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► Med Notes > Cardiology_1 > Flashcards

Cardiology_1 Flashcards

1
Q

Truncus arteriosus gives rise to what?

A

ascending aorta and pulmonary trunk

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2
Q

bulbus cordis gives rise to what?

A

smooth parts (outflow tract) of left and right ventricles

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3
Q

primitive ventricle gives rise to what?

A

trabeculated left and right ventricles

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4
Q

primitive atria give rise to what?

A

trabeculated left and right atria

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5
Q

left horn of sinus venosus gives rise to what?

A

coronary sinus

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6
Q

right horn of SV gives rise to what?

A

smooth part of right atrium

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7
Q

right common cardinal vein and right anterior cardinal vein give rise to what?

A

SVC

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8
Q

what happens in the normal development of the truncus arteriosus?

A

neural crest migration → truncal and bulbar ridges that spiral and fuse to form the aorticopulmonary (AP) septum→ ascending aorta and pulmonary trunk

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9
Q

what are the truncus arteriosus pathologies?

A
  1. TGA • 2. ToF • 3. TA
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10
Q

what is the defect in transposition of the great vessels?

A

failure to spiral

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11
Q

what is the TA defect in tetralogy of Fallot?

A

skewed AP septum development

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12
Q

what is the defect in persistent TA?

A

partial AP septum development

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13
Q

3 steps in embryologic formation of interventricular septum?

A
  1. muscular ventricular septum forms- opening= interventricular foramen • 2. AP septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular foramen • 3. Growth of endocardial cushions separates atria from ventricles and contributes to both atrial separation and membranous portion of the interventricular septum
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14
Q

improper neural crest migration into the TA can result in what?

A

transposition of the great arteries or a persistent TA

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15
Q

in interventricular septum development, membranous septal defect causes what?

A

an initial left to right shunt, which later reverses to a right to left shunt due to onset of pulmonary hypertension (Eissenmenger’s syndrome)

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16
Q

8 steps in interatrial septum development?

A
  1. foramen primum narrows as septum primum grows toward endocardial cushions • 2. perforations in septum primum form foramen secundum (foramen primum disappears • 3. foramen scundum maintains right to left shunt as septum secundum begins to grow • 4. septum secundum contains a permanent opening (foramen ovale) • 5. foramen secundum enlarges and upper part of septum primum degenerates • 6. remaining portion of septum primum forms the valve of the foramen ovale • 7. septum secundum and septum primum fuse to form the atrial septum • 8. foramen ovale usually closes soon after birth because of ↑ LA pressure
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17
Q

what happens in pathology of interatrial septal development?

A

patent foramen ovale, caused by failure of the septum primum and septum secundum to fuse after birth

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18
Q

when is there fetal erythropoiesis in the yolk sac?

A

3-10wk

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19
Q

when is there fetal erythropoiesis in the liver?

A

6wk-birth

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20
Q

when is there fetal erythropoiesis in the spleen?

A

15-30wk

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21
Q

when is there fetal erythropoiesis in the bone marrow?

A

22wk-adult

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22
Q

mnemonic for fetal erythropoiesis?

A

young liver synthesizes blood

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23
Q

structure of HbF?

A

α2γ2

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24
Q

structure of HbA?

A

α2β2

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25
Q

O2 content of fetal blood in the umbilical vein?

A

PO2~30 • 80% saturated with O2

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26
Q

O2 sat of umbilican arteries?

A

low

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27
Q

sites of 3 important shunts of fetal circulation?

A
  1. ductus venosus • 2. foramen ovale • 3. ductus arteriosus
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28
Q

action of shunt at ductus venosus in fetal circulation?

A

blood entering the fetus through the umbilical vein is coducted via the ductus venosus into the IVC to bypass the hepatic circulation

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29
Q

action of the shunt at the foramen ovale in fetal circulation?

A

most oxygenated blood reaching the heart via the IVC is diverted through the foramen ovale and pumped out the aorta to the head and body

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30
Q

action of the shunt at the ductus arteriosus in fetal circulation?

A

deoxygenated blood entering the RA from the SVC enters the RV, is expelled into the pulmonary artery, then passes through the ductus arteriosus into the descending aorta

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31
Q

what happens to fetal circulation at birth when the infant takes a breath?

A

↓ resistance in pulmonary vasculature causes ↑ LA pressure vs RA pressure→ • foramen ovale closes (now called fossa ovalis) → • ↑ in O2 leads to ↓ in prostaglandins, causing closure of ductus arteriosus

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32
Q

what helps close PDA?

A

indomethacin

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33
Q

what keeps PDA open?

A

PGE1, PGE2

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34
Q

post natal derivative of the umbilical vein?

A

ligamentum teres hepatis, contained in falciform ligament

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35
Q

postnatal derivatives of umbilical arteries?

A

medial umbilical ligaments

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36
Q

postnatal derivatives of ductus arteriosus?

