cardio review

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cardiac output(CO) formula: rate of O2 consumption/
(arterial O2 content - venous)
mean arterial pressure (MAP) formula: MAP = CO - TPR

MAP also = 1/3 systolic + 2/3 diastolic
stroke volume (SV) formula: SV = CO/ HR

SV also = EDV-ESV
cardiac output variables: SV CAP
->SV is affected by Contractility, Afterload and Preload
contractility/SV increases due to: increased catecholamines (high activity of Ca pump in SR)
increased [Ca]i
decreased [Na]e
digitalis admin (increases intracellular Na which leads to increased [Ca]i)
contractility/SV decreases due to: B1 blockers
heart failure
acidosis
hypoxia/hypercapnea
Ca channel blockers
force of contraction [starling curve: is proportional to the initial length of cardiac muscle fiber [PRELOAD]
ejection fraction (EF) formula: EF = SV/EDV = (EDV-ESV)/EDV

EF is an index of ventricular contractility
EF should be >/= 55%
resistance/pressure/flow formula: change in P = Q x R

Q = flow, R = resistance

R= 8 x viscosity x length/
pi radius ^4

*viscostity increased in
polycythemia, high protein and hereditary spherocytosis
JVP waves: a: atrial contraction
c: RV contraction(when tricuspid bulges back into RA)
v: increased atrial pressure due to atrial filling against closed tricuspid valve
cardiac myocyte vs skeletal myocytes: cardiac muscle:
-> AP has a plateau
-> nodal cells SPONTANEOUSLY depolarize [automaticity]
-> myocytes are electrically coupled via gap jxns
**contraction is due to extracellular Ca
AP in atrial/ventricular myocytes and purkinje fibers: phase O: rapid upstroke (Na)
1: intial repol (inactivation of Na channels)
2: plateau (Ca influx balances slowly increasing K efflux)
3: rapid repol (massive K efflux due to slow K channels and closure of Ca channels)
4: resting potential (K and Ca leak currents + Na/K ATPase and Na/Ca exchanger)
AP in pacemaker cells: phase 0: upstroke due to Ca channels... NO fast Na channels
2: no plateau (pointy)
4: slow diastolic depol (I-f accounts for automaticity of SA/AV nodes)

**slope of phase 4 in SA node determines heart rate**
wolf parkinson white syndrome: accessory conduction pathway from atria to ventricle
bypasses the AV node
**see a DELTA WAVE before QRS complex
can lead to SVTs
1st degree AV block: PR interval prolonged (>200 msec)

is asymptomatic
2nd degree AV block: mobitz type 1:
->progressive lengthening of PR until a beat is dropped. asymptomatic
mobitz type 2:
->dropped beats not proceeded by change in PR length. is symptomatic: 2 P waves to 1 QRS
3rd degree AV block [complete heart block]: atria and ventricles beat independantly.
P waves have no relation to QRS.
atrial rate > ventricular
*Tx = pacemaker

rate of ventricular beat: 30-45
stroke volume is increased (high pulse pressure)
O2 demand in heart: high O2 demand drives increased blood flow, NOT increased extraction of O2
fluid pressure [hydrostatic] starling forces: Pc = capillary fluid pressure
-> fluid out of capillary

Pi = interstitial fluid pressure
-> fluid into capillary
colloid pressure starling forces: pi-c: plasma colloid osmotic p
-> moves fluid into capillary

pi-i: interstitial colloid p
-> moves fluid out of capillary
right to left shunts: =early cyanosis (blue babies)

Teratology of Fallot
Transposition of great arteries
Truncus arteriosus
left to right shunts: VSD (#1 congenital anomaly)
ASD (loud S1, fixed split S2)
PDA (close w/indomethacin)
teratology of Fallot: PROVe
Pulmonary a. stenosis (Px feature)
RVH
Overriding aorta (overrides VSD)
VSD

*pts suffer 'cyanotic spells'
caused by anteriosuperior displacement of aorta
transposition of great vessels: aorta leavse RV and pulm trunk leaves LV (posterior)
not compatible with life unless shunt is present to mix systemic and pulm circulations (VSD, pDA or pFO)
coarctation of aorta: infants: aortic stenosis proximal to insertion of DA

adults: distal to DA.
-> notching of ribs, HTN in upper extremities, weak pulses in lower extremities
-> 3:1 male to female ratio

**ass'd with Turner Syndrome
patent DA: in fetal pd, shunt R to L (bypasses pulmonary circulation)

birth = lung resistance drops and shut becomes L to R which causes RVH and R heart failure

