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lecture 6 Flashcards

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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
common cause for elevated PVR
COPD
26
stenotic mitral valve
pulmonary artery wedge pressure (or left atrial pressure) is elevated
27
transthoracic M-mode echocardiogaphy
1 dimensional, can be used to observe mitral valve leaflets and measure myocardial shortening and radial thickening
28
transthoracic two dimensional echocardiography
oscillating beam over pie shaped sector of the heart
29
three dimensional echocardiography
3D echocardiography is used for quantification's of LV volume and EF and quantification if mitral valve area in mitral stenosis
30
doppler echocadiography (doppler ultrasound)
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
31
transesophageal pulse doppler
information of pulmonary venous flow into left atrium and measure coronary flow, stenotic regurgitant valve lesions, intracardiac shunts
32
readinuclide ventriculography (RVN)
visualization of heart chambers, evaluate CAD, valvular heart disease, congenital heart disease and cadiomyopathy, determine Ejection fraction
33
radionuclide myocardial perfusion imaging (MPI)
dye taken up by myocardial cells. can see defects of MI
34
gold standard for measuring ejection fraction
MRI
35
positron emission tomography
reveals blood flow through specific areas of heart, gold standard for measuring myocardial viability
36
how is sounds generated
oscillations of blood, movements of heart walls, blood vessels and valves, and turbulence in flowing column of blood
37
Where to place stethoscope
All physician Take Money (2,2,4,5)
38
S1 and S2
closing of all 4 valves
39
S3 and S4
two weaker sounds
40
S1
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
S2
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
S3
rapid ventricular filling during diastole, weaker sound
43
S4
during atrial contraction, usually NOTICEABLE in diseases conditions
44
what is heard in mitral valve stenosis or narrowed?
opening snap
45
Murmurs
hear during through cardiac cycle, caused by turbulent flow of blood
46
systolic murmur
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
diastolic murmur
aortic valve fails to close fully, blood regurgitates into left ventricle during diastole
48
aortic and pulmonic stenosis (systolic murmur)
murmur peaks whenpressure differential across valve is at maximum, hemodynamic, ESV elevated and left ventricle hypertrophied
49
Mitral or tricuspid valve regurgitation (systolic murmur)
holosystolic murmur, lasts through systole and early diastole. large v wave in left atrial pressure curve in mitral insufficiency
50
mitral valve prolapse (systolic murmur)
mitral valve flaps billow back into left atrium causing a click
51
diastolic murmur, Aortic and tricuspid regurgitation
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
Austin Flint mid-diastolic murmur
severe aortic regurgitation when blood jets back into anterior leaflet of open mitral valve, similar effect as mitral stenosis
53
diastolic murmur: mitral and tricuspid stenosis
filling murmur characterized by diastolic crescendo, ceases at S1. Pressure in left atrium at diastole is usually higher than left ventricle at diastole
54
continuous murmur: patent ductus arteriosus "machinery murmur"
revered blood flow from aorta into low pressure pulmonary artery is continuous, murmur heard during systole and diastole. More intense in systole
55
1 peripheral resistance
79.9 dynes.sec cm-5
56
resistance equation shows what?
resistance increases directly with fluid viscosity and tube length, resistance of tube decreases with increasing radius raised to the forth power
57
the fourth power law
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
resistance is dependent on
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
difference between velocity and flow rate
velocity: cm/sec, flow rate: ml/sec
60
velocity in a tube
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
highest cross sectional area
capillaries, so have a low velocity of flow
62
lowest cross sectional area
aorta, higher velocity of flow
63
viscosity
friction of fluid, unit it poise
64
1 poise
1 dyne per second per square cm
65
anomalous viscosity
viscosity increases as flow rate becomes slower
66
Fahraeus Lindquist effect
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
reynolds number
transition from laminar flow to chaotic flow (turbulent) can be predicted. Proportional to velocity
68
effect of pressure in tubes
increased intraluminar pressure can increase their diameter, decrease resistance to flow
69
effect of pressure in tubes
decrease leads to decreased diameter as elastic rebound of vessel walls tends to close on lumen
70
critical closing pressure
pressure at which blood flow stops
71
sympathetic stimulation to CCP
increases CCP
72
sympathetic inhibition to CCP
abolishes much or normal tone of blood vessels and decreases CCP
73
distensibility
percentage increase in volume cause by 1 mm HG rise in pressure
74
compliance
increase in volume for a give increase in pressure
75
delayed compliance or stress relaxation
initial elastic distension associated with rise in pressure, then smooth muscle fibers begin to get longer in length and their tension decreases
76
reverse stress relaxation
same volume of blood is suddenly removed causing sudden drop in pressure, but is then gradually restored (elastic recoil)
77
how is MAP maintained in hemorrhages?
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
pathological changes in central venous and atrial pressure: a wave
absent in atrial fibrillation, elevated tricuspid stenosis, cannon a waves
79
pathological changes in central venous and atrial pressure: v wave
larger and earlier in tricuspid insufficiency
80
pathological changes in central venous and atrial pressure: y descent
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
causes of edema
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
pulmonary edema
imbalance of starling forces, damage to alveolar capillary barrier, lymphatic obstruction, idiopathic
83
cardiogenic pulmonary edema
elevated pulmonary venous pressure (left heart failure or mitral valve stenosis), elevated CVP, death can occur
84
permeability pulmonary edema
permeability changes arising from endothelial injury

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