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First Aid Cardiology > First Aid - Cardiology (369) > Flashcards

First Aid - Cardiology (369) Flashcards

1
Q

what vessel supplies the SA and AV nodes?

A

Right Coronary Artery (80% of the time)

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2
Q

what vessel supplies the posterior left ventricle?

A

circumflex artery

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3
Q

what vessel supplies the apex and anterior interventricular septum?

A

the left anterior descending

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4
Q

what vessel supplies the the posterior septum?

A

posterior descending/interventricular artery

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5
Q

what vessel supplies the right ventricle?

A

the acute marginal artery

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6
Q

what is the most common site of coronary artery occlusion?

A

the LAD (left anterior descending), which supplies the anterior interventricular septum

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7
Q

when do the coronary arteries fill?

A

diastole

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8
Q

enlargement of the left atrium can result in?

A

dysphagia (due to compression of the esophageal nerve) or hoarseness (due to compression of the recurrent laryngeal nerve

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9
Q

what is the equation for cardiac output?

A

stroke volume x heart rate

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10
Q

what is the fick principle?

A

cardiac output = (rate of O2 consumption)/(arterial O2 content - venous O2 content)

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11
Q

what arethe equations for mean arterial pressure?

A

(cardiac output) x (total peripheral resistance) OR 2/3 diastolic + 1/3 systolic pressure

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12
Q

what is the equation for pulse pressure?

A

systolic pressure - diastolic pressure

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13
Q

pulse pressure is a rough correlate for?

A

stroke volume

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14
Q

what are the equations for determining stroke volume?

A

CO/HR or EDV-ESV

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15
Q

what variables affect stroke volume?

A

contractility, afterload, preload

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16
Q

what factors can increase contractility (and therefore stroke volume)?

A
  1. catecholamines (increase the activity of Ca++ pump) in SR)
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17
Q

what factors can decrease contractility (and therefore stroke volume)?

A
  1. beta blockade (decreased cAMP)
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18
Q

the preload is equal to the?

A

ventricular end diastolic volume

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19
Q

the afterload is equal to the?

A

mean arterial pressure (proportional to peripheral resistance)

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20
Q

venodilators (like nitroglycerine) have what effect on preload?

A

decrease preload

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21
Q

vasodilators (like hydralazine) have what affect on afterload?

A

decrease afterload

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22
Q

what factors increase preload?

A

exercise, increased blood volume (overtransfusion) and excitement (sympathetics)

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23
Q

what is starling’s curve?

A

force of contraction is equal to the initial length of cardiac muscle fiber (preload)

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24
Q

what is the equation for ejection fraction?

A

EF=SV/EDV=(EDV-ESV)/EDV

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25
Q

the ejection fraction is an index of?

A

ventricular contractility

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26
Q

what is an approximate normal ejection fraction?

A

> 55%. Decreases in heart failure

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27
Q

ohms law states?

A

change in pressure = the flow times the resistance

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28
Q

what are factors can cause increased viscosity?

A

polycythemia, hyperproteinemic states (multiple myeloma) and hereditary spherocytosis

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29
Q

what vessels account for most of the peripheral resistance?

A

arterioles

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30
Q

what is happening during isovolumetric contraction?

A

mitral valve closes, pressure is increasing in ventricle until aortic valve opens

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31
Q

define systole?

A

aortic valve is open, blood is leaving heart

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32
Q

what is isovolumetric relaxation?

A

period between aortic valve closing and mitral valve opening

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33
Q

what is happening during S1:

A

mitral and tricuspid valved close

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34
Q

what is happening during S2?

A

aortic and pulmonary valve closure

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35
Q

what is happening in S3?

A

in early diastole during rapid ventricular filling phase. Associated with increased filling pressure and more common in dilated ventricles (normal for pg women and kids)

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36
Q

S4 is associated with

A

ventricular hyprtrophy. Left atrium may push against stiff LV wall

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37
Q

jugular venous pulse a wave:

A

atrial contraction

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38
Q

jugular venous pulse c wave?

A

RV contraction (closed tricuspid bulging into atrium

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39
Q

jugular venous pulse v wave?

A

increased right atrial pressure due to filling against closed tricuspid valve

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40
Q

what normal physiologic process can cause S2 splitting?

A

aortic closes before pulmonic. Inspiration increases this difference

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41
Q

what is associated with wide splitting?

A

pulmonic stenosis or right bundle branch block

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42
Q

what is associated with fixed splitting?

A

ASD

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43
Q

what is associated with paradoxical splitting?

A

aortic stenosis and left bundle branch block

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44
Q

what is the mechanism of normal S2 splitting

A

inspiration leads to drop in intrathoracic pressure, which increases the capacity of the pulmonary circulation. The pulmonic valve closes later to accommodate the more blood entering the lungs. Aortic valve closes earlier because of decreased blood return to heart

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45
Q

right sternal border sounds:

A

during systole: aortic stenosis, flow murmur and aortic valve stenosis

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46
Q

left sternal border sounds:

A

during systole: hypertrophic cardiomyopathy. During diastole: aortic regurg, pulmonic regurg

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47
Q

where would you listen for an ASD?

A

pulmonic area (upper right sternal border) during systole

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48
Q

where would you listen for mitral valve issues?

A

5th rib, halfway to axilla (the only non-peristernal location)

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49
Q

what happens to the quality of right sided heart sounds with inspiration?

A

they increase

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50
Q

What are the pathologic systolic heart sounds?

A

Aortic/pulmonic stenosis

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51
Q

What are the pathologic diastolic heart sounds?