A

ligamentum arteriosum

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37
Q

postnatal derivative of ductus venosus?

A

ligamentum venosum

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38
Q

postnatal derivative of foramen ovale?

A

fossa ovalis

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39
Q

postnatal derivative of allantois?

A

urachus-median umbilical ligament

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40
Q

what is the urachus part of?

A

the allantoic duct between the bladder and the umbilicus

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41
Q

what finding is a remnant of the urachus?

A

urachal cyst, or sinus

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42
Q

postnatal derivative of the notochord?

A

nucleus pulplosus of intervertebral disc

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43
Q

LCX supplies what?

A

lateral and posterior walls of left ventricle

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44
Q

LAD supplies what?

A

anterior 2/3 of interventricular septum, anterior papillary muscle, and anterior surface of left ventricle

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45
Q

PD supplies what?

A

posterior 1/3 of interventricular septum and posterior walls of ventricles

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46
Q

acute marignal artery supplies what?

A

right ventricle

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47
Q

SA and AV nodes are usually supplied by what?

A

RCA

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48
Q

frequency and features of right dominant coronary circulation?

A

85% • PD arises from RCA

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49
Q

frequency and features of left-dominant coronary circulation?

A

8% • PD arises from LCX

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50
Q

frequency and features of codominant circulation?

A

7% • PD arises from both LCX and RCA

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51
Q

coronary artery occlusion most commonly occurs where?

A

in LAD

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52
Q

when do coronary arteries fill?

A

during diastole

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53
Q

most posterior part of the heart is what?

A

LA

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54
Q

enlargement of LA can cause what?

A

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

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55
Q

transesophageal echocardiography is useful for diagnosing what?

A

LA enlargement • aortic dissection • thoracic aortic aneurysm

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56
Q

equations for cardiac output?

A

CO= SV x HR • • Fick’s: • CO= (rate of O2 consumption)/((arterial O2 content)- (venous O2 content))

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57
Q

equation for MAP?

A

MAP= CO x TPR • • MAP= 2/3 diastolic pressure + 1/3 systolic

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58
Q

pulse pressure=?

A

systolic pressure - diastolic pressure

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59
Q

pulse pressure is proportional to what?

A

stroke volume

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60
Q

equations for stroke volume?

A

SV = CO/HR = EDV - ESV

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61
Q

during the early stages of exercise CO is maintained by what?

A

↑ HR and ↑ SV

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62
Q

during the late stages of exercise, CO is maintained by what?

A

↑ HR only (SV plateaus)

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63
Q

what happens during exercise if HR is too high?

A

diastolic filling is incomplete and CO ↓

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64
Q

cardiac variables that affect stroke volume?

A

SV CAP • Stroke Volume affected by Contractility, Afterload, and Preload

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65
Q

↑ SV when what?

A

↑ preload, ↓ afterload, ↑ contractility

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66
Q

contractility (and SV) ↑ with what?

A
  1. catecholamines • 2. ↑ intracellular Ca++ • 3. ↓ extracellular Na+ • 4. Digitalis
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67
Q

how do catecholamines ↑ contractility?

A

↑ activity of Ca++ pump in sarcoplasmic reticulum

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68
Q

how does a ↓ in extracellular Na+ ↑ contractility?

A

↓ activity of Na+/Ca++ exchanger

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69
Q

how does digitalis ↑ contractility?

A

blocks Na+/K+ pump → ↑ intracellular Na+ →↓ Na+/Ca++ exchanger activity → ↑ intracellular Ca++

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70
Q

contractility and SV ↓ with what?

A
  1. β blockade • 2. heart failure (systolic dysfunction) • 3. acidosis • 4. hypoxia/hypercapnia (↓PO2/↑PCO2) • 5. Non-dihydropyridine Ca++ channel blockers
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71
Q

effect of anxiety, exercise, and pregnancy on SV?

A

↑

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72
Q

myocardial O2 demand is ↑ by what?

A

↑ afterload (proportional to arterial pressure) • ↑ contractility • ↑ heart rate • ↑ heart size (↑wall tension)

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73
Q

preload = ?

A

ventricular EDV

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74
Q

afterload=?

A

MAP (proportional to peripheral resistance)

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75
Q

agents that ↓ preload?

A

vEnodilators (nitroglycerin)

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76
Q

agents that ↓ afterload?

A

vAsodilators (hydrAlazine)

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77
Q

preload ↑ with what?

A
  1. exercise (slightly) • 2. ↑ blood volume (overtransfusion) • 3. excitement (↑ sympathetic activity)
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78
Q

on Starling curve, force of contraction is proportional to what?

A

end-diastolic length of cardiac muscle fiber (preload)

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79
Q

on Starling curve, what are the factors that increase contractility?

A

sympathetic stimulation • catecholamines • digoxin

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80
Q

on starling curve, which factors ↓ contractility?

A

loss of myocardium (MI) • β blockers • Ca++ channel blockers

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81
Q

equation for EF?

