. Coronary arteries
3. Popliteal arteries
4. Internal carotid
5. Circle of willis

True or false: atheromas are dynamic lesions
1. can get neovasculartization
2. enlarge atheromas through cell death, ECM remodeling, and thrombi
3. calcification

Name 3 things that can happen to atherosclerotic plaques that can cause clinical problems.
1. Acute plaque change
-rupture, ulcerate and erode
-hemorrhage into plaque
2. Atheroembolism
-piece of plaque breaks off and lodges distally
3. Aneurysm
-due to weakened media

How can acute atherosclerotic plaque change lead to occlusion of a vessel?
1. Plaque can rupture, ulcerate, erode
->leads to acute thrombosis ->occlusion
2. Can get hemorrhage into the plaque
-> acute plaque expansion -> occlusion

What is the natural history of atherosclerosis?
1. pre-clinical phase
-slowly evolving lesion over decades
-fatty streak-> fibrofatty plaque -> advanced/vulnerable plaque

2. Clinical phase
-acute plaque change
-in middle age-elderly
-outcomes include aneurysm/rupture, occlusion by thrombosis, critical stenosis (due to progressive plaque growth)

Name 4 causes of decreased blood flow that can cause myocardial ischemia.
1. athlerosclerosis of coronary arteries
2. Hypotension
3. CO poisoning
-due to decreased O2 carrying capacity
4. Aortic regurgitation
-> low diastolic perfusion pressure

Define ischemic heart disease
-generic term for related syndromes that result from myocardial ischemia
-4 main types
1. Angina pectoris
2. Acute MI
3. Chronic ischemic heart disease
-scarring due to AMI -> CHF
4. Sudden death

True or false: myocardial ischemia results from an imbalance between cardiac blood supply and myocardial oxygen demand
-inadequate coronary perfusion often results from acute plaque change
What is the significance of collaterals in ischemic heart disease?
-slow progression of atherosclerotic lesion in coronary artery allows for collateral vessels to form in the heart
-impt b/c
1. may tolerate larger atheroscerlotic lesions
2. may be protective to the myocardial during acute MI

Name the 3 most frequently occluded coronary vessels.
1. LAD
-left anterior descending
2. RCA
-right coronary artery
3. Left circumflex

What is the underlying cause of an acute ischemic event in acute coronary syndrome?
1. Acute plaque change
-rupture or alteration with thrombosis
-hemorrhage into plaque
-acute plaque change is unpredictable and frequently happens in vessels that are NOT the most occluded (ex. less than 50% stenosis)

Define angina pectoris
=intermittent chest pain caused by transient and reversible ischemia
-3 types
1. stable
2. unstable
3. prinzmetal or variable angina

Define stable angina pectoris
=chest pain due to increased O2 demand
-greater than 70% vessel stenosis
-underlying cause is fixed atherosclerotic narrowing (not acute plaque change)
-pain relieved by:
1. rest
2. vasodilators

Define unstable angina pectoris
=increased frequency or intensity of chest pain or pain occurs with less exertion
-most often due to plaque disruption
-associated with subsequent MI (slow heart attack)

Define prinzmetal/variable angina.
=chest pain occuring at rest due to coronary artery spasm
-can happen in:
1. atherosclerotic vessels
2. normal vessels
-treat with:
1. Ca channel blockers
2. nitroglycerin

Define myocardial infarction
=necrosis of heart muscle due to ischemia
=heart attack
-most caused by atherosclerosis
-any coronary artery occlusion can cause MI
-most MIs caused by acute coronary artery thrombosis

Describe the sequence of events that lead to coronary artery occlusion in a typical MI
1.acute plaque change
2. platelets adhere and release cytokines
3. vasospasm
4. clot formation
5. occlusion

Name 6 clinical features that are associated with acute MI
1. Severe, crushing, substernal chest pain
-radiates to jaw, neck, stomach, left arm
-pain lasts longer than 20 min, not relieved by NG
2. Pulse weak and thready
3. Diaphoresis (inappropriate sweating)
4. Nausea
-posterior wall MIs
5. SOB

Name 4 enzymes released from necrotic myocardium during acute MI.
1. Troponin I and T
2. Myoglobin
-released early
3. Creatine kinase
4. lactate dehydrogenase

Compare the myocardial response to ischemia between seconds and minutes.
-aerobic glycolysis stops, no more ATP
-accumulate waste products

-loss of contractility
-EM changes: mitochondrial swelling
-rapid reperfusion can maintain cell viability
-irreversible damage to myocardium occurs about 40 minutes later

True or false: myocardial ischemia causes electrical instability
-can lead to ventricular fibrillation and sudden death
What zone of the myocardium is most vulnerable during ischemia?
-most vulnerable b/c farthest from coronary arteries
True or false: transmural infarcts are most common.
What structural changes can be seen between 0-30 minutes of myocardial ischemia.
-no gross or microscopic changes
-EM: can see mitochondrial swelling, relaxation of microfibils, glycogen loss
-myocardial cells lose contractility within 1 minute

What microscopic change occurs in myocardium between 30 minutes and 4 hours of ischemia?
=waviness of myocardial fibers
-after 40 minutes, you get irreversible changes to myocardium
-no gross changes can be seen yet>

What gross changes become apparent 4-12 hours after myocardial ischemia?
1. occaisional mottling
-microscopically see beginning of coagulative necrosis, edema, hemorrhage

What are the key microscopic changes seen in myocardium with in 12 hrs-1 day after ischemia?
1. coagulative necrosis
2. pyknosis of nuclei
3. contraction band necrosis
4. beginning of neutrophil infiltration

When do you start to see mottling with yellow/tan center in myocardium after ischemia?
=gross changes in myocardium
-1-3 days
Why is 3-7 days post-MI the most worrisome time period?
-b/c that is the time when the heart is most likely to rupture
-heart is soft and least scarred
-gross appearance: little myocardium left, soft yellow/tan center with hyperemic border

When do we see granulation appear in infarcted myocardium?
=1-2 weeks post-MI
-this is when infarcted area is maximally soft
When do we see scarring of infarcted myocardium
=2-8 weeks post-MI
-scarring is from heart border -> inward
-associated with collagen deposition and decreased cellularity

What are the consequences of reperfusion of infarcted myocardium?
1. reperfusion w/in 1-2 hours
-no necrosis but myocardium may be "stunned" but full recovery
2. Repefusion may actually make myocardial injury worse
-microvascular injury-> increased hemorrhage
-radical oxygen
-reperfusion is can happen spontaneously with NO intervention

Name 8 clinical complications that can follow an MI
1.Cardiogenic shock
2. arrhythmias
3. myocardial rupture
4. pericarditis
5. infarct expansion
6. mural thrombosis
7. ventricular aneurysm
8. Chronic IHD/CHF

What influences the presence of complication following an acute MI?
1. size of infarct
2. site of infarct
3. thickness of MI
-75% of patients have some type of post-MI complication
-anterior infarcts are in general worse than posterior infarcts

Name 3 complications associated with large, transmural MI.
1.cardiogenic shock
2. arrhythmias
3.late CHF

Define cardiogenic shock
=pump failure
-post-MI complication (15%)
-usu associated with left ventricular infarcts
-heart can't pump enough blood for itself -> chain rxn
-70% associated mortality

Describe rupture as a post-MI complication
-happens in 1-5% of MIs
-rapidly fatal
-most likely to happen 3-7 days post MI
1. ventricular free wall
2. ventricular septum
-> left right shunt
3. papillary muscle rupture
-mitral valve regurge

Who is most likely to have heart rupture following an acute MI?
1. older (great than 60 yo)
2. female
-have thinner heart walls
3. 1st MI
-Prior MIs actually protective because scar tissue doesn't rupture as easily

Describe post-MI aneurysms.
-thin, scarred ventricular wall
-bulges out during systole
-> poor contractile ability
-typically anteroseptal
-later complication seen 1-2 weeks post MI

Describe post-MI pericarditis.
-fibrinous pericarditis
-typically seen early post-MI (2-3 days)
-usually resolves
-manifestation of myocardial inflammation

Describe post-MI mural thrombosis.
-poor contractility and endocardial inflammation -> thrombosis of endocardium
-can be huge
-if thrombus is detached or fragmented -> thromoboembolism

Describe CHF as post-MI complication
=chronic ischemic heart disease
-scarring and loss of contractility -> reduced cardiac function
-failure of left ventricular fxn leads to
1. pulmonary edema and vasculature congestion
2. systemic hypotension

Describe sudden cardiac death
-sudden death can happen without death or within 1-24 hrs of symptom onset
-may be first manifestation of IHD
-may not be related to IHD (myocarditis, pulmonary HTN, congenital abnormalities)
3. most often due to lethal arrhythmia

Define heart failure
Def. #1= syndrome in which a cardiac disorder prohibits the delivery of sufficient output to meet the perfusion requirements of the metabolizing tissues

-Def #2: syndrome in which cardiac dysfxn is associated with reduced exercise tolerance, high incidence of ventricular arrhythmias, and shortened life span

True or false: heart failure is a common endpoint of many cardiac conditions
Why do we get heart failure (mechanics)?
1. Systolic dysfxn
-heart not contracting like it should -> decreased CO
-this normally happens
2. Diastolic dysfxn
-heart contracts normally but relaxation is abnormal
3. Valve failure

Name 3 mechanisms the cardiovascular system can adopt to deal with decreasing contractility or increased burden.
1. Activation of neurohumoral systems
-sympathetic ANS
2. Frank-Starling mechanism
3. Structural changes to the heart

Name 3 neurohumoral systems that get activated by decreased myocardial contractiliy or increased hemodynamic burden.
1. Sympathetic ANS
-release NE
-increases HR, myocardial contractility, vascular resistance
2. Renin-Angiotensin-aldosterone
3. ANP

Define ANP
=atrial natriuretic peptide (ANP)
-polypeptide hormone released in setting of atrial distension
-causes vasodilation, natriuresis, and diuresis
-helps alleviate volume/pressure overload

Describe the volume/pressure changes that take place in CHF.
1. Decreased contractility/etc -> decreased cardiac output
2. heart unable to eject venous blood delievered to it -> increased end-diastolic ventricular volume -> increased end-diastolic pressures -> elevated venous pressures
Describe the Frank-Starling mechanism
-increased EDP causes cardiac muscle fibers to stretch -> increased volume of cardiac chamber
-longer cardiac muscle fibers contract more forcibly -> increased CO
-this mechanism may allow for compensation for CHF for awhile

Contrast compensated and decompensated heart failure
Compensated heart failure
-when dilated ventricle able to maintain CO at level that meets body's needs by Frank-Starling mechanism

Decompensated HF
-increased dilation of heart -> increased wall tension -> increased O2 demand
-this taxes an already compromised myocardium and it eventually poops out
-decompensated when unable to generate CO sufficient for body's needs

Contrast concentric vs eccentric hypertrophy
-thickness of ventricular wall increases w/o increase in size of chamber
-pressure overload states

eccentric hypertrophy
-increase in heart size in addition to increase in wall thickness
-volume overload

Name 2 ways that heart failure leads to increased O2 demand
1. hypterophy
-increased myocardial cell mass
2. increased wall tension due to ventricular dilation by Frank-Starling mechanism
-impt because increased O2 demand in a failing heart increases susceptibility to ischemic injury

Name 4 common causes of left-sided cardiac failure
1. ischemic heart disease
2. systemic hypertension
3. mitral or aortic valve disease
4. primary disease of myocardium

True or false: left-sided heart failure is the most common cause of right-sided heart failure

-L CHF causes pulmonary congestion and increased pulmonary arterial pressure
-can also get R CHF w/o L CHF (lung diseases, tricuspid alve disease)

Describe the morphological changes to the heart seen in left heart failure
1. left ventricle usually hypertrophied and dilated
2. Can see fibrosis of myocardium
3. Can get secondary enlargment of left atrium

In what type of left heart failure do we NOT see left ventricle hypertrophy
-mitral valve stenosis
Where are the extracardiac effects of left heart failure most seen?
-in the lungs
-backed up -> increased pressure retrogradely transmitted pulmonary veins -> capillaries -> congestion and edema

What are the clinical symptoms associated with left heart failure?
1. Dyspnea (breathlessness)
-from fluid in lungs
2. Orthopnea
-difficulty breathing when lying down (b/c increased venous return to heart from legs)
3. Paroxysmal nocturnal dyspnea
-waking up from asleep b/c trouble breathing

What are the clinical signs of left heart failure?
1. cardiomegaly
2. tachycardia
3. 3rd heart sound (S3)
3. fine rales at base of lung
-with progressive HF
4. systolic murmur/mitral regurg
5. atrial fibrillation
"irregularly irregular" heartbeat

Define atrial fibrillation
=uncoordinated, chaotic contraction of atrium
-"irregularly irregular" heartbreat
-can see in left CHF b/c enlargement of left atrium

