Lectures 7+8

Initiation of cardiac cycle

Begins with spontaneous action potential from SA node

Cardiac cycle duration

Length of one heartbeat calculated as 60 divided by heart rate

Atrial contraction role

Contributes 10–20% of ventricular filling with most filling passive

Inflow phase

AV valves open and semilunar valves closed allowing ventricular filling

Isovolumetric contraction

All valves closed with increasing ventricular pressure and no volume change

Outflow phase

Semilunar valves open and blood is ejected from ventricles

Isovolumetric relaxation

All valves closed with decreasing pressure and constant volume

Phase 1 atrial systole

Atria contract increasing ventricular volume and pressure slightly, initiated by p wave, av open, sl closed, venous a wave

Phase 2 isovolumetric contraction

Ventricles contract with all valves closed and rapid pressure rise, exceeds atria, when LV > aortic pressure, aortic valve opens, venous c wave

Phase 3 rapid ejection

Semilunar valves open and blood rapidly exits ventricles, aortic pressure inc → max, t-wave begins/atria fills

Phase 4 reduced ejection

Decreasing ventricular contraction leads to reduced blood ejection, pressure in vent+ exits dec., venous return continues

Phase 5 isovolumetric relaxation

All valves closed and pressure falls with no volume change, venous v wave when atria full

Phase 6 rapid filling

AV valves open and ventricles fill quickly due to pressure gradient

Phase 7 reduced filling (diastasis)

Slow filling as pressure gradient decreases, 90% filled by end, aortic/pulmonary pressures still falling

ECG relationship to cycle

P wave → atrial contraction QRS → ventricular contraction T wave → ventricular relaxation

End diastolic volume (EDV)

Maximum ventricular volume at end of filling

End systolic volume (ESV)

Volume remaining after ventricular contraction

Stroke volume (SV)

Volume ejected per beat calculated as EDV minus ESV

Atrial A wave

Measured in jugular vein, atrial systole, blood regurgitate into veins when atria contract, causing increase in pressure

Atrial C wave

Measured in jugular vein, bulging of tricuspid valve (just closed) backward into the right atrium during isovolumetric ventricular contraction

Atrial V wave

Measured in jugular vein, mirrors rise in atrial pressure before the tricuspid valve opens during systole

Pressure volume loop

Graph of ventricular pressure versus volume during cardiac cycle

Width of PV loop

Represents stroke volume (sv= edv-esv)

Dicrotic notch

Brief increase in aortic pressure after semilunar valve closure

Heart sound 1/lub (S1)

Isovolumetric contraction, closure of mitral and tricuspid valves

Heart sound 2/dub (S2)

Isovolumetric relaxation, closure of aortic and pulmonary valves

S3 Heart Sound

Early ventricular filling, nromal in children and young adults associated with ventricular dilation

S4 Heart Sound

Atrial contraction, associated with stiff, low compliant ventricle (hypertrophy, ischemia)

Cardiac output (CO)

Volume of blood pumped by the heart per minute

Cardiac output equation

CO = heart rate X stroke volume

Normal cardiac output

Approximately 5 liters per minute in a resting adult

Venous return (VR)

Volume of blood returning to the heart per minute, should equal cardiac output

Mean arterial pressure

Diastolic pressure - 1/3 pulse pressure OR cardiac output x systemic vascular resistance

Systemic vascular resistance (SVR)

Resistance to blood flow in systemic circulation influencing afterload, increase SVR= increase MAP

Determinants of cardiac output

Heart rate, stroke volume, contractility, preload and afterload, = total volume of blood ejected form left ventricle per minute, = HR x SV, changes to meet body’s need for O2/nutrients

Heart rate effect on CO

Increased heart rate increases cardiac output, established by SA node

Contractility (inotropy)/effect on CO

Force of contraction at a given preload affecting stroke volume, direct relationship with ventricular output/CO, increased contractility increases cardiac output

Afterload/effect on CO

Resistance the heart must overcome to eject blood inversely related to output/ increased afterload decreases cardiac output

Preload/effect on CO

Initial stretching of cardiac muscle related to EDV, increased preload increases cardiac output via Frank Starling mechanism

Frank Starling law

Stroke volume increases with increased ventricular filling (EDV)

Length tension relationship

Greater fiber stretch leads to stronger contraction

Cardiac function curve

Relationship between cardiac output and right atrial pressure (venous return= increase in right atrial pressure, EDV and end diastolic fiber length, leads to increase in CO)

Enhanced cardiac function

Occurs with increased HR contractility or decreased afterload

Depressed cardiac function

Occurs with decreased HR contractility or increased afterload

Venous return equation

VR equals pressure gradient between venous pressure and right atrial pressure divided by resistance

Driving force for venous return/factors influencing

Difference between venous pressure and right atrial pressure/Muscle contraction & presence of valves, decreased venous compliance, respiratory activity, vena cava compression

Factors increasing/decreasing venous return

Increasing: muscle/respiratory pump, decreased venous compliance decreasing: vena cava compression and increased right atrial pressure

Vascular function curve

Relationship between venous return and right atrial pressure

Mean systemic pressure

Pressure in circulation when heart stops determining venous return baseline (pressure in circulatory system if heart were stopped, determined by blood volume/distribution)

Equilibrium point of CO and VR

Intersection of cardiac and vascular function curves

Effect of blood volume on cardiac/vascular function curves

Increased volume increases CO VR and right atrial pressure

Effect of inotropic agents

Increase CO + VR and decrease right atrial pressure, no change in vascular function

Effect of total peripheral resistance

Changes both cardiac and vascular function curves affecting CO

Myocardial metabolism

Primarily aerobic using fatty acids and glucose for ATP production

Oxygen extraction by heart

Heart extracts about 50 percent of delivered oxygen

Factors increasing oxygen demand

Increased heart rate contractility, afterload and preload

Myocardial ischemia

Occurs when oxygen supply is less than demand leading to dysfunction or infarction