A

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

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82
Q

EF is an index of what?

A

ventricular contractility

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83
Q

normal EF?

A

> =55%

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84
Q

EF ↓ in what?

A

systolic heart failure

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85
Q

ΔP =?

A

Q x R

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86
Q

equation for resistance?

A

resistance = (driving pressure ΔP)/(Flow Q)= (8ηl)/πr^4

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87
Q

equation for total resistance of vessels in series?

A

0

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88
Q

1/Toral Resistance of vessels in parallel?

A

= 1/R1 + 1/R2 + 1/R3…

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89
Q

viscosity ↑ in what?

A
  1. polycythemia • 2. hyperproteinemic states (multiple myeloma) • 3. hereditary spherocytosis
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90
Q

viscosity ↓ in what?

A

anemia

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91
Q

pressure gradient drives blood flow where?

A

from high pressure to low pressure

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92
Q

resistance is proportional to what?

A

viscosity and vessel length

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93
Q

viscosity is inversely proportional to what?

A

the radius to the 4th power

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94
Q

what accounts for most of total peripheral resistance?

A

arterioles

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95
Q

what vessels regulate capillary flow?

A

arterioles

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96
Q

where is the operating point of the heart on the cardiac and vascular function curve?

A

intersection where cardiac output and venous return are equal

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97
Q

what causes the operating point of the heart on the cardiac and vascular function curve to shift straight down?

A

↑ TPR, hemorrhage before compensation can occur

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98
Q

what causes the operating point of the heart on the cardiac an vascular function curve to shift straight up?

A

↓ TPR, exercise, AV shunt

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99
Q

what causes the operating point of the heart to shift downward and rightward along the venous return curve on the cardiac and vascular function curve?

A

heart failure • narcotic overdose

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100
Q

what causes an upward shift in the CO curve?

A

NAME?

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101
Q

what causes a downward shift in the CO curve?

A

NAME?

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102
Q

what causes a rightward shift in the venous return curve?

A

↑ blood volume

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103
Q

what causes a leftward shift in the venous return curve?

A

↓ blood volume

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104
Q

what is the X intercept of the venous return curve?

A

mean systemic filling pressure

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105
Q

what are the 5 phases of the left ventricle in the cardiac cycle?

A
  1. isovolumetric contraction • 2. systolic ejection • 3. isovolumetric relaxation • 4. rapid filling • 5. reduced filling
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106
Q

what is isovolumetric contraction?

A

period between mitral valve closure and aortic valve opening

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107
Q

what is the period of highest O2 consumption during the cardiac cycle?

A

isovolumetric contraction

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108
Q

what is systolic ejection?

A

period between aortic valve opening and closing

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109
Q

what is isovolumetric relaxation?

A

period between aortic valve closing and mitral valve opening

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110
Q

what is rapid filling?

A

period just after mitral valve opening

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111
Q

what is reduced filling?

A

period just before mitral valve closure

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112
Q

what causes a rightward EDV expansion without an upward pressure expansion in the LV cardiac cycle P/V curve?

A

↑preload → ↑SV

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113
Q

what causes a leftward ESV expansion with an upward pressure expansion on a LV cardiac cycle P/V curve?

A

↑ contractility • ↑ SV • ↑ EF • ↓ ESV

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114
Q

what causes a leftward ESV contraction with an upward pressure expansion on a LV cardiac cycle P/V curve?

A

↑ afterload • ↑ aortic pressure • ↓ SV • ↑ ESV

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115
Q

what causes S1 sound?

A

mitral and tricuspid valve closure

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116
Q

S1 is loudest where?

A

at mitral area

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117
Q

what causes S2 sound?

A

aortic and pulmonary valve closure

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118
Q

where is S2 loudest?

A

at left sternal border

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119
Q

when is S3 heard?

A

in early diastole during rapid ventricular filling phase

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120
Q

S3 is associated with what?

A

↑ filling pressures (MR, CHF)

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121
Q

S3 is more common in which types of ventricles?

A

dilated ventricles, but normal in children and pregnant women

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122
Q

when do you hear S4?

A

atrial kick in late diastole

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123
Q

what causes S4?

A

high atrial pressure • LA must push against stiff LV wall

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124
Q

S4 associated with what?

A

ventricular hypertrophy

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125
Q

what does JVP a wave correspond to?

A

atrial contraction

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126
Q

what does the JVP c wave correspond to?

A

RV contraction (closed tricuspid valve bulging into atrium)

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127
Q

what does the JVP x descent correspond to?

A

atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction

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128
Q

what does the JVP v wave correspond to?

A

↑ right atrial pressure due to filling against closed tricuspid valve

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129
Q

what does the JVP y descent correspond to?

A

blood flow from RA to RV

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130
Q

what happens in normal splitting?

A

inspiration → • drop in intrathoracic pressure → • ↑ venous return to the RV → • ↑ RV stroke volume → • ↑ RV ejection time → • delayed closure of the pulmonic valve

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131
Q

what else contributes to the delayed closure of the pulmonic valve in normal splitting?