Name causes of right CHF
1. left CHF
2. lung disease/pulmonary vascular damage
3. pulmonic or tricuspid valve disease
4. congenital heart disease (w R-> L shunt)

Where are the extracardiac effects of right heart failure seen?
-in systemic venous system and portal venous system
1. congestive hepatomegaly (nutmeg liver)
-chronic congestion can cause central liver cirrhosis
2. congestive spenomegaly
3. pleural and pericardial effusions
-fluid accumulation
3. Peripheral edema

True or false: you only see pleural effusions in right sided heart failure
-can see in both left and right sided HF
-can only see pulmonary edema with left HF

What are the clinical symptoms associated with right heart failure?
1. few respiratory symptoms
2. Hepatosplenomegaly
3. Peripheral edema
4. Pleural effusion
5. Ascites

What is the revised staging system for heart failure (A,B,C,D)?
=continuum to classify patients
1. Stage A
-at risk of HF but no structure heart disease or symptoms
2. Stage B
-structural heart disease but no symptoms
-EF less than 40%
3. Stage C
-structural heart disease with controllable symptoms
4. Stage D
-refractory heart failure that require specialized intervention

Name 8 risk factors for developing symptomatic heart failure.
1. ischemic heart disease
2. hypertension
3. overweight
4. diabetes
5. smoking
6. dyslipidemia
7. valvular heart disease
8. renal insufficiency/microalbuminuria

Why is symptomatic heart failure just the tip of the iceberg?
-b/c there is HF that is asymptomatic (stages A and B)
-that was the problem with old classification system (asymptomatic not included)
-asymptomatic HF is 1-5% of population
-high risk of developing future, symptomatic HF

Describe the working hypothesis of HF
-some event (AMI, onset of HTN) -> initial decrease in LV performance, increase wall stress -> activation of RAAS and SNS -> remodeling of progressive worsening of LV fxn AND peripheral vasoconstriction/hemodynamic changes -> CHF
Name some specific structural changes that take place during myocardial remodeling leading to HF.
1. myocyte hypertrophy
2. fibrosis, chamber dilation
3. collagen strut dissolution
4. apoptosis of myocytes
5. cell necrosis
6. neurocrine activation
7. cytokine release
8. increased wall stress
9. chamber dysxfxn

True or false: heart failure symptoms are insensitive and nonspecific
Name some congestive symptoms of CHF
-respiratory symptoms prominent in L CHF
1. SOB, dyspnea, cough
2. swelling of legs, ankles, abdomen
3. chest congestion, discomfort, orthopnea
4. weight gain due to fluid retention
5. early satiety
6. nocturnal, exertional or "emotional" cough
7. recumbent anxiety, insomnia

Name some symptoms of CHF associated with low cardiac output.
1. dyspnea
-due to tissue hypoperfusion
2. Fatigue, malaises, tiredness
3. weight loss
-unexplained, muscle wasting
4. poor endurance
-mental or physical
5. memory or concentration impairment
6. sleep disturbance
7. Daytime oligouria, recumbent nocturia
-remember that heart failure signs and symptoms are insensitive and non-specific

True or false: heart failure can sometimes first present as frequent urination at night
Name 5 major effects of the renin-angiotensin-aldosterone system
-from activation of AT1 Rs by Ang II
1. vasoconstriction
2. sodium retention
3. increase aldosterone release
4. increased SNS
5. increased cellular growth
-these effects opposite to those of natriuretic peptides (ANP, BNP)

Name 6 major effects of the natriuretic peptide system
1. vasodilation
2. sodium excretion
3. Decreased aldosterone levels
4. inhibition of RAAS
5. inhibition of SNS
6. antiproliferative of vascular SM cells

Name some physical exam signs associated with heart failure.
1. distended neck veins (JVP) or abdominojugular reflux
2. rales or evidence of pleural effusion (L >R)
3. LV or RV S3
4. Ascites, lower extremity edema
5. Cool (vasoconsticted) extremities
6. low carotid volume, low pulse pressure, pulsus alternans

How do we treat symptomatic heart failure?
1. Tx underlying disease
2. Diuretics
3. ACE inhibitors
4. Beta blockers
5. Digitalis
6. Dietary salt restriction

How do we treat patients with refractory heart failure (stage D)?
1. everything we would use before
-also need special interventions
1. Mechanical assist devices
2. heart transplant
3. continuous IV inotropic infusions for palliation
4. hospice

Why is symptom relief not enough for heart failure?
1. b/c HF also limits fxnal capacity and impairs quality of life
2. HF is progressive
-symptoms do not always correspond with ejection fraction
-sometimes death even with presence of minimal or absence of progressive symptoms

How do we assess patient with heart failure
1. Assess LV fxn
-echocardiogram, radionucleotide ventriculogram
2. Assess volume status if ejection fraction is less than 40%
3. If showing symptoms and signs of fluid retention, start diurectic in addition to ACE I, Beta blocker
4. If no signs/symptoms of fluid rention, start ACE I

Name 3 drugs that reduce mortality in CHF.
1. ACE Inhibitors
-inhibits RAAS
2. Beta Blockers
-inhibit RAAS
-suppress SNS activation
3. Spironolactone
-inhibit aldosterone

Who should be on ACE Inhibitors?
1. all patients with current or prior symptoms of HF and reduced LVEF
2. ALL patients with hx of MI regardless of LEVF or if they have HF
3. Patients with reduced LVEF and no symptoms of HF (even if no MI)

Name 4 complications associated with ACE Inhibitors.
1. hypotension
2. renal dysfxn
3. hyperkalemia
4. cough

Who should be on Angiotension Receptor blockers (ARB)?
-anyone who should be on an ACE inhibitor but is not able to tolerate it
Who should be on beta blockers?
1. anyone with hx of MI even if no HF
2. stable, symptomatic HF patients
3. Anyone with reduced LVEF no symptoms or MI
-Beta blockers work better in presence of symptomatic HF unless Hx of MI

Name 3 beta blockers shown to reduce mortality in CHF.
1. Bisoprolol
2. caridilol
3. sustained release metoprolol

True or false: African Americans with CHF should be on hydralazine-nitrate in addition to other drugs because the are more dependent on the NO (nitrous oxide) system
-has shown to be beneficial in AA
True or false: inotropes should be used vigorously in tx of heart failure
-these are a double-edged sword
-ex. digitalis should only be used for acute HF
-these drugs do NOT prolong life

Who should be on heart transplant list?
1. severe heart disease despite adequate medical therapy
-includes no other surgical options
2. absence of noncardiac conditions (cancer, diabetes) that would limit life expectancy

Who should have implantable cardioverter-defibrillators?
1. Patients with ischemic heart disease and ejection fraction less than 35%
-doesn't matter if have symptoms or arrhythmias
2. patients w/o IHD, EF less than 35% and
a. significant HF
b. sign. arrhythmia

What are the 3 major cellular changes in the transition from LV dysfxn to heart failure?
1. myocyte apoptosis
2. myocyte slippage
3. myocyte elongation, hypertrophy

True or false: BNP levels should be used in the assessment of CHF.
-levels go way up in CHF
-wall stress triggers increased txn and production of BNP -> released into bloodstream

Name 5 types of injury that can cause valvular disease.
1. Degeneration w/calcification
2. post-inflammtory scarring
-rheumatic heart disease
3. infective endocarditis
4. Myxomatous degneration
-mitral valve prolapse
5. Non-infective vegetations

Describe dengeneration of the heart valve with calcification.
-caused by wear and tear to the heart
-normal blood calcium
-calacification makes heart valve stiff
-aortic valve mostly affected
-if normal heart valve, can see valvular disease due to calcification usu. 70-80 years
-if have congenital anomaly (ex bicuspid valve), degeneration w/ calcification can lead to valvular disease earlier

True or false: rheumatic heart disease is a common cause of valvular disease in industrialized countries.
-false. Used to be a major cause but incidence in industrialized countries has decreased due to:
1. antibiotics
2. improved general health
-post-inflammatory scarring due to RHD still major cause in developing nations

Name 5 types of lesions that predispose valve to infective endocarditis.
-healthy hearts usually don't get infective endocarditis
1. RHD
2. other acquired valvular lesions
3. hypertrophic cardiomyopathy
4. congenital heart disease
5. surgically implanted device
-ex prosthetic valve

Myxomatous degeneration is the same thing as _______
=mitral valve prolapse
-developmental defect of connective tissue
-condition may also be seen in:
1. Ehlers-Danos
2. Marfan's syndrome

Who gets non-infective vegetations of the heart valves?
=sterile vegetations NOT due to microorganisms
1. debilitates patients
2. Some types of cancer
3. Hypercoaguable states (ex DIC)

Name 4 types of disorders that can cause mitral regurgitation.
1. post-inflammatory scarring (RHD)
2. infective endocarditis
3. Abnormalities of chordae and papillary muscle
4. left ventricular enlargement

Who is more likely to get tricuspic and pulmonic valve disorders?
=right heart valve disorders usu do not cause significant disease b/c lower pressure system
1. IV drug users
-inject stuff into veins -> travels to right heart first
-vegetations predominantly on right side
2. Congenital anatomic anomalies

True or false: complications are seen in less than 10% of prostethic valve patients within 10 years of post-op
-complications seen in about 50%
-Complications include:
1. thromboembolism
2. infective endocarditis
3. structural deterioration
4. hemolysis

Describe the pathophysiology behind mitral regurg
-incompetent mitral valve permits blood flow from ventricle to atrium in systole
-variable blood volume is regurged
-MR enhances left ventricular emptying (EF increased)
-As MR becomes chronic, LV end-diastolic volume iincreases -> increased volumes in pressure in left atrium
-can take years for significant pathophysiology to develop

Describe the symptoms of mitral regurg
1. Asymptomatic
-some pts with mild MR can be asymptomatic whole lives
2. severe MR, not many symptoms until LV fails
3. may take as long as 2 decades for symptoms
4. when LV begins to fail, damage often irreversible

A holosystolic murmur is characteristic of _______.
=mitral regurg
What PEX findings will you see with mitral regurg?
1. brisk, hyperdynamic arterial pulses
-carotid, LV
2. displaced LV impulse
3. Holosystolic murmur

Characterize a holosystolic murmur.
-seen with MR
1. blowing
2. high pitched
3. loudest at apex with radiation to axilla

How do we treat Mitral regurg patients?
1. vasodilators
-reduce volume of blood regurg into LA
2. diruretics for HF
3. digitalis for HF
Careful assessment of LV fxn
1. valve replacement
2. valve reconstruction/repair

How do vasodilators help manage mitral regurg
-these are afterload reducing agents that make it easier for the LV to pump blood forward as opposed to backward into ventricle -> less blood going into LA
Why is timing so important for surgery to correct mitral regurg?
1. because the valves only last so long so you don't want to do it too early
2. there is also a decline in LV function after surgery -> HF and death
What are 3 advantages associated with mitral valve reconstruction?
1. no anticoagulation
2. no risk of embolism from prosthetic valve
3. no artificial valve
-no endocarditis
-no valve failure

Name 3 causes of acute mitral regurgitation.
1. endocarditis
2. ischemic dysfxn of a papillary muscle
3. malfunction of a prosthetic valve

How do you treat acute mitral regurgitation?
1. vasodilators
2. intraaortic balloon pump
3. early surgery
-valve reconstruction works best

Define Mitral valve prolapse
=myxomatous degeneration
-common but variable clinical syndrome that results from diverse pathogenic mechanisms of one or more portions of mitral valve apparatus
-causes mitral regurg
-seen in 3-5% of people
-more frequent in women
- can be associated with heritable disorders of connective tissue

Define valvular stenosis
=failure of a valve to open completely, obstructing forward flow
-usu. chronic process caused by abnormality in cusps of the valve
Define valvular insufficiency
=regurgitation, incompetence
-failure of valve to close completely, allowing reversed flow
-can appear acutely
-can be due to abnormality with the valve cusps or abnormality of supporting structures

Define murmur
=abnormal heart sounds due to abnormal flow through diseased heart valves
True or false: acquired stenosis of the aortic and mitral valves account for approx. 2/3 of all valve disease
What is the pathological hallmark of a calcified heart valve?
-most often aortic valve -> stenosis
=yellow calcium nodules on outflow side of valve cusps
-with aortic valve stenosis, calcium nodules eventually lead to outflow obstruction -> left ventricular pressure overload -> LV hypertrophy

What are the complications/symptoms from a stenosed aortic valve due to calcification?
1. Angina
-from ischemia b/c of LV hypertrophy
2. Syncope
-b/c poor perfusion to the brain
3. CHF

What is the pathological hallmark of mitral valve prolapse?
1. ballooning/hooding of valve cusps (balloon back into left atrium during systole)
2. Affected valve leaflets are enlarged, thick, and rubbery (floppy)
3. Chordae tendinae can be elongated, thinned, or even ruptured

