Step 1 - CV 1

jaudry's version from 2015-05-24 06:47


Question Answer
Structures inside carotid sheathInternal Jugular Vein (lateral), Common carotid Artery (medial), 3. Vagus Nerve (posterior)
Circumflex artery suppliesposterior left ventricle
Left anterior descending artery suppliesapex and anterior interventricular septum
Acute marginal artery suppliesright ventricle
Posterior descending/interventricular artery (PD) supplies posterior septum - 80% of the time it arises from RCA, 20% of the time from the CFX
SA and AV nodes are supplied bythe RCA
Most common coronary artery occlusionLAD - supplying anterior interventricular septum
Coronary arteries fill duringdiastole.
left atrium enlargement can causedysphagia (due to compression of the esophagealnerve) or hoarseness (due to compression of the recurrent laryngeal nerve, a branch of the vagus).
CO and exerciseinitially increases b/c of increase in HR and SV - after prolonged exercise it increases as increase in SV
CO and very high HRdiastolic filling will become incomplete and CO↓ (e.g. Ventricular tachycardia)
sv * hr
CO x TPR = (2/3 diastolic + 1/3 systolic)
Pulse pressuresystolic - diastolic . . Proportional to stroke volume
Fick principlerate of O2 consumption / (arterial O2 content - venous O2 content)
sv = edv-esv
Stroke volume increased by
↑ contractility, ↑ preload, ↓ afterload - increases in anxiety exercise, pregnancy
Stroke volume decreased by↓preload, ↓contractility, ↑afterload
Contractility increased byCatecholamines (↑ activity of Ca pump in SR), ↑intracellular Ca, ↓extracellular Na (↓activity of Na/Ca exchanger), Digitalis (↑intracellular Na),
Contractility decreases withBeta 1 blockade, Heart failure, Acidosis, Hypoxia/hypercapnia, Non-dihydropyridine Ca+2 channel blockers
Myocardial O2 demand increased by↑ preload n afterload, ↑contractility, ↑heart rate, ↑heart size (↑wall tension)
Preload =ventricular EDV (decreased by venodilators, increases with ↑ blood volume(iv serum), with dim TPR: exercise , shunt a-v, grossese)
Afterload =MAP (proportional to peripheral resistance) (decreased by vasodilators(arterial))
Myocardium contractile stateCirculating catecholamines, digitalis and sympathetic stimulation increase it . . Pharmacologic depressants, Loss of myocardium (MI) decrease it
Ejection fraction (EF) =SV/EDV = (EDV-ESV)/ EDV - normally > 55%
Organ removal=↑ TPR , ↓CO


Question Answer
Resistance equation =driving pressure/flow = (8 x viscosity x length) / pi x radius^4
Viscosity increases inpolycythemia, hyperproteinemia, Hereditary spherocytosis
Isovolumetnc contraction phaseperiod between mitral closure and aortic valve opening; period of highest 02 consumption
Systolic ejection phaseperiod between aortic valve opening and closing
Isvolumetrlc relaxation phaseperiod between aortic valve closing and mitral valve opening
Rapid filling phase period just after mitral valve opening
Reduced filling phaseperiod just before mitral valve closure
S1mitral and tricuspid valve closure - Loudest at mitral area.
S2aortic and pulmonary valve closure - Loudest at left sternal border.
S3In early diastole during rapid ventricular filling phase Associated with ↑ filling pressures and more common in dilated ventricles (but normal in children and pregnant women) .
S4("atrial kick")-in late diastole. High atrial pressure. associated with ventricular hypertrophy. Left atrium must push against stiff LV wall
Jugular venous pulse (JVP)3 parts -a wave- atrial contraction . . .c wave- RV contraction (tricuspid valve bulging into atrium). . . v wave- ↑ atrial pressure due to filling against closed tricuspid valve