A

↓ pulmonary impedance ( ↑ capacity of the pulmonary circulation)

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132
Q

what does normal splitting sound like?

A

A2 and P2 are close during expiration, • A2 and P2 are only slightly more separated during inspiration

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133
Q

wide splitting is seen in which conditions?

A

those that delay RV emptying (pulmonic stenosis, RBB block)

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134
Q

what happens in wide splitting?

A

delay in RV emptying causes delayed pulmonic sound (regardless of breath)

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135
Q

what does wide splitting sound like?

A

an exaggeration of normal splitting • Ex: A2 and P2 are split as wide as normal inspiration • Ins: A2 and P2 are split much wider than normal

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136
Q

fixed splitting is seen in what?

A

ASD

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137
Q

what happens in fixed splitting?

A

ASD → left to right shunt → ↑ RA and RV volumes → ↑ flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed

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138
Q

paradoxical splitting is seen in what?

A

conditions that delay LV emptying (aortic stenosis, LBB block)

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139
Q

what happens in paradoxical splitting?

A

normal order of valve closure is reversed so that P2 sound occurs before A2.

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140
Q

what does paradoxical splitting sound like?

A

on inspiration, P2 closes later and moves closer to A2, thereby ‘paradoxically’ eliminating the split

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141
Q

what can cause a systolic murmur in the aortic area?

A

aortic stenosis • flow murmur • aortic valve sclerosis

142
Q

where is the aortic auscultation area?

A

2nd intercostal space RSB

143
Q

what causes a systolic ejection murmur in the pulmonic area?

A

pulmonic stenosis • flow murmur (ASD, PDA)

144
Q

where is the pulmonic area for ausculation?

A

2nd interspace LSB

145
Q

what causes a pansystolic murmur at the tricuspid area?

A

tricuspid regurgitation • ventricular septal defect

146
Q

what causes diastolic murmur at the tricuspid area?

A

tricuspid stenosis • ASD

147
Q

where is the tricuspid area for auscultation?

A

5th interspace LSB

148
Q

what causes a systolic murmur in the mitral area?

A

mitral regurgitation

149
Q

what causes a diastolic murmur in the mitral area?

A

mitral stenosis

150
Q

where is the mitral area for auscultation?

A

5th interspace mid clavicular line

151
Q

what causes diastolic murmur at the left sternal border?

A

aortic regurgitation • pulmonic regurgitation

152
Q

what causes systolic murmur at left sternal border?

A

hypertrophic cardiomyopathy

153
Q

what are the auscultation findings in ASD?

A

pulmonary flow murmur • diastolic rumble (tricuspid) • blood flow across the ASD doesn’t cause a murmur because there is no pressure gradient • murmur → louder diastolic murmur of pulmonic regurgitation from dilation of pulmonary artery

154
Q

the continuous, machine-like murmur of PDA is best appreciated where?

A

left infraclavicular region

155
Q

what is the effect of inspiration on ausculation?

A

↑ intensity of right heart sounds

156
Q

what is the effect of expiration on auscultation?

A

↑ intensity of left heart sounds

157
Q

what is the effect of hand grip maneuver on auscultation (↑ systemic vascular resistance)?

A

↑ intensity of MR, AR, VSD, MVP murmurs • ↓ intensity of AS, hypertrophic cardiomyopathy murmurs

158
Q

what is the effect of the vasalva maneuver (↓ venous return) on auscultation?

A

↓ intensity of most murmurs • ↑ intensity of MVP, hypertrophic cardiomyopathy murmurs

159
Q

what is the effect of rapid squatting (↑ venous return, ↑ preload, ↑afterload with prolonged squatting)?

A

↓ intensity of MVP, hypertrophic cardiomyopathy murmurs

160
Q

conditions associated with systolic heart sounds include what?

A

aortic/pulmonic stenosis • mitral/tricuspid regurgitation • VSD

161
Q

conditons associated with diastolic heart sounds include what?

A

aortic/pulmonic regurgitation • mitral/tricuspid stenosis

162
Q

what does mitral/tricuspid regurgitation sound like?

A

holosystolic, high-pitched “blowing murmur”

163
Q

mitral regurgitation is loudest where?

A

at apex and radiates to toward axilla

164
Q

mitral regurgitation sound is enhanced by what?

A

maneuvers that ↑ TPR (squatting, hand grip) or LA return (expiration)

165
Q

MR is often due to what?

A

ischemic heart disease, mitral valve prolapse, LV dilation

166
Q

where is tricuspid regurgitation loudest?

A

loudest at tricuspid area and radiates to right sternal border

167
Q

tricuspid regurgitation sound enhanced by what?

A

maneuvers that ↑ RA return (inspiration)

168
Q

TR can be caused by what?

A

RV dilation

169
Q

rheumatic fever and infective endocarditis can cause which heart sounds?