Name 2 causes of myxomatous mitral valve
=mitral valve prolapse
1. intrinsic defect in connective tissue/remodeling
2. Secondary to other heart defects/disease (IHD)

True or false: most cases of mitral valve prolapse are picked up incidentally on physical exam
-b/c many people with mitral valve prolapse are asymptomatic
What are the symptoms associated with mitral valve prolapse?
1. asymptomatic
2. chest pain
3. palpitations
4. autonomic dysfxn
5. anxiety neurosis

A midsystolic click followed by a murmur is characteristic of _____.
=mitral valve prolapse
-if valsalva, click and murmur will happen earlier in systole
How do we treat patients with mitral valve prolapse?
1. reassure asymptomatic patients w/o MR
2. Beta blockers if have chest pain or palpitations
3. Endocarditis prophylaxis with MR and echo findings

Name 4 complications of mitral valve prolapse.
-usually benign
1. Progressive mitral regurgitation
-15% of MVP over 10-15 years
-more likely with louder murmurs and clicks
2. Rupture of chordae tendineae
-makes MR worse
3. Endocarditis
4. Cerebral emboli -> TIA, acute hemiplegia, cerebellar infarcts

Name the 4 most common causes of aortic stenosis.
1. senile, calcific aortic stenosis
-most common in US
2. rheumatic aortic stenosis
3. congenital aortic stenosis
4. bicuspid aortic stenosis

How does the heart initially compensate for aortic stenosis?
-as aortic valve narrows, only way to maintain normal flow across the valve is by developing a systolic pressure gradient between LV and aorta
-LV > aorta
-this maintains cardiac output although higher pressures in LV cause it to hypertrophy, which can have deleterious effects

What are the 3 major symptoms of aortic stenosis?
1. Angina
2. Syncope
3. Heart failure
-usually long latency asymptomatic period in disease progression before onset of symptoms

A late peaking harsh systolic ejection murmur heard best at the base and radiating to the carotids is characteristic of _______.
=aortic stenosis
-crescendo-decrescendo murmur
-severity of the stenosis depends on how late the murmur peaks

What are the 4 major physical exam findings associated with aortic stenosis?
1. Slow rising carotid pulse (parvus et tardus)
2. Prominent LV impulse (heav)
3. 4th heart sound
4. late peaking harsh systolic ejection murmur
-best heart at base and radiating to carotids

True or false: aortic stenosis is a surgical disease

1. old age or LV dysfxn are NOT contraindication to valve replacement
-LV will be ok after surgery (compared with MR)

Who should get an aortic stenosis valve replacement surgery?
1. Aortic valve area
Why do you have to be careful in the management of aortic stenosis?
-because you have a fixed aortic valve that isn't able to compensate for an increased stroke volume
-so you want to be careful to not abruptly decrease afterload or preload
Describe the pathological findings of acute rheumatic fever
1. Aschoff bodies
2. fibrinous pericarditis
3. small vegetations (verrucae) on valves

Define Aschoff bodies
=characteristic lesions of rheumatic fever and rheumatic heart disease
=perivascular, fibrinoid, necrosis-surrounded inflammatory cells
-can be found in any of the 3 layers of the heart

Describe the pathologic findings in chronic rheumatic heart disease
1. Diffuse and dense scarring of valves
-leaflet thickening and fibrosis
-permanent dysfxn
-mitral valve most commonly affected
2. Fish mouth/ buttonhole stenoses
-from commissural fusion of leaflets of valves
3. Aschoff bodies replaced by fibrous scar

Name some complications associated with rheumatic fever and RHD.
1. mitral (and other) valve stenosis
2. increased risk of infective endocarditis
3. arrhythmias

Define infective endocarditis
=heart infection characterized by microbial invasion or heart valves or mural endocardium
-results in bulky, friable vegetations
-can be subclassified as acute or subacute
-can develop on normal heart valves but injured heart valves are predisposed to infection

Describe acute endocarditis
-rapid progressing, destructive heart infection
-offending organism is highly virulent
-normal heart valve attacked
-death in 50% in days to weeks despite interventions
-fever, chills, weakness, lassitude
-+/- murmurs
-diagnose with blood cultures, echocardiograph findings, etc

Describe subacute endocarditis
-infections of heart valves and/or wall by low virulence microbes
-disease appears insiduously
-disease course over weeks-months
-most patients recover w/antibiotics
-may not have fever
-nonspecific fatigue, wt loss, flulike syndrome, splenomegaly

Define Nonbacterial thrombotic endocarditis
-characterized by depositions of small, sterile vegetations
-vegetations made up of fibrin, platelets, and blood components
-deposits on cardiac valves
-vegetations can give rise to emboli to brain, heart
-no inflammation

Who gets nonbacterial thrombotic endocarditis?
1. Debilitated patients
2. Some cancers
-ex mucinous adenocarcinomas
3. Hypercoaguable states
-ex DIC

Define carcinoid heart disease
=cardiac manifestation of a systemic syndrome
-symptoms caused by bioactive compounds released by carcinoid tumor
-flushing, diarrhea, dermatitis, bronchoconstriction
-usu affects right heart endocardium and valves
-glistening white plaques on valve and endocardium

What are the advantages and disadvantages of a mechanical heart valve?
1. durability
1. life long anticoagulation (blood thinners)
2. can cause RBC hemolysis b/c of shear stress
3. risk of infection

What are the advantages and disadvantages of bioprosthetic heart valve?
1. don't require life long anti-coagulation
1. not as durable
2. can develop stenosis
3. Valves can tear or fail

What is the major cause of mitral valve stenosis?
1. rheumatic heart disease
-post-inflammatory scarring
What are the major causes of aortic stenosis?
1. Degeneration and calcification
2. RHD
-majority have co-existing mitral valve disease

Define hypertrophic cardiomyopathy
=hypertrophied, non-dilated LV in absence of another cardiac or systemic disease that could produce a similar magnitude of hypertrophy
-most common cause of sudden death in young athletes
-most common cardiovascular disease

Describe the pathology of hypertrophic cardiomyopathy
-marked increase in hypertrophy w/small cavities
-disproportionate involvement of interventricular septum (asymmetric hypertrophy)
-abnormal stiffness of LV with impaired ventricular filling (but reduced SV)
-disorganization of myocyte architecture

What are the symptoms of hypertrophic cardiomyopathy?
1. Dyspnea
2. Angina
3. Syncope
4. Sudden death
-can be first symptom

What are the PEX signs of hypertrophic cardiomyopathy?
1. carotid pulse that rises briskly then declines in midsystole as gradient develops, followed by secondary rise
2. prominent apical precordial impulse
3. sometimes double apical impulse as result of S4
4. Systolic murmur

Describe the murmur heard with hypertrophic cardiomyopathy
1. harsh crescendo-decrescendo
2. Ejection
3. heart best between apex and L sternal border; radiates to axilla but not neck
4. labile in intensity and duration
5. can use maneuvers to distinguish from aortic stenosis murmur
-murmur increases with valsalva
-murmur decreases when lying down

How do we treat hypertrophied cardiomyopathy?
1. No digitalis
2. No exercise
3. Surgery
-septal myectomy: remove part of the hypertrophied muscular septum
-alcohol septal ablation: induce MI in septum-> tissue dies and thins out

What are some of the complications of hypertrophic cardiomyopathy?
1. sudden cardiac death
(prob due to ischemia)
2. peripheral embolic events (stroke)
3. heart failure death
4. bacterial endocarditis

What are the consequences of mitral valve stenosis?
1. LV diastolic pressure usu normal
2. Giant left atrium
3. Pulmonary HTN

Characterize platelets
-small, non-nucleated
-normal count: 150,000-400,000 /uL blood
-lifespan 7-10 days in circulaton
-concentrate on periphery of blood vessel during laminar blood flow
-can release TXA2, serotonin, ADP, ATP when activated

Name 4 factors that cause platelet activation
1. catecholamines
2. stress
3. hemodynamic turbulence
4. plaque disruptions
5. exposed collagen (endothelial injury)
6. thrombin

Name 2 substances released by platelets that induces platelet aggregation and vasoconstriction
1. TXA2
2. serotonin (5HT)
Name 2 factors released by endothelium that promotes SM relaxation and inhibit platelet aggregation
1. NO
2. PGI2
-disease states that cause endothelial dysfxn (ex atherosclerosis) impair release of NO and PGI2 -> increased vasoconstriction and platelet aggregation

How do we assess the activity of PGI2 and TXA2?
-we can measure the breakdown products
Describe platelet response to endothelial injury
-injury -> exposed collagen
1. platelet adhesion
vWF binds subendothelial collagen and plts bind vWF
2. Platelet activation
-activated platetlets release 5HT and ADP which bind and activate adjacent plts
3. Platelet aggregation
-GP IIb/IIIa R bind fibrinogen -> platelet plugs

Exposure of subendothelial collagen due to injury results in:

1. Adhesion, activation, and aggregation of platelets
2. Activation of extrinsic coag pathway via tissue factor/factor VII
3. activation of intrinsic coag pathway via factor XII

Name 3 mechanisms in the body to limit coagulation
1. Heparan sulfate-antithrombin III
2. thrombomodulin/protein C/protein S
3. Fibrinolysis by tPA and urokinase activating plasmin

Describe the heparan sulfate-antithrombin III system
-natural anti-coagulant system
-heparan sulfats bind ATIII -> conformational change -> increased ATIII binding to thrombin, factors XIIa, XIa, Xa, IXa
How do tPA and urokinase influence fibrinolysis?
-enzymes released by endothelial cells
-convert plasminogen -> plasmin
-plasmin cleaves fibrin -> finbrin degredation products
-these enzymes have short half life to keep fibrinolysis in check

How does aspirin act as an antiplatlet therapy?
-irreversibly blocks Cox-1 by acetylation of PG -> can't make TXA2 for life of platelet
-non-specifically inhibits Cox-1 so less PGI2 being made but affects TXA2 more than PGI2 -> favors vasodilation and anti-platelet aggregation
-causes prolonged bleeding time

Name 4 antiplatelet therapies.
1. Aspirin
2. Depyridamole
3. Clopidogrel/thienopyridine compounds
4. GP IIb/IIIa inhibitors

How does dipyridamole act as anti-platelet therapy?
-inhibits PDE to increase intracellular cAMP -> decreased plt responsiveness to activation
-also blocks uptake of adenosine (inhibitor of plt aggregation) from bloodstream
How does clopidogrel act as anti-platelet therapy?
=thienopyridine compound
-block ADP Rs on plts to prevent ADP-induced platelet activation and aggregation
-prodrug converted by cytochrome P450
-blocks P2Y12 -> plt aggregation blocked

How do GP IIb/IIIa inhibitors act as anti-platelet therapy?
-directly inhibit plt aggregation by blocking cross-linking by fibrinogen (block fibrinogen binding to GP IIb/IIIa R on activated plts)
-3 drugs (1 is monoclonal Ab, 2 others are peptide competitive inhibitors)
-can have bleeding complications

Name 3 important anti-coagulant therapies.
1. Heparin
2. Warfarin (Coumadin)
3. Direct thrombin inhibitors

Define heparin
-anti-coagulant therapy
-poor GI absp so SubQ or IV
-can be either unfractionated or low molecular wt
-binds antithrombin III -> conformational change -> ATIII binds and inactivates thrombin and factor X
-activity of heparin assessed by APTT (activated partial thromboplastin time)

What's the difference between unfractionated heparin and low molecular weight heparin
-longer chain, can bind to and inactivate thrombin
-crude admixture of different chain lengths -> makes hard to predict dose-response

-shorter chain
-doesn't complex well with thrombin so inactivates factor X
-more homogeneity in chain length -> more predictable response

How does warfarin act as anti-coagulation therapy?
-prevents reduction of Vit K to active form
-> inhibits formation of Vit K dependent coag proteins (prothrombin, VII, IX, X, protein C, protein S)
-Assess activity with PT (prothrombin time)
-factor VII depleted at 5 hrs, others lag behind -> not sufficient for anti-coag
-can take 3-5 days to be fully effective

How do direct thrombin inhibitors act as anti-coagulation therapy?
-Bind thrombin and sequester it from cleaving fibrinogen to form clot
Name 2 types of thrombolytic therapies
1. Streptokinase
2. Tissue plasminogen activator (tPA)
How does streptokinase work as a thrombolytic therapy?
-streptokinase activates plasmin -> digestion of fibrin, fibrinogen, factors V and VIII
-associated with bleeding problems that can be minor or major (ex hemorrhagic stroke)
-can also get allergic rxns

How does tPA work as a thrombolytic therapy?
-selectively activates plasmin associated with fibrin clots -> degredation of fibrin and thrombus
-less systemic plasminogen activation effects
-can be used in early AMI and stroke
-increased risk of intracerebral hemorrhage

