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First Aid Cardiovascular


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SA and AV nodes are supplied by...
Right Coronary Artery (RCA)
Inferior portion of the LV is most commonly supplied by...
RCA via the Patent Ductus Artery (= right dominant)
coronary artery occlusion most commonly occurs where?
Left anterior descending artery
The Left Anterior Desc. Artery supplies what?
anterior interventricular septum
Compare/ Contrast Red and Pale Infarcts
Red (hemorrhagic) infarcts occur in loose tissues with collateral blood supplies, such as lungs, intestine, or following perfusion; REd = REperfusion

Pale infarcts occurs in solid tissues with single blood suppy such as brain, heart, kidney, and spleen
What are the characteristics of Dilated (congestive) Cardiomypathy?
most common cardiomyopathy (90% cases)

etiologies include Alcohol abuse, Beriberi, Coxsackie disease, Cocaine use, Chaga's disease, Doxorubicin toxicity, peripartum cardiomyopathy and hemochromatosis

the heart dilates and looks like a baloon in chest x ray

systolic dysfxn ensues
During what part of the Cardiac Cycle to coronary arteries fill?
Describe Hypertrophic cardiomyopathy
hypertrophy often asymmetric and involving the intraventricular septum

50% of cases are familial and are inherited as an autosomal dominant trait

cause of sudden death in young athletes

Walls of LV are thickened and chamber becomes banana shaped on x-ray; diastolic dysfxn ensues
What is Restrictive/ Obliterative Cardiomyopathy?
A cardiomyopathy caused by sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis, and endomyocardial fibrosis
Outline the pathological mechanisms of the following CHF abnormalities...

1. Dsypnea on exertion

2. Cardiac Dilation

3. Pulmonary Edema, paroxysmal nocturnal dyspnea
1. Failure of the LV output to Increase during exercise

2. greater ventricular end- diastolic volume

3. LV failure leading to increased pulmonary venous pressure which casues pulmonary distention and transudation of fluid.
Hemosiderin- laden macrophages ("heart failure cells") are visible
What is the most posterior part of the heart and why is it clinically important?
the left atrium, enlargement of the LA can cause dysphagia
Outline the pathological mechanisms of the following CHF abnormalities...

1. orthopnea (shortness of breath when supine)

2. hepatomegaly (nutmeg liver)

3. Ankle, sacral edema
1. pooling of blood in the lungs in supine position adds volume to congested pulmonary vascular system; increased venous return not put out by LV

2. increased central venous pressure leads to increased resistance to portal flow; rarely, leads to "cardiac cirrhosis"

3. RV failur causes an increase in venous pressure that leads to fluid transudation
What is cardiac tamponade?
compression of the heart by fluid in the pericardium leading to a decreased CO

equilibration of pressures in all 4 chambers

Pulsus paradoxus; ECG shows electrical alternans (beat to beat alterations in the QRS complex height)
Describe the cause and course of acute bacterial endocarditis?
S. aureus(high virulence)

large vegetations appear on the valves

rapid onset
Describe the course and cause of Subacute bacterial endocarditis?
Viridans Streptococcus (low virulence)

smaller vegetations appear on congenitally abnormal or diseased valves

may be a sequelae of dental procedures

more insiduous onset
How does Bacterial Endocarditis Present?
Bacteria FROM JANE

Roth's Spots (round white spots on retina surrouded by hemmorhage)
Osler's nodes (tender raised lesions on fingers/toes)
Janeway lesions (small erythromatous lesions on palms or soles)
Nail Bed Hemorrhage
What part of the heart does Bacterial Endocarditis mostly affect?

How is it diagnosed?
mitral valve is most frequently involved
tricuspid valve endocarditis is associated with IV drug use

multiple blood cultures are necessary for diagnosis (continuous bacteria)
What are some complications of Bacterial Endocarditis?

Is Endocarditis only due to bacterial infection?
complications include chordae rupture, gloeruloneprhitis, suppurative pericarditis, emboli

Endocarditis may also be nonbacterial secondary to metastasis or renal failure (marantic/ thrombotic endocarditis)
What is Libman Sacks Endocarditis?
vegetations are found on both sides of valve (--> mitral valve stenosis) but do not embolize

seen in lupus

SLE causes LSE
What is Rheumatic Fever? What does it cause?
a consequence of pharyngeal infection with group A B-hemolytic streoptococci

late sequelae include rheumatic Heart disease which affects heart valves -mitral>aortic>>tricuspid (high pressure valves are affected the most)

immune mediated, not direct effect of bacteria
RHD is associated with what physiological findings?
Aschoff bodies, migratory polyarthritis, erythema marginatum, and elevated ASO titers
What are signs and symptoms of Rheumatic fever/ RHD?