A

MR or TR

170
Q

what does Aortic stenosis sound like?

A

crescendo-decrescendo systolic ejection murmur following ejection click • radiates to carotids/heart base

171
Q

what causes ejection click in aortic stenosis?

A

EC due to abrupt halting of valve leaflets

172
Q

pressure gradient in aortic stenosis?

A

LV» aortic pressure during systole

173
Q

pulse findings in aortic stenosis?

A

pulsus parvus et tardus’ • pulses are weak with a delayed peak

174
Q

aortic stenosis can lead to what?

A

Syncope, Angina, Dyspnea on exertion (SAD)

175
Q

aortic stenosis is due to what?

A

age related calcific aortic stenosis or bicuspid aortic valve

176
Q

what does VSD sound like?

A

holosystolic, harsh sounding murmur

177
Q

where is VSD loudest?

A

tricuspid area

178
Q

VSD sound can be accentuated how?

A

hand grip maneuver due to increased afterload

179
Q

what does MVP sound like?

A

late systolic crescendo murmur with midsystolic click

180
Q

what causes MC?

A

sudden tensing of the chordae tendineae

181
Q

what is the most frequent valvular lesion?

A

MVP

182
Q

MVP is best heard where?

A

over apex

183
Q

when is MVP loudest?

A

S2

184
Q

severity of MVP?

A

usually benign

185
Q

MVP can predispose to what?

A

infective endocarditis

186
Q

MVP can be caused by what?

A

myxomatous degeneration • rheumatic fever • chordae rupture

187
Q

MVP enhanced by what?

A

maneuvers that ↓ Venous return (standing or vasalva)

188
Q

what does aortic regurgitation sound like?

A

immediate high pitched “blowing” diastolic decrescendo murmur

189
Q

pulses in AR?

A

wide pulse pressure when chronic; can present with bounding pulses and head bobbing

190
Q

AR is often due to what?

A

aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever

191
Q

what ↑ murmur in AR?

A

hand grip

192
Q

effect of vasodilators on AR?

A

↓ intensity of murmur

193
Q

what does MS sound like?

A

follows opening snap • delayed rumbling late diastolic murmur

194
Q

what causes OS in MS?

A

abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips

195
Q

pressure gradient in MS?

A

LA»LV during diastole

196
Q

MS often occurs secondary to what?

A

rheumatic fever

197
Q

chronic MS can result in what?

A

LA dilation

198
Q

MS sound is enhanced by what?

A

maneuvers that ↑ LA return (expiration)

199
Q

what does PDA sound like?

A

continuous machine like murmur

200
Q

when is PDA loudest?

A

S2

201
Q

PDA is often due to what?

A

congenital rubella or prematurity

202
Q

where is PDA best heard?

A

left infraclavicular area

203
Q

ventricular action potential also occurs where?

A

in bundle of His and Purkinje fibers

204
Q

what happens in Phase 0 of ventricular action potential?

A

rapid upstroke- voltage gated Na+ channels open

205
Q

what happens in Phase 1 of ventricular action potential?

A

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

206
Q

what happens in Phase 2 of ventricular action potential?

A

plateau-Ca++ influx through voltage gated Ca++ channels balances K+ efflux • Ca++ influx triggers Ca++ release from sarcoplasmic reticulum and myocyte contraction

207
Q

what happens in phase 3 of ventricular action potential?

A

rapid repolarization= massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage gated Ca++ channels

208
Q

what happens in phase 4 of the ventricular action potential?

A

resting potential- high K+ permeability through K+ channels

209
Q

difference between cardiac muscle AP and skeletal muscle?

A
  1. cardiac muscle AP has a plateau, which is due to Ca++ influx and K+ efflux, myocyte contraction occurs due to Ca++ induced Ca++ release from the sarcoplasmic reticulum • 2. cardiac nodal cells spontaneously depolarize during diastole resulting in automaticity due to If channels • 3. Cardiac myocytes are electrically coupled to eachother by gap junctions
210
Q

what do If chanels do?

A

funny current channels responsible for a slow, mixed Na+/K+ inward current

211
Q

what is the direction of the leak currents in cardiac ventricular myocytes?

A

K+ out • Na+, Ca++ in

212
Q

pacemaker action potential occurs where?

A

in the SA and AV nodes

213
Q

what happens in phase 0 of the pacemaker action potential?

A

upstroke- opening of VG Ca++ channels • fast VG Na channels are permanently inactivated because of the less negative resting voltage of these cells

214
Q

permanent fast VG Na channel inactivation in the pacemaker cells results in what?

A

slow conduction velocity that is used by the AV node to prolong transmission from the atria to the ventricles

215
Q

what happens in Phase 2 or pacemaker potential?

A

plateau is absent

216
Q

what happens in phase 3 of the pacemaker potential?

A

inactivation of the Ca++ channels and ↑ activation of K+ channels→ ↑ K+ efflux

217
Q

what happens in phase 4 of the pacemaker potential?

