Introduction to Hemodynamic and
Electrophysiology of Heart :
CARDIOVASCULAR HEMODYNAMICS
Haemodynamics is the term used to describe the interactions of the physiological
parameters that govern the behaviour of the CVS.
Introduction
• The cardiovascular system is concerned with the circulation of the blood. Essentially it
consists of heart, which works as pump, and the blood vessels, which carry the blood.
• The word hemodynamics – means circulation of blood in the human body.
Coronary Blood Flow
• Resting coronary blood flow in human average is approximately 225ml/minute(
0.7 to 0.8 ml/gm) of the heart muscle.
• During the diastole, cardiac muscle relaxes completely and no longer obstructs the
blood flow through left ventricular capillaries.
• This is phasic changes in coronary blood flow during cardiac muscle compression.
• During cardiac contraction – Intra myocardial pressure in the inner layer of the heart
muscle is so much greater than the outer layer.
Control of Coronary Blood Flow:
• Oxygen demand is a major factor in local blood flow regulation.
• Determinants of oxygen consumption.
• Importance of increase in coronary blood flow in response to myocardial oxygen usage.
• Reactive hyperemia in coronary system.
Nervous control
Stroke Volume
• The amount of blood pumped by the left ventricle of the heart in one contraction.
Normally only about 2/3rd of the blood in the ventricle is expelled with each beat.
Cardiac Output
• Flow of blood is usually measured in l/min.
• Total amount of blood flowing through the circulation = Cardiac output (CO)
Cardiac Output = Stroke Volume × Heart Rate = 5 L/min.
• Influenced by blood pressure (force of blood against side wall) & resistance (Blood
viscosity, Vessel length, Vessel Elasticity, Vasoconstriction/Vasodilation).
Blood Pressure Regulation
• Blood pressure is determined by vascular resistance and cardiac output.
• Vascular resistance is regulated at the level of the arterioles, influenced by neural and
hormonal inputs.
• Cardiac output is determined by heart rate and stroke volume, which is strongly
influenced by blood volume.
• Blood volume in turn is regulated mainly by renal sodium excretion or resorption.
• Renin, a major regulator of blood pressure, is secreted by the kidneys in response to
decreased blood pressure in afferent arterioles. In turn, renin cleaves angiotensinogen to angiotensin I; subsequent peripheral catabolism produces angiotensin II, which regulates
blood pressure by increasing vascular smooth muscle cell tone and by increasing adrenal aldosterone secretion and, consequently, renal sodiumresorption.
ELECTROPHYSIOLOGY OF HEART
Physiology of Cardiac Muscle
• Three Major types of cardiac muscle fiber:
1.Atrial muscle.
2.Ventricular muscle.
3.Specialized excitatory and conductive muscle fibers.
o The specialized excitatory and conductive fibers contract feebly because they
contain few contractile fibrils. Exhibit automatic rhythmical electrical discharge in
the form of action potentials.
Atherosclerosis:
• Atherogenesis is driven by interplay of vessel wall injury and inflammation. The multiple
risk factors for atherosclerosis all cause endothelial cell dysfunction and influence
smooth muscle cell recruitment and stimulation.
• Atherosclerotic plaques develop and grow slowly over decades. Stable plaques can
produce symptoms related to chronic ischemia by narrowing vessels, whereas unstable
plaques can cause dramatic and potentially fatal ischemic complications related to acute
plaque rupture, thrombosis, or embolization.
• Stable plaques tend to have a dense fibrous cap, minimal lipid accumulation, and little
inflammation, whereas “vulnerable” unstable plaques have thin caps, large lipid cores,
and relatively dense inflammatory infiltrates.
Action Potential in Cardiac Muscle
Phase 0 (Rapid Depolarization)
Phase 1 (Early Repolarization)
Phase 2 (Plateau)
Phase 3 (Repolarization)
Phase 4 (Resting Membrane Potential)
Heart Failure
• CHF occurs when the heart is unable to provide adequate perfusion to meet the
metabolic requirements of peripheral tissues; inadequate cardiac output usually is
accompanied by increased congestion of the venous circulation.
• Left-sided heart failure is most commonly secondary to ischemic heart disease, systemic
hypertension, mitral or aortic valve disease, or primary diseases of the myocardium;
symptoms are mainly a consequence of pulmonary congestion and edema, although
systemic hypoperfusion can cause renal and cerebral dysfunction.
• Right-sided heart failure is most often due to left heart failure and, less commonly, to
primary pulmonary disorders; signs and symptoms are related chiefly to peripheral
edema and visceral congestion.
Arrhythmias
• caused by ischemic or structural changes in the conduction system
or by myocyte electrical instability. In structurally normal hearts, arrhythmias are due to mutations in ion channels that cause aberrant repolarization or depolarization.
• Sudden cardiac death (SCD) most frequently is due to coronary artery disease leading to
ischemia.
Myocardial irritability typically results from non-lethal ischemia or from
pre-existing fibrosis from previous myocardial injury. SCD less often is due to acute
plaque rupture with thrombosis that induces a rapidly fatal arrhythmia.