A

Aortic/pulmonic regurgitation

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52
Q

Heart Murmurs: MItral/Tricuspid Regurgitation (MR/TR)

A

Holosystolic, high pitched blowing murmur

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53
Q

What increases a mitral regurgitation murmur?

A

Maneuvers that increase TPR (squatting, hand grip) or LA return (exhalation)

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54
Q

What are the common causes of mitral regurgitation?

A

Ischemic heart disease, mitral valve prolapse, LV dilation, rheumatic fever

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55
Q

What are the common causes of tricuspid regurgitation?

A

RV dilation, endocarditis, rheumatic fever

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56
Q

Heart Murmurs: Aortic Stenosis

A

Crescendo-decresendo systolic ejection murmur following ejection click (due to abrupt halting of valve leaflets)

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57
Q

What is the cause of an ejection click in aortic stenosis?

A

Abrupt halting of valve leaflets

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58
Q

What are the common causes of aortic stenosis?

A

Age-related calcific aortic stenosis or bicuspid aortic valve

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59
Q

Heart Murmurs: Ventricular Septal Defect

A

Holosystolic, harsh sounding murmur

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60
Q

Heart Murmurs: MItral Prolapse

A

Late systolic crescendo murmur with midsystolic click (due to sudden tension of chordae tendineae)

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61
Q

What is the most common cause of midsystolic click in mitral prolapse?

A

Sudden tensing of the chordae tendineae

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62
Q

What are the common causes of mitrial prolapse?

A

Myxomatous degeneration, rheumatic fever, or chordae rupture.

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63
Q

Heart Murmurs: Aortic Regurgitation

A

Immediate, high pitched blowing diastolic murmur with wide pulse pressure, bounding pulses and head bobbing

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64
Q

What are the common causes of aortic regurgitation?

A

Aortic root dilation, bicuspid aortic valve or rheumatic fever.

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65
Q

What medications can decrease the intensity of the aortic regurgitation murmur?

A

Sasodilators

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66
Q

Heart Murmur: Mitral Stenosis

A

Following opening snap (due to tensing of chordae tendineae)

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67
Q

What are the common causes of mitral stenosis?

A

rheumatic fever

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68
Q

Heart Murmur: Patent Ductus Arteriosus

A

Continuous machine like mumur

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69
Q

What are the common causes of PDA?

A

Congenital rubella or prematurity

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70
Q

describe the role of calcium in cardiac muscle contraction:

A

cardiac muscle contraction depends on extracellular calcium, which enters during the plateau of action potential and stimulates calcium release from SR.

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71
Q

compare cardiac muscle to skeletal muscle

A

cardiac has a plateau (due to calcium influx), cardiac nodal cells spontaneously depolarize during diastole, cardiac myocytes are electrically coupled to each other by gap junctions

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72
Q

what is happening in phase 0 of the ventricular action potential?

A

rapid upstroke. Opening of voltage gated Na+ channels

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73
Q

what is happening in phase 1 of the ventricular action potential?

A

initial repolarization. Inactivation of voltage-gated Na+ channels. Voltage gated K+ channels begin to open

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74
Q

what is happening in phase 2 of the ventricular action potential?

A

plateau. Ca++ influx through voltage gated Ca++ channels balances K+efflux. Ca++ influx triggers Ca++ release from SR and myocyte contraction

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75
Q

what is happening during phase 3 of the ventricular action potential?

A

rapid reploarization. Massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca++ channels

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76
Q

what is happening during phase 4 of the ventricular action potential?

A

resting potential. High K+ permeability through K+ channels

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77
Q

where does the pacemaker action potential take place?

A

the SA and AV nodes

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78
Q

phase 0 of the pacemaker action potential?

A

upstroke. Opening of voltage gated Ca++ channels. These cells lack fast voltage-gated Na+ channels, results in slow conduction velocity that is used by AV node to prolong transmission from the atria to ventricles

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79
Q

describe phase 2 of the pacemaker action potential?

A

no plateau

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80
Q

describe phase 3 of the pacemaker action potential?

A

inactivation of the Ca++ channels and increased activation of K+ channels, increasing K+ efflux

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81
Q

describe phase 4 of the pacemaker action potential?

A

slow diastolic depolarization, membranse potential spontaneously depolarizes as Na+ conductance increases. . This accounts for the automacity of the SA and AV nodes.

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82
Q

what phase of the of the pacemaker action potential determines heart rate?

A

phase 4

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83
Q

what does administration of Ach or adenosine do to diastolic depolarization and heart rate?

A

decreases heart rate

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84
Q

the P wave represents?

A

atrial depolarization

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85
Q

what is a normal PR interval?

A

less than 200 ms

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86
Q

what does the QRS complex represent?

A

ventricular depolarization (normally less than 120 ms)

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87
Q

what is happening during the QT interval?

A

mechanical contraction of the ventricles

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88
Q

what does the T wave represent?

A

ventricular repolarization

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89
Q

what does T -wave inversion indicate?

A

a recent MI

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90
Q

what might cause a U wave on ekg?

A

hypokalemia or bradycardia

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91
Q

what is torsades de pointes?

A

ventricular tachycardia characterized by sinusoidal waveforms on ECG. Can progress to v-fib

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92
Q

what is Jervell and Lange-Nielsen syndrome?

A

congenital long QT syndrome due to defects in cardiac sodium and potassium channels. Presents with severe congenital sensorineural deafness

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93
Q

what is wolff-parkinson-white syndrome?

A

ventricular preexcitation syndrome. Accessory conduction pathway from atria to ventricle (bindle of kent) bypassing AV node. Ventricles partially depolarize early, making a delta wave on EKG. May lead to recurrent entry and supraventricular tachycardia

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94
Q

describe the trace of A fib:

A

chaotic and erratic baseline (irregularly regular) with no discrete P waves. Irregularly spaced ORS complexes.