A

slow diastolic depolarization- membrane potential spontaneously depolarizes as Na+ conductance ↑ (If different from Ina in phase 0 of ventricular action potential)

218
Q

phase 4 of the pacemaker potential accounts for what?

A

automaticity of SA and AV nodes

219
Q

slope of phase 4 in the SA node determines what?

A

HR

220
Q

effect of ACh/adenosine on SA node?

A

↓ the rate of diastolic depolarization and ↓ HR

221
Q

effect of catecholamines on SA node?

A

↑ depolarization and ↑ heart rate

222
Q

effect of sympathetic stimulation on SA/AV node?

A

↑ the chance that If channels are open and thus ↑ HR

223
Q

P wave corresponds to what?

A

atrial depolarization

224
Q

atrial repolarization in ECG?

A

masked by QRS complex

225
Q

PR interval corresponds to what?

A

conduction delay through AV node

226
Q

normal PR interval?

A

<200 ms

227
Q

QRS complex correspondes to what?

A

ventricular depolarization

228
Q

normal duration of QRS complex?

A

<120s

229
Q

QT interval corresponds to what?

A

mechanical contraction of the ventricles

230
Q

T wave corresponds to what?

A

ventricular repolarization

231
Q

T wave inversion may indicate what?

A

recent MI

232
Q

ST segment corresponds to what?

A

isoelectric, ventricles depolarized

233
Q

U wave is caused by what?

A

hypokalemia • bradycardia

234
Q

relative speed of conduction in the heart?

A

purkinje > atria > ventricles > AV nodes

235
Q

relative speed of conduction in the pacemaker cells?

A

SA node> AV> Bundle of his/purkinje/ventricles

236
Q

what is the conduction pathway in the heart?

A

SA node → atria → AV node → common bundle→ bundle branches→ purkinje fibers→ ventricles

237
Q

dominant pacemaker in heart?

A

SA node pacemaker inherent dominance with slow phase of the upstroke

238
Q

what is the delay in the AV node?

A

100ms delay- atrioventricular delay; allows time for ventricular filling

239
Q

what happens in torsades de pointes?

A

ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG, can progress to ventricular fibrillation

240
Q

what predisposes to torsades de pointes?

A

anything that prolongs the QT interval

241
Q

treatment for torsades de pointes?

A

magnesium sulfate

242
Q

congenital long QT syndromes are most often due to what?

A

defects in cardiac sodium or potassium channels

243
Q

what condition has long QT syndrome that presents with severe sensorineural deafness?

A

Jervell and Lange-Nielsen syndrome

244
Q

how does atrial fibrillation look?

A

chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes

245
Q

atrial fibrillation can result in what?

A

atrial stasis and lead to stroke

246
Q

tx for atrial fibrillation?

A

rate control • anticoagulation • possible cardioversion

247
Q

what does atrial flutter look like?

A

a rapid succession of identical, back-to-back atrial depolarization waves • ‘saw tooth’ appearance

248
Q

pharmacologic conversion to sinus rhythm in atrial flutter?

A

Class IA, IC, or III antiarrhythmics

249
Q

rate control in atrial flutter?

A

β-blocker or calcium channel blocker

250
Q

what does ventricular fibrillation look like?

A

a completely erratic rhythm with no identifiable waves

251
Q

severity of ventricular fibrillation?

A

fatal arrhythmia without immediate CPR and defibrillation

252
Q

features of 1st degree AV block?

A

prolonged PR interval >200ms • asymptomatic

253
Q

features of 2nd degree AV block Mobitz type I (Wenckebach)?

A

progressive lenghtening of the PR interval until a beat is dropped • usually asymptomatic

254
Q

features of Mobitz type II?

A

dropped beats that are not preceded by a change in the length of the PR interval

255
Q

severity of Mobitz type II?

A

these abrupt, nonconducted p waves result in a pathologic condition

256
Q

mobitz type II is often found as what?

A

2:1 block, where there are >=2 p waves to 1 QRS

257
Q

mobitz type II often treated with what?

A

pacemaker

258
Q

mobitz type II may progress to what?

A

3rd degree block

259
Q

what happens in 3rd degree (complete) heart block?

A

the atria and ventricles beat independently of each other • both p waves and QRS complexes are present, though P waves bear no relation to the QRS complexes

260
Q

which rate is faster in 3rd degree heart block?

A

atrial rate is faster than ventricular rate

261
Q

3rd degree heart block is usually treated with what?

A

a pacemaker

262
Q

which disease can result in 3rd degree heart block?

A

Lyme disease

263
Q

ANP is released from where?

A

atrial myocytes

264
Q

ANP is released in response to what?

A

↑ blood volume and pressure

265
Q

ANP causes what?

A

generalized vascular relaxation and ↓ Na+ reabsorption at the medullary collecting tubule

266
Q

effect of ANP on renal blood flow?