How do we use antiplatelet, anticoagulant, and thrombolytic therapy for STEMI pts?
1. PCI preferred when cath lab available
-give with adjuvant heparin and GP IIb/IIIa
2. Thrombolytic therapy (tPA)
-good if given within 12 hrs of STEMI
-benefit anterior wall MI> inferior wall
-adjuvant LMWH
3. ASA + clopogrel indefinitely

How do we use anti-platelet, anticoagulant, thromboytic therapy for unstable angina?
No full clot occlusion -> don't need immediate thrombolytic or PCI
1. antiplatelet (ASA, ticlopidine)
2. anticoag (heparin)
-increased risk of bleeding w/combo ASA + heparin but more effective
-this also how you treat non-STEMI MI

_______ is the drug of choice for secondary prevention of MI.
-heparin has same effects but aspirin cheaper and safer
What type of tx should be used following CABG to reduce incidence of saphenous vein occlusion.
Define PCI
=percutaneous coronary intervention
-cardiac catheterization using balloon angioplasty
-restenosis prevented by:
1. drug-eluting stents
2. antiplatet agents (ASA + clopidogrel) + GP IIb/IIIa inhibitors

True or false: tPA used in acute stroke has no risk of cerebral hemorrhage
What effect does atrial fibrillation have on hemodynamics?
atrial fibrillation=loss of atrial contractions
-predisposes to blood stasis ->activation of coag system -> can form emboli
-give anticoag (heparin) to people with a fib + risk factors
-give ASA (less effective but less risk of bleeding) to those with a fib + no factors or contra-indications to anticoag therapy

How do we prevent DVT and PE?
-given to surgical pts, hospitalized AMI or HF
-initial full dose + chronic tx

What are the key differences between the SA and AV nodal APs and the AP of the cardiac myocytes.
1. Phase 0
-myocytes: steep upslope due to opening voltage gated Na channels
-AV,SA nodes: not as steep upslope due to opening of voltage gated Ca channels
2. Phase 4
-SA,AV nodes: have depolarization/upslope due to increased Na conductance
-accounts for automaticity (able to beat on own)
-myocytes don't have this

Name the 3 major mechanisms of arrhythmias
1. Disorders of impulse formation
-altered normal automaticity
-abnormal automaticity
-triggered activity
2. Disorders of impulse conduction
-conduction block
3. combined disorders of impulse formation and conduction

Define arrhythmia
=large, heterogenous group of conditions in which there is abnormal electrical activity in the heart
-heart can beat:
1. too fast (tachycardia)
2. too slow (bradycardia)
3. regularly
4. irregularly

What are some common symptoms that can be associated with arrhythmias?
1. Palpitations
=abnormal awareness of heart beat
-most common

If arrhythmia causes heart to beat too fast, too slow, or too weak to supply body's needs (not enough CO) -> can get symptoms of low BP
1. dizziness/lightheadedness
2. syncope

Describe altered normal automaticity
=mechanism of arrhythmia due to disordered impulse formation
-inappropriate discharge rate from normal pacemaker cells (SA, AV)
-can be too fast, too slow
-ex. jxnal tachycardia

Describe abnormal automaticity
=mechanism of arrhythmia due to disordered impulse formation
-Cells that should not spontaneously discharge (myocytes, H-P cells)
-can see 24-72 hrs after MI b/c ischemia can cause abnormal automaticity (accelerated idoventricular rhythm, VT)

Describe triggered activity
=mechanism of cardiac arrhythmias due to disordered impulse formation
-AP potential induce subsequent oscillations in membrane potential
-can be:
1. Early after depolarization (EADs)
2. Delayed after depolarization (DADs)

Define EADs
=early after depolarization
-triggered activity that can cause arrhythmia
-previous APs trigger with either prolonged phase 2 or membrane voltage fluctuations trigger early depolarizations BEFORE cell has fully repolarized
-EADs occur in ventricular tissue and can lead to VT
-can be congenital or acquired

Name some causes of EADs
=early afterdepolarizations
1. familial long QT syndrome
-prolonged ventricular APs

1. drugs
-anti-arrhythmics (sotalol, doretilide)
2. ischemia
3. hypocalcemia
4. hypothermia
-at risk for VT

When is sinus bradycardia inappropriate?
-arrhythmia of slowed HR due to altered normal automaticity
-Inappropriate when:
1. persistent
2. HR does not increase with exercise
-diagnose with treadmill test
-symptoms: fatigue, dyspnea, syncope
-longterm treatment: pacemaker

True or false: bradycardias and tachycardias can both decrease cardiac output (CO)
-bradycardia decreases CO by decreasing HR
-tachycardia decreases CO by decreasing SV (due to suboptimal filling b/c heart pumping so fast)

Define reentry.
=disorder of impulse conduction that can lead to arrhythmias
-happens when a group of cells not activated by initial depolarization wave is activated retrogradely, then serve as bridge to activate areas recovered from depolarization (moves anterograde)
-may continue indefinitely

What are the 3 requirements for re-entry
=impulse conduction disorder that can lead to arrhythmias
1. Dispersion of repolarization
-not all cells recover at same rate
2. unidirectional conduction block
3. slow conduction

How does heart block cause arrhythmias?
-injury to the specialized conduction tissues impairs the coordinated fxn of the heart
-different heart blocks develop depending on where injury took place
Define delayed afterdepolarizations (DADs)
=depolarizations that occur after the cell has repolarized (phase 3)
-disorders of impulse generation triggered by previous APs that can lead to arrhythmias
-can see DADs with digitalis toxicity

Name 2 major types of bradyarrythmias.
1. Sinus bradycaria
2. AV block
-1st degree
-2nd degree
-Type I (Wenckenbach)
-Type II (Mobitz)
-3rd degree

Define first degree AV block
=bradyarrhythmia due to disorder of impulse conduction
-long PR interval (=delay greater than 200ms from onset of P wave to onset of QRS complex)
-usu benign and doesn't need tx

Define second degree AV block
=bradyarrhythmia characterized by intermittent conduction of P waves to the ventricle
-2 subtypes
1. Wenckebach (type I)
2. Mobitz (type II)

Define Wenckebach heart block
=2nd degree AV block= bradyarrhythmia
-heart block at level of AV node
-progressive lengthening of PR interval prior to dropped QRS (some P waves not getting conducted to ventricle)
-often benign and does not usually progress to type II

Define Mobitz (type II) heart block
=2nd degree AV block
-block in the Purkinje system (below AV node and bundle of His)
-fixed PR interval and intermittent dropped beats (no QRS)
-risk of progressing suddenly to complete heart block
-may need pacemaker

Define 3rd degree AV block
-complete disruption of conduction between atria and ventricles
-atria and ventricles activated independently at different, fixed rates
-block can be located anywhere in conduction system
-RR interval is constant
-Symptoms of decreased CO (fatigue, dyspnea, syncope)
-At risk for sudden death
-need pacemaker

Define SVT
=supraventricular tachycardia
-tachycardias involving the atria or AV node
-arrhythmias with a rate greater than 100 bpm

Name 6 different SVTs
=supraventricular tachycardias
-arise from either atria or AV node
1. sinus tachycardia
2. atrial tachycardia
3. atrial flutter
4. atrial fibrillation
5. AV node reentrant tachycardia (AVNRT)
6. Atrioventricular reentrant tachycardia (AVRT)

Define sinus tachycardia
=arrhythmia greater than 100 bpm due to altered normal automaticity
-can be:
1. physiologic
-exercise, catecholamines, pain, fever
-leave alone
2. inappropriate
-tachycardia out of proportion to stimuli
-tx with beta blockers or SA node ablation

Define atrial tachycardia
-arrhythmia due to abnormal automaticity (cells in L or R atria start firing spontaneously)
-see negative P waves on ECG
-often has symptoms (palpitations, lightheaded)
1. Ca channel blockers
2. Beta blockers
3. Class IC agents (flecaminde)
-usu ablation required for a cure

Define atrial flutter.
=arrhythmia due to reentry around tricuspid valve annulus
-ECG shows saw tooth pattern with 2:1 or 4:1 conduction (P: QRS)
-can see rapid fluttering in JVP
-complication: thrombosis
-tx: ablation

How do atrial flutter and atrial fibrillation differ?
=both involve atria going fast
1. Location of arrhythmia origin
-Atrial flutter generated in R atria
-A fib usu generated in L atria
2. Mechanism
-Atrial flutter: reentry
-Atrial fib: abnormal automaticity or reentry (depends on if paroxysmal vs persistent)

Contrast paroxysmal and persistent atrial fibrillation
=2 types of atrial fibrillation (tachycardic arrhythmias)
-a frib starts and stops spontaneously
-due to spontaneous firing of pulmonary veins (abnormal automaticity)
-easier to do ablation vs persistent

-a fib that doesn't stop spontaneously
-due to reentry
-ablation harder to cure a fib

How do we treat atrial fibrillation?
1. Rate control
-use beta blockers, Ca blockers, or anticoagulation to take away risk factors for bad events
2. Rhythm control
-aggressively attempt to restore and maintain normal sinus rhythm with electrical cardioversion, antiarrhythmic drugs, ablation

Define AV node reentrant tachycardia (AVNRT)
-tachycardia due to reentry in AV node
-ECG shows pseudo R' waves immediately after QRS (atrial activation at end of QRS)
-wavefront goes down slow pathway -> activates H-P cells and ventricles -> then travels up fast pathway and depolarizes atria
-tx with Class II beta blockers, Class IV Ca channel blockers, ablation

Define atrioventricular reentrant tachycardia (AVRT)
-tachycardia that involves reentry both through AV node and accessory pathway
-can be part of Wolf-Parkinson White syndrome
-ECG shows delta waves (ventricular excitation immediately after P wave)
-tx with antiarrhythmic drugs (block conduction in accessory pathway), ablation (tx of choice for symptomatic patients)

Name 3 things that can terminate an AVRT
=tachycardia due to reentry by AV node and accessory pathway
1. Valsalva
2. carotid sinus massage
3. IV adenosine

Name 3 ventricular tachycardias
1. Premature ventricular contractions (PVCs)
2. Ventricular tachycardia (VT)
3. Ventricular fibrillation (VF)

Define PVCs
=premature ventricular contractions
-spontaneous ventricular depolarizations NOT preceeded by a P wave
-arise from ventricle and don't follow normal conduction
-usually don't need tx unless symptomatic
-tend to be benign

Define VT
=ventricular tachycardia
-medical emergency that requires immediate ID and defibrillation
-can be very fatal
-if survive, should get ICD (implanted defibrillator)
-Can be:
1. monomorphic
-1 pattern/consistent amplitude QRS
2. polymorphic
-amplitude of QRS varies in regular pattern
-if long QT interval at baseline -> torsades de pointes

Define VF
=ventricular fibrillation
-medical emergency requiring immediate defibrillation
-if survive should get ICD
-ventricular depolarizations with no consistent pattern

Name the 4 classes of antiarrhythmic drugs
class 1=Na channel blockers
class 2= beta adrenoceptor blockers
class 3= K+ channel blockers
class 4= Ca channel blockers

Describe common features of antiarrhythmic drugs
-best suited to tx tachycardia
-separated into 4 classes by major mechanism
-digoxin is NOT classified as antiarrhythmic
-all antiarrhythmic drugs can also cause arrhythmias

Which 2 classes of antiarrhythmic drugs can be especially proarrhythmic?
1. Na channel blockers
2. K+ channel blockers
-except amiodarone
-induced arrhythmias can be fatal

How do Na channel blockers act as antiarrhythmics?
1. slow conduction in cells (block phase 0)
2. suppress automaticity (phase 4 block)
Name 4 Na channel blockers used as antiarrhythmic drugs
1. quinidine
2. procainamide
3. lidocaine
-has some CNS toxicity
4. flecainide

Define Flecainide
=class I antiarrhythmic drug
-Na channel blocker
-tx suppression of a fib
-exhibits use-dependence (greater efficacy at faster HR)
-use dependence b/c has slow dissociation rate so Na channel blocked for greater proportion of time at faster rates

Describe use of beta blockers as anti-arrhythmic drugs.
Used for
1. rate control
-a fib, slow AV nodal conduction
2. arrythmia prevention
-reduce mortality in patients after MI b/c suppress ventricular arrhythmias
-side effects: bronchospasm, bradycardia, hypotension, worsening of CHF

How do K+ channel blockers act as antiarrhythmic drugs?
-block outward phase 3 currents -> prolong AP duration and depolarization
-reverse use dependence (greater effect at slower HR)
-ca also tx tachycardias

Name 3 important K+ channel blockers for treating arrhythmias.
1. Amiodarone
2. Sotalol
3. Dofetillide

_______ is the most effective antiarrhythmic drug
-K+ channel blocker
-can prevent a fib, reduce post MI arrhythmias
-long half life (50 days)
-some irreversible, serious side effects
-should try drugs w/less side effects first (even though less effective) and if those don't work, then put pt on amiodarone