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95
Q

what are the risks and treatments of A fib?

A

atrial stasis leading to stroke. Tx with beta blockers/calcium-channel blockers, and warfarin (prophylaxis against thromboembolism)

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96
Q

describe the trace of atrial flutter:

A

a rapid succession of identical, back to back atrial depolarization waves. “sawtooth”

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97
Q

tx for atrial flutter?

A

Class IA, IC or III antiarrhythmics

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98
Q

describe first degree AV block:

A

the PR interval is prolonged (>200) asymptomatic

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99
Q

describe second degree heart block, Mobitz type I, wenkebach:

A

progressive lengthening of PR interval until a beat is ‘dropped’ (P wave not followed by a QRS complex) usually asymptomatic

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100
Q

describe second degree heart block, Mobitz type II

A

dropped beats are not preceded by a change in PR interval. Abrupt, non-conducted P waves result in a pathologic condition.

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101
Q

describe a third degree heart block:

A

the atria and ventricles beat independently of each other. Both P waves and QRS complex are present, but the P waves bear no relation to the QRS complex.

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102
Q

tx for third degree heart block?

A

a pacemaker

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103
Q

infectious cause of third degree heart block?

A

lyme disease

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104
Q

describe V fib:

A

a completely erratic rhythm with no identifiable waves. Fatal without immidiate CPR and defribillation

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105
Q

what does decreased MAP do to the JGA?

A

JGA senses decreased MAP, stimulates the renin-angiotensin system, angiotensin II causes vasoconstriction and increased TPR, aldosterone increases blood volume, increasing cardiac output.

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106
Q

what does decreased MAP do to the baroreceptors?

A

decreases firing rate, increasing sympathetic activity

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107
Q

what does increased sympathetic activity do to cardiac output and TPR?

A

stimulation of beta 1’s increase heart rate and contractility, increase CO. Stimulation of alpha 1’s cause venoconstriction, increasing venous return and cardiac output, and alpha stimulation also causes arteriolar vasoconstriction increasing TPR

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108
Q

what causes the release of ANP?

A

ANP is released from the atrial in response to increased blood volume and atrial pressure.

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109
Q

what does increased ANP cause?

A

relaxation of vasculature. Constricts efferent renal arterioles and dilates afferent arterioles, promoting diuresis.

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110
Q

by what nerve does the aortic arch receptor transmit information?

A

vagus

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111
Q

by what nerve does the carotid sinus receptor transmit information?

A

glossopharyngeal to solitary nucleus of medulla.

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112
Q

what affect does hypotension have on the baroreceptors?

A

hypotension causes a decrease in arterial pressure, decreasing stretch, decreasing afferent baroreceptor firing, increasing efferent sympathetic firing and decreasing efferent parasympathetic stimulation, leading to vasoconstriction, increased heart rate and BP.

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113
Q

what happens when you massage the carotid?

A

increase pressure on carotid artery, increasing streth, increasing the afferent baroreceptor firing rate and decreasing heart rate

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114
Q

to what stimuli do the peripheral chemoreceptors respond?

A

decreased PO2 (

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115
Q

what stimuli do the central chemoreceptors respond?

A

changes in pH and PCO2 in brain interstitial fluid. Does not respond to P02.

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116
Q

what vessel supplies the SA and AV nodes?

A

the RCA (80% of the time)

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117
Q

what vessel supplies the posterior left ventricle?

A

circumflex artery

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118
Q

what vessel supplies the apex and anterior interventricular septum?

A

the left anterior descending

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119
Q

what vessel supplies the the posterior septum?

A

posterior descending/interventricular artery

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120
Q

what vessel supplies the right ventricle?

A

the acute marginal artery

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121
Q

what is the most common site of coronary artery occlusion?

A

the LAD, which supplies the anterior interventricular septum

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122
Q

when do the coronary arteries fill?

A

diastole

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123
Q

enlargement of the left atrium can result in?

A

dysphagia (due to compression of the esophageal nerve) or hoarseness (due to compression of the recurrent laryngeal nerve

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124
Q

what is the equation for cardiac output?

A

stroke volume x heart rate

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125
Q

what is the fick principle?

A

cardiac output = (rate of O2 consumption)/(arterial O2 content - venous O2 content)

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126
Q

what arethe equations for mean arterial pressure?

A

(cardiac output) x (total peripheral resistance) OR 2/3 diastolic + 1/3 systolic pressure

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127
Q

what is the equation for pulse pressure?

A

systolic pressure - diastolic pressure

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128
Q

pulse pressure is a rough correlate for?

A

stroke volume

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129
Q

what are the equations for determining stroke volume?

A

CO/HR or EDV-ESV

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130
Q

what variables affect stroke volume?

A

contractility, afterload, preload

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131
Q

what factors can increase contractility (and therefore stroke volume)?

A

catecholamines (increase the activity of Ca++ pump) in SR), increased intracellular calcium, decreased extracellular sodium (decreased activity of the Na+/Ca++ exchanger), digitalis (increased intracellular Na+, resulting in increased Ca++)

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132
Q

what factors can decrease contractility (and therefore stroke volume)?

A

beta blockade (decreased cAMP), heart failure (systolic dysfunction) acidosis, hypoxia/hypercapnea, and non-dihydropyridine Ca++ channel blockers

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133
Q

the preload is equal to the?

A

end diastolic volume

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134
Q

the afterload is equal to the?

A

mean arterial pressure (proportional to peripheral resistance)

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135
Q

venodilators (like nitroglycerine) have what effect on preload?

