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66 Cards in this Set

  • Front
  • Back
Acute marginal artery supplies?
Right ventricle
Posterior descending artery supplies?
Supplies posterior 1/3 of IV septum and posterior ventricular walls
LAD supplies?
Anterior IV septum, anterior papillary muscle, anterior LV
Left circumflex coronary artery (LCX) supplies?
L. ventricle (lateral and posterior wall)
Left-dominant coronary circulation - PDA from which artery?
Left circumflex artery (LCX)
Right-dominant coronary circulation - PDA from which artery?
Right coronary artery
Coronary arteries fill during
Diastole
Enlargement of right atrium - clinical signs (2)
1) Dysphagia (compression of esophagus)
2) Hoarseness (L recurrent nerve compression)
MAP
MAP = CO x TPR = 2/3 P(diastole) + 1/3 P(systole)
Venodilator effect on preload
Decrease preload
Vasodilator effect on afterload
Decrease afterload
Ejection Fraction
EF = SV/EDV = (EDV - ESV)/EDV
Measures ventricular contraction
Resistance calculation
R = (8 x viscosity x length) / ( pi x r^4)
Isovolumetric contraction
Between mitral valve closure and aortic valve opening; highest O2 consumption
Isovolumetric relaxation
Between aortic valve closing and mitral valve opening
S3 heart sound
Early diastole, increased filling pressure, dilated ventricles
S4 heart sound
Late diastole, ventricular hypertrophy (high atrial pressure)
JVP - waves
a, c, x, v, y
JVP a wave
atrial contraction
JVP c wave
RV contraction
JVP x descent
atrial relaxation
JVP v wave
Increased right atrial pressure
JVP y descent
blood flow from R atrium to R ventricle
Normal splitting
Inspiration --> Increased R ventricle filling --> Increased ejection time --> Split pulm and aortic valve closure
Wide splitting
Delayed RV empyting (plum stenosis, right bundle branch block)
Fixed splitting
ASD - Left-to-right shunt increases R heart volumes
Paradoxical splitting
Delay L ventricle emptying (aortic stenosis, left bundle branch block); P2 sound before A2
Hand grip maneuver
Increase afterload; Increase intensity of regurgitation murmurs, VSD, mitral valve prolaspe
Valsalva maneuver
Decrease preload; Increase intensity of mitral valve prolapse
Mitral regurgitation
Holosystolic, high-pitchted "blowing" murmur; loudest at apex, radiates toward axilla; enhanced by handgrip, expiration; due to IHD, MVP, LV dilation
Tricuspid regurgitation
Holosystolic high-pitched "blowing" murmur; loudest at LLSB, radiates to right sternal border; enhanced by inspiration
Aortic stenosis
Crescending-decrescendo systolic ejection murmur with ejection click; radiation to carotids; pulsus parvus et tardus; syncope, angina, dyspnea; calcified aortic valves, bicuspid valves
VSD
Holosystolic, harsh murmur; loudest at LLSB, enhanced by handgrip
Mitral valve prolapse
Late systolic crescendo murmur, midsystolic click; apex, loudest at S2; enhanced by Valsalva
Aortic regurgitation
High-pitched "blowing" diastolic decrescendo murmur; enhance with hand grip; bounding pulses
Mitral stenosis
Opening snap, rumbling late diastolic murmur; secondary to rheumatic fever; enhanced by expriation
PDA
Continuous, machine-like murmur loudest at S2; left infraclavicular area; congenital rubella
Phase 0 of pacemaker AP
Opening of voltage-gated Ca++ channels --> Ca++ influx
Phase 3 of pacemaker AP
Inactivation of Ca++ channels, activation of K+ channels --> K+ efflux
Phase 4 of pacemaker AP
Funny current - Na+ influx into cell; slope determines HR (Sympathetic stimulation increase funny current channels opening, increase HR)
Phase 0 of ventricular AP
Voltage-gated Na+ channels open --> Na+ influx
Phase 1 of ventricular AP
VGNa+ channels inactivated, K+ channels open
Phase 2 of ventricular AP
VGCa++ channels open --> Ca++ influx balance K+ efflux; PLATEAU
Phase 3 of ventricular AP
VGC++ channels close, slow VGK+ channels open --> K+ efflux
Phase 4 of ventricular AP
Resting potential (K+ channels open)
Jervell and Lange-Nielsen syndrome
Prolonged QT interval, deafness
PR interval
AV conduction delay (< 200 msec)
QT interval
Ventricular mechanical contraction
T wave
Ventricular repolarization
U wave
Caused by hypokalemia, bradycardia
Atrial flutter
Identical atrial depolarization waves; "sawtooth" appearance; treat with class IA, IC, III
Ventricular fibrillation
Erratic rhythm, no identifiable waves; fatal
1st degree AV block
Prolonged PR interval (> 200 msec); asymptomatic
2nd degree Mobitz type I AV block
Progressive lengthening of PR interval until a beat is "dropped" - no QRS interval following P wave
2nd degree Mobitz type II AV block
Dropped QRS with normal PR interval; pathologic, treated with pacemaker
3rd degree AV block (complete)
P waves and QRS are present independently; pathogenic - treat with pacemaker; Lyme disease
ANP
Efferent renal arteriole contract, afferent arteriole dilation --> opposes effects of aldosterone
Aortic arch receptors - transmit via which nerve?
Vagus
Carotid sinus receptors - transmit via which nerve?
Glossopharyngeal
Baro- and chemo-receptor nerves lead to which CNS nucleus?
Solitary nucleus of medulla
Carotid sinus - which receptor type?
Baroreceptor
Carotid body - which receptor type?
Chemoreceptor
Baroreceptor response to hypotension
Decreased stretch --> decrease baroreceptor firing --> Stimulate SNS and depress PSNS --> Vasocontraction, Increased BP, HR
Baroreceptor response to stretch
Increased stretch --> increase baroreceptor firing --> Stimulate PSNS, depress SNS --> Decrease BP, HR
Peripheral chemoreceptors respond to
Decreased PO2 (< 60 mmHg)
Increased PCO2
Decreased pH
Central chemoreceptors respond to
pH and PCO2 changes in brain interstitial fluid; NO direct response to PO2!