Cardio Physiology

eesohbel's version from 2015-08-02 19:08

Equations to memorize

Question Answer
Fick PrincipleCO = (rate of O2 consumption) / (arterial O2 - venous O2)
MAPMAP = 2/3 diastolic + 1/3 systolic
MAPaverage arterial pressure during a single cardiac cycle
Pulse pressureSystolic pressure - Diastolic pressure
total resistance of vessels in seriesR1 + R2 etc.
total resistance of vessels in parallel1/R1 + 1/R2...
removal of a organdecreases CO and increases TPR

Cardio principles

Question Answer
increases in pulse pressurehyperthyroidism, AR, exercise, obstructive sleep apnea, aortic stiffening
decreases in pulse pressureaortic stenosis, cardiogenic shock, cardiac tamponade, advanced HF
Increase PreloadExercise, Transfusion, Pregnancy
What decreases preload?nitroglycerin (dilate veins)
What decreases afterload?vasodilators (dilate arteries ↓ TPR)
What increases contractility?Catecholamines (Beta 1 receptors NE, epi)
What decreases contractility?Heart failure, Beta blockers, Acidosis, Hypoxia, Hypercapnia, Non-dihydropyridine CCB's
What effect do non-dihydropyridine CCB's have on the heart?Decrease contractility [verapamil, diltiazam]
How do you increase COIncrease contractility, Increase preload, Decrease afterload
Ejection fractionNormal >50%
Decreased ejection fractionSystolic HF (normal in diastolic HF)
organ removalincreases TPR and decreases CO
AV fistulaincreases CO and preload and decreases TPR (also seen in sepsis)
decrease afterloadvasodilators (ex. hydralazine)


Question Answer
anterior surface of heartRV
posterior part of heartLA
atrial enlargement can causedysphagia due to compression of esophagus or hoarseness due to compression of laryngeal nerve (branch of vagus)
when does coronary blood flow peak?early diastole
what supplies SA and AV node?RCA --so infarct may cause bradycardia or heart block

PV loops

Question Answer
increase in preloadincreases stroke volume
increase in afterloaddecreases stroke volume
increase in contractilityincreases stroke volume
increases ESVincrease in afterload
decreases ESVincrease contractility
area of PV loopstroke work
stroke work increasesoxygen demand

Heart sounds

Question Answer
S1mitral and tricuspid closure
S2aortic and pulmonary closure
S3in early diastole. associated with increased volume
when is S3 normalin children and pregnant women
S4in late diastole, associated with filling pressures


Question Answer
a waveatrial contraction.
c waveRV contraction
x descentatrial relaxation and downward displacement of closed tricuspid
v waveincreased right atrial pressure due to filling against closed tricuspid
y descentRA emptying into RV
absent a waveatrial fibrillation
large a wavetricuspid stenosis
X descentabsent in tricuspid regurgitation

Murmur Enhanced by

Question Answer
HOCMvalsalva (decreased venous return), sudden standing (Decrease preload)
what causes earlier onset of MVP valsalva (decreased preload)
what causes later onset of MVPrapid squatting (increased preload) and hand grip (increased afterload)
MRsquatting (increased preload), hand grip (increased TPR), expiration ( increased LA return)
TRinspiration (increased RA return)
mitral stenosisincreased LA return
Hand grip increases afterload increasesintensity of MR, AR, VSD,
Hand grip decreasesHOCM
ASrapid squatting (increases preload)

Where Do You Hear Me

Question Answer
Aortic stenosisupper right sternal border
flow murmurupper right sternal border
aortic valve sclerosisright upper sternal boarder
pulmonic stenosisupper left sternal border
flow murmur (ASD)upper left sternal border
tricuspid regurglower left sternal border
tricuspid stenosislower left sternal border
apexmitral regurg
apexmitral stenosis
PDAleft intraclavicular area


Question Answer
Wide splittingdecreased ability of the RV to empty blood exaggerated delay in pulmonic valve closure in inspiration and expiration (abnormal)
Fixed splittingshunting of blood from left to right (ex. ASD) results in consistent delay in pulmonic closure. (A2 and P2 same gap in expiration and inspiration)
Paradoxical splittingdecreased ability of LV to empty blood results in delayed closure of aortic valve. (P2 comes before A2; and A2 and P2 are closer together in inspiration. A2 and P2 further apart during expiration because left sided)
Inspirationright sided murmurs get worst
Expirationleft sided murmurs get worst

General Heart Murmurs

Question Answer
crescendo-decrescendo systolic ejection murmuraortic stenosis
holosystolic, blowing murmurmitral/tricuspid regurgitation
midsystolic click with late systolic crescendo murmurMVP
holosystolic, harsh sounding murmurVSD
high pitched blowing early diastolic decrescendo murmurAR
follows opening snap with delayed rumbling late diastolic murmurMS
continuous machine like murmurPDA