A

they decrease it

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136
Q

vasodilators (like hydralazine) have what affect on afterload?

A

they decrease it

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137
Q

what factors increase preload?

A

exercise, increased blood volume and excitement (sympathetics)

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138
Q

what is starling’s law?

A

force of contraction is equal to the initial length of cardiac muscle fiber (preload)

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139
Q

what is the equation for ejection fraction?

A

EF=SV/EDV=(EDV-ESV)/EDV

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140
Q

the ejection fraction is an index of?

A

ventricular contractility

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141
Q

what is an approximate normal ejection fraction?

A

55%. Decreases in heart failure

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142
Q

ohms law states?

A

change in pressure = the flow times the resistance

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143
Q

what are factors can cause increased viscosity?

A

polycythemia, hyperproteinemic states (multiple myeloma) and hereditary spherocytosis

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144
Q

what vessels account for most of the peripheral resistance?

A

arterioles

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145
Q

what is happening during isovolumetric contraction?

A

mitral valve closes, pressure is increasing in ventricle until aortic valve opens

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146
Q

define systole?

A

aortic valve is open, blood is leaving heart

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147
Q

what is isovolumetric relaxation?

A

period between aortic valve closing and mitral valve opening

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148
Q

what is happening during S1:

A

mitral and tricuspid valved close

149
Q

what is happening during S2?

A

aortic and pulmonary valve closure

150
Q

what is happening in S3?

A

in early diastole during rapid ventricular filling phase. Associated with increased filling pressure and more common in dilated ventricles (normal for pg women and kids)

151
Q

S4 is associated with

A

ventricular hyprtrophy. Left atrium may push against stiff LV wall

152
Q

jugular venous pulse a wave:

A

atrial contraction

153
Q

jugular venous pulse c wave?

A

RV contraction (closed tricuspid bulging into atrium

154
Q

jugular venous pulse v wave?

A

increased right atrial pressure due to filling against closed tricuspid valve

155
Q

what normal physiologic process can cause S2 splitting?

A

aortic closes before pulmonic. Inspiration increases this difference

156
Q

what is associated with wide splitting?

A

pulmonic stenosis or right bundle branch block

157
Q

what is associated with fixed splitting?

A

ASD

158
Q

what is associated with paradoxical splitting?

A

aortic stenosis and left bundle branch block

159
Q

what is the mechanism of normal S2 splitting

A

inspiration leads to drop in intrathoracic pressure, which increases the capacity of the pulmonary circulation. The pulmonic valve closes later to accommodate the more blood entering the lungs. Aortic valve closes earlier because of decreased blood return to heart

160
Q

right sternal border sounds:

A

during systole: aortic stenosis, flow murmur and aortic valve stenosis

161
Q

left sternal border sounds:

A

during systole: hypertrophic cardiomyopathy. During diastole: aortic regurg, pulmonic regurg

162
Q

where would you listen for an ASD?

A

pulmonic area (upper right sternal border) during systole

163
Q

where would you listen for mitral valve issues?

A

5th rib, halfway to axilla (the only non-peristernal location)

164
Q

what happens to the quality of right sided heart sounds with inspiration?

A

they increase

165
Q

what are the pathologic systolic heart sounds:

A

aortic/pulmonic stenosis, mitral/tricuspid regurg

166
Q

what are the pathologic diastolic heart sounds:

A

aortic/pulmonic regurg, mitral/tricuspid stenosis

167
Q

holosystolic, high pitched ‘blowing’ murmur?

A

mitral/tricuspid regurg

168
Q

what can increase a mitral regurg murmur?

A

maneuvers that increase TPR (squatting, hand grip) or LA return (exhalation)

169
Q

common causes of mitral regurg?

A

ischemic heart disease, mitral valve prolapse or LV dilation

170
Q

common causes of tricuspid regurg?

A

RV dilation or endocarditis. Also rheumatic fever

171
Q

crescendo-decresendo systolic ejection murmur following ejection click, radiating to carotids:

A

aortic stenosis

172
Q

what is the cause of an ejection click?

A

abrupt halting of valce leaflets

173
Q

common causes of aortic stenosis?

A

age-related calcific aortic stenosis or bicuspid aortic valve

174
Q

pulses weak compare to heart sounds?

A

aortic stenosis

175
Q

holosystolic, harsh sounding murmur loudest at tricuspid area?

A

VSD

176
Q

late systolic crescendo murmur with midsystolic click?

A

mitral prolapse

177
Q

what is the most common cause of midsystolic click?

A

sudden tensing of the chordae tendineae

178
Q

mitral proplase can predispose to what?

A

endocarditis

179
Q

causes of mitrial prolapse:

A

myxomatous degeneration, rheumatic fever, or chordae rupture.

180
Q

immediate, high pitched blowing diastolic murmur with wide pulse pressure, bounding pulses and head bobbing:

A

aortic regurg

181
Q

causes of aortic regurg:

A

aortic root dilation, bicuspid aortic valve or rheumatic fever.

182
Q

what medications can decrease the intensity of the aortic regurg murmur?

A

vasodilators

183
Q

opening snap, followed by delayed rumbling late in diastole:

A

mitral stenosis

184
Q

common cause of mitral stenosis:

A

rheumatic fever

185
Q

continuous machine-like murmur:

A

PDA

186
Q

common causes of PDA

A

congenital rubella or prematurity

187
Q

describe the role of calcium in cardiac muscle contraction:

A

cardiac muscle contraction depends on extracellular calcium, which enters during the plateau of action potential and stimulates calcium release from SR.

