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Cardiology - Physiology

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ibench85lbs's version from 2016-07-16 15:36

Cardiac output

Question Answer
CO=SVxHR
Fick principleCO = rate of O2 consumption/(arterial O2 content - venous O2 content)
MAP =COxTPR (total peripheral resistance) = 2/3 diastolic pressure + 1/3 systolic pressure
Pulse pressure =systolic pressure - diastolic pressure
pulse pressure is directly related to stroke volume, Inversely proportional to arterial compliance
SV=CO/HR = EDV-ESV
CO during exercise is maintained by↑ HR and ↑ SV during early stages of exercise
↑ HR during late stages (SV plateaus)
Catecholaminesincrease contractility via ↑ activity of Ca pump in sarcoplasmic reticulum
↑ intracellular Caincreases contractility
↓ extracellular Naincreases contractility via ↓ activity of Na/Ca exchanger
Digitalisincreases contractility via blocking Na/K pump → ↑ intracellular Na → ↓ Na/Ca exchanger activity → ↑ intracellular Ca
B1-blockadedecreases contractility via ↓ cAMP
Acidosis, Heart failure with systolic dysfunction↓ contractility
Hypoxia/hypercapnea↓ contractility
Non-dihydropyridine Ca channel blockers↓ contractility
Preload =ventricular EDV ( depends on venous tone and circulating blood)
Preload ↑ withExercise (slightly
↑ blood volume
Excitement (↑ sympathetic activty)
Afterload =MAP (proportional to peripheral resistance)
VEnodilators↓ prEload
(e.g., nitroglycerin)
VAsodilators↓ Afterload (Arterial)
e.g., hydrAlAzine)
Starling HypothesisForce of contraction is proportional to end diastolic length of cardiac muscle fiber (preload)
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Blood flow

Question Answer
Ejection fractionEF=SV/EDV = (EDV-ESV)/EDV
EF is an index ofventricular contractility
EF is normally>=55%
Pressure =Q (flow) x R (resistance)
Resistance isdirectly proportional to viscosity and vessel length
inversely proportional to radius to the 4th power
Resistance in series vs. in parallelSeries: R1+R2+R3
Parallel: 1/R1+1/R2+1/R3
What vessel type determines most of the total peripheral resistance?Arterioles → regulates capillary flow
Viscosity depends mostly on what?Hematocrit
Viscosity ↑ inPolycythemia
Hyperproteinemic state (multiple myeloma)
Hereditary spherocytosis
Viscosity ↓ inanemia
X-intercept of venous return curvemean systemic filling pressure
X axis of cardiac and vascular function curvesRight atrial pressure or EDV
Y axis of cardiac and vascular function curvesCO or venous return
Period of highest cardiac O2 consumptionIsovolumentric contraction - period between mitral valve closing and aortic valve opening
How does ↑ preload affect the cardiac cycle?↑ EDV → ↑ SV
How does ↑ afterload affect the cardiac cycle?↑ aortic pressure → ↓ SV (can't push as much blood out against higher pressures) → ↑ ESV
How does ↑ contractility affect the cardiac cycle?↓ ESV → ↑ SV → ↑ EF
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Heart Sounds

