Cardiac Output April 28, 2017 Cardiac Output

Cardiac output volume of blood pumped by each ventricle per minute C.O = HEART RATE x SROKE VOLUME (H.R X S.V) typically about 5,500 ml (or 5.5 liters) per minute which is about equal to total blood volume; so, each ventricle pumps the equivalent of total blood volume each minute under resting conditions BUT maximum may be as high as 25 - 35 liters per minute April 28, 2017 Cardiac Output

Cardiac reserve the difference between cardiac output at rest & the maximum volume of blood the heart is capable of pumping per minute permits cardiac output to increase dramatically during periods of physical activity April 28, 2017 Cardiac Output

Cardiac Index Cardiac output in liters/min per square meter of body surface area CO varies widely with level of body activity level of body metabolism, whether a person is exercising age, size of the body Increases approximately in proportional to the surface area of the body CO is 20 – 30% less in female April 28, 2017 Cardiac Output

Cardiac Index Vs age 4 - 3 - Cardiac index L/min/M2 2 - 1- 80 10 4 - 3 - 2 - 1- Cardiac index L/min/M2 80 10 April 28, 2017 Cardiac Output Age (years)

Regulation of cardiac output At rest heart pumps 4 – 6 liters per minute. Volume pumped by the heart is regulated by: Intrinsic cardiac regulation in response to change in volume of blood flowing into the heart. Autonomic nervous system Frank – Starling law of the heart Explains the intrinsic ability of the heart to adapt to changing volume of inflowing blood CO = stroke vol. X HR April 28, 2017 Cardiac Output

Regulation of Stroke volume If the HR remain constant CO increases in proportion to SV Stroke volume is the result of the balance between force of contraction and afterload. intrinsic control related to amount of venous return extrinsic control related to amount of ANS activity April 28, 2017 Cardiac Output

Intrinsic control of stroke volume Increased end-diastolic volume increased strength of cardiac contraction increased stroke volume The increase in strength of contraction due to an increase in end-diastolic volume is called the Frank-Starling law of the heart: April 28, 2017 Cardiac Output

Frank-Starling law of the heart Increased end-diastolic volume increases stretching of of cardiac muscle increases strength of contraction increases stroke volume April 28, 2017 Cardiac Output

Frank-Starling law of the heart There is a relation between initial length and total tension in cardiac muscle similar to that in skeletal muscles. There is optimal length at which the tension developed is maximal. April 28, 2017 Cardiac Output

Starling Law of the Heart Stroke Volume End diastolic fiber length April 28, 2017 Cardiac Output

Effects of Hypertrophy on SV Myocardial hypertrophy Increases the force of contraction Physical exercise & sustained elevation of arterial pressure leads to repeated bouts of increased CO As a result in increased synthesis of contractile proteins and enlargement of cardiac myocytes As each cell enlarges the ventricular wall thickens and is capable of greater force development. April 28, 2017 Cardiac Output

Effects of Afterload on SV The force against which the ventricular muscle fibers must shorten. In normal circumstances, after load can be equated to the aortic pressure during systole. If the arterial pressure is suddenly increased a ventricular contraction.(at a given level of contractility and EDFL) Produce a lower stroke volume. April 28, 2017 Cardiac Output

Intrinsic control of stroke volume End diastolic volume Depends on venous return Venous return is the amount of blood returning to the heart through the veins April 28, 2017 Cardiac Output

Extrinsic control of stroke volume Increased sympathetic stimulation > increased strength of contraction of cardiac muscle Parasympathetic stimulation has little effect in reducing the strength of ventricular contraction April 28, 2017 Cardiac Output

Increased sympathetic stimulation release of norepinephrine increased permeability of muscle cell membranes to calcium Activation of more cross-bridges Giving stronger contraction April 28, 2017 Cardiac Output

Regulation of heart rate Role of ANS Changes in heart rate: Parasympathetic stimulation reduces heart rate Sympathetic stimulation increases heart rate April 28, 2017 Cardiac Output

Parasympathetic stimulation Increased parasympathetic stimulation release of acetylcholine at the SA node increased permeability of SA node cell membranes to potassium 'hyperpolarized' membrane fewer action potentials and, therefore, fewer contractions) per minute April 28, 2017 Cardiac Output

Sympathetic stimulation Increased sympathetic stimulation release of norepinephrine at SA node decreased permeability of SA node cell membranes to potassium membrane potential becomes less negative (closer to threshold) more action potentials (and more contractions) per minute April 28, 2017 Cardiac Output

Sympathetic stimulation Strong sympathetic stimulation increases HR up to 180 – 200 in adult and even 250 in young people Sympathetic nerve fibers to the heart discharge continuously at slow rate that maintains pumping at about 30% above that with no sympathetic stimulation April 28, 2017 Cardiac Output

Effect of nervous stimulation to CO Max. sympathetic stimulation Normal sympathetic stimulation CO L/min Zero sympathetic stimulation Parasympathetic stimulation Rt atrial pressure (mmHg) April 28, 2017 Cardiac Output

Regulation of CO April 28, 2017 Cardiac Output