188
Q

compare cardiac muscle to skeletal muscle

A

cardiac has a plateau (due to calcium influx), cardiac nodal cells spontaneously depolarize during diastole, cardiac myocytes are electrically coupled to each other by gap junctions

189
Q

what is happening in phase 0 of the ventricular action potential?

A

rapid upstroke. Opening of voltage gated Na+ channels

190
Q

what is happening in phase 1 of the ventricular action potential?

A

initial repolarization. Inactivation of voltage-gated Na+ channels. Voltage gated K+ channels begin to open

191
Q

what is happening in phase 2 of the ventricular action potential?

A

plateau. Ca++ influx through voltage gated Ca++ channels balances K+efflux. Ca++ influx triggers Ca++ release from SR and myocyte contraction

192
Q

what is happening during phase 3 of the ventricular action potential?

A

rapid reploarization. Massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca++ channels

193
Q

what is happening during phase 4 of the ventricular action potential?

A

resting potential. High K+ permeability through K+ channels

194
Q

where does the pacemaker action potential take place?

A

the SA and AV nodes

195
Q

phase 0 of the pacemaker action potential?

A

upstroke. Opening of voltage gated Ca++ channels. These cells lack fast voltage-gated Na+ channels, results in slow conduction velocity that is used by AV node to prolong transmission from the atria to ventricles

196
Q

describe phase 2 of the pacemaker action potential?

A

no plateau

197
Q

describe phase 3 of the pacemaker action potential?

A

inactivation of the Ca++ channels and increased activation of K+ channels, increasing K+ efflux

198
Q

describe phase 4 of the pacemaker action potential?

A

slow diastolic depolarization, membranse potential spontaneously depolarizes as Na+ conductance increases. . This accounts for the automacity of the SA and AV nodes.

199
Q

what phase of the of the pacemaker action potential determines heart rate?

A

phase 4

200
Q

what does administration of Ach or adenosine do to diastolic depolarization and heart rate?

A

decreases heart rate

201
Q

the P wave represents?

A

atrial depolarization

202
Q

what is a normal PR interval?

A

less than 200 ms

203
Q

what does the QRS complex represent?

A

ventricular depolarization (normally less than 120 ms)

204
Q

what is happening during the QT interval?

A

mechanical contraction of the ventricles

205
Q

what does the T wave represent?

A

ventricular repolarization

206
Q

what does T -wave inversion indicate?

A

a recent MI

207
Q

what might cause a U wave on ekg?

A

hypokalemia or bradycardia

208
Q

what is torsades de pointes?

A

ventricular tachycardia characterized by sinusoidal waveforms on ECG. Can progress to v-fib

209
Q

what is Jervell and Lange-Nielsen syndrome?

A

congenital long QT syndrome due to defects in cardiac sodium and potassium channels. Presents with severe congenital sensorineural deafness

210
Q

what is wolff-parkinson-white syndrome?

A

ventricular preexcitation syndrome. Accessory conduction pathway from atria to ventricle (bindle of kent) bypassing AV node. Ventricles partially depolarize early, making a delta wave on EKG. May lead to recurrent entry and supraventricular tachycardia

211
Q

describe the trace of A fib:

A

chaotic and erratic baseline (irregularly regular) with no discrete P waves. Irregularly spaced ORS complexes.

212
Q

what are the risks and treatments of A fib?

A

atrial stasis leading to stroke. Tx with beta blockers/calcium-channel blockers, and warfarin (prophylaxis against thromboembolism)

213
Q

describe the trace of atrial flutter:

A

a rapid succession of identical, back to back atrial depolarization waves. “sawtooth”

214
Q

tx for atrial flutter?

A

Class IA, IC or III antiarrhythmics

215
Q

describe first degree AV block:

A

the PR interval is prolonged (>200) asymptomatic

216
Q

describe second degree heart block, Mobitz type I, wenkebach:

A

progressive lengthening of PR interval until a beat is ‘dropped’ (P wave not followed by a QRS complex) usually asymptomatic

217
Q

describe second degree heart block, Mobitz type II

A

dropped beats are not preceded by a change in PR interval. Abrupt, non-conducted P waves result in a pathologic condition.

218
Q

describe a third degree heart block:

A

the atria and ventricles beat independently of each other. Both P waves and QRS complex are present, but the P waves bear no relation to the QRS complex.

219
Q

tx for third degree heart block?

A

a pacemaker

220
Q

infectious cause of third degree heart block?

A

lyme disease

221
Q

describe V fib:

A

a completely erratic rhythm with no identifiable waves. Fatal without immidiate CPR and defribillation

222
Q

what does decreased MAP do to the JGA?

A

JGA senses decreased MAP, stimulates the renin-angiotensin system, angiotensin II causes vasoconstriction and increased TPR, aldosterone increases blood volume, increasing cardiac output.

223
Q

what does decreased MAP do to the baroreceptors?

A

decreases firing rate, increasing sympathetic activity

224
Q

what does increased sympathetic activity do to cardiac output and TPR?

A

stimulation of beta 1’s increase heart rate and contractility, increase CO. Stimulation of alpha 1’s cause venoconstriction, increasing venous return and cardiac output, and alpha stimulation also causes arteriolar vasoconstriction increasing TPR

225
Q

what causes the release of ANP?

A

ANP is released from the atrial in response to increased blood volume and atrial pressure.

226
Q

what does increased ANP cause?

A

relaxation of vasculature. Constricts efferent renal arterioles and dilates afferent arterioles, promoting diuresis.

227
Q

by what nerve does the aortic arch receptor transmit information?

A

vagus

228
Q

by what nerve does the carotid sinus receptor transmit information?

A

glossopharyngeal to solitary nucleus of medulla.