Name 6 side effects of amiodarone
=most effective antiarrhythmic drug
-K+ channel blocker
1. pulmonary fibrosis
2. visual side effects
3. irreversible retinal degeneration
4. hypothyroidism
5. liver enzyme elevations
5. peripheral neuropathy
6. photosensitivity

Name 2 anti-arrhythmic drugs that you need to check for QT interval prolongation when first starting on drug
-K+ channel blockers
1. Sotalol
2. Dofetillide
-long QT -> increased risk of torsades de pointes

How do Ca channel blockers act as antiarrhythmics?
-block phase 0 upstroke in AV nodal cells -> slow conduction through AV node in a fib
-should NOT be given post MI
How does digoxin act when used to tx arrhythmias?
-binds and inhibits Na/K ATPase
-enhances vagally mediated slowing of AV node
-not classified as an antiarrhythmic drug!
-given as adjunct with beta blockers or Ca channel blockers

How does adenosine tx arrhythmias?
-short acting agent
-blocks AV nodal conduction for approx 3-5 seconds -> terminates AV node-dependent arrhythmias

Why is anticoagulant therapy used in arrhythmias?
-prevent formations of clot (ex atrial fib) that could embolize
-both heparin and warfarin used
Pacemakers are used to tx __________
1. infection
2. pacemaker mediated tachycardia
3. pacemaker syndrome (loss of synchrony between atria and ventricles)

Name the primary and secondary indications for ICDs.
=implantable defibrillators
1. Long QT syndrome
2. LV dysfxn (EF less than 30-35%)
Secondary indications
1. patients that survive VF or VT

Describe use of ablation to tx arrhythmias.
-surgery using radiofrequency energy to burn tissue and create block in slow pathway
-can treat most arrhythmias effectively
-first line indications:
1. atrial flutter
2. AV node reentrant tachycardia
3. Atrioventricular reentrant tachycardia (WPW)

Define Torsades des pointes
=ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG
-can progress to Vfib
-Can result from anything that prolongs QT interval
-frequently either due to drugs or congenital (familial long QT syndrome)

Define Wolff-Parkinson-White syndrome

=tachycardia caused by reentry due to accessory pathways
-accessory conduction pathway from atria to venticle bypasses AV node
-ventricles can partially depolarize earlier
-on ECG see delta wave right after P wave
-can cause SVT

True or false: the cause of pericardial disease is often never identified
-can be either isolated phenomenon or complication of a variety of systemic disorders, trauma, drugs
True or false: removing the pericardium is life-threatening.
-you can remove the pericardium and patients will be fine
Name 4 ways that pericardial disease presents:
1. Acute fibrinous pericarditis (dry)
2. Pericardial effusion without cardiac compression
3. Cardiac tamponade
4. Constrictive pericarditis

Name 4 functions of the pericardium
1. limits distension of cardiac chambers
2. Prevents excessive torsion and displacement; minimizes friction with surrounding structures, barrier to spread of infection
3. Equalize gravitational, inertia, and hydrostatic forces
4. Modulate stucture, fxn, and gene expression

Describe signs and symptoms of acute pericarditis
1. Chest pain and quality
-over anterior chest
-sudden onset
-pleuritic (sharp and exacerbated by inspiration)
2. Sitting and leaning forward on chair
3. Fever
4. Pericardial friction rub
5. ECG changes (diffuse ST elevation)
-need at least 2 features +/- pericardial effusion

Name 4 categories of causes of acute pericarditis
1. Infectious
-viral most common (Echo or cocksackie)
2. Idiopathic
-prob viral
3. Secondary
-post MI
-cardiac surgery
-mediastinal radiation
-drug induced
4. Systemic disorders
-lupus, connective tissue disease

Describe the chest pain in pericarditis
-occurs over anterior chest
-often pleuritic (sharp and exacerbated by inspiration)
-pain can be difficult to distinguish from MI
-may decrease in intensity when patient sits up
-may radiate, esp to trapezius edge

Describe 4 pathological states of acute pericarditis
-early inflamm. response with all types
2. Serofibrinous
-most common
-rough and shaggy
-uremia, rheumatic fever, viral
-roughened b/c of deposition of fibrin
3. Purulent
4. Hemorrhagic
-TB or neoplasm

Describe the ECG changes that accompany acute pericarditis
4 stages
1. Diffuse ST elevation
-PR depression at times
2. Normalization of ST and PR segments
3. Development of diffuse T wave inversions
4. Normalization

How do we differentiate ECG changes in acute pericarditis from those of acute MI?
1. Diffuse ST elevation in acute pericarditis
2. No reciprocal changes (vs. AMI)
3. ST elevation and T wave changes do NOT occur simultaneously in acute pericarditis

How do we treat acute pericarditis?
1. ASA or NSAIDs
2. Steroids if refractory
3. Hospitalize high risk pts (high fever, evidence of cardiac tamponade,immunosuppressed)
-10-30% of patients develop either recurrent or incessant disease, usu with pericardial effusion

Define pericardial effusion
=accumulation of transudate, exudate, or blood in pericardial space
-many conditions that cause pericarditis produce chronic pericardial effusion (TB, uremia, neoplasia, CTD)
-in transplant patients, associated with increased incidence of acute rejection

Name 4 conditions that are associated with pericardial disease.
1. CHF
2. valvular disease
3. MI
4. cancer
-also common after cardiac surgery

If you suspect a pericardial effusion, what should you do?
1. Establish presence of effusion
-done with Echo
2. Assess hemodynamic impact
-make sure stable
-elevated neck veins on PEX suggest hemodynamic compromise
3. Establish cause

Name 2 characteristic ECG findings with pericardial effusion

1. Electical alternans
-swinging of heart in wave of pericardial fluid
-seen more often with large effusion
2. Low voltage of QRS complexes
-short-circuiting of cardiac potentials by fluid surrounding heart

______ is the tool of choice to diagnose a pericardial effusion
How would you distinguish pericardial effusion from pulmonary edema?
-the 2 may look similar on chest xray
-look at BNP levels
-BNP levels will be elevated in pulmonary edema due to heart failure

True or false: the clinical features of a pericardial effusion depend on speed of fluid accumulation
1. Slow accumulation
-large fluid volumes can be tolerated
2. Rapid accumulation
-cardiac tamponade
-can use echo to evaluate for cardiac tamponade

State the clinical definition of cardiac tamponade
=life-threatening caused by fluid under pressure around the heart
-fluid can rapidly accumulate
-increased pressure from fluid can prevent heart from relaxing completely between beats
-sudden drop in CO
-fluid can be blood, purulence, effusion

List symptoms of cardiac tamponade
=due to sudden drop in CO
1. Hypotension
2. shock
3. abnormal heart rhythms
4. death

State the hemodynamic definition of cardiac tamponade.
=hemodynamic continuum characterized by: 1. elevated and equal ventricular diastolic, atrial, and pericardial pressure
2. pulsus paraodoxus
3. Arterial hypotension

True or false: 100mL of fluid accumulation is sufficient to cause cardiac tamponade
-as long as accumulates rapidly
Name 3 major causes of cardiac tamponade
1. Hemopericardium causes
-trauma, aortic aneurysm, iatrogenic (CPR, cardiac cath, anti-coag drugs)
2. Neoplasm
-causes mixture of serous and blood
3. Pericarditis
-from radiation therapy, infections, drug rxns (hydralazine, procainamide)

Name the 3 components of Beck's triad for tamponade
1. Hypotension
2. JVP elevation
3. Muffled heart sounds

Define pulsus paradoxus
=an abnormally large decrease in systolic BP (> 10 mmHg) on inspiration= exaggerated normal response
-can see in other conditions besiders tamponade and some tamponade does not show pulsus paradoxus
-limitation of outward expansion of RV causes bulge of interventricular septum when blood flows into RV during inspiration -> decreases LV volume -> large decrease in stroke volume ->large decrease in systolic BP

How do you measure pulsus paradoxus?
-Elevate pressure in BP cuff above systolic pressure, slowly bleed air until Korsakoff sounds
-sounds only audible during expiration
-continue to release air until beats heard with both inspiration and expiration
-if systolic difference between 2 points is greater than 10mm Hg -> pulsus paradoxus

Name 3 cariac tamponade conditions without pulsus paradoxus
1. LV dysfxn
2. ASD
3. Aortic insufficiency

Name 6 conditions other than cardiac tamponade that can show pulsus paradoxus
1. Constrictive pericarditis
3. RV infarct
4. Pulmonary embolus
5. Circulatory shock
6. Pleural effusions

What is the cardinal sign on echo of cardiac tamponade?
-diastolic collapse of RV, late diastolic RA collapse
Name 3 ways to remove fluid in cardiac tamponade
=a medical emergency!
1. pericardiocentesis
2. Surgery
3. Percutaneous balloon pericardiotomy

Define pericardial constriction
-results from scarring with consequent loss of elasticity of pericardial sac
-compression does NOT occur until the cardiac volume approximates that of the pericardium, which occurs in mid-late diastole
-as a result majority of ventricular filling occurs rapidly in early diastole
-pericardium will be thick and calcified

Name 6 causes of pericardial constriction
1. Idiopathic
2. Following CABG
-most common
3. Following radiotherapy
4. Post infectious
5. Neoplasm
6. Connective tissue disorder

Name some symptoms and signs of pericardial constriction
-due to decreased CO
1. Weakness
2. Fatigue
-fluid retention
3. Peripheral edema and ascites
4. elevated JVP
5. Pericardial "knock"
6. wasting/cachexia
7. Pulsatile hepatomegaly
8. no pulsus paradoxus

Define pericardial "knock"
=heart sound in pericardial constriction
-early in diastole (right after S3)
-heard in pts with severe calcific constriction
-can sometimes see calcification on chest xray

How do you distinguish cardiac tamponade and pericardial constriction with JVP recordings?
1. Tamponade
-show blunted Y descent
2. constrictive pericarditis
-show accentuated Y descent

Name some clinical features of restrictive cardiomyopathies
1. stiff and inelastic ventricle fills with great difficulty
2. fatigue
3. exertional dyspnea
4. chest pain

Describe restrictive cardiomyopathy
-presents same as constrictive pericarditis but NOT curable
-rigid ventricles that impair filling but normal size and systolic fxn
-ventricular stiffness due to:
1. fibrosis or scarring of endomyocardium
2. infiltration of myocardium by an abnormal substance

Name some causes of restrictive cardiomyopathy.
1. Amyloidosis
2. Sarcoidosis
3. Hemochromatosis and other storage diseases
-lead to abnormal relaxation of ventricle because muscle is NOT working right

Define aneursym
localized abnormal dilation of a blood vessel or of the heart wall
Can be:
1. True vs false
2. True can be saccular vs fusiform

Name the 2 most common causes of aneurysms
1. Atherosclerosis
2. Cystic medial degeneration
Other causes:
-congenital defects (berry aneurysm)
-infections (syphillis)

_________ is the most common site for atherosclerotic aneurysms

=abdominal aorta
-usually below renal arteries but above bifurcation of aorta
-usu seen in men in 50s
-risk factors: fam hx, HTN, atherosclerosis
-could be linked to genetic defects in structural proteins

Contrast true vs false aneurysm
-involves all 3 layers of arterial wall or attenuated heart wall

-breach in a vascular wall leading to extravascular hematoma that communicates with the intravascular space
-ex. ventricular free wall rupture after MI that's contained by percardial adhesion

Define arterial dissection
=when blood enters the wall of the artery as a hematoma and separates the layers of the blood vessel
-dissections can be associated with other causes than aneurysm

Contrast saccular vs fusiform aneurysms
=macroscopic classifications of aneurysms by shape and size

Saccular= spherical outpouchings
-involve only portion of vascular wall
-after contain thrombi

Fusiform= diffusion, circumferential dilation of a long vascular segment

Define mycotic aneurysm
=aneurysm caused by infection
-infection weakens wall of aortic
-complications include
1. thrombosis
2. rupture

How can infection cause aneurysms?
=mycotic aneurysm
1. embolization of septic thrombus (infective endocarditis)
2. extension of adjacent suppurative process
3. organisms directly affecting arterial wall

How does atherosclerosis cause an aneurysm?
=atherosclerosis weakens the media
-plaques compress the media
-interfere with nutrient and waste diffusion
-wall becomes necrotic and weak ->dilation

Name the 2 variants of abdominal aortic aneurysms.
1. Inflammatory
-lots of periaortic fibrosis
-lots of lymphocytes and plasma cells
-sometimes giant cells

2. Mycotic AAA
-Can be bacterial (ex Salmonella)
-microorganisms lodge in wall of aorta -> degeneration and necrosis of the wall -> weakening

How can an abdominal aortic aneurysm present clinically?
1. Pulsatile abdominal mass
2. Death
Name 4 complications of abdominal aortic aneurysms.
1. Rupture
-massive, often fatal hemorrhage
2. Obstruction of branch vessel -> ischemia
3. Embolism
4. Compression of abdominal structures
-ex ureter