A

constricts efferent renal arterioles and dilates afferent arterioles (cGMP mediated), promoting diuresis and contributing to the escape from aldosterone mechanism

267
Q

aortic arch baroreceptors transmit info where?

A

via vagus nerve to solitary nucleus of medulla (responds only to ↑ BP)

268
Q

carotid sinus baroreceptor transmits info where?

A

via glossopharyngeal nerve to solitary nucleus of medulla (responds to ↑ and ↓ in BP)

269
Q

what happens at baroreceptors in response to hypotension?

A

↓ arterial pressure → • ↓ stretch → • ↓ afferent baroreceptor firing→ • ↑ efferent sympathetic firing and ↓ efferent parasympathetic stimulation → • vasoconstriction, ↑ HR, ↑ contractility, ↑ BP

270
Q

baroreceptors are important in the response to what?

A

severe hemorrhage

271
Q

effect of carotid massage on baroreceptors?

A

↑ pressure on carotid artery → ↑ stretch → ↑ afferent baroreceptor firing → ↓ HR

272
Q

baroreceptors contribute to which reaction?

A

Cushing reaction

273
Q

what happens in Cushing reaction?

A

triad of hypertension, bradycardia, and respiratory depression

274
Q

mechanism of Cushing reaction?

A

↑ ICP constricts arterioles→ cerebral ischemia and reflex sympathetic increase in perfusion pressure (hypertension)→ ↑ stretch → reflex baroreceptor induced-bradycardia

275
Q

what happens in stimulation of peripheral chemoreceptors?

A

carotid and aortic bodies are stimulated by ↓ PO2 (<60mmHg), ↑ PCO2, and ↓ pH of blood

276
Q

what happens in stimulation of central chemoreceptors?

A

are stimulated by changes in pH and PCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2

277
Q

central chemoreceptors do not directly respond to what?

A

PO2

278
Q

what is the organ with the largest blood flow?

A

Lung (100% of CO)

279
Q

what is the organ with the largest share of systemic cardiac output?

A

liver

280
Q

which organ has the highest blood flow per gram of tissue?

A

kidney

281
Q

which organ has the largest arteriovenous O2 difference?

A

heart

282
Q

why does heart have the largest arteriovenous O2 difference?

A

becuase O2 extraction is 80%

283
Q

how is O2 demand met in heart?

A

↑ O2 demand is met by ↑ coronary blood flow, not by ↑ extraction of O2

284
Q

what is the normal pressure in the RA?

A

<5

285
Q

what is the normal pressure in the RV?

A

25-May

286
Q

what is the normal pressure in the PA?

A

25-Oct

287
Q

what is the normal pressure in the LA?

A

<12

288
Q

what is the normal pressure in the LV?

A

130/10

289
Q

what is the normal pressure in the aorta?

A

130/90

290
Q

PCWP is a good approximation of what?

A

left atrial pressure

291
Q

when is PCWP> LV diastolic pressure?

A

mitral stenosis

292
Q

how is PCWP measured?

A

Swan Ganz catheter

293
Q

what is autoregulation?

A

how blood flow to an organ remains constant over a wide range of perfusion pressures

294
Q

what are the factors determining autoregulation in the heart?

A

Local metabolites (vasodilatory)-CO2, adenosine, NO

295
Q

what are the factors determining autoregulation in the brain?

A

Local metabolites (vasodilatory)-CO2 (pH)

296
Q

what are the factors determining autoregulation in the kidneys?

A

myogenic and tubuloglomerular feedback

297
Q

what are the factors determining autoregulation in the lungs?

A

hypoxia causes vasoconstriction

298
Q

what are the factors determining autoregulation in skeletal muscle?

A

local metabolites- lactate, adenosine, K+

299
Q

what are the factors determining autoregulation in the skin?

A

sympathetic stimulation most important mechanism-temperature control

300
Q

what determines fluid movement through capillary membranes?

A

starling forces

301
Q

what are the 4 starling forces?

A

Pc • Pi • πc • πi

302
Q

what is Pc?

A

capillary pressure- pushes fluid out of capillary

303
Q

what is Pi?

A

interstitial fluid capillary- pushes fluid into capillary

304
Q

what is πc?

A

plasma colloid osmotic pressure- pulls fluid into capillary

305
Q

what is πi?

A

interstitial fluid colloid osmotic pressure-pulls fluid out of capillary

306
Q

equation for net filtration pressure?

A

Pnet= [(Pc - Pi) - (πc - πi)]

307
Q

what is Kf?

A

filtration constant (capillary permeability)

308
Q

what is Jv?

A

net fluid flow= Kf x Pnet

309
Q

what is edema?

A

excess fluid outflow into interstitium

310
Q

edema is commonly caused by what?

A

↑ capillary pressure (heart failure) • ↓ plasma proteins (nephrotic syndrome, liver failure) • ↑ capillary permeability (toxins, infections, burns) • ↑ interstitial colloid osmotic pressure (lymphatic blockage)

311
Q

what is the most common cause of early cyanosis?