229
Q

what affect does hypotension have on the baroreceptors?

A

hypotension causes a decrease in arterial pressure, decreasing stretch, decreasing afferent baroreceptor firing, increasing efferent sympathetic firing and decreasing efferent parasympathetic stimulation, leading to vasoconstriction, increased heart rate and BP.

230
Q

what happens when you massage the carotid?

A

increase pressure on carotid artery, increasing streth, increasing the afferent baroreceptor firing rate and decreasing heart rate

231
Q

to what stimuli do the peripheral chemoreceptors respond?

A

decreased PO2 (

232
Q

what stimuli do the central chemoreceptors respond?

A

changes in pH and PCO2 in brain interstitial fluid. Does not respond to P02.

233
Q

what is the Cushing reaction?

A

increased ICP constricts arterioles, causing cerebral ischemia, leading to systemic hypertension and reflex bradycardia.

234
Q

what is cushing triad?

A

hypertension, bradycardia and respiratory depression

235
Q

what organ gets the largest share of systemic output?

A

liver

236
Q

what organ gets the highest blood flow per gram of tissue?

A

kidney

237
Q

how is the O2 demand of the heart met?

A

O2 extraction is always 100%. Demand is met by increasing coronary blood flow, not by increasing extraction of O2

238
Q

what factors determine regulation of blood flow to the heart?

A

local metabolites - O2, adenosine and NO

239
Q

what factors determine regulation of blood flow to the brain?

A

local metabolites - CO2 (pH)

240
Q

what factors determine regulation of blood flow to the kidneys?

A

myogenic and tubuloglomerular feedback

241
Q

what factors determine regulation of blood flow to the lungs?

A

hypoxia causes vasoconstriction (this is unique)

242
Q

what factors determine regulation of blood flow to the skeletal muscle?

A

local metabolites – lactate, adenosine, K+

243
Q

what factors determine regulation of blood flow to the skin?

A

sympathetic stimulation is the most important. Temperature control

244
Q

name the 4 starling’s forces:

A

capillary pressure, interstitial pressure, plasma colloid pressure and interstitial fluid colloid osmotic pressure

245
Q

what is the equation for net filtration pressure?

A

[(Pc-Pi) - (πc-πi)

246
Q

what is edema?

A

excess fluid flow into interstitium

247
Q

what are the common causes of edema?

A

increased capillary pressure (heart failure), decreased plasma proteins (liver failure/nephrotic syndrome), increased capillary permeability (toxins, infections, burns), increased interstitial fluid colloid osmotic pressure (lymphatic blockage)

248
Q

right to left shunts cause?

A

early cyanosis. Blue babies.

249
Q

5 T’s of right to left shunts:

A

tetralogy of Fallot, Transposition of great vessels, truncus arteriosis, tricuspid atresia, and total anomalous pulmonary venous return

250
Q

what is persistant trunctus arteriosus?

A

failure of truncus arteriosus to divide into pulmonary trunk and aorta

251
Q

what is tricuspid atresia?

A

characterized by absence of tricuspid valve and hypoplastic right ventricle. Requires both ASD and VSD for viability

252
Q

what is TAPVR?

A

total anomalous pulmonary venous return. Pulmonary vein drains into right heart circulation (SVC, coronary sinus, etc)

253
Q

name the 3 types of left to right shunts:

A

VSD, ASD and PDA

254
Q

what is the most common congenital cardiac anomaly?

A

VSD

255
Q

what medication is given to close a PDA?

A

indomethacin

256
Q

what is eisenmenger’s syndrome?

A

uncorrected VSD, ASD or PDA causes compensatory vascular hypertrophy, which results in progressive pulmonary hypertension. As pulmonary resistance increases, the shunt reverses from left to right to right to left, which causes late cyanosis (clubbing and polycythemia)

257
Q

what are the 4 issues in tetralogy of fallot?

A

pulmonary stenosis (most inportant for prognosis), right ventricular hypertrophy, overiding aorta and VSD

258
Q

S/S of tetralogy of fallot?

A

early cyanosis is caused by r-l shunt across VSD. R-L shunt exists because of the increased pressure caused by stenotic pulmonic valve. X-Ray: boot shaped heart (because of RVH). Pt suffers cyanotic spells. Pt squats to improve symptoms

259
Q

embryology of tetralogy of fallot:

A

anterosuperior displacement of the infundibular septum

260
Q

describe the transposition of the great vessels:

A

aorta leaves RV, pulmonary trunk leaves left ventricle, keeping the pulmonary and systemic circulations separate. Not compatible with life without a PDA, VSD or patent foramen ovale to allow for mixing of blood

261
Q

embryology of transposition of the great vessels:

A

failure of the aorticopulmonary septum to spiral

262
Q

infantile coarctation of the aorta s associated with what chromosomal anomaly?

A

turner

263
Q

where is the coarctation in infantile type CotA?

A

proximal to insertion of ductus arteriosum

264
Q

notched ribs, hypertension in arms, weak pulse in legs:

A

adult type coarctation of the aorta

265
Q

coarctation of the aorta can cause what type of murmur?

A

aorti regurg

266
Q

coarctation of the aorta is associated with what valve abnormality?

A

bicuspid aortic valve

267
Q

what is the ductus arteriosus?

A

normal fetal R - L shunt. When an infant takes her first breath lung resistance decreases and PDA should close.

268
Q

what is a patent ductus arteriosus?

A

DA doesn’t close and a left to right shunt forms, causing RVH and failure.

269
Q

how do you maintain a patent ductus arteriosus?

A

PGE

270
Q

continuous machine-like murmur:

A

PDA

271
Q

late cyanosis in lower extremities?

