Cardiac Cycle-Chapter 9• Beginning of one heart beat to

the next.– Includes a cycle of

contraction and relaxation• Systole: contraction• 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)

• Opposing pressures in atria/ventricles/ large arteries

Phases of Cardiac Cycle-step by step-800mSec- only 370mSec for Systoles

• Quiescent period/ Diastasis– Quiescent period/ Diastasis– 430mSec430mSec– all chambers relaxedall chambers relaxed– AV valves openAV valves open– blood flowing into ventriclesblood flowing into ventricles

• Atrial systole- 100mSecAtrial systole- 100mSec– SA node fires, atria depolarizeSA node fires, atria depolarize– P wave appears on ECGP wave appears on ECG– atria contract, force additional atria contract, force additional

blood into ventriclesblood into ventricles– ventricles now contain ventricles now contain end-end-

diastolic volume (EDV) of diastolic volume (EDV) of about 120 ml of bloodabout 120 ml of blood

– Heart sound 4 occursHeart sound 4 occurs

P

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 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

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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 Cycle (cont’d)

Figure 9-5; Guyton & HallHeart sounds are from turbulent blood!

4th

Cardiac Output (CO)

• Amount ejected by a ventricle in Amount ejected by a ventricle in 1 minute1 minute

• CO = HR x SVCO = HR x SV• Resting values, usually about 4 Resting values, usually about 4

to 6L/minto 6L/min• Vigorous exercise Vigorous exercise CO to 21 CO to 21

L/min for fit person and up to 35 L/min for fit person and up to 35 L/min for world class athleteL/min for world class athlete

• Cardiac reserve: difference Cardiac reserve: difference between maximum and resting between maximum and resting COCO

Volumes and Fraction

• End diastolic volume = 120 ml• End systolic volume = 50 ml• Ejection volume (stroke volume) = 70 ml• Ejection fraction = 70ml/120ml = 58%

(normally 60%)• If heart rate (HR) is 70 beats/minute, what is

cardiac output?• Cardiac output = HR * stroke volume

= 70/min. * 70 ml = 4900ml/min.

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

• 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.

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.

25

20

15

10

5

0-4 0 +4 +8

Car

diac

Out

put (

L/m

in)

Right Atrial Pressure (mmHg)

(Parasympatheticstimulation)

No sympathetic and no parasympathetic stimulation

sympathetic stimulation

Maximum sympathetic stimulation

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!

Factors Influencing CO

Figure 14-31: Factors that affect cardiac output

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 derived from foxglove plant. It has a (-,+) effect, neg chronotropic and positive inotropic effect; slows heart rate but increases force of contraction. Is 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?

Na+ Na+

K+

Ca++Na+

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.

• Glycosides (eg. digoxin) inhibit the Na/K ATPase…increase intracellular Na+decrease Na+ gradientdecrease Na+/Ca2+ counter-transportincrease intracellular Ca2+