Erythema marginatum
Valvular damage
ESR increased
Red hot joints (polyarthritis)
Subcutaneous nodules
St. Vitus' dance (Chorea)
What is pericarditis and why is it clinically important?
inflammation of the mesothelial sac which encloses the heart

clinically important b/c:
1. it is a cause of chest pain
2. the associated exudates may produce cardiac tamponade
3. organized effusions may cause chronic impairment of diastolic filling (consrtictive pericarditis - firbous obliteration of the pericardial space)
What characterizes Serous pericarditis?
clear fluid with low proetein content and lttle inflammation

caused by SLE, rheumatoid arthritis, viral infection, uremia

usually heals w/o residuum
Describe Fibrinous pericarditis
fluid w/ higher protein content and more inflammation

associated with uremia, some viral infections, MI, and rheumatic fever

heals with fibrous adhesions
What are the causes and findings associated with Hemorrahgic pericarditis?
caused by TB, malignancy (melanoma)

blood tinged exudate, pericardial pain, friction rub, ECG changes(diffuse ST elevations in all leads),pulsus paradoxus, distant heart sounds

can resolve w/o scarring or lead to chronic adhesive or chronic constrictive pericarditis
Describe the primary endocardial diseases.
1. Endocardail fibroelastosis - diffuse thickening of the endocardium only by proliferation of elastic an collagen fibers; occurs in first 2 yrs of life and is fatal; us. associated with congenital heart defects

2. Endomyocardial fibrosis (Davie's disease) - thickening of endocardium and myocardium by collagenous scar; affect either or both ventricles; identical to Loefflers endocarditis

3. Carcinoid Heart Disease - R sided endocardial proliferation and fibrosis -> tricuspid insufficiency, stenosis and/or pulmonic stenosis
What is the most common primary cardiac tumors in adults and children?
Myxomas- 90% in adults in the atria (mostly LA); usually described as a "ball valve" obstruction in the LA

Rhabdomyomas - associated with tuberous sclerosis in children

metastasis is the most comon heart tumor
What is syphilitic heart disease?
occurs when teritary syphilis disrupts the vaso vasorum of the aorta leading to dilation of the aorta and valve ring

often affects the aortic root and ascending aorta

associated with tree bark appearance of the aorta
What are major complications of Syphilitic Heart disease?
can result in aneurysm of the ascending aorta or aortic arch and aortic valve imcompetence
What is Breuger's disease?
also known as thromboangitis obliterans

an idiopathic, segmental, thrombosing vasculitis of intermediate and small peripheral vessels and veins

usually seen in heavy smokers
What pathological findings are associated with Buerger's Disease?

How is it treated?
intermittent claudication, superficial nodular phlebitis, cold sensitivity (Raynauds phenomenon), severe pain in affected part

may lead to gangrene

treated by cessation of smoking
What is Takayasu's arteritis and what findings are associated with it?
the "pulseless disease"

due to thickening of the aorta and/or proximal great vessels; primarily affects young asian females

associated with an elevated ESR
How does Takayasu's arteritis present?
"FAN MY SKIN On Wednesday"

Night Sweats
SKIN nodules
Occular disturbances
Weak pulses in upper extremeties (esp ulnar and radial pulse)
What is Temporal (Giant Cell) arteritis?
the most common vasculitis that affects medium and small arteries, usually branches of the carotid

half of patients have systemic involvement and polymylagia rhuematica (proximal muscle pain, periarticular pain)

usually affects elderly females and responds well to steroids
How does Temporal (Giant Cell) arteritis present and what findings are associated with it?
unilateral headache, jaw claudication, impaired vision (due to occlusion of the opthalamic artery, can lead to blindness)

associated with elevated ESR

TEMporal = signs near the TEMles
What is Kawasaki disease?
an acute, self limiting disease of infants/kids

acute necrotizing vasculitis of small/ medium vessels

P/W fever, congested conjuctiva, changes in lips/oral mucosa, lymphadenitis

may develop coronary aneurysms
Breifly describe each of the following ANCA positive vasculitides...