Question Answer
S1Mitral and tricuspid valve closure
Loudest at mitral area (apex)
S2Aortic and pulmonary valve closure (aortic first, pulmonic second)
Loudest at left sternal border
S3sound during early diastole when ventricles are filling rapidly
Louder with ↑ filling pressures (mitral regurgitation, CHF)
More common in dilated ventricles
Normal in children and pregnant women
S4late diastole
Indicates high atrial pressure
Louder with ventricular hypertrophy (LA must push against stiff LV)
a wave (JVP)atrial contraction
c wave (JVP)RV contraction (closed tricuspid valve bulging into atrium)
x descent (JVP)atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
v wave (JVP)↑ right atrial pressure due to filling against closed tricuspid valve
happens just before S3
y descent (JVP)blood flow from RA to RV
Explanation for normal splittingInspiration → drop in intrathoracic pressure → ↑ venous return to the RV → increased RV SV → ↑ RV ejection time → delayed closure of pulmonic valve
↓ pulmonary impedance (↑ capacity of pulmonary circulation) also contributes to delayed closure of pulmonic valve
Wide splittingseen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block)
an exaggeration of normal splitting (regardless of breath)
Fixed splittingSeen in ASD
ASD → left-to-right shunt → ↑ RA and RV volumes → ↑ flow through pulmonic valve such that pulmonic closure is greatly delayed (regardless of breath)
Paradoxical splittingSeen in conditions that delay LV empyting (aortic stenosis, left BBB)
P2 sound occurs before A2 (abnormal)
Therefore the normal delay in P2 during inspiration simply brings P2 so close to the delayed A2 that they sound as one
Inspiration does what to heart sounds?↑ intensity of right heart sounds
Expiration does what to heart sounds?↑ intensity of left heart sounds (brings heart closer to chest wall)
Hand grip does what to heart sounds?↑ systemic vascular resistance
↑ intensity of MR, AR, VSD, MVP murmurs (late onset of murmur/click)
↓ intensity of AS, hypertrophic cardiomyopathy murmurs
Valsalva(phase II) & standing does what to heart sounds?↓ venous return
↓ intensity of most murmurs (including AS), intensity of MVP(earlier onset murmur/click)
↑ hypertrophic cardiomyopathy murmurs
Rapid squatting does what to heart sounds?(↑ venous return, ↑ preload, ↑ afterload with prolonged squatting)
↓hypertrophic cardiomyopathy murmurs, ↑ MVP murmur intensity (later onset of click/murmur) and AS murmur
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Murmurs

Question Answer
Mitral regurgitationHolosystolic, high-pitched "blowing murmur"
Loudest at apex and radiates toward axilla
Enhanced by maneuvers that ↑ TPR (squatting, hand grip) or LA return (expiration)
Often due to ischemic heart disease, mitral valve prolapse, LV dilation, rheumatic fever, or infective endocarditis
Tricuspid regurgitationHolosystolic, high-pitched "blowing murmur"
Loudest at tricuspid area and radiates to right sternal border
Enhanced by maneuvers that ↑ RA return (inspiration)
TR can be caused by RV dilation, rheumatic fever, or infective endocarditis
Aortic StenosisCrescendo-decrescendo systolic ejection murmur following ejection click (EC due to abrupt halting of valve leaflets)
LV >> aortic pressure during systole
Radiates to carotids/heart base
"Pulsus parvus et tardus" - pulses are weak with a delayed peak
Can lead to Syncope, Angina, and Dyspnea on exertion
Louder with squatting, softer with standing and fist pump
Often due to age-related calcific aortic stenosis or bicuspid aortic valve.
VSDHolosystolic, harsh-sounding murmur
Loudest at tricuspid area
enhanced with hand grip maneuver d/t increased afterload
Mitral valve prolapseLate systolic crescendo murmur with midsystolic click (MC d/t sudden tensing of chordae tendineae)
Most frequent valvular lesion - usually benign
Best heard over apex just before S2
Occurs earlier by maneuvers that ↓ venous return (standing, valsalva)
Can predispose to infective endocarditis
Causes: myxomatous degeneration, rheumatic fever, chordae rupture
Aortic regurgitationImmediate high-pitched "blowing" diastolic decrescendo murmur
Wide pulse pressure when chronic - bounding pulses and head bobbing
Causes: aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever
↑ murmur during hand grip
Vasodilators ↓ intensity of murmur
Mitral stenosisDelayed rumbling late diastolic murmur following opening snap (OS d/t abrupt halt in leaflet motion in diastole after rapid opening d/t fusion at leaflet tips)
LA>>LV pressure during diastole
Often 2° to rheumatic fever
Chronic MS → LA dilation
Enhanced by ↑ LA return (expiration)
decreased interval between S2 & OS correlates with ↑ severity

PDAContinuous machine-like murmur
Loudest at S2 (time-point), over left infraclavicular area
Often d/t congenital rubella or prematurity
ASDWide & fixed splitting of S2 that doesn't change with respiration
HOCSystolic ejection murmur accentuated by standing
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Action potentials