*continuous machine like murmur

patency = low O2 tension, PGE
congenital cardiac defects: 22q11: truncus arteriosus, teratology of fallot
Ts21: ASD or VSD
rubella: septal defects, pDA
turner's: coarctation of aorta
marfan's: aortic insufficiency
mom w/DM: transposition of great vessels
monckeburg arteriosclerosis: calcification of arteries, especially radial or ulnar.

usually benign
arteriolosclerosis: hyaline thickening of small arteries due to essential hypertension
ONION SKINNING in malignant HTN
cardiovascular system is derived from which cell layer?: mesoderm

paired endocardial heart tubes from in cephalic region
primitive embryonic heard dilates into five areas (starting at weeks 5-8):: from cranial to caudal
-truncus arteriosus: proximal aorta and proximal pulm artery
-bulbus cordis: smooth parts of right ventricle and LV
-primitive ventricle: RV, LV
-primitive atrium: RA and LA
-sinus venosus (R and L): smooth part of RA, coronary sinus, oblique vein
pathophysiology of teratology of Fallot: aberrant development of aortico-pulmonary septum [which should normally divide aorta and pulmonary trunk]
development of aortic arches: 6 paired aortic arches at 1st
->arch 3: common carotids
->4: aorta and proximal subclavian artery
->6: DA and pulmonary trunk
developent of veins: vitelline veins: ductus venosus carries O2 blood from placenta to fetus
L umbilical vein: ligamentum teres hepatis
R umbilical vein: regresses
paradoxical emboli: originate in the venous circulation and pass through pFO or ASD to produce symptoms on arterial side
situs inversus: all body's organs are transposed

associated with Kartagener's syndrome [immotile cilia]
Eisenmerger's syndrome: change of L to R to R to L shunt secondary to increasing pulmonary HTN

often result of chronic response to VSD
acquired arteriovenous fistula: decreased TPR leads to increased CO (increased HR and SV)

diastolic bp falls b/c blood rapidly exits arterial system

but mean bp is relatively normal b/c regulating mechanisms are normal
change in pulse pressure with arteriosclerosis: increases (b/c arteries have hardened... need to push harder [higher systolic bp] to get the blood out)
type of endocarditis in pts with SLE: Libman-Sacks
->small granular vegetations consisting of fibrin develop on mitral and aortic valves
->leads to aortic stenosis
premortum thrombus: look for Lines of Zahn (composed of platelets)
->b/c has formed over a period of time

often due to atrial fibrillation
pathology of repeated episodes of stable angina: gradual loss of myocytes
->small patches of fibrosis and vacuolization
->usually in subendocardial area (poorly perfused)
thoracic outlet syndrome with the presence of a cervical rib: subclavian artery compressed btwn scalenus anterior and the rib
=pain and tingling on affected side
effect of severe anemia: wide pulse pressure
->resting CO is increased due to increased SV and HR

also see tachycardia
causes of decreased pulse pressure: aortic valve obstruction
cardiac tamponade
heart failure
mitral valve obstruction
effect of malignant hypertension on arteriole structure: arteriolar rarefaction
=dissolution and loss of arterioles
-due to long term over-perfusion of tissues

also, arteriolar wall to lumen ratio INCREASES (thicker wall)
syphilitic aneurysm: massive dilation of aortic root with absence of atherosclerosis

histo = plasma cell lesion in vasa vasorum that supply the aorta [eventually obliterate it and cause aneurysm]
cyanosis: only from R-L shunt
signs of cardiac tamponade: decreased arterial pressure
small, quiet heart
hypotension, tachypnea, tachycardia, increased JVP
*pulsus paradoxus
signs of pericarditis: sharp, knife like pain
->usually related to breathing
diffuse STEs and upright T waves
pericardial rub MAY be present
location of femoral vein on CT: medial to femoral artery
('venous toward the penis')
typical bp of someone with aortic regurgitation: wide pulse pressure (160/80)

systemic pressure drops during diastole b/c blood flows back thru aorta into LV
most common cause of sudden cardiac death (SCD): ischemic heart disease

*in younger patients, the non-atherosclerotic causes are more common
->hypertrophy, MVP, myocarditis, dilated cardiomyopathy, etc
Kawasaki disease: 'mucocutaneous lymph node syndrome'
leading cause of acquired heart disease in kids in the US
all sizes of arteries affected
*risk of coronary artery aneurysm
positive result in starling equation: =net fluid leaving capillaries

(Pc-Pi) - (pi c - pi i)
Dressler's syndrome: autoimmune phenomenon several weeks post-MI

