Exam 1 Cardio I Flashcards
explain pulmonary and systemic circulation
Pulmonary circulation- right ventricle propels blood through the blood vessels in the lungs and accomplishes exchange of O2 and CO2.
Systemic circulation- left ventricle propels blood through blood vessels in other tissues of the body.
What type of muscle is cardiac muscle? Describe how the muscle mass is a “syncytium” (what does this mean? why is it needed for the heart to be an effective pump?).
This is involuntary striated muscle. Contractions are controlled by built-in “pacemakers”.
Cardiac muscle makes an electrical syncytium. This is a big difference from voluntary muscle. Cardiac muscle is made of individual cells connected either in series or in parallel to each other, connecting mechanically at structures called intercalated disks. The cells are connected electrically at these disks through gap junctions which allow ions to diffuse from cell to cell, making the muscle mass a “syncytium”, meaning that APs can easily travel from cell to cell.
As one cell is excited, the AP spreads to (effectively) all other cells, allows wave of excitation to pass over the myocardium to produce a synchronous contraction.
This is necessary for the heart to act effectively as a pump.
How do the syncytiums of the atria and ventricles relate to each other/communicate?
How does cardiac muscle differ from skeletal at the sarcomere level?
Why is the abundance of mitochondria significant?
The atrium and ventricles make in effect two separate syncytiums, since they are insulated from each other by a fiber bundle. Electrical excitation travels from the atrium to ventricles by way of specialized connective tissue, the A-V bundle.
At the sarcomere level, cardiac muscle is similar to striated muscle. The SR is less dense, different Ca++ release mechanisms
Abundance of mitochondria = indicates a high oxidative capacity.
How does the ‘wave-form’ of the action potential in cardiac muscle differs from the AP in a neuron or skeletal muscle? What are the currents responsible for the plateau phase? What are the phases 0 - 4?
The ‘wave-form’ of the action potential in cardiac muscle differs from the AP in a neuron or skeletal muscle; it starts with a rapid depolarization as we have seen before, but is followed by a “plateau” phase prolonging the depolarization, followed by the repolarization.
Phase 0= Na+ enters through fast Na+ channels to generate upstroke.
Phase 1= efflux of K+ through voltage-gated channels generates early and partial repolarization.
Phase 2= during plateau, net influx of Ca++ through Ca++ channels (L-type Ca channels- “L” stands for long duration, these are voltage-gated channels) is balanced by efflux of K+.
Phase 3= efflux of K+ through leak and voltage-gated channels now predominate.
Phase 4= efflux of K through leak channels slightly exceeds the influx of K through these same channels.
What role does Ca++ plays in K+ permeability during cardiac muscle contraction?
The role Ca++ plays in K+ permeability: opening Ca++ in phase 2 appears to reduce K+ permeability via a yet to be described mechanism. When the Ca++ permeability falls in phase 3, K+ permeability increases back to baseline.
How does cardiac muscle’s use of Ca2+ for contraction differ from skeletal muscle’s? With what does this provide cardiac muscle?
Cardiac muscle differs from skeletal muscle in use of Ca++. Skeletal muscle contraction is initiated by Ca release from sarcoplasmic reticulum. This is true of cardiac muscle, but Ca also flows into reticulum from T-tubules. This provides extra Ca and increases strength of cardiac muscle contraction. This also means cardiac muscle contraction is strongly influenced by extracellular calcium.
What events lead to the ca2+-dependent cardiac contraction and relaxation?
Cardiac muscle AP prolonged plateau due to voltage-gated L-type Ca2+ channel.
Contraction: Influx triggers opening SR Ca2+ channels, promotes actin/myosin interaction for contraction.
For relaxation: SERCA helps reuptake of Ca2+ into SR by ATP dependent process. 3Na-1Ca antiporter uses Na gradient to extrude Ca (against gradient). ATP-dependent Ca2+ pump also removes Ca2+.
SERCA=sarco/endoplasmic reticulum Ca2+ ATPase, or Ca-ATPase
*Long-duration AP in cardiac muscle overlaps contraction.
Why do cardiac APs have long refractory periods? What are the two phases? How can they be pathological?
Long refractory period is protective against tetanus in cardiac muscle.
Note there is an absolute refractory of .25 to .3 sec, which mirrors the prolonged plateau of the AP. Then there is a relative refractory period of .05 sec during which it is difficult but possible to the tissue. This can result in an early or premature contraction, a situation that arises in several pathologies.
What are the functions of the AV valves (name them) and semilunar valves (name them)?
