Cardiovascular System5

Cardiac Output Volume of blood ejected by each ventricle in 1 minute Cardiac Output = Heart Rate (beats/minute) x Stroke Volume (mL/beat) Cardiac output varies with the body’s state of activity. Cardiac reserve is the difference between resting and maximal CO

Cardiac output Cardiac Index: the cardiac output per square meter of body surface area. the normalized data for different size individuals the normal range is about 3.0 – 3.5 L/min/m2

MEASUREMENT OF CARDIAC OUTPUT 1. THE FICK METHOD: VO 2 = ([O 2 ] a - [O 2 ] v ) x Flow Flow = VO 2 [O 2 ] a - [O 2 ] v Spirometry (250 ml/min) Arterial Blood (20 ml%) Pulmonary Artery Blood (15 ml%) CARDIAC OUTPUT PERIPHERAL BLOOD FLOW VENOUS RETURN PULMONARY BLOOD FLOW

CARDIAC OUTPUT (Q) = VO 2 [O 2 ] a - [O 2 ] v 250 ml/min 20 ml% - 15 ml% = = 5 L/min . Q = HR x SV . SV = Q HR . = 5 L/min 70 beats/min = 0.0714 L or 71.4 ml CARDIAC INDEX = Q m 2 body surface area . 5 L/min 1.6 m 2 = = 3.1 L/min/m 2

Measurement of cardiac output 2. Indicator dilution method 3. Doppler Echocardiography

Factors Affecting Cardiac Output

Heart Rate Pulse = surge of pressure in artery Infants have HR of 120 bpm or more Normal range of the heart rate 60 – 100 beats/min Tachycardia: resting adult HR above 100 stress, anxiety, drugs, heart disease or  body temp. Bradycardia: resting adult HR < 60 in sleep and endurance trained athletes

Regulation of Heart Rate Positive chronotropic factors increase heart rate Negative chronotropic factors decrease heart rate

Regulation of Heart Rate 1. Vital centers of medulla Cardiac Center Cardioaccelerator center Activates sympathetic neurons that increase HR Cardioinhibitory center Activates parasympathetic neurons that decrease HR Cardiac center receives input from higher centers (hypotha-lamus), monitoring blood pressure and dissolved gas concentrations

Regulation of the Heart rate 2. Neural regulation Parasympathetic stimulation - a negative chronotropic factor Supplied by vagus nerve, decreases heart rate, acetylcholine is secreted and hyperpolarizes the heart Sympathetic stimulation - a positive chronotropic factor Supplied by cardiac nerves. Innervate the SA and AV nodes, and the atrial and ventricular myocardium. Increases heart rate and force of contraction . Epinephrine and norepinephrine released. 3.Hormonal regulation Epinephrine and norepinephrine from the adrenal medulla. Occurs in response to increased physical activity, emotional excitement, stress

SA node establishes baseline (sinus rhythm) Modified by ANS If all ANS nerves to heart are cut, heart rate jumps to about 100 b/min Basic heart rate established by pacemaker cells

Regulation of Stroke Volume SV: volume of blood pumped by a ventricle per beat SV= end diastolic volume (EDV) minus end systolic volume (ESV); SV = EDV - ESV EDV = end diastolic volume amount of blood in a ventricle at end of diastole ESV = end systolic volume amount of blood remaining in a ventricle after contraction Ejection Fraction - % of EDV that is pumped by the ventricle; important clinical parameter = stroke volume / end diastole volume X 100%,it s hould be about 55-60% or higher

Factors Affecting Stroke Volume EDV - affected by Venous return - vol. of blood returning to heart Preload – amount of stretch on the ventricular myocardium prior to contraction (=EDV ) ESV - affected by Contractility – myocardial contractile force due to factors other than EDV. After load – back pressure exerted by blood in the large arteries leaving the heart.

Frank-Starling Law of the Heart Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume;  EDV leads to  stretch of myocardium.  preload   stretch of muscle   force of contraction   SV If SV is increased, then ESV is decreased!! Slow heartbeat and exercise increase venous return (VR) to the heart, increasing SV VR changes in response to blood volume, skeletal muscle activity, alterations in cardiac output  VR   EDV and  in VR   in EDV Blood loss and extremely rapid heartbeat decrease SV

Frank –starling curve Left ventricle (LV) function curve, or Frank - Starling curve (1914): Normal range of the LVEDP, 5-6 mmHg Optimal initial preload, 15-20 mmHg (Sarcomere, 2.0 – 2.2 µm )

Factors influencing Venous return

Total Peripheral Resistance ( TPR) Total Peripheral Resistance: Impedance to the ejection of blood from ventricle. Afterload. In order to eject blood, pressure generated in the ventricle must be greater than pressure in the arteries. Pressure in arteries before ventricle contracts is a function of TPR. SV inversely proportional to TPR. Greater the TPR, the lower the SV.

Contractility- Extrinsic factors influencing SV Contractility is the increase in contractile strength, independent of stretch and EDV Referred to as extrinsic since the influencing factor is from some external source Increase in contractility comes from: Increased sympathetic stimuli Certain hormones Ca 2+ and some drugs Agents/factors that decrease contractility include: Acidosis Increased extracellular K + Calcium channel blockers

Effects of Hormones on Contractility Epi, NE, and Thyroxine all have positive ionotropic effects and thus  contractility Digitalis elevates intracellular Ca ++ concentrations by interfering with its removal from sarcoplasm of cardiac cells Beta-blockers ( propanolol, timolol ) block beta-receptors and prevent sympathetic stimulation of heart (neg. chronotropic effect)

Factors Involved in Regulation of Cardiac Output

RIGHT ATRIAL PRESSURE AND VENOUS RETURN Venous return RA pressure Venous return from the periphery depends on the pressure difference between the peripheral pressure and right atrial pressure. Thus as right atrial pressure (central venous pressure) rises venous return will fall Venules Right atrium 25 mm Hg ∆P = 25 mm Hg 0 mm Hg 25 mm Hg ∆P = 20 mm Hg 5 mm Hg

GUYTON’S ANALYSIS OF THE INTACT CIRCULATION Two relationships have been established: A rise of right atrial pressure will more effectively fill the heart in diastole, increase stroke work and thus increase flow in the circulation (assume afterload and heart rate are constant) A rise of right atrial pressure will hinder venous return and thus decrease flow in the circulation. But in the intact circulation venous return must equal cardiac output Venous return RA pressure Cardiac output RA pressure

GUYTON’S ANALYSIS OF THE INTACT CIRCULATION Thus right atrial pressure exerts conflicting effects on flow in the intact circulation. But: cardiac out put = venous return. Thus: the two curves can be superimposed to yield an equilibrium point for the circulation. Cardiac output = venous return RA pressure cardiac function curve equilibrium point vascular function curve

Cardiovascular System5

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