lecture 6 Flashcards
cardiac catheterizations
used to elevate and diagnose CAD, cardiomyopathies, pulmonary hypertension, valve defects and congenital heart abnormalities
normal cardiac output is
5.6 liters/min
how to increase cardiac output
sympathetic stimulation and myocardial hypertrophy coupled with increased stroke volume
sympathetic stimulation involves
dromotropic-> conduction velocity increased
chronotropic-> heart rate increased
inotropic-> myocardial contractility
lusitropic-> rate of relaxation increased
cardiac out is reduced by
arrhythmias, valvular insufficiency, increased afterload, reduced myocardial contractility, preload elevated beyond point of starling’s law’s
What three variables are measured using fick method?
oxygen consumption, oxygen in mixed venous blood, oxygen in arterial blood.
thermal dilution
area under curve represents flow in pulmonary artery and can be equated to left ventricular output, provided there is no shunts
techniques to calculate cardiac output
thermal dilution, doppler method, Fick method, three d echo ventriculography
doppler method
can use cross sectional area of aorta combined with flow velocity to calculate cardiac input. can also use data to calculate preload and afterload
three D echo ventriculography
determines stroke volume by computing EDV and ESV
determining intracardiac pressure
Swan-Ganz catheterization
How is left atrial pressure estimated?
catheterize right heart, pass through branch of pulmonary artery and record pulmonary capillary wedge pressure (PCWP)
lowest pressure in in
the atrium
pulmonary trunk pressure should be the same as
right ventricle, if lower-> pulmonary stenosis
when is the best time to measure intracardiac pressure?
during expiration
SVR stands for
systemic vascular resistance, resistance in the vascular system is governed mainly by radius of the vessel (Poiseulle’s law)
PVR
pulmonary vascular resistance
SVR and PVR relation
SVR is usually ten times the PVR
Pulmonary hypertension
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
systemic hypertension
rise of TPR (or SVR) coupled with normal cardiac output leads to elevation of mean arterial pressure
mitral stenosis
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
Aortic stenosis
a much higher ventricular pressure is required to pump out normal cardiac output through a narrowed aortic valve
hepatic portal hypertension
increase in resistance to flow through liver, if flow is maintained, then must be elevation of pressure in hepatic portal vein
what does a diminished A-V oxygen difference mean?
increased cardiac output
common cause for elevated PVR
COPD
stenotic mitral valve
pulmonary artery wedge pressure (or left atrial pressure) is elevated
transthoracic M-mode echocardiogaphy
1 dimensional, can be used to observe mitral valve leaflets and measure myocardial shortening and radial thickening
transthoracic two dimensional echocardiography
oscillating beam over pie shaped sector of the heart
three dimensional echocardiography
3D echocardiography is used for quantification’s of LV volume and EF and quantification if mitral valve area in mitral stenosis
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
transesophageal pulse doppler
information of pulmonary venous flow into left atrium and measure coronary flow, stenotic regurgitant valve lesions, intracardiac shunts
readinuclide ventriculography (RVN)
visualization of heart chambers, evaluate CAD, valvular heart disease, congenital heart disease and cadiomyopathy, determine Ejection fraction
radionuclide myocardial perfusion imaging (MPI)
dye taken up by myocardial cells. can see defects of MI
gold standard for measuring ejection fraction
MRI
positron emission tomography
reveals blood flow through specific areas of heart, gold standard for measuring myocardial viability
how is sounds generated
oscillations of blood, movements of heart walls, blood vessels and valves, and turbulence in flowing column of blood
Where to place stethoscope
All physician Take Money (2,2,4,5)
S1 and S2
closing of all 4 valves
S3 and S4
two weaker sounds
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
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
S3
rapid ventricular filling during diastole, weaker sound
S4
during atrial contraction, usually NOTICEABLE in diseases conditions
what is heard in mitral valve stenosis or narrowed?
opening snap
Murmurs
hear during through cardiac cycle, caused by turbulent flow of blood
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)
diastolic murmur
aortic valve fails to close fully, blood regurgitates into left ventricle during diastole
aortic and pulmonic stenosis (systolic murmur)
murmur peaks whenpressure differential across valve is at maximum, hemodynamic, ESV elevated and left ventricle hypertrophied
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
mitral valve prolapse (systolic murmur)
mitral valve flaps billow back into left atrium causing a click
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
Austin Flint mid-diastolic murmur
severe aortic regurgitation when blood jets back into anterior leaflet of open mitral valve, similar effect as mitral stenosis
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
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
1 peripheral resistance
79.9 dynes.sec cm-5
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
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
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
difference between velocity and flow rate
velocity: cm/sec, flow rate: ml/sec
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
highest cross sectional area
capillaries, so have a low velocity of flow
lowest cross sectional area
aorta, higher velocity of flow
viscosity
friction of fluid, unit it poise
1 poise
1 dyne per second per square cm
anomalous viscosity
viscosity increases as flow rate becomes slower
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
reynolds number
transition from laminar flow to chaotic flow (turbulent) can be predicted. Proportional to velocity
effect of pressure in tubes
increased intraluminar pressure can increase their diameter, decrease resistance to flow
effect of pressure in tubes
decrease leads to decreased diameter as elastic rebound of vessel walls tends to close on lumen
critical closing pressure
pressure at which blood flow stops
sympathetic stimulation to CCP
increases CCP
sympathetic inhibition to CCP
abolishes much or normal tone of blood vessels and decreases CCP
distensibility
percentage increase in volume cause by 1 mm HG rise in pressure
compliance
increase in volume for a give increase in pressure
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
reverse stress relaxation
same volume of blood is suddenly removed causing sudden drop in pressure, but is then gradually restored (elastic recoil)
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
pathological changes in central venous and atrial pressure: a wave
absent in atrial fibrillation, elevated tricuspid stenosis, cannon a waves
pathological changes in central venous and atrial pressure: v wave
larger and earlier in tricuspid insufficiency
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
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
pulmonary edema
imbalance of starling forces, damage to alveolar capillary barrier, lymphatic obstruction, idiopathic
cardiogenic pulmonary edema
elevated pulmonary venous pressure (left heart failure or mitral valve stenosis), elevated CVP, death can occur
permeability pulmonary edema
permeability changes arising from endothelial injury
