Lecture 17 Cardiac Cycle
Clinical note: Third degree AV block: impulse does not go through AV node; atria act on their own (fast), ventricles act on their own (slow): will see three low hills before the QRS peak.
The same picture in your homework packet p.2 is the same one on the exam. You have to draw in the blanks on the exam and answer some questions.
Cardiac Cycle
• Beginning of one heart beat to the next. Electrical and mechanical events.
– Includes a cycle of contraction and relaxation
• Systole: contraction; there are ventricular and atrial contractions and relaxation, but clinically it refers to the ventricles.
• Diastole: relaxation (filling)
• Blood will only move from one chamber to the next if the pressure in the first chamber exceeds the second!
• Timing is EVERYTHING!
Principles of Pressure and Flow
• Measurement: compared to force generated by column of mercury (mmHg) – sphygmomanometer
• Change in pressure gradient creates a change in volume (Boyle’s law)
• Boyle’s Law: Increased pressure à decreased volume (inverse relationship)
• Opposing pressures in atria/ventricles/ large arteries
• Fluid only flows from high pressure to low pressure
• What factors affect pressure and blood flow?
• Length of vessels
• Radius of vessel
• Viscosity of blood
When you put your lips on a straw, you create low pressure in your mouth, high pressure in your soda, fluid moves into your mouth.
Phases of Cardiac Cycle-step by step-800mSec- only 370mSec for Systoles
• Quiescent period/ Diastasis– 430mSec
– all chambers relaxed
– AV valves open from the pressure.
– There is higher pressure in atria than the ventricles, so blood flows into ventricles
• Atrial systole- 100mSec
– SA node fires, atria depolarize
– P wave appears on ECG
– atria contract, force additional blood into ventricles
– ventricles now contain end-diastolic volume (EDV) of about 120 ml of blood
– Heart sound 4 occurs
Isovolumic Contraction of Ventricles
• Atria repolarize and relax
• Ventricles depolarize
• QRS complex appears in ECG
• Ventricles contract
• Rising pressure closes AV valves
• Heart sound S1 occurs
• No ejection of blood yet (no change in volume)
Ventricular Ejection
• Rising pressure opens semilunar valves
• Stroke volume: amount blood ejected, ~ 70 ml
• Rapid and reduced ejection phases
• SV/EDV= ejection fraction,
– at rest ~ 60%
– during vigorous exercise as high as 90%
– diseased heart < 50%
• End-systolic volume: amount left in heart (50ml)
• Ventricular systole lasts 270mSec
Isovolumic Relaxation of Ventricles
• T wave appears in ECG
• Ventricles repolarize and relax (begin to expand)
• Semilunar valves close
• AV valves remain closed
• Ventricles expand but do not fill
• Heart sound S2 occurs
Ventricular Filling
• AV valves open
• Ventricles fill with blood - 3 phases
– rapid ventricular filling - high pressure
– diastasis - sustained lower pressure
– filling completed by atrial systole
• Heart sound S3 may occur
Cardiac Output (CO)
• Amount ejected by a ventricle in 1 minute: CO = HR x SV
• Resting values, usually about 4 to 6L/min
• Vigorous exercise CO to 21 L/min for fit person and up to 35 L/min for world class athlete
• Cardiac reserve: difference between maximum and resting CO
Be familiar with the above photo. Understand what happens during the pQRST complex, what the volume and pressure is during each phase of the cardiac cycle.
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Not all of the blood is ejected from the ventricles during contraction. If you start will 120 ml of blood in the ventricles and eject 70 ml. you will have 50 ml left over as the end systolic volume.
If you want a greater stroke volume, increase the venous return. That provokes the Frank-Starling mechanism, the length-tension relationship. What goes in must come out. Water from a faucet into a water balloon causes tension in the latex. Your heart does not keep stretching until it pops. As the blood pools it creates weight. When they contract, the more sag that they have promotes a greater force. The more venous return there was, the greater the stroke volume on the next contraction. If blood dams up in the blood vessels, you will have edema. If this back-up is in the vessels on the left side of the heart, it will result in pulmonary edema.
Blood flows from high pressure area to low pressure area. If the pressure of the blood in the vessels is high, the ventricles have to generate a greater pressure to eject the blood. If there has not been enough time for the heart to hypertrophy, the heart has to work harder to overcome that pressure.