->fibrinous pericarditis
dilated cardiomopathy: 90% of all cardiomyopathies
Alcohol, Beriberi, Coxsackie B, Cocaine, Chagas', Doxorubicin toxicity [chemo], peripartum, hemochromatosis
-> SYSTOLIC dysfunction
hypertrophic cardiomyopathy: often asymmetric, involves intraventricular septum
50% familial (AD)
sudden death in young athletes
loud S4**, strong apical impulse, systolic murmur
treat with B-blockers
-> DIASTOLIC dysfunction
restrictive/obliterative cardiomyopathy: sarcoidosis, amyloidosis, postradiation, Loffler's
MR: holosystolic
high pitched, 'blowing'
loudest at apex
AS: crescendo-decrescendo systolic, following an ejection click
LV >> aortic pressure in systole
radiates to carotids, apex
*pulsus parvus et tardus*
VSD: holosystolic
MVP: late systolic murmur
midsystolic click
#1 valvular lesion
AR: high pitched blowing diastolic
associated with wide pulse pressure
MS: delayed rumbling late diastolic
follows opening snap
LA >> LV during diastole (takes a lot to open the stenotic MV)
**tricuspid stenosis murmur gets louder with INSPIRATION** (b/c more blood to lungs)
pDA murmur: continuous, machine like

throughout systole and diastole

loudest at S2 (aortic/pulmonic close)
'heart failure cells': hemosiderin laded macrophages
cause of orthopnea in CHF: increased venous return in supine position

exacerbates pulmonary vascular congestion (= SOB)
virchow's triad: stasis
hypercoagulability
endothelial damage

leads to DVTs
features of cardiac tamponade: compression of heart by fluid leads to low CO
equilibration of pressures in all 4 chambers**
hypotension, high JVP, pulsus paradoxus
Aschoff bodies: =granulomas with giant cells

found in rheumatic heart disease

also see Anitschkow's cells (activated histiocytes)
hydralazine: increases cGMP: sm musc relaxation
vasodilates arterioles > veins
REDUCED AFTERLOAD
SEs: tachycardia, fluid retention, lupus like syndrome
CCBs: block L-type Ca channels
->reduced cardiac contractility
nifedipine better vascular sm muscle
verapamil better heart muscle
SEs: cardiac depression, edema, flushing, constipation
nitroglycerine, isosoribde dinitrate: release NO in smooth muscle: increased cGMP
veins >> arteries
REDUCED PRELOAD
for angina, pulmonary edema
digoxin: inhibits Na/K/ATPase
->increased Na-i leads to increased Ca-i (b/c Na won't come in using Na/Ca antiport)
EKG changes
->low QT, scooping of ST, T wave inversion*
used for CHF, a-fib (low AV)
SEs
-> n/v, van gogh vision, arrhymthmias
Digoxin drug interaction: increased [ ] with renal failure
hypokaleima potentiates effects (low K = more K out, Na in)
quinidine decreases clearance

*treat Dig toxicity with K+ admin (or Mg+)
beta blockers with intrinsic sympathomimetic activity: acebutolol and pindolol

not recommended for pts with angina (can exacerbate)
CCBs to avoid in those with CHF: verapamil
->1st gen CCB that has strong negative inotropic effect
dilitiazem
->mild to mod negative inotrope

*amlodipine and felodipine are used in CHF pts (can actually increase contractility)
treatment of WPW: don't use an agent that slows AV node conduction (will increase propensity to go to bypass tract)

DO use ibutilide (K channel blocker)
->disrupts reentry circuits and increases refractory period of the bypass tract
acute treatment of atrial fibrillation: dilitiazem (IV)
-inhibits Ca into vascular sm muscle and myocardium
-AV node blocker

*amiodarine takes 1-3 weeks to work properly
most common cardiac anomaly in Ts21: endocardial cushion defect (??)

or maybe ASD/VSD

20% have congenital cardiac abnormalities
mean linear velocity of a RBC is lowest in what vessels?: capillaries (have the largest cross-sectional area)

velocity from highest to lowest:
aorta > vena cavae > large veins > small arteries > arterioles > small veins > venules > capillaries
Churg-Strauss syndrome: aka allergic granulomatosis and angiitis
variant of PAN--> ass'd with asthma and eosinophilia
vascular lesions, granulomas, GI vasculitis
polyarteritis nodosa (PAN): affects small/med arteries
->esp GI tract and kidneys
fibrinoid necrosis of vessels w/ polys, eos, monos
often young adult males
Tx: steroids, cyclophosphamide
severe anemia's affects on vessels: hypoxia causes dilation of small arterioles and arteries
also: low blood viscosity, decreased PVR, low splanchnic blood flow
most common primary cardiac tumor in children: rhabdomyoma

composed of cells that resemble skeletal muscle

**common in kids with tuberous sclerosis
mechanism of cocaine-induced hypertension: blocks re-uptake of NE
arterioles account for ___% of total peripheral resistance: 50% (greatest fall in bp occurs as blood goes thru arterioles)

