Cardiac Performance Flashcards

1
Q

Cardiac performance

A

. How well the heart performs this pump function

. Described in terms of functional parameters (stroke volume, stroke work, CO)

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2
Q

Stroke volume

A

. Volume of blood ejected during a single cardiac contraction
SV = EDV-ESV

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3
Q

Cardiac output

A

. Blood flow per unit time

CO = SV X HR

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4
Q

Cardiac index

A

. CO divided by the body surface area

. Compensates that the large the individual generally the greater the CO

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5
Q

Stroke work

A

. Amount of work the heart does during a single contraction
SW = VPP X SV
. VPP: ventricular pulse pressure (peak pressure minus end-diastolic pressure)
. Under physiological conditions, the right ventricular stroke volume is equal to the left, but the RV stroke work is not equal to LV

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6
Q

Factors that overall performance of ventricle depends on

A

. Preload
. Afterload
. Contractility
. HR

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7
Q

Preload

A

. Consists of forces acting to stretch cardiac mm. Fibers prior to onset of contraction (at end of diastole)
. Determines max resting fiber length in mm.
. Preload of whole heart determined by tension in ventricular wall at end of diastole which depends on Law of LaPlace (T = Pr)

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8
Q

Ventricular filling time

A

. Time available for passive filing (both rapid and reduced) to occur
. Filling time dependent on HR
. Most filling occurs during rapid filling phase
. Normally filling time is adequate to not limit perfusion of organs
. As HR inc., time available for diastolic filling dec.
. If ventricular contractility inc. w/ inc. HR stroke volume may not dec. w/ inc. HR, but stay the same or even inc. w/ inc. HR until filling time becomes limiting at very high HRs
. Situation (inc. contractility plus inc. HR) will lead to inc. in CO, the magnitude of which can be large when exercising

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9
Q

What occurs when diastolic filing time decreases to less than 0.1 sec?

A

. Occurs due to excessively rapid HR
. Time available for completion of rapid filling phase of cardiac cycle is no longe adequate
. Primary functional implication of inadequate ventricular filing time is that it results in an inability to maintain adequate CO due to reduction in SV at very high HR

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10
Q

Ventricular compliance

A

. Property of the heart that allows it to be expanded or distended
. One large change in volume produces a relatively small change in pressure
C = DeltaV/DeltaP
. As compliance dec., a given change in volume will produce an abnormally large change in pressure
. Change affects pressure gradient required for passive and active ventricular filling to occur and continue
. Myocardial compliance is dec. in conjunction w/ ventricular hypertrophy and ischemia
. Not significantly affected by altered sympathetic or parasympathetic tone

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11
Q

The value of passive pressure that develops during ventricular filling depends on ____

A

. Compliance of ventricle
. Normally back pressure is of minor importance in terms of ventricular filling
. However, when there is abnormally low ventricular compliance (high EDV), diastolic pressure assoc. w/ ventricular filling can be more important in limiting ventricular filling

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12
Q

Ventricular filling pressure

A

. Intrathoracic pressure and central venous pressure affect venous return to RA and affect LV function by influence RV stroke volume.
. Inc. in central venous pressure/Neg. intrathoracic pressure will inc. pressure gradient and enhance filling of RV
. This affects RV stroke volume ultimately LV filling and LV stroke volume

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13
Q

Atrial contractility

A

. Atrial systole only accounts for 15-20% ventricular filling at rest
. Changes in atrial contractility normally minor factors in EDV, but importance include. When diastolic filling time becomes limited
. Atrial systole can account for up to 40% of filling at high HRs
. Lack of effective contraction is not life threatening but reduces exercise capacity

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14
Q

Pericardial restraint

A

. Pericardium protects against LV distension during volume overload
. Maintains alignment of heart w/ great vessels
. Provides lubricated surface against which ventricles move
. Accumulation of fluid or fibrosis restricts or limits ventricular filling
. At the same time ventricular compliance will be reduced
. Meaning that as ventricle fills there will be disproportionate inc. in ventricular end-diastolic pressure

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15
Q

Frank-Starling Mechanism

A

. Defines relationship between EDV and ventricular pressure development
. Intrinsic mechanism for regulation of cardiac function
. If ventricles are filled to a greater extent than normal, subsequent contraction is more forceful than normal
. Systolic inc. w/ inc. EDV
. SV also inc. w/ inc. EDV
. Creates starling curve

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16
Q

EDV is dependent on ___

A

. Body position
. When supine, there is very little diastolic reserve volume so EDV can’t be substantially inc. by inc. venous return so alterations in EDV to alter cardiac function
. When standing there is a sizeable diastolic reserve volume and EDV can be inc. significantly as venous return is enhanced
. Diastolic reserve = volume of blood that could be returned to the heart

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17
Q

Pressure-volume loop

A

. Describes function of heart when ventricular muscle is allowed to shorten and blood is ejected
. Ventricular pressure inc. to overcome pressure in the aorta and ventricular volume falls and blood is being ejected
. Intraventricular pressure is highest at peak of ejection then falls
. After aortic valve closes, intraventricular pressure continues to fall as ventricle relaxes isovolumetrically
. Filling occurs and EDV begins to inc. again
. Dimensions fo pressure-volume loop depend on EDV, afterload, and myocardial contractility