Why are the papillary muscle and chordae tendineae important? Which heart sound is what? (1st and 2nd)
Mnemonic for heart valves?
A-V valves (tricuspid & mitral) prevent backflow from ventricles during systole.
Semilunar valves (aortic and pulmonary) prevent backflow from aorta and pulmonary arteries during ventricular diastole. *Valves operate passively
The papillary muscle and chordae tendineae: Rather than pull the valves open, these function to keep the AV valves from bulging inward during ventricular systole. If these rupture or break, it can lead to lethal cardiac incapacity. Chordae tendineae support (subjected to higher mechanical stress).
First heart sound is closure of A-V valves, second heart sound is closure of aortic and pulmonary valves
Mnemonic for heart valves: Try Pulling My Aorta.
How are the atria “primer pumps”?
Atria as primer pumps: blood flows continuously into atria, with 80% continuing directly into the ventricles. Atrial contraction pushes the remaining 20% of blood that fill the ventricle. This acts as a ‘pump primer’.
Identify the component waves of atrial pressure.
Atrial pressure: A-wave is atrial contraction it occurs towards the end of diastole period, in between the P and peak of R.
C-wave is ventricular contraction (causing backflow). It occurs during beginning of systole period.
V-wave is at end of ventricular contraction while A-V valves are closed and blood is flowing into the atrium, occurs after systole period.
Describe ventricular pumping. What is the isometric/isovolumic contraction period? What is the isometric/isovolumic relaxation period?
What are the two ejection periods?
Compare the volumes of blood at the end of diastole vs during systole.
Ventricles as pumps: During ventricular systole, blood collects in atria. With the end of contraction, pressure falls, A-V valve opens, and blood enters. Note last third of filling is atrial systole.
With onset of ventricular contraction, pressure rises causing A-V valve closure (.02 to .03 seconds needed to raise pressure to point where aortic and pulmonary valves open). This period is called isometric contraction or isovolumic contraction. With contraction comes a period of rapid ejection (1st third-70% of blood) and period of slow ejection (2nd two thirds of blood).
Isovolumic relaxation: pressure in aortic and pulmonary arteries closes aortic and pulmonary valves. For .03 to .06 sec, ventricle muscle continues to relax but there is no change in volume.
End diastolic volume: 110 to 120 ml, blood is filling ventricle during diastole. During systole, this goes down to 70ml (the stroke volume).
Equation for pulse pressure (what is it)?
Equation for mean arterial pressure (explain)?
Pulse pressure= arterial systolic pressure – diastolic pressure
Mean arterial pressure= diastolic pressure + 1/3 pulse pressure. The mean arterial pressure isn’t simply the average of systolic and diastolic pressures since a greater fraction of the cardiac cycle (2/3 of the cycle) is spent in diastole.
Describe work output of heart. What is the primary purpose?
Work output of heart: “stroke-work output”: amount of energy heart converts to work during each BEAT. Work output from heart is primarily to move blood from low-pressure veins to high-pressure arteries, known as ‘volume-pressure work’, or ‘external work’.
“Minute-work output” is energy converted to work in 1 MINUTE, or stroke work output times heart rate per minute.
This figure from the text is graphical analysis of left ventricular pumping. The diastolic pressure curve is determined by filling the heart with progressively greater volumes of blood before ventricular contraction starts- the ‘end-diastolic pressure’. The systolic pressure curve is determined by recording the systolic pressure achieved during ventricular contraction at each volume of filling.
Note that up to @150ml, the diastolic pressure doesn’t rise much, meaning up to this point it is easy for blood to flow from atrium to ventricle- above 150ml, the walls of the ventricle are stretched and pressure rises rapidly. Systolic pressure increases even at lower volumes, maxing at @150-170mls. Above this volume, systolic pressure can fall. Why? The tissue is so stretched that the actin/myosin filaments are too far apart. Left ventricle pressure gets up to 250 to 300 mmHg, right ventricular pressure maxes out at 60 to 80 mmHg.
- What is the approximate stroke volume represented on a graph?
- What is the effect on loop with an increase in end-diastolic volume (pre-load)? What is effect on stroke volume?
Stroke volume is width of pressure loop.
End-diastolic volume , or “preload”, is volume of blood contained in the ventricle just before contraction. Increasing this volume means more fluid (blood) enters the ventricle during diastole, and shifts the curve to the right. Frank-Starling relationship holds that as end-diastolic volume increases, stroke volume increases (everything coming in gets pumped out). Note the increase in the width of the pressure-volume loop.