Question Answer
Normal splittinginspiration leads to drop in Intrathoracic pressure, which ↑ capacity of pulmonary circulation. Pulmonic valve closes later to accommodate more blood entering lungs; aortic valve closes earlier because of ↓ return to left heart.
Wide splittingseen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block). Delay in RV emptying causes delayed pulmonic sound (regardless of breath). An exaggeration of normal splitting.
Fixed splittingseen in ASD. ASD leads to left-to-right shunt and therefore ↑ flow through pulmonic valve such that regardless of breath, pulmonic closure is greatly delayed.
Paradoxical splittingseen in conditions that delay LV emptying (aortic stenosis, left bundle branch block). Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound. Therefore on inspiration, the later P2 and earlier A2 sounds move closer to one another, "paradoxically" eliminating the split.
Things to hear in aortic areasystolic murmurs - Aortic stenosis, flow murmur (VSD), aortic valve stenosis
Things to hear at pulmonic areassystolic ejection murmur: pulmonic stenosis, flow murmur (ASD) (PDA)
Things to hear at tricuspid areapansystolic murmurs: tricuspid regurg, VSD, Diastolic murmurs: Tricuspid stenosis, Atrial septal defect
Things to head at Mitral areaSystolic murmur: mitral regurg, Diastolic murmurMitral stenosis
Things to hear along left sternal borderAortic regurg, pulmonic regurg, hypertrophic cardiomyopathy
Mitral/tricuspid regurg murmurHolosystolic, high-pitched "blowing murmur." 2. Mitral - Ioudest at apex and radiates toward axilla. Enhanced by maneuvers that increase TPR(e.g., squatting, hand grip) or LA return (e.g., expiration). MR is often due to ischemic heart disease, mitral valve prolapse, or LV dilation. 3. Tricuspid - loudest at tricuspid area and radiates to right sternal border. Enhanced by maneuvers that ↑ RA return (e.g., inspiration). TR is due to RV dilation or endocarditis. Rheumatic fever can cause both.
Aortic stenosis murmurCrescendo-decrescendo systolic ejection murmur following ejection click (EC; due to abmpt halting of valve lea Bets). LV >> aortic pressure during systole. Radiates to carotids/apex. "Pulsus parvus et tardus" - pulses weak compared to heart sounds. Can lead to syncope. Often due to age-related calcific aortic stenosis or bicuspid aortic valve
VSD murmurHolosystolic, harsh-sounding murmur, Loudest at tricuspid area
Mitral prolapse murmurLate systolic crescendo murmur With midsystolic click (MC; due to sudden tensing of chordae tendineae). Most frequent valvular lesion. Loudest at S2. Usually benign . Can predispose to infective endocarditis. Can be caused by myxomatous degeneration, rheumatic fever, or chordae rupture. ENHANCED
by maneuvers that ↑ TPR (e.g., squatting, hand grip)
Aortic regurg murmurImmediate high-pitched "blowing" dIastolic murmur. Wide pulse pressure when chronic; can present with bounding pulses and head bobbing. Often due to aortic root dilation, bicuspid aortic valve, or rheumatic fever
Mitral stenosis murmurFollows opening snap (OS; due to tensing of chordae tendineae). Delayed rumbling late diastolic murmur LA » LV pressure during diastole. Often occurs 2° to rheumatic fever. Chronic can result in LA dIlation. Enhanced by expiration
PDA murmurContinuous machine-like murmur - loudest at S2


Question Answer
Cardiac myocyte physiologyCardiac muscle contraction is dependent on extracellular calcium, which enters the cells during plateau of action potential and stimulates calcium release from the cardiac muscle sarcoplasmic reticulum (calcium-induced calcium release),
In contrast to skeletal muscle, cardiac muscle1. action potential has a plateau, which is due to Ca2+ influx 2, nodal cells spontaneously depolarize, resulting in automaticity due to funny channels 3. myocytes are electrically coupled to each other b) gap Junctions
Ventricular action potential Phase 0 =rapid upstroke- voltage-gated Na+ channels open,
Ventricular action potential Phase 1 = initial repolarization - inactivation of voltage-gated Na+ channels, Voltage gated K+ channels begin to open,
Ventricular action potential Phase 2 = plateau-Ca2+ influx through voltage-gated Ca2+ channels balances K+ eflux, Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction
Ventricular action potential Phase 3 = rapid repolarization- masslve K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels,
Ventricular action potential Phase 4 =resting potenial - high K+ permeability through K+ channels,
Pacemaker Phase 0 =upstroke-opening of voltage-gated Ca2+ channels. Fast v oltage gated Na channels are present in pacemaker cells but permanently inactivated b/c of the resting voltage of pacemaker cells. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.
Pacemaker Phase 2 =plateau is absent.
Pacemaker Phase 3 =inactivation of the Ca2+ channels and ↑ activation of K+ channels → ↑ K+ efflux.
Pacemaker Phase 4 =slow diastolic depolarization- membrane potential spontaneously depolarizes as Na+ conductance ↑ (funny channels different from INa). Accounts for automaticity of SA and AV nodes. The slope of phase 4 in the SA node determines hea rt rate. ACh ↓, the rate of diastolic depolarization and ↓, heart rate, while catecholamines ↑depolarization and AUGMENTE
heart rate. Sympathetic stimulation ↑ the chance that If channels are open.