1. Microscopic polyangiitis

2. Primary pauci-immune crescentic glomeulonephritis

3. Churg-Strauss syndrome
1. similar to Wegener's but lacks granulomas; P- or C-ANCA

2. Vasculitis limited to kidney

3. granulomatous vasculitis w/ eosinophilia; involves lung, heart, skin, kidneys, nerves; often seen i atopic patients
Describe Wegener's granulomatosis and the findings associated with it.
characterized by focal necrotizing vasculitis and necrotizing granulomas in the lung and upper airway and by necrotizing glomerulonephritis

C-ANCA is a strong marker of the disease

chest x-ray may reveal large nodular densities

hematuria and red cell casts
How does Wegener's granulomatosis present and how is it treated?
perforation of the nasal septum, chronis sunusitis, otitis media, mastoditis, cough, dyspnea, hemoptysis, hematuria

treated with cyclophosphamide & corticosteroids
Describe Polyarteritis nodosa and the findings associat with it.
characterized by necrotizing immune complex inflammation of medium-sized muscular arteries, typically involving renal and visceral vessels; lesions are of different ages

Hep B seropositivity in 30% of patients
multiple aneurysms and constrictions on arteriograms
NOT assocaited with ANCA
How does Polyarteritis nodosa present and how is it treated?
presents with fever, weight loss, malaise, abdominal pain, melena, headache, mylagia, hypertension, neurologic dysfunciton, cutaneuous eruptions

treated with corticosteroids and cyclophosphamide
What the three Congenital Heart Defects cause RIGHT to LEFT shunt?
1. Tetralogy of Fallot (most common cause of early cyanosis)

2. Transposition of Great Vessels

3. Truncus arteriosus

the three T's
early cyanosis --> "blue babies"
children may squat to increase venous return
What are three congenital Heart defects that lead to LEFT to RIGHT shunts?
1. VSD - most common congenital cardiac anomoly

2. ASD - loud S1; wide, fixed split S2

3. Patent Ductus Arteriosus - close with Indomethacin

Late cyanosis --> blue kids INC. pulmonary resistancedue to arteriolar thickening.
--> progressive pulomonary hypertension; R-->L shunt (Eisemenger's)
Riddle me this: What is Eisenmenger's Syndrome?
Uncerrected VSD, ASD, or PDA leads to progressive pulmonary hypertension.

As pulmonary resistance increases, the shunt changes from L-->R, to R-->L, which causes late cyanosis (clubbing and polycythemia)
What is Tetralogy of Fallot?
1.Prove stenosis
2.Right Ventricular Hypertrophy
3.Overriding aorta (overrides the VSD)
4. VSD

This leads to early cyanosis from a R-->L shunt across the VSD. On X-ray, boot shaped heart due to RV hypertrophy. Patients suffer "cyanotic spells."
The cause of Tetralogy of Fallot is anterosuperior displacement of the infundibular septum.
What causes Transposition of the Great Vessels?
Failure of the aorticopulmonary septum to spiral.
Describe what happens when Great Vessels are Transposed.
Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior) --> separation of systemic and pulmonary circulations
Is Transposition of the Great Vessels compatible with life?
Not compatible with life unless a shunt is present to allow adequte mixing of blood (e.g., VSD,PDA,or patent foramen ovale)

Without surgical correction, most infants die within the first months of life
Describe Coarction of the Aorta?
relatively common malformation characterized by constriciton of aorta proximal (preductal) or distal (postductal) to ductus arteiosus

Requires development of extensive collateral circulation to deliver blood into descending aorta

M:F ratio 3:1
check femoral pulses on physical exam
Compare and contrast findings in Adult and Infantile Coarction of the Aorta.
Infantile type - aortic stenosis proximal to insertion of the ductus arteriosus (pre-ductal)
INfantile is IN close to the heart

Adult Type - stenosis is distal to ductus arteriosus (postductal.) results in increased BP in upper extremities, and weak pulses in the lower extremities, with increased risk of cerebrovascular accident.
ADult: Distal to Ductus
What causes a Patent Ductus Arteriosus?
Failure of the ductus arteriosus to close after birth.
Describe the pathology of a PAtent Ductus Arteriosus?
In the fetal period, shunt is R-->L(normal).
In neonatal Oeriod, lung resistance decreases and shunt becomes L-->R (blood flow from aorta to Pulm Artery) with subsequent RV hypertrophy and failure.

Associated with a machine like murmur
How is a Patent Ductus maintained physiologically?
Patency is maintained by PGE synthesis and low O2 pressure
How is a Patent Ductus maintained pharmacologically? How is it closed?
PGE is used to keep PDA open, which may be necessary to sustain life in such conditions as Transposition of the Great Vessels.

