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Physiology I: Cardiovascular System > Lectures 28 & 29: Cardiac Mechanics > Flashcards

Lectures 28 & 29: Cardiac Mechanics Flashcards

1
Q

Extracellular calcium is necessary for

A
  • Normal contractility
  • Excitability
  • Ca 2+ is the link between electrical and mechanical activation of the heart
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2
Q

Ca2+- induced Ca2+-release

A
  • Calcium enters during action potential
  • Acts as trigger for calcium release from SR rather than binding troponin
  • Directly triggering shortening process
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3
Q

Plasma membrane Ca2+ channel (L-Type, DHPR)

A
  • Channel does not physically interact with the Ca2+- release channel (RYR) in the SR
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4
Q

Relaxation (lusitropy) steps

A
  • SR Ca2+ ATPase (SERCA) sequesters Ca into the SR
  • Na+/Ca2+ exchanger and a sarcolemmal Ca2+ ATPase also mediate Ca2+ efflux
  • An amount of calcium equal to that which entered must exit the cell on a beat-to-beat basis at constant contractility
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5
Q

Na+/Ca2+ exchanger (NCX)

A
  • Exchanges 1 Ca2+ for 3 Na+
  • Direction of net Ca2+ flux determined by magnitude of Na and Ca gradients and Vm
  • [Na+]o, [Na+]i, [Ca2+]o are constant on a beat-to-beat basis
  • [Ca2+]i varies between 0.1μM and 10 mM; Vm varies between -85 and 20 mV
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6
Q

Na+/Ca2+ exchanger (NCX) mediates

A
  • Ca2+ efflux at rest
  • Ca2+ influx during early part of action potential
  • Shifts to net efflux as [Ca2+]i and Vm change
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7
Q

A decrease in the magnitude of the Na gradient

A
  • Occurs with digoxin
  • Results in the exchanger mediating a larger calcium influx on a beat-to-beat basis
  • Thus, enhancing contractility
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8
Q

Myocardial contractility (intrinsic regulation) definiton

A
  • Change in peak isometric force at a given initial fiber length
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9
Q

Effects of changes in preload - the Starling effect

A
  • Heterometric regulation

- Involves length changes

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10
Q

Homeometric changes

A
  • Independent of length of fibers such as contractility changes
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11
Q

The ejection fraction

A
  • Ratio of the volume of blood ejected from the left ventricle per beat (stroke volume) to the volume of blood in the left ventricle at the end of diastole
  • Used clinically as an index of contractility
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12
Q

Stroke volume

A
  • Volume of blood ejected from the left ventricle per beat
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13
Q

Cardiac hypertrophy

A
  • Progressive and sustained enlargement of the heart
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14
Q

Pericardial effusion

A
  • Slow progressive increase in pericardial fluid
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15
Q

Cardiac hypertrophy and pericardial effusion can cause

A
  • Gradual stretching of the intact pericardium
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16
Q

Importance of myocardial contractility

A
  • Enables the heart to adapt to alterations in venous return
  • Keeping the cardiac output of two ventricles matched
  • Keeping pulmonary and systemic circuits in balance
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17
Q

Heart failure

A
  • Preload can be substantially increased because of the poor ventricular ejection
  • Increased blood volume caused by fluid retention
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18
Q

Essential hypertension

A
  • High peripheral resistance augments the afterload

- Via decreasing the peripheral runoff of the blood from the arterial system

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19
Q

Heart rate will influence stroke volume through

A
  • Temporal effect on diastolic filling time

- The greater the filling time, the greater the stroke volume

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20
Q

With increasing HR, encroachment into filling time leads to

A
  • Reduced EDV
  • Reduced SV
  • Reduced Q
21
Q

Temporary alterations in myocardial contractility may occur via interval-strength factors

A
  • Staircase or treppe
  • Rest potentiation
  • Post-extra systolic potentiation
22
Q

Afterload stresses

A
  • Increasing afterload (aortic pressure as in hypertension)

- Decreases stroke volume, ejection velocity and ejection time

23
Q

Afterload stresses decreases stroke volume, ejection velocity and ejection time, which means

A
  • Myocardial fibers need a longer time to develop the tension required to overcome the greater afterload
24
Q

Contractility changes (homeometric regulation; inotropy)

A
  • Decreases in extracellular calcium ions, increases in sodium gradients by increase in external sodium or decrease in internal sodium
25
Q

Decreases in calcium entry (via L-type calcium channels) during homeometric regulation

A
  • Reduces contractile force at any given sarcomere length
26
Q

The Na+ and Ca2+ ions that enter and the K+ ions that leave during the action potential (homeometric contractility)

