CARDIAC OUTPUT & VENOUS RETURN Lecture – 7 Dr. Zahoor Ali Shaikh

CARDIAC OUTPUT What is Cardiac Output? It is volume of the blood pumped out by each ventricle per minute .It is about 5 – 5.5 Lit/min Cardiac Output [COP ] = Heart rate × Stroke volume = 70 beats/min × 70ml/beat = 4900 ml/min ≈ 5liters/min COP of each ventricle is same.

CARDIAC OUTPUT [COP] COP increases during exercise, and depending on exercise, it can increase to 20–25 liters/min [up to 35 liters/min is recorded in trained athlete during heavy exercise]. How ? - By increasing stroke volume and heart rate.

CARDIAC INDEX What is Cardiac Index ? It is cardiac output per minute per square meter of body surface area. Normal Cardiac Index = 3.2 Liter /min/ sq meter body surface area. What is Cardiac Reserve ? It is the difference between cardiac output at rest and maximum volume of blood that heart can pump per minute.

REMEMBER THE FOLLOWING DEFINITIONS WHICH WE WILL USE DURING DISCUSSION OF COP Stroke Volume: It is a volume of blood pumped out by each ventricle per beat. It is about 70 - 80 ml. Stroke volume (SV) = EDV – ESV End Diastolic Volume: Volume of blood in each ventricle at the end of diastole. It is about 120 – 130 ml. End Systolic Volume: Volume of blood in each ventricle at the end of Systole. It is about 50 to 60 ml

Ejection fraction (EF) is the percentage of ventricular end diastolic volume (EDV) which is ejected with each stroke. EF = SV (EDV – ESV) EDV X 100 75 X 100 = 62.5% 120 Normal ejection fraction is about 60 – 65 %. Ejection fraction is good index of ventricular function.

CARDIAC OUTPUT [COP] As cardiac output depends on heart rate and stroke volume, we will discuss each one. HEART RATE [No. of beats per minute] Normal heart rate = 70 beats/min [60 to 100]. Heart rate above 100 is called Tachycardia. Heart rate below 60 is called Bradycardia. Heart rate is determined by autonomic nervous system effect on SA – Node.

CARDIAC OUTPUT [COP] Effect of Autonomic Nervous System on Heart

CARDIAC OUTPUT [COP] Control of Heart Rate Heart rate is 70 beats/min, when there is sympathetic and parasympathetic ANS effect on SA –Node. If all autonomic nerves to the heart are blocked, Heart Rate [HR] at rest will increase to 100 beats/min, which is inherent rate of SA – Node spontaneous discharge when there is no influence of ANS.

CARDIAC OUTPUT [COP] Control of Heart Rate Our Heart Rate is 70/min as normal rate of SA – Node discharge because of dominant effect of parasympathetic ANS on SA – Node.

CARDIAC OUTPUT [COP] We will discuss Stroke Volume: STROKE VOLUME It is amount of blood pumped out by each ventricle per beat. Stroke volume can be increased by TWO mechanism: 1. INTRINSIC CONTROL – by increasing venous return to the heart 2. EXTRINSIC CONTROL – due to the sympathetic stimulation of the heart

CARDIAC OUTPUT [COP] STROKE VOLUME [cont] Both factors( Intrinsic and Extrinsic ) increase stroke volume by increasing the strength of heart contraction. First, we will see mechanism of INTRINSIC control – when there is increase in end – diastolic volume, it results in increased stroke volume. It is due to length – tension relationship of cardiac muscle.

FRANK STARLING LAW OF THE HEART When there is increase in initial length of cardiac muscle fiber [within physiological limits], there will be increased force of contraction. OR When there is increased end- diastolic volume [EDV], there is increased stroke volume [SV]. This is INTRINSIC relationship between EDV and SV, it is known as ‘Frank Starling Law of the Heart’.

FRANK STARLING LAW OF THE HEART Mechanism of Cardiac Length – Tension Relationship When there is increase in the length of cardiac muscle fiber to the optimal length, there is maximum sliding of actin and myosin and we get maximum contraction.

CARDIAC OUTPUT [COP] EXTRINSIC CONTROL [factors outside the heart] Extrinsic control is through sympathetic stimulation. Sympathetic stimulation and epinephrine increases heart contractility, at any given end – diastolic volume. Increased contractility results from increased Ca2+ influx triggered by nor- epinephrine and epinephrine.

CARDIAC OUTPUT [COP] EXTRINSIC CONTROL [cont] Example : Normally EDV 135ml ESV 65ml Therefore, SV 70ml Under sympathetic stimulation EDV 135ml ESV 35ml SV 100ml Frank Starling Curve shifts to the left by sympathetic stimulation.