Indomethacin is used to close the PDA.
What cardiac defects are associated with 22q11 syndromes?
Truncus arteriosus
tetralogy of Fallot
What Cardiac Defects are assocaited with Down Syndrome?
What Cardiac defects are associated with Down Syndrome and Congenital Rubella?
DS - Septal Defects, PDA

CR - Coarction of the Aorta
WHat cardiac defects are associated with offspring of diabetic mothers?
Transposition of the great Vessels
P wave of ECG represents...
atrial depolarization
What does the PR interval represent?
conduction delay through the AV node
What factors influence the lenght of the PR interval?
conduction velocity thru the AV node (e.g. heart block) heart rate
QRS complex respresents...
ventricular depolarization
Normal length of the QRS segment?
<120 msec
What occurs during the QT interval?
mechanical contraction of the ventricles
T wave represents...
ventricular repolarization
What is the ST segment?
period when the ventricles are depolarized it is isoelectric
On the ECG, atrial repolarization is masked by what?
QRS complex
A U wave on an ECG is caused by what?
What does An ECG tracing show in Atrial Fibrillation?
Chaotic and erratic baseline with no discrete P waves in between irregularly spaced QRS complexes
Atrial Flutter shows what on ECG?
a rapid succession of identical, back to back atrial depolarization waves. The identical appearance accounts for the "sawtooth" appearance of the flutter waves
What are the ECG tracings of 1st Degree Heart Block?
The PR interval is prolonged (> 200 msec). 1st Degree Heart Block is Asymptomatic
ECG tracings of 2nd degree heart block, Mobitz type I, show what?
Progressive lengthening of the PR Interval until a beat is dropped (a P wave not followed by a QRS complex) Usually asymptomatic
2nd degree heart block, Mobitz type II, shows what on ECG?
dropped beats that are not preceded by a change in the length of the PR interval (compared to Type I) These abrupt, nonconducted P waves result in a pathologic condition. Often found as 2:1 block, where there a 2 P waves to QRS response. May progress to 3rd- degree block
3rd degree/ Complete Heart block ECG tracings show what?
The atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P Waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate. Usually treat with a pacemaker
ECG tracings of Ventricular Fibrillation show?
a completely erratic rhythm with no identifiable waves. Fatal arrythmia without immediate defibrillation.
What is Wolff-Parkinson-White syndrome?
Accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing AV node. As a result, venticles begin to partially depolarize earlier, giving rise to characteristic delta wave on ECG. May result in reentry current leading to supraventricular tachycardia.
Phase 0 of the Cardiac Action potential?
rapid upstroke caused by transient increase in Na conductance --> Na+ channels open
What occurs during Phase 1 of the Ventricular Axn Potential?
Initial repolarization - cuased by outward current Inactivation of Na+ Channels, decrease in Na+ conductance Voltage Gated K+ channels begin to open
Phase 2 of Ventricular AP?
Plateau: inward currents apporx = outward currants Ca++ influx thru voltage gated channles balance K+ efflux Ca++ influx triggers another Ca++ release from sarcoplasmic reticulum and myocyte contraction
Phase 3 of Ventricular AP?
Rapid Repolarization massive K+ efflux due to openings of voltage gated slow K+ channels and closure of voltage gated Ca++ channels
Phase 4 Ventricular AP?
resting potential high K+ perm thru K+ channels, membrane potential approaches K equilibirium
Where does the Pacemaker action potential occur?
in the SA and AV nodes
Describe Phase 0 of the pacemaker action potential.
Upstroke opening of voltage gated Ca++ channels. These cells lack fast voltage gated Na+ channels. results in a slow conduction velocity that is used by the AV node to prolong transmissionfrom the atria to the ventricles
Phase 1 and 2 of the pacemaker AP
dont exist...gotcha!!
Phase 3 of the Pacemaker AP
Replorization increase in K+ conductance --> outward K+ current
Describe Phase 4 of the Pacemaker AP
Slow Diastolic Depolarization membrane potential spontaneously depolarizes as Na+ conductance INCrease Accounts for automaticity of SA and AV nodes. THe slope of phase 4 in the SA node determines heart rate. ACh DECreases and Catecholamines INCrease the rate of diastolic depolarization, decreasing or increasing heart rate, respectively.
What are the effects of PsNS activity on the heart?
Negative Chronotropic Effect - DEcreases heart rate by decreasing rate of Phase 4 depolarization Neg. dromotropic efx - DEcreases condxn velocity thru AV node, increases the PR interval Negative ionotropic effect on the ATRIA ONLY
Effects of SNS activity on the Heart?
Positve chronotropic efx - increases heart rate Positive Dromotropic efx - increases condxn velocity thru the AV node, decreases PR interval Positive Ionotropy Constriction of SKIN and SPLANCHNIC bv's relaxation of Skeletal m. bv
The PsNS acts by what neurotransimitter and what types of receptors in the Cardiovascular system?
Acetylcholine, which acts at muscarinic receptors PsNS innervates the SA, AV nodes and atria only
SNS acts by what neurotransmitter and receptor in the heart and CV system?
Norepinephrine acts at B1 receptor in the heart a1 receptors in vascular SM B2 in Skeletal bvs

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