Heart sounds

Question Answer
Shorter interval between A2 and OS for MS is more or less severe?More severe. Recall, OS is from the abrupt tensing of the valve leaflets as the mitral valve reaches its maximum diameter during forceful opening -> Pressure in LA will increase -> pressure causes the valve to open more forcefully, hence shorter interval.
opening snapMS
mid systolic clickMVP
Mitral stenosisopening snap with low diastolic rumble
opening snap and low diastolic rumbleMS
crescendo-decrescendo systolic ejection murmurAS
aortic stenosiscrescendo-decrescendo systolic ejection murmur loudest at heart base (R sternal border)
holosystolic high-pitched blowing murmurMR and TR
mitral regurgholosystolic high-pitched blowing murmur radiates toward axilla
tricuspid regurgitationholosystolic high-pitched blowing murmur radiates to R sternal border
mid systolic click followed by systolic murmurMVP
mitral valve prolapsemid systolic click followed by systolic murmur
VSDholosystolic, harsh-sounding murmur
holosystolic harsh sounding murmurVSD
high-pitched blowing early diastolic decrescendo murmurAortic regurgitation
patent ductus arteriosuscontinuous machine-like murmur loudest at S2 (pulmonic area)
ASDloud S1 with wide, fixed split S2
loud S1 with wide, fixed split S2ASD
machine like murmurPDA
paradoxical splitAS, LBBB: inspiration decreases the split (delayed aortic valve closure)
wide splitPS, RBBB (delayed RB emptying)
which murmurs are benign?split S1, split S2 with inspiration, S3 < 40 y.o, Early quiet systolic
water hammer or head bobbingaortic regurg due to wide pulse pressure
which murmurs are heard best with inspiration?right sided (I in Inspiration and rIght)
which murmurs are heard best with expiration?left sided (E in Expitaion and lEft)
which murmurs are increased with hand grip?AR and MR (increase SVR increase afterload)
which murmurs are increased with valsalva?hypertrophic cardiomyopathy! (increase intrathoracic pressure, decrease afterload)
which murmurs are decreased with valsalva?AS, AR, MS, MR
what murmurs are heard best in left lateral decubitus?mitral (regurg and stenosis), left S3 and left S4
S3Normal in young patients, LV failure in old patients
S4Atria contracting against a stiff ventricle due to ventricular hypertrophy. [AS, HTN, fibrosis post-MI, HOCM]
Which auscultatory finding indicates worse severity of mitral regurgitation?S3 gallop
S3 gallopLarge volume of regurged flow entering the ventricle during diastole
Sign of worse mitral regurg

More on Valvular Disorders

Question Answer
loudest at heart baseAS
radiates to carotidsAS
pulses parvus et tardusAS (pulses are weak with delayed peak).
where does aortic stenosis radiate to?carotids
which valvular defect is associated with pulsus parvus et tardus ?aortic stenosis
loudest at apex and radiates toward axillaMR
Often due to ischemic heart diseaseMR (post MI, MVP, LV dilatation)
can be caused by RF and infective endocarditisfavors mitral (stenosis and regurg) but all valves are susceptible
which murmur radiates to axilla?mitral regurg
what commonly causes tricuspid regurg?RV dilatation
which murmur radiates to R sternal border?tricuspid regurg, aortic stenosis
which murmurs can be caused by Rheumatic fever and infective endocarditismostly mitral but all valves can be involved
due to sudden tensing of chord tendineaeMVP midsystolic click
best heard over apexMVP
loudest just before S2MVP
associated with chord ruptureMVP
most common valvular lesion?MVP
associated with marfan or Ehlers-danlos?MVP
due to aortic root dilation, bicuspid aortic valve, endocarditis, RFAS
progresses to L Heart failureAR
severe chronic aortic regurgitationlong diastolic murmur and hyper-dynamic pulse (widening PP, head bobbing, pulsatile nail beds)
decreased interval between S2 and OS is a worse prognosismitral stenosis
what can chronic MS cause?LA dilatation
best heard at L infraclavicular areaPDA
what does inspiration do to heart sounds?increases venous return to RA so increases intensity of R heart sounds (Pulmonic and Tricuspid)
what does handgrip/rapid squat/passive leg raise/ alpha agonists do to heart sounds?increases afterload/preload. Increased intensity of MR, AR, AS, VSD murmurs, Decreased HCM, Later onset MVP click
what does valsalva/ sudden standing/ nitroglycerine admin do to heart sounds?decrease preload/afterload, decrease intensity of most murmurs (including AS), increase HCM intensity, MVP earlier onset of click
asymmetric hypertrophy of the septum compared to the free wallHCM
symptoms of ASweak delayed peripheral pulse, syncope, angina, SOB
causes of ASbicuspid aortic valve, senile calcification, ARF with MS, tertiary syphilis
symptoms of MSpulmonary congestion, a-fib, cough
causes of MSARF, infective endocarditis, mitral annular calcification, congenital
causes of MRARF, infective endocarditis, ischemic heart disease, LV dilation, MVP
MVPlarge floppy billowing MV
causes of MVPidiopathic, inherited
which patients are most likely to have tricuspid endocarditisIV drug users