Contractility is related to the amount of calcium in the cell. The more calcium present, the greater the contraction can be.
Factors that Affect Stroke volume
• EDV- dependent on filling time (diastole) and venous return
– Skeletal pumping
– Respiratory pumping
• ESV-
– Preload- degree of stretching
• Frank-Starling Principle: more in, more out
– Contractility of the ventricle
• Availability of calcium; positive and negative inotropy
– Afterload- amount of tension ventricle must exert to eject; affected by peripheral vasculature; if greater ESV then there was less stroke volume
Frank-Starling Mechanism
• What goes in, must come out
• Within physiological limits the heart pumps all the blood that comes to it without excessive damming in the veins.
• Length-tension relationship of cardiocytes.
• Extra stretch on cardiac myocytes makes actin and myosin filaments interdigitate to a more optimal degree for force generation.
The Frank-Starling Mechanism happens in skeletal and smooth muscle as well. If you stretch before you lift weights, you stretch the actin and myosin filaments apart, allows for more force of contraction. When smooth muscle is stretched, it also puts out more calcium and you get greater contractility.
How much blood your kidney can filter depends on the blood pressure. Your kidneys regulate their filtering when your BP increases so that you don’t have to urinate every time you exercise.
The sympathetic system affects your end diastolic volume. How does it change the contractility? When it releases epinephrine or norepinephrine, leads to cAMP, leads to alteration of phosphorylation on the calcium permeability. The force of contraction increases, influences stroke volume.
Autonomic Effects on Heart
• Sympathetic stimulation causes increased HR + increased contractility with HR = 180-200 and C.O. = 15-20 L/min.
• Parasympathetic stimulation decreases HR markedly and decreases cardiac contractility slightly. Vagal fibers go mainly to atria.
• Fast heart rate (tachycardia) can decrease C.O. because there is not enough time for heart to fill during diastole.
So what happens to the Cycle when the heart rate increases?
• All phases are shortened; Diastole pays the biggest price!
• Reduced by almost 75% at 200bpm
• What does that mean? Less Filling!
If the heart rate increased too much, the cardiac cycle is too short, stroke volume is low, CO decreases. The heart gets perfused when it is relaxing. If it is contracting vigorously because stoke volume has declined, Baroreceptors (monitor degree of stretch in blood vessels) are not firing. When there is more stroke volume, it leads to more stimulation of Baroreceptors, send signals to medulla oblongata. Parasympathetic system stimulates reflex arc; the cardiac inhibitory centers, and heart rate declines. More stroke volume, greater stretch, stimulates cardiac inhibitory centers. If stroke volume is low, provokes a reflex to stimulate cardiac stimulation centers.
A high heart rate (when stroke volume is decreased by blood loss, etc) can actually lead to a higher heart rate; this is a dangerous situation.
Drugs Affecting CO
• Atropine- parasympathetic blocking (blocks muscarinic AchR) agent, (+,+)
• Pilocarpine- drug that causes cholinergic neurons to release ACH. Since Ach decreases heart rate, it causes (-, ) effect on heart.
• Propranalol- Reversible, competitive blocker of Beta1 receptor. So blocks sympathetics effect of heart (-,-) Decrease heart rate and force of contraction, and lowers blood pressure.
Drugs Affecting CO (2)
• Digoxin (shorter ½ life) or Digitoxin- come from group of drugs derived from digitalis. Digitalis is derived from foxglove plant. It has a (-, +) effect, neg chronotropic and positive inotropic effect; slows heart rate but increases force of contraction. Ii is the only drug with this effect on heart.
– Increases intracellular concentration of Ca.
– Increase force of contraction by inhibiting Na+/K+ pump. So cells start to accumulate Na.
– Disadvantage of using digitalis is that it’s extremely toxic. The optimal dose is very close to lethal dose- stops heart
Q: How do cardiac glycosides
increase cardiac contractility?
• Glycosides (eg. Digoxin) inhibit the Na/K ATPase…
l increase intracellular Na+
l decrease Na+ gradient
l decrease Na+/Ca2+ counter-transport
l increase intracellular Ca2+
Digoxin has been a cornerstone for the treatment of heart failure for decades and is the only oral inotropic support agent currently used in clinical practice.