The document summarizes key aspects of cardiac physiology including the cardiac cycle, myocardial action potential, coronary circulation, and jugular venous pulse (JVP). It describes the electrical and mechanical events of the heart during one cardiac cycle as represented by an electrocardiogram (ECG) and pressures. It also discusses the anatomy and regulation of coronary blood flow to meet metabolic demand of the myocardium.
3. Modern concept of circulation & heart as generator of
circulation was advanced by Harvey in 1628.
Field of cardiac physiology has developed to include
• physiology of heart as pump
• cellular & molecular biology of cardiomyocyte, &
• regulation of cardiac function by neural & humoral
factors
4. Basic anatomy of heart consists of 2 atria & 2 ventricles -
provide 2 separate circulations in series.
Pulmonary circulation, low-resistance & high-
capacitance vascular bed, receives output from right side
heart, chief function - bidirectional gas exchange.
Systemic circulation, high resistance, receives output from
left side heart & provides output for systemic circulation,
delivers O2, nutrients & removes CO2 & metabolites from
tissue beds.
5. CARDIAC CYCLE
Sequence of electrical & mechanical events during
course of single heart beat.
1. Electrical events represented by ECG
2. Mechanical events represented by left atrial & left
ventricular pressure pulses correlated in time with
aortic flow & ventricular volume
6. Electrical events of pacemaker & specialized
conduction system are represented by ECG at body
surface & is result of differences in electrical potential
generated by heart at sites of surface recording.
7. P wave action potential initiated at SA node is
propagated to both atria by specialized conduction
tissue, it leads to atrial systole (contraction) & P wave
of ECG
P-R interval.. PR interval can be used to measure
delay between atrial & ventricular contraction at
level of AV node
8. From distal His bundle, electrical impulse
propagated through left & right bundle branches
finally to Purkinje system fibers
Electrical signals are transmitted from Purkinje
system to individual ventricular cardiomyocytes.
9. Spread of depolarization to ventricular myocardium
is manifested as QRS complex on ECG.
Depolarization is followed by ventricular
repolarization and appearance of T wave on ECG.
10.
11. LATE DIASTOLE
Mitral & tricuspid valves - open, aortic & pulmonary
valves -closed
Blood flows into heart throughout diastole
Rate of filling declines as ventricles become
distended, —especially when heart rate is low—
cusps of AV valves drift toward closed position
Pressure in ventricles remains low
12. Atrial Systole
It pumps additional blood into ventricles, but about
70% of ventricular filling occurs passively during
diastole
Contraction of atrial muscle that surrounds the
orifices of SVC,IVC & pulmonary veins narrows
their orifices; however, there is some regurgitation of
blood into veins during atrial systole
13. Ventricular Systole
Mitral & tricuspid valves close
Intraventricular pressure rises sharply as myocardium
presses on blood in ventricle .
14. This isovolumetric (isovolumic, isometric)
ventricular contraction lasts about 0.05 s, until
pressures in left & right ventricles exceed pressures
in aorta (80 mm Hg ) & pulmonary artery (10 mm
Hg) & aortic & pulmonary valves open
AV valves bulge into atria, causing a sharp rise in
atrial pressure
15. When aortic pulmonary valves open, phase of
ventricular ejection begins
Rapid at first, slowing down as systole progresses.
Intraventricular pressure rises to a maximum ,then
declines before ventricular systole ends
Peak left ventricular pressure is about 120 mm Hg, &
peak right ventricular pressure is 25 mm Hg or less
16. Late in systole, the aortic pressure actually exceeds
the ventricular, but for a short period momentum
keeps the blood moving forward
The AV valves are pulled down by the contractions of
the ventricular muscle, and atrial pressure drops
17. Amount of blood ejected by each ventricle per stroke
at rest is 70–90 mL.
End-diastolic ventricular volume is about 130 mL.
Thus, about 50 mL of blood remains in each
ventricle at end of systole (end-systolic ventricular
volume), the ejection fraction, percent of EDVV-
that is ejected with each stroke, is about 65%.
Ejection fraction is a valuable index of ventricular
function.