How do we estimate the risk of rupture with abdominal aortic aneursysm?
-risk increases as size of aneurysm increases
1. 0-4cm ~0 risk
2. 4-5cm ~1% risk of rupture per year
3. 5-6cm ~11% risk
4. >6cm ~ 25% rupture

How are abdominal aortic aneurysms treated?
1. Surgery
-want to treat BEFORE rupture b/c only 5% risk of mortality (vs 50% risk once aneurysm has ruptured)
Define syphyilitc aneurysm
=manifestation of tertiary syphillis
-occurs in thoracic aorta and aortic arch
-due to inflammation of vasa vasorum of aorta -> ischemic medial injury -> dilation and formation of aneurysm
-can result in aortic insufficiency -> LV hypertrophy -> usually die of CHF

Describe the pathologic hallmarks of syphillitic aneurysm
1. dilation of aorta
2. tree bark (contraction of fibrous scars -> wrinkling of intima)

1. Vaso vasorum surrounded by inflammatory cells
2. destruction of elastic tissue and scar formation
3. ischemic changes in aortic media

Define aortic dissection
=tear in intima with hemorrhage into wall of the aorta
-most often thoracic aorta
-may rupture adventitia and bleed
-when ruptures can cause massive hemorrhage or cardiac tamponade
-very lethal
-may or may not be associated with dilation of aorta

Who is at risk of aortic dissections?
-2 groups of people
1. HTN men (age 40-60)
**HTN is major risk factor (90% of cases)
2. People with connective tissue abnormalities (ex Marfan's)

-Other causes:
1. Iatrogenic
2. pregnancy (why unknown)

What is the sequence of events in an aortic dissection?
1. intimal tear
2. hemorrhage into aortic media
3. extension of hemorrhage
4. rupture

What are the pathological changes seen with HTN in aortic dissection?
-HTN involved in 90% of cases
1. medial hypertrophy of vaso vasorum
2. matrix degenerative changes (elastic fragmentation)
3. loss of medial SM
=cystic medial degneration
-these changes do not guarantee dissection (like plaque rupture)

What is the defect in Marfan's syndrome
=autosomal dominant disorder
-defect in fibrillin (ECM scaffolding protein required for normal elastic tissue synthesis)
-elongated skeletal bones, ocular findings, CV manifestations (increased risk of aortic dissection and aneurysms)

Define cystic medial degeneration
-histological lesion that can lead to aortic dissection
-characterized by:
1. elastic tissue fragmentation
2. separation of elastic and SM parts of media by cystic spaces filled with ECM components
-can be seen in pts with Marfans, pts with dissection due to HTN

Describe the clinical course of aortic dissection.
=abrupt onset of "tearing" chest pain
that radiates to the back
-can be misdiagnosed as AMI
-most common cause of death is rupture
-dissection to the aortic root can cause:
1. cardiac tamponade
2. aortic insufficiency
3. MI
4. extension of dissection in great arteries of neck, coronary, renal, mesenteric, iliac

Define Bakeley type 1, 2, 3
=classifications of aortic dissections based on location of aorta affected
-closer to aortic valve =worse
-type A lesions
-involve either ascending aorta only (type 1) or ascending and descring aorta (type 2)
-most dangerous
-need immediate anti-hypertensive
-now survival 65-70%

-type B lesions
do NOT involve ascending aorta at all (type 3)

Define vasculitis
=inflammation of vessel walls
-occurs in diverse clinical settings
-virtually any type of vessel in any tissue can be affected
-most usually involve small vessels (arterioles -cap-venules)
-there are some disorders that characteristically affect one vessel type (ex large vessel diseases)

How are types of vasculitis grouped/subclassified?
1. infectious vs noninfectious
2. vessel size
3. role of immune complexes
4. presence of autoantibodies
-lots of clinical and pathologic overlap among the different disorders

Name the 3 major mechanisms involved in noninfectious vasculitis
1. immune complex deposition
2. antineutrophil cytoplasmic antibodies (ANCAs)
3. anti-endothelial antibodies

Describe immune complex associated vasculitis
immune complex=Ab bound to Ag
-possible Ag: drugs (penicillins), viral particles, serum proteins
-immune complexes deposit in vessel walls and attract complement
1. SLE
2. Hypersensitivity drug rxns

Define ANCA
=antineurtrophilic cytoplasmic antibodies
-circulating antibodies that react with neutrophil cytoplasmic agents (autoantibodies)
-can be directed against enzymes in primary neutrophil granules, monocyte lysosomes, and endothelial cells
-2 types
1. c-ANCA
2. p-ANCA

Contrast c-ANCA and p-ANCA
c-ANCA= cytoplasmic ANCA
-against serine proteinase 3, a neutrophil granule constituent
-Wegener's granulomatosis
2. p-ANCA= perinuclear ANCA
-against myeloperoxidase (MPO)
-other types of vascultitis

Describe the role of ANCAs in pathophysiology of vasculitis
ANCAs=autoantibodies against cytoplasmic components of neutrophils
-levels of ANCAs go up with increased disease activity and severity
-if tx, levels go down
-how they work is unknown, but thought to activate neutrophils that then release ROS and proteolytic enzymes

Anti-endothelial cell antibodies are associated with certain types of vasculitis, including _________.
=Kawasaki disease
Define Giant cell arteritis
=most common vasculitis
-chronic, usu granulomatous inflammation of large-small sized arties
-usu vessels in head (esp temporal arteries)
-seen in older patients
-presents with nodular tender arteries at temple
-sometimes presents with blindness
-associated with involvement of opthalmic artery

Describe the microscopic pathology of Giant cell arteritis.
-lesions are focal
-giant cells and lymphocytes with fragmented internal elastic lamina
-sometimes just nonspecific arteritis
-healed lesions show collagen deposition and scar
-pathogenesis is unknown but likely autoimmune with T cells mediated

What are the clinical features of giant cell arteritis?
1. Vague symptoms: fever, fatigue
2. Facial pain or headache
3. Tender nodularities
in temple
4. Worst: abrupt onset of blindness
-due to involvement of opthalmic artery
-tx with steroids

Environmental risk factors have the greatest impact for development of congenital heart disease between _____ and ______ weeks of gestation
4-9 weeks
Name 4 risk factors for developing congenital heart defects.
-80% of congenital heart disease is due to unknown cause
1. Genetics
-multifactorial inheritance

Environmental factors
1. Maternal viral infections (rubella)
2. Chronic maternal EtOH abuse
3. drugs

Name 3 important shunts during fetal development?
1. Ductus venosus
-oxygenated blood bypasses the liver
2. Foramen ovale
-oxygenated blood for ductus venosus diverted to left heart and cerebral circulation while deoxygenated blood from SVC diverted to systemic circulation and umbilical arteries
3. Ductus arteriosus
-blood bypasses high resistance pulmonary bed via ductus arteriosus into systemic circulation

How do the fetal shunts close after birth?
1. Ductus vensosus
-collapses when blood flow ceases after removal of placenta
-becomes fibrotic
2. Foramen ovale
-flap valve closes when LA pressure increase due to increased transpulmonary blood flow at birth
3. Ductus arteriosus
-active constricts when blood oxygen saturation increases at birth
-becomes fibrotic

Name 9 clinical and pathologic features associated with congenital heart disease
1. failure to thrive
2. impaired growth
3. respiratory distress
4. cyanosis
5. finger clubbing
6. polycythemia
7. heart failure
8. pulmonary HTN
9. infective endocarditis

Name the 3 major categories of congenital heart disease
1. Obstructive lesions
2. Right-left shunts
3. Left-right shunts

Describe the group characteristics of congenital heart disease with obstructive lesions
-25% of CHD
-acyanotic pts
-pressure gradient across stenotic region
-common lesions:
1. pulmonic stenosis
2. aortic stenosis
3. coarctation of the aorta

Describe the group characteristics of congenital heart defects due to Left->Right shunts
-40% of CHD
-acyanotic pts (but show late cyanosis)
-communication between systemic and pulmonary circulation ->increased transpulmonary blood flow
-common lesions
1. ASD
2. VSD
3. PDA
-O2 saturation of blood increases in right heart chamber at level of the shunt
-increased pressure and volume in pulmonary circulation -> RV hypertrophy

Name 2 factors the influence a left->right shunt in congenital heart disease
1. Compliance of heart chambers connected by the defect
2. size of defect

-these 2 factors determine:
1. volume of shunt
2. direction of shunt

Describe the group characteristics of right-left shunts in congenital heart disease.
-20% of cases
-check mucous membranes and nail beds
2. Desaturated blood bypasses the pulmonary circulation and enters directly into systemic circulation
3. can also see polycythemia

Name 3 types of congenital heart defects involving right-left shunts
=where desaturated blood bypasses lungs and goes straight into systemic circulation
1. Tertralogy of Fallot
2. Transposition of the great vessels
3. Tricuspid atresia
#2 and 3 not compatible with life unless shunting (ex PDA) is present; need early surgery

Name 3 examples of congenital heart defects involving left-right shunts
1. Atrial septal defect
2. ventricular septal defect
3. Patent ductus arteriosus

What are the 2 key anatomic features of a right-left congenital shunt?
1, communication between pulmonary and systemic circulations
2. obstruction is present -> increased resistance in right heart
Define Atrial septal defect
-L-R congential shunt
-10% of congenital heart defects
-incrreased pulomonary blood flow
-isolated ASD may not be symptomatic until 30 years later
-3 types
1. secundum (90%)
-in region of fossa ovalis
2. primum
3. sinus venosus

Name 3 potential complications of atrial septal defect.
1. heart failure
2. paradoxical embolization
3. irreversible pulmonary HTN
-10% of pts

Define ventricular septal defect
-L-R congenital shunt
-most common cardiac anomaly at birth (1/3)
-classified by size and location
-impact of VSD depends on size and presence of pulmonary stenosis
-some small VSDs may close on own
-often associated with other cardiac malformations
-complication of pulmonary HTN (with large defects)
-most VSDs from failure of membranous part of septum to form

90% of VSDs occur in the region of ____________ near the bundle of His
-membranous septum
What physical finding will you get with VSD?
1. loud pansystolic murmur
-often associated with a thrill
Define Patent ductus arteriosus
-L-R congenital shunt
-results when ductus arteriosus remains open after birth
-oxygenated blood flowing out LV gets shunted back to lungs -> volume overload and dilation of LA and LV and pulmonary HTN
-90% PDA are isolated defects
-symptoms of PDA proportional to size of shunt
-if another heart defect present, PDA may be life saving (and may use PG E2 to keep it open until heart surgery to correct other malformations)

How does the ductus arteriosus normally close?
-when SM in wall of ductus arteriosus exposed to oxygenated blood after 1st breath, it actively constricts -> closes ductus
-later fibrous tissue completes closure
Name the murmur characteristic for a PDA?
-continuous "machinery" murmur
-loudest at time of 2nd heart sound
Define Atrioventricular septal defect
-L-R congenital shunt
-present in 1/3 of Down's syndrome
-AV canal fails to develop into atrioventricular valves and close lower portion of AV septum

Define tetralogy of fallot
-R-L shunt
-cyanotic heart disease
-4 features of defects
-untreated pts often survive into adult life
-severity of obstruction to RV outflow determines direction of blood flow
-decreased pulmonary blood flow -> no pulm HTN
-increased aortic volumes

Name the 4 anatomic features of tetralogy of fallot
-all result from anterosuperior displacement of infundibular septum -> abnormal division between pulmonary trunk and aortic root
1. VSD
2. obstruction to RV outflow tract
-either pulmonic stenosis or subpulmonic stenosis
3. Aorta that overrides the VSD
4. RV hyptertrophy

How does the body compensate for a tetralogy of fallot?
-right->left shunt creates hypoxia
1. polycythemia
2. increase hemoglobin concentration
3.RV hypertrophy
-combined with pulmonary stenosis can result in right heart failure and infective endocarditis

Why do kids with tetralogy of fallot like to squat?
-attempting to increase venous return from extremities and increase flow across patent ductus or VSD to right side of circulation
Define transposition of the great arteries

-R->L shunt that causes early cyanosis
-result of abnormal formation of truncal and aortopulmonary septa
-aorta ends up coming off RV and lies anterior to pulmonary artery
-forms separate systemic and pulmonary circulations
-can't live with defect unless some other defect creating a shunt that allows for mixing of blood
-prognosis depends on degree of mixing of blood
-need surgery for longterm survival

Define truncus arteriosus.
-R->L shunt
-failure during development to separate truncus arterosus into aorta and pulmonary artery
-also has VSD
-early systemic cyanosis from mixing of blood
-increased pulmonary blood flow
-surgery needed to prevent irreversible HTN

Define tricuspid atresia
-Congenital R->L shunt
-cyanosis present from birth
-complete occlusion of tricuspid valve orifice
-hypoplasia of RV
-ASD and VSD maintain life when present
-high mortality unless surgical repair