A

Tetralogy of Fallot

312
Q

which congenital heart diseases make up the right to left shunts (early cyanosis)-blue babies?

A

5T’s • Tetralogy of Fallot • Transposition of the great vessels • persistent Truncus arteriosus • Tricuspid atresia • Total anomalous pulmonary venous return

313
Q

features of Persistent Truncus Arteriosus?

A

failure of truncus arteriosus to divide into pulmonary trunk and aorta

314
Q

most patients with persistent truncus arteriosus have what?

A

accompanying VSD

315
Q

tricuspid atresia is characterized by what?

A

absence of tricuspid valve and hypoplastic RV

316
Q

tricuspid atresia requires what for viability?

A

both ASD and VSD

317
Q

what happens in TAPVR?

A

pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc)

318
Q

TAPVR is associated with what?

A

ASD and sometimes PDA to allow for right to left shunting to maintain CO

319
Q

which congenital heart abnormalities make up the left to right shunts (late cyanosis)-blue kids?

A

VSD • ASD • PDA

320
Q

what is the most common congenital cardiac anomaly?

A

VSD

321
Q

findings in ASD?

A

loud S1, wide, fixed split S2

322
Q

what do you use to close PDA?

A

indomethacin

323
Q

what is the frequency of the congenital left to right shunts?

A

VSD > ASD > PDA

324
Q

what happens in Eisenmenger’s syndrome?

A

uncorrected VSD, ASD, or PDA causes compensatory pulmonary vascular hypertrophy, which results in progressive pulmonary hypertension

325
Q

what happens in Eisenmenger’s syndrome as pulmonary resistance increases?

A

the shunt reverses from left to right to right to left, which causes late cyanosis, clubbing, and polycythemia

326
Q

tetralogy of fallot is caused by what?

A

anterosuperior displacement of the infundibular septum

327
Q

what is the mnemonic for the components of ToF?

A

PROVe • 1. Pulmonary infundibular stenosis • 2. RVH • 3. Overriding aorta (overrides the VSD) • 4. VSD

328
Q

what is the most important determinant for prognosis in ToF?

A

pulmonary infundibular stenosis

329
Q

in ToF early cyanosis (tet spells) caused by what?

A

a right to left shunt across the VSD

330
Q

difference between isolated VSD and VSD in ToF?

A

isolated VSDs usually flow left to right (acyanotic) • in tetralogy, pulmonary stenosis forces right to left (cyanotic) flow and causes RVH

331
Q

how does RVH in ToF look?

A

boot shaped heart on CXR

332
Q

patients with ToF learn what compensatory mechanism?

A

squat to relieve cyanotic symptoms

333
Q

why do patients with ToF squat?

A

reduces blood flow to the legs, ↑ PVR, and thus ↓ the cyanotic right to left shunt across the VSD

334
Q

what is the preferred treatment for ToF?

A

early, primary surgical correction

335
Q

what happens in transposition of great vessels?

A

aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior)→ separation of systemic and pulmonary circulations

336
Q

transposition of the great vessels not compatible with life unless what?

A

a shunt is present to allow adequate mixing of blood (VSD, PDA, or patent foramen ovale)

337
Q

transposition of great vessels is due to what?

A

failure of aorticopulmonary septum to spiral

338
Q

prognosis of transposition of great vessels?

A

without surgical correction, most infants die within the first few months of life

339
Q

coarctation of the aorta can result in what?

A

AR

340
Q

what is infantile type of coarctation of the aorta?

A

aortic stenosis proximal to insertion of ductus arteriosus (preductal)

341
Q

preductal coarctation of the aorta is associated with what?

A

Turner syndrome

342
Q

what needs to be checked in infantile coarctation of the aorta?

A

check femoral pulses on physical exam

343
Q

what is adult type coarctation of the aorta?

A

stenosis is distal to ligamentum arteriosum (postductal)

344
Q

postductal coarctation of the aorta is associated with what?

A

notching of the ribs (due to collateral circulation), hypertension in upper extremities, weak pulses in lower extremities

345
Q

postductal coarctation of the aorta is most commonly associated with what?

A

bicuspid aortic valve

346
Q

what is going on in patent ductus arteriosus in the fetal period?

A

shunt is right to left (normal)

347
Q

what happens to patent ductus arteriosus in the neonatal period?

A

lung resistance ↓ and shunt becomes left to right with subsequent RVH and/or LVH and failure (abnormal)

348
Q

patent ductus arteriosus is associated with what finding?

A

continuous machine like murmur

349
Q

in PDA, patency is maintained with what?

A

PGE synthesis and low O2 tension

350
Q

uncorrected PDA can eventually result in what?

A

late cyanosis in the lower extremities (differential cyanosis)

351
Q

when is PDA normal?

A

PDA is normal in utero and only closes after birth

► Med Notes (62 decks)

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