Moderator : Dr V. Chandak
Dr. Tarun Yadav
Heart is functionally divided into right and left pumps
each consisting of an atrium & a ventricle.
The atria serve as both conduits and priming pumps,
whereas the ventricles act as the major pumping
The right ventricle receives systemic venous
(deoxygenated) blood and pumps into the
Left ventricle receives pulmonary venous
(oxygenated) blood and pumps it into the systemic
Four valves normally ensure unidirectional flow
through each chamber.
specialized striated muscle
Serial low-resistance connections (intercalated
disks) between individual myocardial cells.
Electrical activity spreads via specialized
The normal absence of direct connections
between the atria and ventricles except through
the atrioventricular (AV) node delays conduction
and enables atrial contraction to prime the
Myocardial cell membrane is permeable to K+ but is relatively
impermeable to Na+.
Na+–K+ATPase concentrates K+ intracellularly in exchange for
extrusion of Na+ out.
Intracellular Na+ concentration is kept low, whereas
intracellular K+ concentration is kept high.
Relative impermeability to calcium also maintains a high
extracellular to cytoplasmic calcium gradient.
Movement of K+ out & down its concentration gradient results
in a net loss of positive charges from inside the cell.
An electrical potential is established, with the inside of the cell
negative with respect to the extracellular environment.
The resting membrane is the balance
between two opposing forces: the movement
of K+ down its concentration gradient and the
electrical attraction of the negatively charged
intracellular space for the positively charged
–80 to –90 mV
When the cell membrane potential becomes
less negative and reaches a threshold value,
a characteristic action potential
The action potential raises the membrane
potential of the myocardial cell to +20 mV.
Spike in cardiac action potentials is
followed by a plateau phase that lasts .2–
Action potential is due to the opening of
both fast sodium channels (the spike) and
slower calcium channels (the plateau).
The cardiac cycle is traditionally defined
based on events occurring before, during,
and after LV contraction. (0.8 sec)
Left ventricular systole is commonly
divided into three parts:
rapid ejection, and
Isovolumic contraction is the interval between
closure of the mitral valve and the opening of
the aortic valve.
Left ventricular volume remains constant
during this period of the cardiac cycle.
The rate of increase of LV pressure reaches
its maximum during isovolumic contraction.
Pressure in the aortic root declines to its
minimum value immediately before the aortic
Rapid ejection occurs when LV pressure exceeds aortic
pressure and the aortic valve opens.
Approximately two thirds of the LV end-diastolic volume is
ejected into the aorta during this rapid ejection phase of systole.
Aortic dilation occurs in response to this rapid increase in
volume as the kinetic energy of LV contraction is transferred to
the systemic arterial circulation as potential energy.
The compliance of the aorta and proximal great vessels
determines the amount of potential energy that can be stored
and subsequently released to the arterial vasculature during
The normal LV end-diastolic volume is about 120 mL.
The average ejected stroke volume is 80 mL, and the normal
ejection fraction is approximately 67%.
During the period of slower ejection, aortic
pressure may briefly exceed LV pressure.
The reversal of the pressure gradient
between the aortic root and the LV causes
the aortic valve to close, thereby
producing the second heart sound (S2)
Diastole is divided into four phases in the
Isovolumic relaxation defines the period
between aortic valve closure and mitral
valve opening during which LV volume
remains constant. LV pressure falls
precipitously as the myofilaments relax.
When LV pressure falls below left atrial
pressure, the mitral valve opens, and blood
volume stored in the left atrium rapidly enters
the LV driven by the pressure gradient
between these chambers.
This early-filling phase of diastole accounts
for approximately 70 to 75% of total LV stroke
volume available for the subsequent
After left atrial and LV pressures have
equalized, the mitral valve remains open and
pulmonary venous return continues to flow
through the left atrium into the LV.
This phase of diastole is known as diastasis,
during which the left atrium functions as a
Diastasis accounts for no more than 5% of
total LV end-diastolic volume under normal
The final phase of diastole is atrial systole.
Contraction of the left atrium contributes
the remaining blood volume
(approximately 15 to 20%) used in the
subsequent LV systole.
Cardiac output : vol of blood pumped by heart
per minute. It is measure of ventricular systolic
C.O = S V
Stroke volume: vol of blood pumped per
Cardiac index : C I = C O / BSA
normal value 2.5 to 4.2 l / min / m2
DETERMINANTS OF C .O
No of beats per minute
C .O directly proportional to HR
HR is intrinsic function of SA node
HR is modified by autonomic, humoral,
Enhanced vagal activity decrease HR
Enhanced sympathetic activity increase
Intrinsic ability of myocardium to pump in
absence of changes in preload and after
Factors modifying contractility are
exercise, adrenergic stimulation, changes
in Ph, temperature, drugs, ischemia
Frank starling relationship
Relation between sarcomere length and
States that if cardiac muscle is stretched it
develops greater contractile tension
Increase in venous return increases
contractility and CO
Clinical application is relation between
LVEDV and SV
Frank straling relationship
HOW TO ASSESS
Pressure volume loops
Noninvasive like echocardiography,
EF = (LVEDV – LVESV)/ LVEDV
NORMAL – 60 6%
Defined as ventricular load at the end of
diastole before contraction has started
In clinical practice PCWP or CVP are used
to estimate preload
Defined as systolic load on LV after
contraction has began
Aortic compliance is determinant of
afterload e.g. AS or chronic hypertension
both impede ventricular ejection
Measurement of afterload DONE BY
systolic BP or SVR
Wall stress: Laplace law states that wall
stress is product of pressure and radius
divided by wall thickness
wall stress= P R/ 2H
RV load depends on PVR.
External work( stroke work) is work done
to eject blood under pressure. stroke
work= SV P
Internal work is work done to change
shape of heart for ejection. Wall stress
directly proportional to internal work
Both internal work and external work
Determinants of coronary perfusion
Coronary perfusion is intermittent
compared to continous in other organs
CPP = Aortic diastolic pressure –
LV is perfused entirely during diastole
RV is perfused during both systole &
Autoregulation of coronary blood
Coronary blood flow = 250 ml/min at rest
Myocardium regulates its blood supply
between 50 to 170 mmhg
When blood pressure decreases
Blood flow decreases
Vascular smooth muscle relaxation
Blood flow increases
When blood flow decreases
Blood flow increases
Myocardial oxygen balance
Myocardium extracts 65% 02 in arterial
blood compared to 25% in most other
Cannot compensates for reduction in
blood flow by extracting more 02 from Hb
Any increase in demand must be met by
an increase in coronary blood flow
Atrial Natriuretic Peptide
Produced by the atria of the heart.
Stretch of atria stimulates production of
– Antagonistic to aldosterone and angiotensin
– Promotes Na+ and H20 excretion in the urine
by the kidney.
– Promotes vasodilation.
Long term control
After hours of sustained change in BP
Sodium and water retension