Define total anomalous pulmonary venous connection
-R->L congenital shunt
-pulmonary veins do NOT drain into left atrium
-return to heart to heart can have various pathways usually back to right heart
-RA and RV volume and pressure hypertrophy

Name 4 obstructive congenital anomalies
1. coarctation of aorta
2. pulmonic stenosis
3. aortic stenosis
4. bicuspid aortic valve

Define coarctation of the aorta
=obstructive congenital abnormality
-coarctation=narrowing or constriction of aorta
-affects men more than women
-Can be:
1. Preductal location
-infantile type
2. postductal location
-adult type

Define preductal coarctation of the aorta

=infantile aorta
-congential obstructive defect due to narrowing of aorta
-see signs and symptoms early in life
-less common
-requires surgery
-usu severe narrowing
-circulation depends on R->L shunt through PDA
-elevated pulmonary artery pressure
-RV hypertrophy

Define postductal coarctation of the aorta
=congenital obstructive defect
-adult type
-may be asymptomatic and not detected until adulthood
-BP differences between upper and lower extremities
-X ray sign: rib notching
-collateral circulation involving intercostal arteries
-also decreased femoral pulse
-systolic murmur heard in posterior test

Define congenital pulmonic stenosis
-obstructive defect
-RV hypertrophy
-if severe injury, can get jet flow through valve that injuries wall of pulmonary artery
-can involve infundibulum of RV outflow tract and valve cusps
-often associated with other malformations (tet. of fallot)

Define congenital aortic stenosis
-obstructive lesion
-hypoplasia of aorta
-LV hypertrophy
-endocardial fibroelastosis in LV
-> restricts fxn of LV
-group of findings= hypoplastic left heart syndrome
-need surgery for both mild and severe stenosis
-complications: infective endocarditis, hemodynamic complications

Define bicuspid aortic valve
=congenital obstructive defect
-common malformation
-only 2 cusps instead of 3
-cusps can be same size or disproportionate
-usu asymptomatic at birth
-increased risk of later complications
-50% of infants and adults with coarctation of aorta also have bicuspid aortic valve

Name 3 complications that the presence of bicuspid aortic valves increase the risk for.
1. Infective endocarditis
2. Calcific aortic sentosis (men)
3. Dissecting aneurysms of aorta

True or false: congenital heart defects treated with surgery always make the heart essentially normal
-false (or not always true)
-some myocardial hypertrophy and cardiac remodeling may be irreversible
-irreversible changes can lead to problems later in life

Name some genetic factors associated with congenital heart defects
1. Chromosomal abnormalities
-trisomies 13,15,18,21 (Down Syndrome) and Turner syndrome (X monosomy)
2. Mutations in transcription factors
-seen in ASD and VSD
3. Other mutations
-deletions in chromosome 22 associated with outflow tract malformations and malformations of branchial arches (Di George syndrome)

Define shunt
=abnormal communication between chambers or blood vessels
-direction of blood flow in shunt depends on pressure relationships between the 2 compartments

Why do right to left congenital shunts result in prominent cyanosis?
-b/c poorly oxygenated blood bypasses the pulmonary circulation and gets out into systemic circulation
Why do we see late cyanosis with congenital left-right shunts?
-prolonged pulmonary HTN caused by the shunt can raise right heart pressures so that RH pressure> LH pressure --> reversal of flow in the shunt --> unoxygenated blood gets into systemic circulation -> cyanosis
Describe the pathogenesis of ASD.
-congenital heart defect producing L -> R shunt
-ASDs arise from failure of normal formation of atrial septa and forament ovale or failure of foramen ovale to close
Normal development
1. Septum primum grows down toward endocardial cushion with 1 opening between them
2. second opening forms (ostium secundum) and second septum (septum secundum)
3. septum secundum proliferates and turns into foramen ovale
-forament ovale acts as 1 way valve/normal right -> left shunt in utero that gets closed at birth with changes in chamber pressures
-ASDs less likely to spontaneously close but often well-tolerated
-surgery used to prevent potential future complications

Define the ductus arteriosus
-connection between aorta and pulmonary outflow tract during intrauterine life
-permits bloodflow to bypass unoxygenated lungs
-ductus constricts shortly after birth due to:
1. increased arterial oxygenation
2. decreased pulmonary vascular resistance
3. declining levels of PG E2
-in most kids it closes after birth and later forms ligamentum arteriosum
-PDA = failure of ductus to close after birth

Define Takayasu arteritis
=type of vasculitis
-young women, most often Asian
-Granulomatous inflammation of medium -large arteries
-fibrosis of the vessel wall w/luminal narrowing and giant cells
-Aortic arch classically involved and may extend beyond
1. ocular disturbances
2. weak pulses upper extremities
"pulseless disease"

True or false: giant cell arteritis and Takayasu arteritis are often histologically indistinguishable.
-distinguish by age of pt (Takayasu less than 40 yo), location, sex
Describe the histological changes seen in Takayasu arteritis
-thickening of the vessel wall
-intimal hyperplasia
-inflammation of adventitia and media
-inflammation can be granulomatous
-giant cells
-later fibrosis of vessel wall
-vessel wall becomes so thick lumen of vessel narrows

Name 5 clinical features of Takayasu arteritis
1. Low blood pressure and weak pulse (upper extremities lower than lower extremities)
2. ocular disturbances
3. distal aortic involvement: claudication (cramping in legs during exercise due to poor circulation)
4. Renal artery involvement: HTN
5. Variable disease course

Define Polyarteritis nodosa
-systemic vasculitis of small or medium sized muscular arteries
-usu involves renal, other visceral vessels but lung vessels spared
-young adults
-unknown cause

Describe the pathogenesis of polyarteritis nodosa
-transmural necrotizing inflammation of small and medium muscular arteries
-fibrinoid necrosis of vessel wall
-thrombosis of lumen
-Later: fibrosis of wall-> thickens
-May see both early and late stage lesions together

Name 5 potential complications to blood vessels of polyarteritis nodosa
Necrotizing inflammation weakens vessel wall ->
1. aneurysm and possible rupture

Lesions lead to impaired perfusion ->
1. ulcerations
2. infarcts
3. ischemic atrophy
4. hemorrhages

Describe the clinical course of polyarteritis nodosa
-Findings related to ischemia ( malaise, fever, wt loss)
-renal artery involvement major cause of death
-acute -chronic course, episodic
-frequently linked to Hep B Ag circulating in blood
-tx with steroids and cyclophosphamide

Define Kawasaki disease
-mucocutaneous lymph node syndrome
-acute, febrile illness of children
-arteritis of large-medium sized vessels
-May involve coronary arteries leading to MI, rupture, thrombosis
-pathogenesis is unclear

Describe the clinical presentation of Kawasaki disease
-80% in children less than 4 yo
-conjunctival and oral erythema
-edema of hands and feet
-cervical lymphadenopathy
-20% will develop cardiovascular problems (can cause formation of coronary artery aneurysms)
-can reduce rate of coronary artery involement with IVIG

Define Wegener's granulomatosis
=necrotizing vasculitis characterized by triad
1. Acute necrotizing granulomas of upper resp tract (nose, sinus, throat) or lower tract (lungs) or both
2. Necrotizing or granulomatous vasculitis of small-medium sized arteries and veins (esp in lungs are upper airways)
3. Renal disease
-focal necrotizing often crescentric glomerulonephritis
-associated with c-ANCA
-males affected > females
-40-50 yo

Describe clinical presentation of Wegener's granulomatosis
1. Pneumonitis
2. Ulcers of nasopharynx
3. Renal disease
4. Chronic sinusitis
-if untreated, 80% of patients will die within 1 year
-tx with steroids and cyclophosphamide

True or false: the necrotizing granulomas of the lung in Wegener's granulmatosis can stimulate the formation of malignant neoplasms
-can also cause infections
-these babies are destructive!

Define Thromboangiitis obliterans
=Buerger disease -seen in young ( vascular insufficiency -tibial and radial arteries freq affected
Describe the pathogenesis of throboangiitis obliterans
Could be due to:
1. direct toxicity of cigarette smoke to endothelium
2. idiosyncratic immune response to cigarette smoke
-segmental acute and chronic vasculitis
-luminal thrombi containing microabscesses
-inflammation extends to involve neighboring veins and nerves

Describe the clinical features of thromboangiitis obliterans
1. chronic ulceration of digits
2. painful
3. gangrene of fingers and toes
( serial amputations sometimes required)
-cured if quit smoking

Define infectious vasculitis
=localized arteritis caused by direct invasion of infectious agents
-usu due to bacterial (Aspergillus, Mucor )
or fungi
-Can lead to:
1. thrombosis and infarction
2. mycotic aneurysm (dilation of vessel wall caused by growth of fungi, usu result of septic emboli)

Define Varicose veins
=abnormally dilated, tortuous veins
-involves superficial veins of the legs (NOT the deep veins)
1. Males 10-20%
2. Female 25-33%
-Risk factors
1. obesity
2. pregnancy
3. family hx

How do varicose veins develop?
-caused by prolonged increase in pressure
-elevated pressure leads to venous valve incompetence
-dilation of venous walls
-Results in:
1. venous stasis
2. congestion
3. pain
4. edema
5. thrombosis (due to stasis)
-very rare to embolize
-eventually have stasis dermatitis and ulceration

Define stasis dermatitis
-brown coloration of skin (from hemosiderin)
-skin thickened and rough
-complication of varicose veins

Compare thromboplebitis and phlebothrombosis

-interchangeable terms for venous thrombosis with inflammation
-most often seen in deep leg veins (DVT)
Name 6 risk factors for thrombophlebitis
1. CHF
2. pregnancy
3. obesity
4. recent surgery
5. prolonged immobility
6. hypercoagulability

Name Virchow's triad
1. alterations in normal blood flow (stasis)
2. injury to vascular endothelium
3. alterations in constitution of blood (hypercoaguability)

Describe clinical manifestations of thrombophlebitis
-can be difficult to diagnose
-painful, swelling
-use doppler ultrasound to help diagnose
-sometimes, PE is first manifestation
-Tx with anticoagulants and greenfield filter to catch PE if drugs fail

Define Thrombophlebitis migrans
=Trousseau's syndrome
-distinctive from thrombphlebitis
-venous thrombi appear, disappear, and then reappear somewhere else (migratory)
-associated with visceral malignancies (esp pancreatic adenocarcinoma)

Define SVC and IVC syndromes
-due to compression of SVC or IVC
-frequently compression by neoplasms
Describe the findings in SVC syndrome
-compression of SVC
-can be caused by lung or mediastinal malignancies
1. dilation of veins of head, neck, and arms with cyanosis

Describe the findings of IVC syndrome
-compression of IVC
-usually by liver tumors or thrombi
1. marked lower extremity edema, dilation of veins
2. distension of abdominal collateral veins
3. if renal veins involved-proteinuria

Define lymphangitis
=acute inflammation of lymphatic
-usually due to bacteria
-painful, red subcutaneous streaks
-draining lymph nodes enlarged

Define lymphedema
-swelling of lymphatics
-usu due to secondary causes
1. malignant tumors obstructing lymphatics
2. axillary node dissections (breast cancer)
3. postradiation fibrosis
4. filariasis (parasitic infection)
-increased pressure behind obstruction
-increased intersitial fluid

Contrast Myocardial ischemia with Myocardial hypoxia
Myocardial ischemia
-temporary supply/demand imbalance, usu due to a decrease in coronary blood flow, which impairs O2 and substrate delivery and removal of metabolic end products

Myocardial hypoxia
-decreased oxygen supply WITHOUT decreased coronary blood flow

Define myocardial stunning
=sustained (days-weeks) but reversible depression in myocardial fxn due to transient changes without permanent damage
Define hibernating myocardium
=a reversible depression of myocardial fxn related to coronary artery under-perfusion
Define Sudden cardiac death
-unexpected death outside hospital with no or brief (< 1 hr) preceding symptoms -SCD is usu due to cardiac arrhythmias and is not fatal if pt is resuscitated
Name 4 causes of myocardial ischemia
increased myocardial oxygen demand
1. aortic stenosis
2. LV hypertrophy

decreased myocardial oxygen supply
3. reduced oxygen content (anemia)
4. reduced coronary blood flow (spasm or atherosclerosis)

Describe CBF and O2 demands in the heart
-any increase in demand (exercise) is met by increase in coronary blood flow
-most CBF occurs during diastole
-affected by:
1. tachycardia
2. aortic insufficiency
-according to Pouiseille's law, luminal narrowing (affected by radius) affects flow the most

Name the determinants of myocardial O2 demand
1. HR
2. contractility
3. myocardial wall tension
-wall tension influenced by:
1. intra-ventricular pressure
2. ventricular volume
-another way to say #3 is afterload and preload

