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