A
  • Must be removed/taken back up
  • Requires sarcolemmal Na/K pump, Na:Ca exchanger, and Ca2+-ATPase
  • Otherwise get phenomenon called calcium overload
27
Q

Calcium overload

A
  • Depressed contraction due to calcium accumulation in mitochondria
  • Reduces their energy production capability
28
Q

The cardiac cycle consists of

A
  • Period of relaxation (diastole) followed by a period of contraction (systole)
  • During diastole, heart chambers fill with blood
  • During systole, blood is pumped forward into the arteries
29
Q

Events of the cardiac cycle

A
  • Isometric contraction
  • Rapid ejection
  • Reduced ejection (protodiastole)
  • Isometric relaxation
  • Rapid ventricular filling
  • Reduced ventricular filling (diastasis)
  • Atrial systole
30
Q

Isometric contraction

A
  • Contraction is occurring in the ventricles (no emptying)
  • Tension increasing in muscle fibers (no shortening)
  • Instantaneous rise in ventricular pressure (causes AV valves to close)
31
Q

Isometric contraction lasts until

A
  • Sufficient ventricular pressure is built up to push the semilunar valves open against the pressures in the aorta and pulmonary artery
32
Q

Rapid ejection

A
  • Left ventricular pressures rises slightly above 80 mmHg (pulmonary arterial pressure slightly above 8 mmHg)
  • Pushes open the aortic semilunar valve (pulmonic on right side)
  • Blood immediately pours out of the ventricles
33
Q

Reduced ejection (protodiastole)

A
  • During last 1/5 to 1/4 of ventricular systole
  • Almost no blood flows from the ventricles into the large arteries
  • Ventricular musculature remains contracted
  • Arterial pressure falls (almost no blood entering the arteries) even though large quantities of blood are flowing from the arteries through the peripheral vessels
34
Q

Isometric relaxation

A
  • End of systole
  • Ventricular relaxation begins suddenly
  • Intraventricular pressure falls rapidly
  • Elevated pressures in large arteries push blood back toward the ventricles
  • Snaps the aortic and pulmonary valves closed
  • Intraventricular pressures fall back to below the atrial pressures
  • Allowing the AV valves to open
35
Q

Rapid ventricular filling

A
  • With opening of the AV valves and higher pressures in atria, blood flows rapidly into the ventricles
  • First third of diastole
36
Q

Reduced ventricular filling (diastasis)

A
  • Middle third of diastole
  • Small amount of blood normally flows into the ventricles
  • Blood that continues to empty into the atria from the veins
  • Passes on through the atria directly into the ventricles
37
Q

Atrial systole

A
  • Last third of diastole
  • Atria contract, give additional thrust to inflow of blood into the ventricles
  • Ventricles are then ready to begin contraction
  • Blood flows continually from great veins into atria
  • About 70% of this blood directly into the ventricles even before the atria contract
  • Atrial contraction provides the additional 30% filling
  • When atrium is nonfunctional, ventricles can still operate almost normally
38
Q

During the cardiac cycle, the atrial pressure curve shows

A
  • Three major pressure elevations
  • a, c, and v atrial waves
  • Also reflected in venous pulse waves
39
Q

The ‘a’ wave is caused by

A
  • Actual atrial contraction
40
Q

The ‘c’ wave is caused by

A
  • Reflux of blood out of the ventricles during ventricular contraction
  • Tension created on the atrial muscles by the contraction of the ventricles
41
Q

The ‘v’ wave results from

A
  • Slow buildup of blood in the atria during ventricular systole
42
Q

Function of the AV valves

A
  • Prevent backflow of blood from ventricles to atria during systole
43
Q

Function of the semilunar valves

A
  • Prevent backflow from aorta and pulmonary arteries into ventricles during diastole
44
Q

Opening of valves (heart sounds)

A
  • Relatively slow process

- Makes no noise

45
Q

Closure of valves (heart sounds)

A
  • Vibrations of the surrounding fluids give off sound
  • First heart sound = closure of the A-V valves
  • Second heart sound = closure of aortic and pulmonary valves
  • Occasionally, atrial sound can be heard
  • Third sound (sometimes) = middle of diastole, may be caused by blood flowing with a rumbling motion into the almost filled ventricles
46
Q

Split sounds

A
  • Asynchronous valve closures
  • Over the apex of the heart for the AV valves
  • Over the base for the semilunar valves
47
Q

Heart murmurs

A
  • Deformities of the valves
48
Q

Valve lesions (stenosis or incompetence)

A
  • May be congenital or produced by disease (e.g., rheumatic fever)
  • Timing (systolic or diastolic) and character of the murmur provide clues regarding the type of valve damage

Physiology I: Cardiovascular System (12 decks)

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