Question Answer
Ventricular action potentialOccurs in bundle of His and Purkinje fibers
Phase 0: Depolarization - INa (voltage-gated channels)---> Class I antiarrhytmic
Phase 1: inactivation of Na channels, K channels begin to open--->No antiarrhytmic
Phase 2: plateau - ICa & EK; Ca release from sarcoplasmic reticulum → myocyte contraction-->No antiarrhytmic
Phase 3: Repolarization - massive EK through slow channels and closure of Ca channels-->Class III antiarrhytmic
Phase 4: Resting potential - high K permeability through K channels
IfFunny current - spontaneous depolarization (slow INa & IK) of cardiac nodal cells during diastole → automaticity
Slope of If (phase 4 - SA node) determines HR
ACh/adenosine ↓ If → ↓ HR
Catecholamines ↑ If → ↑ HR
Differences between cardiac and skeletal muscleCardiac:
-has AP plateau
-myocyte contraction due to Ca-induced Ca release from SR
-If - spontaneous depolarization keeps automaticity
-myocytes are electrically coupled to each other by gap junctions
Pacemaker action potentialOccurs in SA/AV nodes. Key differences from vent. AP:
Phase 0: slower upstroke d/t ICa - prolongs transmission from atria to vents----> Class IV (Na channels are permanently inactivated d/t less negative resting voltage of these cells: No effect of class I on these slow fibers )
Phase 2: no plateau
Phase 3: inactivation of Ca channels and ↑ activation of K channels → ↑ K efflux
Phase 4: slow diastolic depolarization d/t If:membrane potential spontaneously depolarizes as Na conductance increases --> class II and IV can slow phase IV in these fibers.
ECG P waveatrial depolarization
atrial repolarization is masked by the QRS
ECG PR intervalconduction delay through AV node
normal: <200ms
ECG QRS complexventricular depolarization
normal: <120ms
ECG QT intervalmechanical contraction of the ventricles
ECG T waveventricular repolarization
T-wave inversion → MI
ECG ST segmentisoelectric; ventricles depolarized
ECG U wavecause by hypokalemia, bradycardia
Speed of conductionPurkinje > atria > ventricles > AV node (PAVA)
PacemakesSA>AV>bundle of His/Purkinje/Ventricles
Conduction pathwaySA node → atria → AV node → common bundle → bundle branches → Purkinje fibers → ventricles
AV node delay100ms
allows time for ventricular filling
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Arrhythmias

Question Answer
Torsades de pointesPolymorphic Ventricular tachycardia
Can progress to V fib
Anything that prolongs the QT interval → -->drugs, hypo K, hypo Mg-->↑ risk
Tx: magnesium sulfate
Jervell and Lange-Nielsen syndromeCongenital long QT, autosomal recessive
d/t defects in Ca, Na, K channels
presents with sensorineural deafness
A fibIrregularly irregular w no P waves. Atrial stasis → stroke
Tx: rate control, anticoag, and possible pharmacologic or electrical cardioversion
Atrial flutterRapid succession of identical, back-to-back atrial depolarization waves - "sawtooth" appearance
Conversion to sinus rhythm: class IA, IC, or III antiarrhythmics
Rate control: B-blocker or Ca channel blocker
Definitive Tx: catheter ablation.
Ventricular fibCompletely erratic rhythm with no identifiable waves
Fatal without immediate CPR and defibrillation
1st degree AV blockProlonged PR interval (>200ms) - Benign and Asymptomatic--> No treatment required
2nd degree AV block - Mobitz type 1 (Wenckebach)Progressive lengthening of PR interval until a QRS is skipped. Usually asymptomatic
2nd degree AV block - Mobitz type 2Skipped QRS's without change in PR interval length - Often 2:1 block (Pwaves:QRS's)
Pathologic - may progress to 3rd degree block
Tx with pacemaker
3rd degree (complete) AV blockAtria and ventricles beat independently of each other
P waves and QRS's don't bear any relation to each other
atrial rate is faster
Tx: pacemaker
Lyme disease → 3° heart block
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Cardiology - Physiologic regulation of circulation (by bri1231)