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Cardio > lecture 6 > Flashcards

lecture 6 Flashcards

1
Q

cardiac catheterizations

A

used to elevate and diagnose CAD, cardiomyopathies, pulmonary hypertension, valve defects and congenital heart abnormalities

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2
Q

normal cardiac output is

A

5.6 liters/min

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3
Q

how to increase cardiac output

A

sympathetic stimulation and myocardial hypertrophy coupled with increased stroke volume

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4
Q

sympathetic stimulation involves

A

dromotropic-> conduction velocity increased
chronotropic-> heart rate increased
inotropic-> myocardial contractility
lusitropic-> rate of relaxation increased

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5
Q

cardiac out is reduced by

A

arrhythmias, valvular insufficiency, increased afterload, reduced myocardial contractility, preload elevated beyond point of starling’s law’s

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6
Q

What three variables are measured using fick method?

A

oxygen consumption, oxygen in mixed venous blood, oxygen in arterial blood.

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7
Q

thermal dilution

A

area under curve represents flow in pulmonary artery and can be equated to left ventricular output, provided there is no shunts

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8
Q

techniques to calculate cardiac output

A

thermal dilution, doppler method, Fick method, three d echo ventriculography

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9
Q

doppler method

A

can use cross sectional area of aorta combined with flow velocity to calculate cardiac input. can also use data to calculate preload and afterload

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10
Q

three D echo ventriculography

A

determines stroke volume by computing EDV and ESV

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11
Q

determining intracardiac pressure

A

Swan-Ganz catheterization

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12
Q

How is left atrial pressure estimated?

A

catheterize right heart, pass through branch of pulmonary artery and record pulmonary capillary wedge pressure (PCWP)

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13
Q

lowest pressure in in

A

the atrium

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14
Q

pulmonary trunk pressure should be the same as

A

right ventricle, if lower-> pulmonary stenosis

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15
Q

when is the best time to measure intracardiac pressure?

A

during expiration

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16
Q

SVR stands for

A

systemic vascular resistance, resistance in the vascular system is governed mainly by radius of the vessel (Poiseulle’s law)

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17
Q

PVR

A

pulmonary vascular resistance

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18
Q

SVR and PVR relation

A

SVR is usually ten times the PVR

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19
Q

Pulmonary hypertension

A

Elevated pressure in pulmonary arteries. if there is a rise in pulmonary vascular resistance (which is normally low) and unchanged cardiac output, can be increase in pressure across pulmonary circuit

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20
Q

systemic hypertension

A

rise of TPR (or SVR) coupled with normal cardiac output leads to elevation of mean arterial pressure

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21
Q

mitral stenosis

A

there is an increase in resistance to blood flow through mitral valve, generates large diastolic pressure drop across valve (which is normally very small), so observe an elevation of left atrial and pulmonary venous pressure

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22
Q

Aortic stenosis

A

a much higher ventricular pressure is required to pump out normal cardiac output through a narrowed aortic valve

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23
Q

hepatic portal hypertension

A

increase in resistance to flow through liver, if flow is maintained, then must be elevation of pressure in hepatic portal vein

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24
Q

what does a diminished A-V oxygen difference mean?

A

increased cardiac output

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25
Q

common cause for elevated PVR

A

COPD

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26
Q

stenotic mitral valve

A

pulmonary artery wedge pressure (or left atrial pressure) is elevated

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27
Q

transthoracic M-mode echocardiogaphy

A

1 dimensional, can be used to observe mitral valve leaflets and measure myocardial shortening and radial thickening

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28
Q

transthoracic two dimensional echocardiography

A

oscillating beam over pie shaped sector of the heart

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29
Q

three dimensional echocardiography

A

3D echocardiography is used for quantification’s of LV volume and EF and quantification if mitral valve area in mitral stenosis

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30
Q

doppler echocadiography (doppler ultrasound)

A

observing blood turbulence as well as flow, when carried out during exercise good for ventricular wall motion and valve function, and locate areas where arteries are narrowed

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31
Q

transesophageal pulse doppler

A

information of pulmonary venous flow into left atrium and measure coronary flow, stenotic regurgitant valve lesions, intracardiac shunts

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32
Q

readinuclide ventriculography (RVN)

A

visualization of heart chambers, evaluate CAD, valvular heart disease, congenital heart disease and cadiomyopathy, determine Ejection fraction

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33
Q

radionuclide myocardial perfusion imaging (MPI)

A

dye taken up by myocardial cells. can see defects of MI

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34
Q

gold standard for measuring ejection fraction

A

MRI

35
Q

positron emission tomography

A

reveals blood flow through specific areas of heart, gold standard for measuring myocardial viability

36
Q

how is sounds generated

A

oscillations of blood, movements of heart walls, blood vessels and valves, and turbulence in flowing column of blood

37
Q

Where to place stethoscope

A

All physician Take Money (2,2,4,5)

38
Q

S1 and S2

A

closing of all 4 valves

39
Q

S3 and S4

A

two weaker sounds

40
Q

S1

A

closure of atrioventricular valves, can be split into an M1 and T1 sound, and if split is far about could indicate right bundle branch block

41
Q

S2

A

closure of semilunar valves (magnitude increased in hypertension). A2 and P2 components, wide splitting may also indicate right bundle branch block, a P2 A2 sequence indicates left bundle branch block

42
Q

S3

A

rapid ventricular filling during diastole, weaker sound

43
Q

S4

A

during atrial contraction, usually NOTICEABLE in diseases conditions

44
Q

what is heard in mitral valve stenosis or narrowed?