Question Answer
P waveatrial depolarization.
PR intervalconduction delay through AV node (normally < 200 msec).
QRS complexventricular depolarization (normally < 120 msec).
QT intervalmechanical contraction of the ventricles.
T waveventricular repolarization.
T-wave inversionindicates recent Ml.
Atrial repolarization on EKGmasked by QRS complex.
ST segment isoelectric, ventricles depolarized.
U wavecaused by hypokalemia, bradycardia.
Speed of conduction in heartPurkinje > atria > ventricles> AV node
Pacemakers speedSA>AV> bundle of His/Purkinje/Ventricles
Torsades de pointesVentricular tachycardia is characterized by shifting sinusoidal waveforms on ECG -Can progress to V-fib. Anything thai prolongs the QT interval can predIspose SAUF AMIDARONE
CongenItal long QT syndromesmost often due to defects in cardiac sodium or potassium channels. Can present with severe congenital sensorineural deafness (Jervell and Lange- Nielsen syndrome).
Wolff-Parkinson-White syndromeAlso known as ventricular preexcitation syndrome. Accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing AV node. As a result, ventricles begin to partially depolarize earlier, giving rise to characteristic delta wave on ECC. May result in reentry current leading to supraventricular tachycardia.
Atrial fibrillationChaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes. Can result in atrial stasis and lead to stroke. Treat with Beta blocker or calcium channel blocker; prophylaxis against thromboembolism with warfarin (Coumadin).
Atrial flutterA rapid succession of identical, back-to-back atrial depolarization waves. The identical appearance accounts for the "sawtooth" appearance of the flutter waves. Attempt to convert to sinus rhythm. Use class lA, IC, or III antiarrhythmlcs.
1st degree av blockThe PR interval is prolonged (> 200 msec). Asymptomatic.
Mobitz type I AV block (wenckebach)progressive lengthening of the PR interval until a beat is “dropped” (a P wave not followed by a QRS complex) - usually asx
Mobitz type II AV blockDropped beats that are not preceded by a change in the length of the PR interval (as in type I). These abrupt, nonconducted P waves result in a pathologiC condition. It is often found as 2: 1 block, where there are 2 P waves to 1 qRS response. May progress to 3rd degree block.
3rd degree AV block (complete)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 treated with pacemaker. Lyme disease can result in 3rd-degree heart block.
Ventricular fibrillationcomplelely erratic rhythm with no identifiable waves. Fatal arrhythmia Without Immediate CPR and defibrillation


Question Answer
ANPa diuretic, is released from atria in response to ↑ blood volume and atrial pressure. Causes generalized vascular relaxation. Constricts efferent renal arterioles, dilates afferent arterioles. Involved in "escape from aldosterone" mechanism.
Aortic arch transmits viavagus nerve to medulla (responds only to ↑ BP)
Carotid sinus transmits via glossopharyngeal nerve to solitary nucleus of medulla (responds to ↓ and ↑ in BP).
Baroreceptor response to hypotension ↓ arterial pressure→↓ stretch→↓ afferent baroreceptor firing→ ↑efferent sympathetic firing and ↓ efferent parasympathetic stimulation→ vasoconstriction, ↑HR, ↑ contractility, ↑BP. Important in the response to severe hemorrhage.
Baroreceptor response to carotid massage↑ pressure on carotid artery→↑stretch→↑afferent baroreceptor firing→↓HR
Peripheral chemoreceptorscarotid and aortic bodies respond to ↓ Po2 (<60 mmHg). ↑ PcO2 and ↓ pH of blood
Central chemoreceptors respond to changes in pH and PCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2. Do not directly respond to PO2. Responsible for Cushing reaction- ↑ intracrania pressure constricts arterioles→ cerebral ischemia → hypertension (sympathetic response)→ reflex bradycardia
Cushing triadhypertension, bradycardIa, resp depression
Largest share of systemic cardIaC outputLivery
Highest blood Row per gram of tissue.Kidney
Large arteriovenous 02 differenceHeart - because 02 extraction is always - 100%. ↑O2 demand is met by ↑ coronary blood flow, not by ↑ extraction of O2


Question Answer
PCWP pulmonary capillary wedge pressure (in mmHg) is a good approximation of left atrial pressure. In mitral stenosis, PCWP > LV diastolic pressure. - Measured with Swan-Ganz catheter.
Heart autoregulation of blood flowLocal metabolites-O2, adenosine, NO (SURTOUT)
Brain autoregulation of blood flow Local metabolites - CO2 (pH)
Kidney autoregulation of blood flowMyogenic and tubuloglomerular feedback
Lung autoregulation of blood flow Hypoxia causes vasoconstriction
Skeletal muscle autoregulation of blood flow Local metabolites-lactate, adenosine, K+
Skin autoregulation of blood flow Sympathetic stimulation most important mechanism- temperature control
Reasons for edema↑ capillary pressure (↑ Pc; heart failure), ↓ plasma proteins (↓ ᴨc; nephrotic syndrome, liver failure), ↑ capillary permeability (↑ Kf; toxin, infections, burns), ↑interstitial fluid colloid osmotic pressure (↑ᴨ; lymphatic blockage)