Lectures 28 & 29: Cardiac Mechanics Flashcards
Extracellular calcium is necessary for
- Normal contractility
- Excitability
- Ca 2+ is the link between electrical and mechanical activation of the heart
Ca2+- induced Ca2+-release
- Calcium enters during action potential
- Acts as trigger for calcium release from SR rather than binding troponin
- Directly triggering shortening process
Plasma membrane Ca2+ channel (L-Type, DHPR)
- Channel does not physically interact with the Ca2+- release channel (RYR) in the SR
Relaxation (lusitropy) steps
- 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
Na+/Ca2+ exchanger (NCX)
- 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
Na+/Ca2+ exchanger (NCX) mediates
- Ca2+ efflux at rest
- Ca2+ influx during early part of action potential
- Shifts to net efflux as [Ca2+]i and Vm change
A decrease in the magnitude of the Na gradient
- Occurs with digoxin
- Results in the exchanger mediating a larger calcium influx on a beat-to-beat basis
- Thus, enhancing contractility
Myocardial contractility (intrinsic regulation) definiton
- Change in peak isometric force at a given initial fiber length
Effects of changes in preload - the Starling effect
- Heterometric regulation
- Involves length changes
Homeometric changes
- Independent of length of fibers such as contractility changes
The ejection fraction
- 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
Stroke volume
- Volume of blood ejected from the left ventricle per beat
Cardiac hypertrophy
- Progressive and sustained enlargement of the heart
Pericardial effusion
- Slow progressive increase in pericardial fluid
Cardiac hypertrophy and pericardial effusion can cause
- Gradual stretching of the intact pericardium
Importance of myocardial contractility
- 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
Heart failure
- Preload can be substantially increased because of the poor ventricular ejection
- Increased blood volume caused by fluid retention
Essential hypertension
- High peripheral resistance augments the afterload
- Via decreasing the peripheral runoff of the blood from the arterial system
Heart rate will influence stroke volume through
- Temporal effect on diastolic filling time
- The greater the filling time, the greater the stroke volume
With increasing HR, encroachment into filling time leads to
- Reduced EDV
- Reduced SV
- Reduced Q
Temporary alterations in myocardial contractility may occur via interval-strength factors
- Staircase or treppe
- Rest potentiation
- Post-extra systolic potentiation
Afterload stresses
- Increasing afterload (aortic pressure as in hypertension)
- Decreases stroke volume, ejection velocity and ejection time
Afterload stresses decreases stroke volume, ejection velocity and ejection time, which means
- Myocardial fibers need a longer time to develop the tension required to overcome the greater afterload
Contractility changes (homeometric regulation; inotropy)
- Decreases in extracellular calcium ions, increases in sodium gradients by increase in external sodium or decrease in internal sodium
Decreases in calcium entry (via L-type calcium channels) during homeometric regulation
- Reduces contractile force at any given sarcomere length
The Na+ and Ca2+ ions that enter and the K+ ions that leave during the action potential (homeometric contractility)
- Must be removed/taken back up
- Requires sarcolemmal Na/K pump, Na:Ca exchanger, and Ca2+-ATPase
- Otherwise get phenomenon called calcium overload
Calcium overload
- Depressed contraction due to calcium accumulation in mitochondria
- Reduces their energy production capability
The cardiac cycle consists of
- 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
Events of the cardiac cycle
- Isometric contraction
- Rapid ejection
- Reduced ejection (protodiastole)
- Isometric relaxation
- Rapid ventricular filling
- Reduced ventricular filling (diastasis)
- Atrial systole
Isometric contraction
- 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)
Isometric contraction lasts until
- Sufficient ventricular pressure is built up to push the semilunar valves open against the pressures in the aorta and pulmonary artery
Rapid ejection
- 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
Reduced ejection (protodiastole)
- 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
Isometric relaxation
- 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
Rapid ventricular filling
- With opening of the AV valves and higher pressures in atria, blood flows rapidly into the ventricles
- First third of diastole
Reduced ventricular filling (diastasis)
- 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
Atrial systole
- 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
During the cardiac cycle, the atrial pressure curve shows
- Three major pressure elevations
- a, c, and v atrial waves
- Also reflected in venous pulse waves
The ‘a’ wave is caused by
- Actual atrial contraction
The ‘c’ wave is caused by
- Reflux of blood out of the ventricles during ventricular contraction
- Tension created on the atrial muscles by the contraction of the ventricles
The ‘v’ wave results from
- Slow buildup of blood in the atria during ventricular systole
Function of the AV valves
- Prevent backflow of blood from ventricles to atria during systole
Function of the semilunar valves
- Prevent backflow from aorta and pulmonary arteries into ventricles during diastole
Opening of valves (heart sounds)
- Relatively slow process
- Makes no noise
Closure of valves (heart sounds)
- 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
Split sounds
- Asynchronous valve closures
- Over the apex of the heart for the AV valves
- Over the base for the semilunar valves
Heart murmurs
- Deformities of the valves
Valve lesions (stenosis or incompetence)
- 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