A

opening snap

45
Q

Murmurs

A

hear during through cardiac cycle, caused by turbulent flow of blood

46
Q

systolic murmur

A

mitral valve fails to close fully, blood regurgitates into atrium during ventricular systole, can be normal when heard in small children (heard late S1)

47
Q

diastolic murmur

A

aortic valve fails to close fully, blood regurgitates into left ventricle during diastole

48
Q

aortic and pulmonic stenosis (systolic murmur)

A

murmur peaks whenpressure differential across valve is at maximum, hemodynamic, ESV elevated and left ventricle hypertrophied

49
Q

Mitral or tricuspid valve regurgitation (systolic murmur)

A

holosystolic murmur, lasts through systole and early diastole. large v wave in left atrial pressure curve in mitral insufficiency

50
Q

mitral valve prolapse (systolic murmur)

A

mitral valve flaps billow back into left atrium causing a click

51
Q

diastolic murmur, Aortic and tricuspid regurgitation

A

early diastolic murmur, blood flow back into left ventricle during diastole, diastolic murmur at A2 and dies away, elevates EDV and increases SV, forward cardiac output is normal

52
Q

Austin Flint mid-diastolic murmur

A

severe aortic regurgitation when blood jets back into anterior leaflet of open mitral valve, similar effect as mitral stenosis

53
Q

diastolic murmur: mitral and tricuspid stenosis

A

filling murmur characterized by diastolic crescendo, ceases at S1. Pressure in left atrium at diastole is usually higher than left ventricle at diastole

54
Q

continuous murmur: patent ductus arteriosus “machinery murmur”

A

revered blood flow from aorta into low pressure pulmonary artery is continuous, murmur heard during systole and diastole. More intense in systole

55
Q

1 peripheral resistance

A

79.9 dynes.sec cm-5

56
Q

resistance equation shows what?

A

resistance increases directly with fluid viscosity and tube length, resistance of tube decreases with increasing radius raised to the forth power

57
Q

the fourth power law

A

vessels range in diameter from 8-30 mm, and large proportion of smooth muscle in their walls allows them to increase their diameters as much as four fold. So if an arteriole increases its diameter by factor or 4, resistance could drop by a factor of 256, if pressure is maintained, flow rate then increase b factor of 256

58
Q

resistance is dependent on

A

fourth power of radius and area only on the square of radius, so an enormous pressure drop will be seen because their small individual diameters add up to a high resistance

59
Q

difference between velocity and flow rate

A

velocity: cm/sec, flow rate: ml/sec

60
Q

velocity in a tube

A

tube of varying cross-section and constant flow rate, velocity of fluid passing through the tube is inversely related to cross-sectional area of tube

61
Q

highest cross sectional area

A

capillaries, so have a low velocity of flow

62
Q

lowest cross sectional area

A

aorta, higher velocity of flow

63
Q

viscosity

A

friction of fluid, unit it poise

64
Q

1 poise

A

1 dyne per second per square cm

65
Q

anomalous viscosity

A

viscosity increases as flow rate becomes slower

66
Q

Fahraeus Lindquist effect

A

viscosity of blood in smaller for diameter tubes diminishes as diameter of tube decreases. increasing hematocrit does not increase viscosity as much as large tubes, effect may play a role in decreasing resistance to flow of blood in smaller vessels

67
Q

reynolds number

A

transition from laminar flow to chaotic flow (turbulent) can be predicted. Proportional to velocity

68
Q

effect of pressure in tubes

A

increased intraluminar pressure can increase their diameter, decrease resistance to flow

69
Q

effect of pressure in tubes

A

decrease leads to decreased diameter as elastic rebound of vessel walls tends to close on lumen

70
Q

critical closing pressure

A

pressure at which blood flow stops

71
Q

sympathetic stimulation to CCP

A

increases CCP

72
Q

sympathetic inhibition to CCP

A

abolishes much or normal tone of blood vessels and decreases CCP

73
Q

distensibility

A

percentage increase in volume cause by 1 mm HG rise in pressure

74
Q

compliance

A

increase in volume for a give increase in pressure

75
Q

delayed compliance or stress relaxation

A

initial elastic distension associated with rise in pressure, then smooth muscle fibers begin to get longer in length and their tension decreases

76
Q

reverse stress relaxation

A

same volume of blood is suddenly removed causing sudden drop in pressure, but is then gradually restored (elastic recoil)

77
Q

how is MAP maintained in hemorrhages?

A

reduction in venous capacity and action of sympathetic on systemic vascular resistance, shifts blood from venous side to arterial side of circulation, this reduction in venous capacity will maintain central venous pressure, preload and cardiac output and coupled with sympathetic induced increase in SVR, maintain MAP

78
Q

pathological changes in central venous and atrial pressure: a wave

A

absent in atrial fibrillation, elevated tricuspid stenosis, cannon a waves

79
Q

pathological changes in central venous and atrial pressure: v wave

A

larger and earlier in tricuspid insufficiency

80
Q

pathological changes in central venous and atrial pressure: y descent

A

a slow y descent can indicate narrowed of an AV node valve orifice, elevated mean left atrial pressure coupled with a slow y descent=mitral stenosis

81
Q

causes of edema

A

venous pressure increase (failing heart), lowered plasma oncotic pressure (loss of plasma proteins), raised interstitial colloid osmotic pressure (increase endotheilial permeability), and blockage of lymphatics

82
Q

pulmonary edema

A

imbalance of starling forces, damage to alveolar capillary barrier, lymphatic obstruction, idiopathic

83
Q

cardiogenic pulmonary edema

A

elevated pulmonary venous pressure (left heart failure or mitral valve stenosis), elevated CVP, death can occur

84
Q

permeability pulmonary edema

A

permeability changes arising from endothelial injury

Cardio (8 decks)

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