Describe CBF
-controlled by local metabolic factors (esp hypoxia, adenosine)
-exhibits auto-regulation
-exhitis active and reactive hyperemia (vasodilation and increased CBF)
-during systole, mechanical compression of coronary vessels reduced blood flow. After the period of occlusion, blood flow increases to repay the O2 debt (reactive hyperemia)

Define Acute Coronary syndrome
=term broadly defined as a progressive pathological condition
1. unstable angina
2. non-Q wave MI
3. acute MI (ST elevation)
-etiology is usually plaque disruption

Stable plaques have a _________ cap but vulnerable plaques have a _______cap.
-thick fibrous
-thin, friable fibrous cap
-vulnerable plaques can be disrupted in many ways (intimal fissure, break, tear, rent, erosion, or ulceration)

Name 4 causes of plaque rupture
1. Exercise
-esp in previously sedentary when begin exercising
2. Stress
3. Big, fatty meals
4. Inflammation
-enzymes from macrophages and T cells eat away at vulnearable plaques
-seen esp w/ chronic infections

What happens when a vulnerable plaque ruptures?
1. expose necrotic core of plaque and collagen fibers ->serve as a nidus for thrombus formation (plt and fibrin aggregate)
2. Stasis of blood flow
3. more chemical mediators from plts and endothelium (TXA2, serotonin, adp, paf, thrombin tissue factors, ROS) -> promote vasoconstriction and further plt aggregation
4. mechanical obstruction of blood flow => AMI

-plaque disruption and thrombosis found in other myocardial ischemic syndromes than AMI, but tend to be less severe

Describe the contractile abnormalities seen with myocardial ischemia

Impaired contractility in ischemic zone
1. hypokinesis
-shortening reduced
2. Akinesis
-shortening absent
3. Dyskinesis
-paradoxical lengthening

Compensatory hyperfxn in non-ischemic areas
1. Catecholamines
2. neural responses
3. Frank-Starling

Myocardial ischemia leads to a ________ in left end diastolic pressure
-due to:
1. decreased contractility and emptying
2. slower HR
3. incomplete relaxation
4. increased stiffness
-LVEDP ~15-20 mmHg optimal for improving LV fxn (Frank-Starling)

-marked increase in LVEDP causes:
1. pulmonary venous congestion
2. hypoxia
3. increased MVO2
4. shock
5. mortality

Describe the relationship between infarct size and LV fxn
-bigger infarct size correlated with worsening LV fxn
-damage accumulates between acute and old MI
-if infarct size greater than 40% of LV, can go into cardiogenic shock

Contrast Anterior MI and Inferior MI
-Effects and outcome affected by infarct site
Anterior MI
-higher mortality
-usu larger infarct
-sympathetic reflex tachycardia with HTN

Inferior MI
-lower mortality
-smaller infarcts
-RV involvement
-Bezold-Jarisch reflex caused by stim of vagal afferents, results in bradycardia with hypotension, nausea, vomitting

Describe the clinical presentation of an AMI
-pain often more intense
-pain often lasts longer than 20 minutes
-pain vice-like, crushing, squeezing
-associated symptoms: nausea, sweating, dizziness
-may mimic indigestion

Other symptoms
-uneven heartbeat
-heavy sweating
-cyanosis (pal of bluish skin, lips, or fingernails)

True or false: about half of accute MIs have no known trigger
-other triggers
1. emotional upset
2. moderate or heavy physical activity
3. lack of sleep, overeating

Who is more likely to have a silent MI?
-half have no symptoms, other half have atypical symptoms (CHF, CNS manifestations, etc)
-25% diagnosed retrospectively by ECG

Name 6 atypical presentations of acute MI
1. CHF
2. CNS manifestations
-syncope, stroke, TIA
3. sudden mania or psychosis
4. overwhelming weakness
5. acute indigestion
6. peripheral embolization

Name 3 ECG changes with myocardial ischemia
1. ST elevation -ischemia involves >40-50% of wall thickness 2. Q waves -infarction > 40% of wall thickness -can resolve in some cases (inferior wall MI) 3. ST depression/non-Q wave MI -
True or false: ECGs are normal in 20% of myocardial ischemia
-diagnostic of MI in 65%
-but serial ecgs diagnostic in 80-90%

Describe ECG changes in MI seen with serial ECGs
1. ST elevation
2. Loss of QRS amplitude with T wave inversion
3. new Q wave
4. normalization of ST segment

Name 3 biomarkers used to evaluate acute coronary syndrome. Which is best
1. Creatine kinase (CK-MB)
2. myoglobin
3. Troponins
-best b/c
1. specific
2. stay elevated for up to a week

Define acute coronary reperfusion
-reperfusion in clinical myocardial ischemia
-if started within 4-6 hrs of AMI, will have a smaller infarct size, better LV fxn, and improved survival
-some benefit may occur after 6 hrs
1. heterogenity of infarct zone
2. collateral blood flow
3. beneficial effects of healing and remodeling

How do you decide reperfusion options for STEMI pts?
1. Assess time and risk
-time since symptom onset
-risk of STEMI
-risk of fibrinolysis
-time for transport to a skilled PCI lab
2. Select reperfusion tx
-if present in less than 3 hrs and there is no delay to an invasive strategy, than either thrombolytics or balloon is fine

Describe 3 guidelines for care of AMI
1. initial pt eval within 20 min of arrival to ER
2. Thrombolysis within 30 min
3. PTCA 60-90 min

When is fibrinolysis generally preferred to tx AMI?
1. Early presentation (< 3 hrs) -thrombolytics work better when given early 2. Invasive strategy (cath lab) is not an option 3. delay to invasive strategy
When is invasive (cath lab) generally preferred to tx AMI?
1. Skilled PCI lab available and door-balloon time 3 hrs of symptoms onset to clinical presentation 5. diagnosis of STEMI in doubt
Name 7 components of acute phase tx of acute coronary syndrome
-acute=within first 24 hrs
1. ASA
2. Clopidogrel
3. Heparin
4. GP IIb/IIIa inhibitors
5. Beta blockers
6. Nitrates
7. Cath lab

Name 6 long-term tx for acute coronary syndrome
=what the pt goes home on
1. ASA
2. Clopidogrel
3. Beta blockers
4. ACE Inhibitors
5. Statins
6. Risk factor + lifestyle changes

What's the difference between STEMI and Non-STEMI?
1. have symptoms of ischemia
2. show troponin elevation
3. NO ST elevation on ECG

True or false: being on a combination of ASA and heparin increases your risk of MI complications
-it dramatically decreases your risk
Name 2 drugs that reduce myocardial oxygen requirements
1. beta blockers
2. nitrates
-given in tx of AMI (beta blockers given acutely and long-term, nitrates given acutely

How do nitrates reduce myocardial oxygen requirements?
-relax vascular SM -> peripheral venous and arterial vasodilation -> reduced afterload -> reduced ventricular wall stress
How do beta blockers reduce myocardial oxygen requirements?
-inhibit beta adrenergic cardiac stimulation -> reduce contractility -> reduce ventricular wall stress
Why are beta blockers such an important post-MI tx?
1. reduce all-cause mortality
2. reduce risk of sudden death
3. reduce risk of nonfatal reinfarction
-high risk pts often less likely to be treated

Why are ACE Inhibitors important post-MI tx?
-partially prevent ventricular remodeling
Describe cardiogenic shock following an MI?
-7-20% of pts with MI
-most have sustained anterior infarction
-85% mortality
-usu due to infarct extension
-pathological findings include:
1. involvement of LAD
2. stenosis of greater than 75% of all 3 major coronary arteries
4. necrosis in at least 40% of LV

Describe the downward spiral of cardiogenic shock in AMI.
-ischemia causes cardiac dysfxn -> LV fails to pump -> decrease SV and CO
-hypotension from decreased CO along with tachycardia decrease myocardial perfusion -> ischemia exacerbated
-also getting increased diastolic pressure from LV failing to pump -> increased wall stress -> increased MVO2 -> worsens ischemia
-compensatory mechanism from decreased CO (peripheral vasoconstriction to maintain BP and fluid retention) only increase the workload on heart -> more dysfxn
-unless spiral interrupted -> death

Name 3 mechanical causes of cardiogenic shock
1. free wall rupture
2. interventricular septum rupture
3. papillary muscle rupture

Who is more likely to have a free-wall rupture post MI?
elderly hypertensive women without previous intervention
-free wall rupture causes pericardial tamponade
-death usu in minute
-most likely to occur in first week after MI
-early use of thrombolytic agents may reduce incidence

Name 2 clinical characteristics of an interventricular septum rupture
-mechanical cause of post-MI cardiogenic shock
1. heart failure
2. new holosystolic murmur
-diagnosed by Swan (step up in O2 saturation), and echo to visualize rupture
-needs to be tx by surgery

What type of MI most frequently causes rupture of the papillary muscle?
-inferior wall MI
-clinical features
1. pulmonary edema
2. holosystolic murmur
-diagnosis by swam (giant V waves) or echo
-urgent surgery indicated for instability

Define Marfan's syndrome
-inherited connective tissue disorder caused by defect in fibrillin
-autosomal dominant
-at high risk for aneurysms and aortic dissection
-floppy mitral valve
due to loss of fibrillin -> regurg
-long fingers
-spinal abnormalities
-pectus excavatum (depressed chest)
-ocular problems (subluxation of lens)

Define HTN
-systolic BP greater than 140 or diastolic BP greater than 90
-normal BP between 100/60 and 140/90
Who gets Libman Sacks endocarditis?
-people with lupus (SLE)
-vegetations develop on both sides of valve (leading to mitral valve stenosis)
-but vegetations do NOT embolize

Define malignant HTN
-very high BP with swelling of optic nerve behind the eye (papilledema)
-seen commonly in young African American men, women w/toxemia of pregnancy, people with kidney disease
-often preceded by chronic HTN
-HTN is risk for CNS hemorrhage
1. kidney failure
-blood vessels of kidneys susceptible to damage caused by high luminal pressure
2. pulmonary edema

Name some complications of HTN
1. Coronary heart disease
2. Cerebrovascular accidents (strokes,etc)
3. HTNive heart disease
-cardiac hypertrophy and heart failure
4. aortic dissection
5. renal failure

Name 3 types of cardiomyopathies
=weakening of heart muscle or change in heart muscle structure
-often associated w/inadequate pumping or other heart fxnal problems
-3 subtypes
1. dilated
-most common
-cardiomegaly + dilation of all 4 chambers
2. hypertrophic
-hypertrophy (LV>RV)
-asymmetrical hypertrophy of interventricular septum -> obstruction of LV outflow tract
-50% inherited (Autosomal dominant)
3. restrictive
-heart chambers unable to fill properly b/c of stiffness of heart

Name some causes of dilated cardiomyopathy
-most common type of cardiomyopathy (weakening of heart muscle or change in structure)
-cardiomegaly + dilation (looks like balloon on xray)
1. Alcohol abuse
2. Beriberi
3. coxsackie B virus myocarditis
4. chronic cocaine use
5. Chagas' disease
6. Doxorubicin toxicity
7. Peripartum cardiomyopathy

Name some causes of restrictive cardiomyopathy
=infiltrative cardiomyopathy
-heart chambers unable to fill properly b/c of stiffness of the heart
-heart usu normal size
1. sarcoidosis
2. amyloidosis
3. postradiation fibrosis
4. hemochromatosis

Define sarcoidosis
=disease of unknown cause with multi-system inflammation
-usu affects lungs, then eyes and skin
-non-caseating granulomas with Schauman bodies and asteroid bodies in lungs
-granulomas can be in other tissues
-80% present with hilar and mediastinal lymphadenopathy
-can be acute, subacute, or chronic
-can affect almost any organ in body
-tends to affect African Americans and Caucasians, females > males
-onset usu between 20-40 yrs
-prognosis is variable

Describe the clinical presentation of sarcoidosis
-hypersenstivity rxn
-hilar adenopathy
-respiratory sx common b/c lungs often affect (dyspnea, cough, cehest pain)

Dx usu based on clinical sx
-tissue biopsy with noncaseating granulomas distinguishes from TB

Define Amyloidosis
=disorder characterized by extracellular deposits of misfolded proteins that aggregate to form insoluble fibrils
-can be localized of systemic
-associated with a number of inherited and inflammatory conditions
1. monoclonal B cell proli
2. chronic inflammatory diseases (RA)
3. Alzheimer's disease
4. Familial conditions
5. dialysis
-amyloid deposits cause tissue injury and impair normal fxn by causing pressure on cells and tissues
-no inflammatory response caused by deposits

Name 2 complications of syphilitc heart disease
1. Aneurysm of ascending aorta
2. aortic arch and aortic valve incompetence

-tertiary syphilis disrupts vasa vasorum of aorta -> dilation of aorta and valve ring
-often affects aortic root and calcification of ascending arch

Define Eisenmenger's syndrome
-uncorrected VSD, ASD, or PDA leads to progressive pulmonary HTN
-as pulmonary resistance increases, shunt reverses from L->R to R->L
-late cyanosis

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