18
Q

Afterload

A

. Resistance against which ventricle contracts

. Mean aortic pressure generally approximates afterload on intact heart

19
Q

Most common cause of inc. afterload is ___

A

Arterial hypertension

20
Q

Factors influencing afterload

A

. Arterial pressure: greatest effect, as it inc. afterload inc.
. Peripheral vascular resistance: inc., afterload inc.
. Blood viscosity: inc., afterload inc.
. Amount of blood in aorta: mass of blood inc., greater inertia due to column of blood which has to be overcome
. Aortic compliance: reduced, afterload inc.
. Preload: inc. in preload, greater wall tension resulting from ventricular filling has to be overcome during contraction before ventricular pressure can rise

21
Q

Type of relationship between level of afterload and stroke volume a a given level of preload

A

. Inverse
. As afterload inc., SV dec.
. Decreased SV can be compensated fro by subsequent inc. in EDV

22
Q

Contractility

A

. Ability of heart to perform work at any given end-diastolic fiber length
. Independent of starling effect
. Influenced by metabolic condition of cells, ANS, hormones, and HR

23
Q

Acute effects of a positive inotropic intervention on pressure-volume loop

A

. At end of diastole, ventricle is filled to same volume and pressure as before the inc. in contractility
. During systole, the ventricle ejects more blood (inc. SV) due to inc. in contractility
. Inc. SV occurs from age EDV (same preload)

24
Q

Physiological modulation of ventricular contractility in normal heart is dominated by ____

A

ANS
. Inc. sympathetic n. Activity and E release from adrenal gland enhance contractility
. Mediated by beta-adrenergic receptors and cAMP/cAMP protein kinase system

25
Q

Clinical measurements of contractility

A

.dP/dtmax: most accurate indirect measurement of contractility, max rate of pressure change during contraction, it is max. Positive slope of ventricular pressure curve
. Ejection fraction: ratio of stroke volume to EDV (50-75% Normal, contractile dysfunction if below 40%), difficult to measure
Ejection fraction = SV/EDV

26
Q

Heart rate influences on cardiac performance

A

. Inc. contractility: inc. HR directly inc. contractility (Bowditch effect) which causes inc. SV
. Contribution to CO: CO doubles due to contribution of HR

27
Q

Left ventricular stroke work

A

. Equal to the product of left ventricular pressure and stroke volume
LVSW = LVPP X SV

28
Q

Minute work

A

. Left ventricular minute work: product of ventricular stroke work and HR (LVSW X HR)
. Index of heart function that’s provides info about dynamic contractile activity of heart over period of time rather than single beat basis

29
Q

External work vs internal work

A

. External: area of the pressure-volume loop, work done to generate pressure and eject blood
. Internal: work done by heart prior to development of pressure, work done against non-contractile elements of the heart

30
Q

Volume work vs. pressure work

A

. Equal amounts of external work performed by volume loading (inc. preload/EDV) or pressure loading (inc. afterload), the volume-loaded ventricle will have less O2 consumption

31
Q

Cardiac efficiency

A

Worked performed/O2 uptake
. Normally 12-20%
. Most energy dissipated as heat
. For equal amts of external work performed by volume loading, the volume-loaded ventricle will have greater efficiency
. Pressure-loaded heart performs more internal work against non-contractile elements of heart
. Internal work does not contribute to determining efficiency

32
Q

Fick Principle

A

. Flow = quantity consumed(or added)/arterial content-venous content

33
Q

Cardiac output formula

A
. Expressed in L/min 
CO = VO2/aO2-vO2
.VO2: whole body O2 consumption 
.aO2: arterial blood oxygen content 
.vO2: pulmonary artery blood
34
Q

Heart failure

A

. Heart fails to pump adequate CO
. Can occur on right side or left
. Left HF: failure of LV to pump adequately, leads to an inc. pulmonary venous pressure, inc. pulmonary capillary pressure
. Inc. pulmonary capillary pressure leads to inc. filtration of fluid out of capillaries causing pulmonary edema

35
Q

Causes of HF

A
. Coronary artery disease/infarcts
. Hypertension
. Cardiomyopathy
. Abnormal hear valves 
. Arrhythmias
. Congenital heart defects
36
Q

Coronary artery disease/infarcts

A

. Blockage of aa. Leads to inadequate O2 delivery to cardiac mm.
. Causes temporary or permanent damage to the muscle
. Remaining mm. Needs to work harder to pump out same CO
. If heart mm. Is inadequately oxygenated for long enough the heart muscle cells die

37
Q

Hypertension

A

. Inc. in arterial bp (inc. in afterload) makes heart work harder to pump same amount of blood
. To maintain same CO requires ventricle to work harder, requiring more energy and O2
. Chronic hypertension can result in damage to heart mm.

38
Q

Cardiomyopathy

A

. Heart muscle can be damaged by variety of disease processes, drugs, chronic alcohol use, or unknown causes

39
Q

Effective stroke volume

A

. Amount of blood going out to the systemic organs

40
Q

Treatment of heart failure

A

. Lifestyle changes
. Surgery/angioplasty: bypass, angiolasty, heart transplant
. Medications: combination of more than 1 drug

41
Q

Drugs used in them treatment of heart failure

A

. Diuretics: eliminate excess fluid
. Cardiac inotropic drugs: inc. contractility enhancing pumping ability of the heart
. Vasodilators: reduce resistance that the heart pumps against by lowering bp
. Beta-blockers: drugs that block beta-adrenergic receptors in the heart, limits sympathetic stimulation causing lowered bp and dec. HR