A

PDA

272
Q

what vessel supplies the SA and AV nodes?

A

the RCA (80% of the time)

273
Q

what vessel supplies the posterior left ventricle?

A

circumflex artery

274
Q

what vessel supplies the apex and anterior interventricular septum?

A

the left anterior descending

275
Q

what vessel supplies the the posterior septum?

A

posterior descending/interventricular artery

276
Q

what vessel supplies the right ventricle?

A

the acute marginal artery

277
Q

what is the most common site of coronary artery occlusion?

A

the LAD, which supplies the anterior interventricular septum

278
Q

when do the coronary arteries fill?

A

diastole

279
Q

enlargement of the left atrium can result in?

A

dysphagia (due to compression of the esophageal nerve) or hoarseness (due to compression of the recurrent laryngeal nerve

280
Q

what is the equation for cardiac output?

A

stroke volume x heart rate

281
Q

what is the fick principle?

A

cardiac output = (rate of O2 consumption)/(arterial O2 content - venous O2 content)

282
Q

what arethe equations for mean arterial pressure?

A

(cardiac output) x (total peripheral resistance) OR 2/3 diastolic + 1/3 systolic pressure

283
Q

what is the equation for pulse pressure?

A

systolic pressure - diastolic pressure

284
Q

pulse pressure is a rough correlate for?

A

stroke volume

285
Q

what are the equations for determining stroke volume?

A

CO/HR or EDV-ESV

286
Q

what variables affect stroke volume?

A

contractility, afterload, preload

287
Q

what factors can increase contractility (and therefore stroke volume)?

A

catecholamines (increase the activity of Ca++ pump) in SR), increased intracellular calcium, decreased extracellular sodium (decreased activity of the Na+/Ca++ exchanger), digitalis (increased intracellular Na+, resulting in increased Ca++)

288
Q

what factors can decrease contractility (and therefore stroke volume)?

A

beta blockade (decreased cAMP), heart failure (systolic dysfunction) acidosis, hypoxia/hypercapnea, and non-dihydropyridine Ca++ channel blockers

289
Q

the preload is equal to the?

A

end diastolic volume

290
Q

the afterload is equal to the?

A

mean arterial pressure (proportional to peripheral resistance)

291
Q

venodilators (like nitroglycerine) have what effect on preload?

A

they decrease it

292
Q

vasodilators (like hydralazine) have what affect on afterload?

A

they decrease it

293
Q

what factors increase preload?

A

exercise, increased blood volume and excitement (sympathetics)

294
Q

what is starling’s law?

A

force of contraction is equal to the initial length of cardiac muscle fiber (preload)

295
Q

what is the equation for ejection fraction?

A

EF=SV/EDV=(EDV-ESV)/EDV

296
Q

the ejection fraction is an index of?

A

ventricular contractility

297
Q

what is an approximate normal ejection fraction?

A

55%. Decreases in heart failure

298
Q

ohms law states?

A

change in pressure = the flow times the resistance

299
Q

what are factors can cause increased viscosity?

A

polycythemia, hyperproteinemic states (multiple myeloma) and hereditary spherocytosis

300
Q

what vessels account for most of the peripheral resistance?

A

arterioles

301
Q

what is happening during isovolumetric contraction?

A

mitral valve closes, pressure is increasing in ventricle until aortic valve opens

302
Q

define systole?

A

aortic valve is open, blood is leaving heart

303
Q

what is isovolumetric relaxation?

A

period between aortic valve closing and mitral valve opening

304
Q

what is happening during S1:

A

mitral and tricuspid valved close

305
Q

what is happening during S2?

A

aortic and pulmonary valve closure

306
Q

what is happening in S3?

A

in early diastole during rapid ventricular filling phase. Associated with increased filling pressure and more common in dilated ventricles (normal for pg women and kids)

307
Q

S4 is associated with

A

ventricular hyprtrophy. Left atrium may push against stiff LV wall

308
Q

jugular venous pulse a wave:

A

atrial contraction

309
Q

jugular venous pulse c wave?

A

RV contraction (closed tricuspid bulging into atrium

310
Q

jugular venous pulse v wave?

A

increased right atrial pressure due to filling against closed tricuspid valve

311
Q

what normal physiologic process can cause S2 splitting?

A

aortic closes before pulmonic. Inspiration increases this difference

312
Q

what is associated with wide splitting?

A

pulmonic stenosis or right bundle branch block

313
Q

what is associated with fixed splitting?

A

ASD

314
Q

what is associated with paradoxical splitting?

A

aortic stenosis and left bundle branch block

315
Q

what is the mechanism of normal S2 splitting

A

inspiration leads to drop in intrathoracic pressure, which increases the capacity of the pulmonary circulation. The pulmonic valve closes later to accommodate the more blood entering the lungs. Aortic valve closes earlier because of decreased blood return to heart

316
Q

right sternal border sounds:

A

during systole: aortic stenosis, flow murmur and aortic valve stenosis

317
Q

left sternal border sounds:

A

during systole: hypertrophic cardiomyopathy. During diastole: aortic regurg, pulmonic regurg

318
Q

where would you listen for an ASD?

A

pulmonic area (upper right sternal border) during systole

319
Q

where would you listen for mitral valve issues?

A

5th rib, halfway to axilla (the only non-peristernal location)

320
Q

what happens to the quality of right sided heart sounds with inspiration?

A

they increase

321
Q

what are the pathologic systolic heart sounds:

A

aortic/pulmonic stenosis, mitral/tricuspid regurg

322
Q

what are the pathologic diastolic heart sounds:

A

aortic/pulmonic regurg, mitral/tricuspid stenosis

323
Q

holosystolic, high pitched ‘blowing’ murmur?