18. Early Diastole
Once ventricular muscle is fully contracted,already
falling ventricular pressures drop more rapidly
This is the period of protodiastole ,lasts about 0.04sec,
ends when aortic & pulmonary valves close
After the valves close, pressure continues to drop rapidly
during isovolumetric ventricular relaxation
19. Isovolumetric relaxation ends when ventricular
pressure falls below atrial pressure & AV valves
open, permitting ventricles to fill
Filling -rapid at first, then slows as next cardiac
contraction approaches
Atrial pressure continues to rise after the end of
ventricular systole until AV valves open, then drops
and slowly rises again until next atrial systole
20. Length of Systole & Diastole
Cardiac muscle has unique property of contracting &
repolarizing faster when heart rate is high
Duration of systole decreases from 0.27 s at a heart
rate of 65 to 0.16 s, diastole from 0.62sec to 0.14 sec
at a rate of 200 beats/min
THUS, duration of systole is much more fixed than
diastole, & when heart rate is increased, diastole is
shortened to much greater degree
21. This fact has important physiologic and clinical
implications
It is during diastole that heart muscle rests, and
coronary blood flow to the subendocardial portions of
the left ventricle and most of the ventricular filling
occurs
22. At heart rates up to about 180, filling is adequate as
long as there is ample venous return, and cardiac
output per minute is increased by an increase in rate
At very high heart rates, filling may be compromised
such that cardiac output per minute falls and
symptoms of heart failure develop
23.
24. JVP is a vertical height from sternal angle to zone of
transition of distended & collapsed IJV’s
Patient reclining at 45 degree,it is normally 4-5cm
It is an indicator of right mean atrial pressure.
It is the reflection of phasic pressure changes in right
atrium
Consists of three positive waves (a,c,v) and two
negative troughs(x,y)
25.
26. a wave depicts atrial contraction(atrial systole)
c wave depicts bulging of tricuspid valve into the atria
(isovolumetric contraction)
x descent shows atrial relaxation(ventricular systole)
v wave venous filling,(isovolumetric relaxation)
y descent indicates atrial emptying(ventricular filling)
27.
28. The types of action potential in the heart can be separated
into two categories:
fast-response action potentials, which are found in the
His-Purkinje system and atrial or ventricular
cardiomyocytes,
and
Slow response action potentials, which are found in the
pacemaker cells in the SA and AV nodes
29.
30. Phase 0 – Depolarization ( Na influx)
Phase 1 -Transient repolarization(activation of
transient outward K+ current)
Phase 2 -Plateau phase(net influx of Ca2+ through L-
type calcium channels efflux of K+ through K+
channels
Phase 3 -Repolarization(when efflux of K+ from 3
outward K+ currents exceeds the influx of Ca2+)
Phase 4 -Diastole(little ionic changes)
31. Action potentials in SA & AV nodes are largely due
to Ca+, with little contribution by Na influx
So there is no sharp rapid depolarization spike before
plateau,as in other parts of conduction system
When compared with fast-response action potential,
phase 0 is much less steep, phase 1 is absent, phase
2 is indistinct from phase 3
32.
33. ANATOMY
RCA and LCA
RCA - rt atrium, most of rt ventricle & inferior wall
of left ventricle
In 85% cases,RCA gives rise to posterior descending
artery(superior posterior IVS & inferior wall)-Rt
Dominant Circulation
34. LCA –left atrium, most of interventricular septum,
left ventricle
Bifurcates into left anterior descending(septum
&anterior wall) and circumflex artery(lateral wall)
SA node-RCA(60%), LAD(40%)
AV node-RCA(85%),circumflex(15%)
Bundle of His-PDA,LAD
35. Difference between aortic & ventricular pressure
CPP= arterial diastolic pressure – LVEDP
Decrease in aortic pressure ,increase in VEDP
reduces CPP
Increase in heart rate also decrease CPP(because of
reduction in diastolic time)
Endocardium-most vulnerable to ischemia
36. Parallels myocardial metabolic demand
Approx 250ml/min at rest
Myocardium regulates its own blood flow between
perfusion pressures 50 &120mm Hg
Changes in blood flow mainly due to coronary
arterial tone
Hypoxia cause vasodilation(directly or by adenosine
release)
Sympathetic stimulation increases myocardial blood
flow
37. Most important determinant of myocardial blood
flow
Myocardium extracts 65% of oxygen in arterial
blood, compared with 25% in other tissues
Coronary sinus saturation -30%
Myocardium cannot compensate for blood flow
reductions by extracting more O2 from Hb
Increase in demand must be met by increase in CBF