EJECTION FRACTION Ejection Fraction is ratio of Stroke Volume to End – Diastolic Volume. EF = [SV ÷ EDV] × 100 Normal healthy heart has Ejection Fraction of 50 – 75% [55 – 65%] under resting conditions and may go up to 90% during strenuous exercise. A failing heart (cardiac failure)  EF maybe 30% or less.

CARDIAC OUTPUT [COP] Control of Cardiac Output

Frank Starling Curve In Heart Failure

VENOUS RETURN TO THE HEART EDV depends on Venous Return and Venous Return is increased to the heart by: i). Blood Volume ii). Skeletal Muscle Pump iii). Respiratory Pump iv). Increased Sympathetic Veno constriction v). Cardiac suction effect vi). Venous Valves

VENOUS RETURN TO THE HEART i). Increased Blood Volume Veins are capacitance vessels and hold about 60 to 70% of blood, when veins store less blood, more blood is returned to the heart. ii). Skeletal Muscle Pump Muscle contraction compresses the veins. This external venous compression decreases venous capacity and increases venous pressure and moves blood towards the heart.

VENOUS RETURN TO THE HEART iii). Respiratory Pump During respiration, intra-thoracic pressure decreases and is less than atmospheric pressure [-5 mmHg]. This negative chest cavity pressure squeezes blood from the lower veins to the chest, increasing venous returns.

VENOUS RETURN TO THE HEART iv). Increased Sympathetic Vasoconstriction Sympathetic Stimulation causes vasoconstriction, which increases venous pressure and drives more blood to right atrium, therefore, more venous returns and increase EDV. v). Cardiac suction effect Heart plays role in its own filling. During ventricular contraction, AV valves are pulled downward enlarging atrial cavities. Atrial pressure drops below 0 mmHg and increases venous returns.

VENOUS RETURN TO THE HEART vi). Venous Valves In the veins, blood can be driven forward only as large veins have one way valve placed at 2 to 4 cm intervals. These valves prevent back flow of blood that tends to occur when a person stands up.

Summary of Factors Affecting Venous Returns

MEASUREMENT OF CARDIAC OUTPUT Cardiac Output can be measured 1. Fick Principle 2. Dye Dilution Method 3. Doppler Combined with Echocardiography

FICK PRINCIPLE Output of Left Ventricle Oxygen Uptake by lungs ml/min = AO2 - VO2 200 ml / min 200 ml / L – 160 ml / L Art blood – Venous blood [Pul artery] 200 ml/min 40ml / liter = 5 L/min = =

CARDIAC OUTPUT IN EXERCISE Cardiac Output increases to 25 to 30 liters/min because there is - increased muscle pump - increased respiratory pump - increased sympathetic stimulation - increased venomotor tone - increased venous return - increased force of contraction of heart [SV] - increased heart rate

APPLIED HEART FAILURE What is Heart Failure ? It is inability of heart to give cardiac output, sufficient to keep pace with body’s demand. There may be left ventricular failure or right ventricular failure or bi – ventricular failure. Most common cause heart failure is 1. Heart Attack or Myocardial Infarction 2. Working against Increased after load e.g. hyper tension or aortic valve stenosis

PRE LOAD & AFTER LOAD PRE LOAD – load on the heart before contraction i.e. end – diastolic volume. AFTER LOAD – load against which ventricle has to pump i.e. pressure in the artery or arterial blood pressure.

SIGNS OF HEART FAILURE In Left Ventricular Failure – pulmonary congestion or pulmonary edema occurs which causes decrease exchange of O2 and CO2 in the lungs. In Right Ventricular Failure – due to back pressure, there is engorgement of neck veins, peripheral edema, liver enlargement. Heart failure is treated by -- positive Inotropic drugs e.g. digitalis -- diuretics - to get rid of salt and water -- ACE Inhibitors [Angiotensin Converting Enzyme] inhibitors which decrease preload and after load.

LIST OF POSITIVE INOTROPIC & NEGATIVE INOTROPIC - Epinephrine - Nor Epinephrine - Sympathetic Stimulation - Calcium - Caffeine - Digitalis Negative Inotropic - Acetylcholine - Parasympathetic Stimulation - Potassium - Hypoxia - Hypercapnia - Acidosis - Drugs Beta Blocker

WHAT YOU SHOULD KNOW FROM THIS LECTURE Definition of Cardiac Output [COP] Factors Affecting Heart Rate & Stroke Volume Cardiac Index Cardiac Reserve Intrinsic & Extrinsic Control For Stroke Volume Frank Starling Law of Heart Ejection Fraction Factor Affecting Venous Return Heart Failure Positive Inotropic & Negative Inotropic

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