Cardiac Cycle

Beginning of one heart beat to the next including a period of relaxation.

Contracting

Relaxing(filing)

The pressure has to be greater in the chamber that has fluid presently and lower in the chamber it wants to flow into.

That there is an inverse relationship between pressure and volume, Change in pressure gradient creates a change in volume and drives blood flow.

1. Diastasis 2. Atrial systole 3. Isovolumic contraction of ventricles 4. Ventricular ejection 5. Isovolumic relaxation of ventricles 6. Ventricular filling

All chambers are relaxed, AV valves open blood flows into ventricles.

SA node fires, atrial depolarization shown as P wave on EKG, Atrial kick last 20% or blood into ventricle, heart sound 4 heard turbulence caused by blood rushing into ventricles

Volume in ventricles at end of phase 2

Atria repolarize and relax, Ventricles depolarize, QRS complex, Ventricles initiate contraction, raising pressure closes AV valves, Heart sound one turbulence against AV valves

Rising pressure causes aortic and pulmonary semilunar valves to open,

amount ejected in ventricular ejection greater or equal to 70ml

Is a product of sv/edv at rest 60% during vigorous exercise 90% in a diseased heart 50%

amount left in heart after ejection usually 50ml

Appears as T wave, ventricles repolarize, semilunar valve closes, AV valve remains closed, ventricles expand but do not fill, heart sound 2 (turbulence against semilunar valve)

AV valve opens, Heart sound 3,

Rapid ventricular filling, Diastasis, Filling by atrial systole(phase 2)

Caused by turbulence against the AV valves, when isovolumic contraction of ventricles

Turbulence against semilunar valves when isovolumic relaxation of ventricles

Turbulence caused by inrush of blood into ventricles when passive ventricular filling

Turbulence caused by inrush of blood into ventricles when atrial systole

Amount of blood ejected by ventricle per minute

Stroke volume X Heart rate

4-6L/m Vigorous exercise increase CO to 21L/min for fit person and up to 35L/min for world class athlete

Maximum CO- resting CO

EDV and ESV

Filling time (diastole), venous return (the rate of blood flow into the heart from veins), Skeletal pumping(muscular pressure excreted on the veins), respiratory pumping(lower intrathoracic pressure during inspiration takes blood into atria)

End diastolic volume(EDV)- End Systolic volume= Ejection volume(stroke volume)

Preload degree of muscle tension when it begins contraction, Contractility of the ventricle (dependent on CA available positive and negative ionotrophy), After load

Contractile force needed for ventricle ejection affected by peripheral vascular resistance hence the pressure in the vessels needed to be overcome

More in more out

The heart pumps all the blood that comes to it within physiological limits, if there isnt excessive damning of the vessels, Length tension relationship of cardiocytes

Extra stretch on cardiac myocytes make actin and myosin filaments interdigitate to a more optimal degree for force generation

Causes increased HR up to 180-200 bpm Increased force of contraction and CO to 15-20 L/min

Causes decrease in HR and decreased cardiac output and force of contraction

It actually lowers it as the chamber cannot fill completely

The diastolic phase is proptionaly shortened but all are to an extent

Blocks Parasympathetic input (block muscranic AChR agent) (+,+)

Drug that causes cholinergic neurons to release ACh, since ACh decreases HR it has a (-,) effect on HR

Reversible competitive blockers Beta 1 receptor blocks sympathetic effect on HR and force of contraction(-,-) also lower BP

Derived from Foxglove plant, Has a (-,+) effect on Heart i.e. lowers HR(chronotrophy) but increase force of contrations(ionotrophy) only drug with such effects

Digioxin or Digitoxin

They inhibit Na/K ATPase (Na/K pump) increase Na intercellularly, decrease Na gradient, decrease Na/Ca2+ counter transport, increase intercellular Ca2+