A

mitral/tricuspid regurg

324
Q

what can increase a mitral regurg murmur?

A

maneuvers that increase TPR (squatting, hand grip) or LA return (exhalation)

325
Q

common causes of mitral regurg?

A

ischemic heart disease, mitral valve prolapse or LV dilation

326
Q

common causes of tricuspid regurg?

A

RV dilation or endocarditis. Also rheumatic fever

327
Q

crescendo-decresendo systolic ejection murmur following ejection click, radiating to carotids:

A

aortic stenosis

328
Q

what is the cause of an ejection click?

A

abrupt halting of valce leaflets

329
Q

common causes of aortic stenosis?

A

age-related calcific aortic stenosis or bicuspid aortic valve

330
Q

pulses weak compare to heart sounds?

A

aortic stenosis

331
Q

holosystolic, harsh sounding murmur loudest at tricuspid area?

A

VSD

332
Q

late systolic crescendo murmur with midsystolic click?

A

mitral prolapse

333
Q

what is the most common cause of midsystolic click?

A

sudden tensing of the chordae tendineae

334
Q

mitral proplase can predispose to what?

A

endocarditis

335
Q

causes of mitrial prolapse:

A

myxomatous degeneration, rheumatic fever, or chordae rupture.

336
Q

immediate, high pitched blowing diastolic murmur with wide pulse pressure, bounding pulses and head bobbing:

A

aortic regurg

337
Q

causes of aortic regurg:

A

aortic root dilation, bicuspid aortic valve or rheumatic fever.

338
Q

what medications can decrease the intensity of the aortic regurg murmur?

A

vasodilators

339
Q

opening snap, followed by delayed rumbling late in diastole:

A

mitral stenosis

340
Q

common cause of mitral stenosis:

A

rheumatic fever

341
Q

continuous machine-like murmur:

A

PDA

342
Q

common causes of PDA

A

congenital rubella or prematurity

343
Q

describe the role of calcium in cardiac muscle contraction:

A

cardiac muscle contraction depends on extracellular calcium, which enters during the plateau of action potential and stimulates calcium release from SR.

344
Q

compare cardiac muscle to skeletal muscle

A

cardiac has a plateau (due to calcium influx), cardiac nodal cells spontaneously depolarize during diastole, cardiac myocytes are electrically coupled to each other by gap junctions

345
Q

what is happening in phase 0 of the ventricular action potential?

A

rapid upstroke. Opening of voltage gated Na+ channels

346
Q

what is happening in phase 1 of the ventricular action potential?

A

initial repolarization. Inactivation of voltage-gated Na+ channels. Voltage gated K+ channels begin to open

347
Q

what is happening in phase 2 of the ventricular action potential?

A

plateau. Ca++ influx through voltage gated Ca++ channels balances K+efflux. Ca++ influx triggers Ca++ release from SR and myocyte contraction

348
Q

what is happening during phase 3 of the ventricular action potential?

A

rapid reploarization. Massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca++ channels

349
Q

what is happening during phase 4 of the ventricular action potential?

A

resting potential. High K+ permeability through K+ channels

350
Q

where does the pacemaker action potential take place?

A

the SA and AV nodes

351
Q

phase 0 of the pacemaker action potential?

A

upstroke. Opening of voltage gated Ca++ channels. These cells lack fast voltage-gated Na+ channels, results in slow conduction velocity that is used by AV node to prolong transmission from the atria to ventricles

352
Q

describe phase 2 of the pacemaker action potential?

A

no plateau

353
Q

describe phase 3 of the pacemaker action potential?

A

inactivation of the Ca++ channels and increased activation of K+ channels, increasing K+ efflux

354
Q

describe phase 4 of the pacemaker action potential?

A

slow diastolic depolarization, membranse potential spontaneously depolarizes as Na+ conductance increases. . This accounts for the automacity of the SA and AV nodes.

355
Q

what phase of the of the pacemaker action potential determines heart rate?

A

phase 4

356
Q

what does administration of Ach or adenosine do to diastolic depolarization and heart rate?

A

decreases heart rate

357
Q

the P wave represents?

A

atrial depolarization

358
Q

what is a normal PR interval?

A

less than 200 ms

359
Q

what does the QRS complex represent?

A

ventricular depolarization (normally less than 120 ms)

360
Q

what is happening during the QT interval?

A

mechanical contraction of the ventricles

361
Q

what does the T wave represent?

A

ventricular repolarization

362
Q

what does T -wave inversion indicate?

A

a recent MI

363
Q

what might cause a U wave on ekg?

A

hypokalemia or bradycardia

364
Q

what is torsades de pointes?

A

ventricular tachycardia characterized by sinusoidal waveforms on ECG. Can progress to v-fib

365
Q

what is Jervell and Lange-Nielsen syndrome?

A

congenital long QT syndrome due to defects in cardiac sodium and potassium channels. Presents with severe congenital sensorineural deafness

366
Q

what is wolff-parkinson-white syndrome?

A

ventricular preexcitation syndrome. Accessory conduction pathway from atria to ventricle (bindle of kent) bypassing AV node. Ventricles partially depolarize early, making a delta wave on EKG. May lead to recurrent entry and supraventricular tachycardia

367
Q

describe the trace of A fib:

A

chaotic and erratic baseline (irregularly regular) with no discrete P waves. Irregularly spaced ORS complexes.

368
Q

What factors increase myocardial O2 demand?

A

Increased afterload (arterial pressure)

369
Q

Under what circumstances does stroke volume increase?

A

Anxiety

First Aid Cardiology (1 decks)

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