-highest ratio of wall to cross-sectional area to lumen cross-sectional area
leukocytoclastic angiitis: =microscopic PAN
smaller affected vessels
vasculitis w/hemorrhage to skin (palpable purpura)
many fragmented neutrophils
*penicillin is a common trigger
vascular structures that contain the greatest % of total blood volume: venules and veins (64%)
week of gestation when heart forms: 4th week

(heart forms and starts beating almost immediately)

6th week = heart is fully formed (so difficult to prevent congenital malformations b/c heart forms so early)
alpha1 agonists act on...: smooth muscle cells in media of arterioles
leads to increase in intracellular Ca [smooth muscle contraction]
ASD found in Down's syndrome: ostium primum (most common type in general is the ostium secundum)
can also be associated with tricuspid and mitral valve abnormalities

*L-R shunts with late cyanosis (when reversal occurs)
mean systemic filling pressure (MSFP): pressure that exists when heart has been stopped and blood has been redistribuited equally
as MSFP increases, there is more venous return to heart
**venous system is important blood reservoir (normal fxn can be resored w/20% of blood loss)
when O2 consumption of the heart increases, this builds up in heart muscle: adenosine

(ATP degrades to adenosine)

adenosine then dilates vessels allowing increased coronary blood flow
graft vascular disease (aka graft arteriosclerosis): develops years after transplant
intimal thickening of coronary arteries w/out atheroma formation or inflammation
leads to progressive stenosis
chest pain DOES NOT accompany the ischemia--> sudden death
**can't be prevented with current immunosuppresive Tx
this decreases in old age and causes widened pulse pressure: arterial compliance (usually due to hardening by arteriosclerosis)
cardiac complications of fragile X syndrome: mitral valve prolapse and aortic root dilatation
[occur late in adolescence or adulthood]
___% of those with ischemic heart disease will present with death: 25%
Beta-1 selective beta blockers: A BEAM

atenolol, betaxolol, esmolol, acebutalol, metroprolol

non-selective: labetalol (also adds alpha 1), timolol, nadolol
individual cardiac muscles are joined together at: intercalated disks (that contain gap jxns)
fetal umbilical arteries arise from: the fetal iliac arteries (supply unoxygenated blood to the placenta)

umbilical vein takes newly oxygenated blood from placenta to fetal liver then to IVC via the ductus venosus
fibrinous and serofibrionous pericarditis: = Dresseler's syndrome (when following an acute MI)
why is atenolol contra-indicated in DM pts?: b/c it can block the 'warning signs' of hypoglycemia
what is a cystic hygroma??: lymphatic malformations resembling hemangiomas
-->a feature of Turner syndrome that contributes to the 'webbed neck'
(and remember, Turner is associated with coarctation of the aorta)
side effect of metroprolol: dyslipidemia
ovary drainage: R ovary = ovarian vein to IVC

L ovary = ovarian vein to RENAL VEIN to IVC
best drug for initial treatment of hypertrophic cardiomyopathy: beta blocker (metoprolol)

Sx: sustained apical impulse, loud S4, systolic ejection murmur

echo = systolic anterior motion of mitral valve, assymetic LVH, early closing of aortic valve
appearance of amyloidosis: waxy texture of affected organs

histo = positive Congo red staining
TPR: (MAP-RAP) / CO

pressure = flow x resistance

(P = Q x R)
removing an organ will ___ the TPR: INCREASE

(organs are in parallel.. and adding parallel resistances = lower total)
fully compensated aortic coarctation: blood flow normal in upper and lower body
but there is increased arterial pressure in upper body
->lower vascular resistance in lower body (b/c resistance = pressure / flow)
possible finding at autopsy of a SIDS baby: RVH
endocardial fibroelastosis: probably related to intrauterine viral infection (mumps)

thickened endocardium w/fibrous and elastic tissue

LV is most commonly involved

other findings = mural thrombi, flattened trabeculae and stenosed valves

*infantile and adolescent forms
artery commonly damaged in knee dislocations: popliteal artery
-divides into anterior tibial, posterior tibial and peroneal
-emerges from superficial femoral artery
classical findings in ASD: prominent RV impulse
systolic ejection murmur heard in pulmonic area
fixed split S2
*due to abnormal L-R shunt [creates volume overload on R side]
massive PE affects which part of the heart first?: RV
[a saddle PE causes acute cor pulmonale with abrupt RV dilation]

*acute cor pulmonale is a surgical emergency
cardiac tamponade causes build up of fluid in which space?: between the epicardium [visceral pericardium] and parietal pericardium

(aka the pericardial space)
PO agent similar to lidocaine: mexiletine

(class IB anti-arrhythmic for treatment of VT)
Na channel blocker and shortens AP duration

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