Myocardial Action Potential

Question Answer
phase 0rapid upstroke, voltage gated sodium channels open
phase 1initial repolarization, voltage potassium begin to open
phase 2Ca influx
phase 3rapid repolarization, massive potassium efflux
phase 4resting potential, high potassium permeability

Pacemaker action potential

Question Answer
phase 4slow spontaneous diastolic depolarization as sodium conductance increases. slope determines HR.
phase 0opening of voltage gated calcium channel
phase 3repolarization increased activation of potassium channels
slope of phase 4 in SA nodedetermines HR

Localization of a STEMI

Question Answer
inferior wall of the left ventricle formsmost of the diaphragmatic surface of the heart
PDA suppliesinferior wall
LAD suppliesanterior 2/3 on interventricular septum, anterior wall of left ventricle and part of anterior papillary muscle
LCX supplieslateral and posterior walls of left ventricle
acute marginal branches from the right coronary artery supplyright ventricle

Arteries, Walls, EKG leads

Question Answer Column 3
left anterior descendinganterior wallV1-V4, V5
left circumflexlateral wallaVL, V5, V6
right coronaryinferior wall diaphragmaticII, III, aVF
right coronaryposterior wallR precordial EKG V4

Murmur maneuvers

Question Answer
What does handgrip do to circulation?Increases after load
Handgrip increases intensityMR, AR, VSD
Handgrip decreases intensityHCM
handgrip's effect on MVPlater onset of click
What does inspiration do to circulation?Increases venous return to RA
Inspiration increases intensityR sided valve murmurs
Inspiration increases intensitySplitting of S2
What does valsalva do to circulation?Increases intrathoracic pressure - reduces venous return to RA; also reduces systemic pressure if held long enough; Decreases preload and after load
Valsalva decreases intensitymost murmurs
Valsalva increases the intensityHCM
Causes earlier onset of click in MVPValsalva
What does rapid squatting do to circulation?Increases venous return, increases preload
Rapid squatting decreases intensityHCM
Rapid squatting increases intensityAS
MVP and rapid squattinglater onset fo click
whenever HOCM is decreased, MVPhas a later onset of click
Causes later onset of click in MVPRapid squatting
Heard best in left lateral decubitus positionMS
Heard best in left lateral decubitus positionMR
Heard best in left lateral decubitus positionLeft sided S3
Heard best in left lateral decubitus positionLeft sided S4
Enhanced by expirationMS

Miscellaneous Physiology

Question Answer
hypoxia in lungscauses vasoconstriction
WPWbypasses rate slowing AV node. Widened QRS and shortened PR
in Torsadesdo not cardiovert
Conduction pathwaySA node to atria to Av node to common bundle to bundle branches to fascicles to Purkinje fibers to ventricles
Speed of conductionPark At Ventura Avenue (Purkinje, Atria, Ventricles, AV node)
ANPreleased in response to increased blood volume and atrial pressure. acts via cGMP. causes vasodilation and decreases sodium reabsorption at the RCT.
ANP's effect on kidneydilates afferent renal arterioles and constricts efferent arterioles. increases GFR
BNPreleased from ventricular myocytes. Longer half life than ANP. Used for diagnosing HF.
responds to a decrease and increase in BPcarotid sinus
responds to a increase in BPaortic arch
hypotension and baroreceptorcauses a decrease in stretch which increases efferent sympathetic firing leads to increased HR and contractility
carotid massageincreases pressure on carotid sinus, increases stretch increases afferent baroreceptor firing, decreases HR
PCWPLA pressure
carotid sinustransmits via glossopharyngeal nerve to increase and decrease in BP
aortic archtransmits via vagus. responds only to an increase in BP
sympatheticincreases HR, contractility and BP
parasympatheticdecreases HR
pressure in RA0/8
pressure in RV4/25
pressure in pulmonary artery9/25
pressure in left atrium2/12
pressure in left ventricle9/130
pressure in aorta70/130


Question Answer
edema in heart faillureincreased capillary hydrostatic pressure 2 much fluid
edema in nephrotic syndromelose protein because pee it out. oncotic pressure in capillary is too low!
edema in post renal obstructionincreases bowman's space hydrostatic. equivalent of intersititum
examples of lymphatic blockagebreast cancer, axillary node resection, elephantiasis

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