Control of Cardiac Output PDF

University of Zakho Dr. Majeed Tahir Ahmed Internal Medicine specialist M.B.ch.B., F..B.M.S. University of Zakho Control of cardiac output Cardiac Output Cardiac Output (CO) is the amount of blood the heart pumps from each ventricle per minute. It's value is almost same for b...

University of Zakho Dr. Majeed Tahir Ahmed Internal Medicine specialist M.B.ch.B., F..B.M.S. University of Zakho Control of cardiac output Cardiac Output Cardiac Output (CO) is the amount of blood the heart pumps from each ventricle per minute. It's value is almost same for both the ventricles and is about 5L/min in normal adult. Of the total CO: 75 % is distributed to the vital organs – Liver, kidney, brain, lung, heart CO = HR x SV Cardiac index : is the cardiac output per square meter of body surface area. Normal value is about 3L/min /M2. Physiological variations of cardiac output  PATHOLOGICAL VARIATION OF CARDIAC OUTPUT Pathological increase: 1. Hyperthyroidism 2. Fever Pathological decrease: 1. Hypothyroidism 2. Hypovolemia 3. Haemorrhage 4. Myocardial infarction  Why cardiac output is vital to our well-being ? - Simply cardiac output is intimately connected to energy production. -Sufficient perfusion to tissues yield an abundant energy supply -Poor tissue perfusion result in critical of energy and often diminished function. - Sufficient cardiac output is necessary to deliver adequate supply of oxygen and nutrient to tissues Cardiac output varies widely with the level of activity of the body. The following factors, directly affect cardiac output: 1. The basic level of body metabolism 2. Whether the person is exercising, 3. The person’s age, and 4. Size of the body  stroke volume The amount of blood pumped by the left ventricle of the heart in one contraction. The stroke volume is not all the blood contained in the left ventricle; normally, only about two-thirds of the blood in the ventricle is expelled with each beat. Together with the heart rate, the stroke volume determines the output of blood by the heart per minute - When the heart contracts strongly, the end - systolic volume can be decreased to as little as 10 to 20 milliliters. - Conversely, when large amounts of blood flow into the ventricles during diastole, the ventricular end - diastolic volumes can become as great as 150 to 180 milliliters in the healthy heart. REGULATION OF STROKE VOLUME Regulated by three variables: 1. End diastolic volume (EDV): Volume of blood in the ventricles at the end of diastole. - Sometimes called preload - Stroke volume increases with increased EDV. 2. Total peripheral resistance: Frictional resistance in the arteries. -called after load -Inversely related to stroke volume 3. Contractility: Strength of ventricular contraction - Stroke volume increases with contractility. Stroke volume = EDV – ESV Normal values for a resting healthy individual about 60- 100mL. - Ejection fraction (EF) – percentage of the EDV that is ejected per cardiac cycle. EF% = (SV / EDV) x 100 Normal ejection fraction is about 55-75%.  Heart rate (HR) also affects SV. Changes in HR alone inversely affects SV. However, SV can increase when there is an increase in HR (during exercise for example) when other mechanisms are activated, but when these mechanisms fail, SV cannot be maintained during an elevated HR. These mechanisms include increased venous return, venous constriction, increased atrial and ventricular inotropy and enhanced rate of ventricular relaxation.  Preload Preload, also known as the left ventricular end-diastolic pressure (LVEDP), is the amount of ventricular stretch at the end of diastole. Preload increases in: 1.Exercise 2.. Increasing blood volume (over transfusion, polycythemia) 3. Neuroendocrine excitement (sympathetic tone). 4. Arteriovenous fistula  Factors affecting preload Preload is affected by venous blood pressure and the rate of venous return. And explain by two main body pumps. - Respiratory pump : During inspiration intra –pleural pressure decrease and abdominal pressure increases leading to squeezing local abdominal veins, allowing thoracic veins to expand and increase blood flow towards the right atrium and increasing preload.. -Skeletal muscle pump - In the deep veins of the legs, surrounding muscles squeeze veins and pump blood back towards the heart. This occurs most notably in the legs. Once blood flows past valves it cannot flow backwards and therefore blood is “milked” towards the heart  Afterload Afterload is the pressure the heart must work against to eject blood during systole (ventricular contraction). Afterload is proportional to the average arterial pressure. As aortic and pulmonary pressures increase, the afterload increases on the left and right ventricles respectively  Factors affecting afterload 1. Systemic and pulmonary hypertension: both Increases after load because both ventricles must work harder to eject blood into the systemic and pulmonary circulation. 2. Aortic and pulmonary stenosis and regurgitation also increase after load 3. Increase vascular resistance also increase after load  REGULATION OF CARDIAC OUTPUT It means maintaining a constant cardiac output around 5 liters/min under normal conditions and adjusting the cardiac output as per the physiological demands.  Factors affect cardiac out put 1. Heart rate 2. stroke volume. - Primary factors: include blood volume reflexes, autonomic innervation, and hormones. -Secondary factors: include extracellular fluid ion concentration, body temperature, emotions, sex, and age Primary Factors 1.Blood Volume Reflexes Two heart reflexes respond to changes in blood volume: the atrial reflex and the ventricular reflex. Atrial/Bainbridge Reflex The atrial reflex, also referred to as the right heart reflex or Bainbridge reflex, is triggered by an increase in venous return to the heart. Baroreceptors in the superior and inferior venae cavae sense pressure changes and send impulses to the SA node, increasing heart rate. Ventricular Reflex Whereas the atrial reflex affects heart rate, the ventricular reflex affects stroke volume. The amount of blood ejected is dependent on the amount of blood filling the ventricle during diastole(Frank-Starling Law ). The Frank–Starling law of the heart Overview it’s the relationship between stroke volume and end diastolic volume. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant. As a larger volume of blood flows into the ventricle, the blood stretches the cardiac muscle fibers, leading to an increase in the force of contraction. The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return and arterial blood supply , without depending upon external regulation to make alterations. Mechanisms Increased venous return increases the ventricular filling (end-diastolic volume) and therefore preload, which is the initial stretching of the cardiac myocytes prior to contraction. Myocyte stretching increases the sarcomere length, which causes an increase in force generation and enables the heart to eject the additional venous return, thereby increasing stroke volume.  Factors Affecting Frank–Starling Physiology Factors leading to an increase in LVEDV and CO, thus shifting the Starling curve up and left, include: 1. Volume expansion: administration of crystalloid, colloid, or blood components. 2. Avoiding increases in the intrathoracic pressure (from positive pressure ventilation or tension pneumothorax) or increases in the pericardial pressure (from effusions or tamponade ) 3. Augmenting venous tone and venous return to the heart. - In contrast, factors leading to a decrease in LVEDV and CO, thus shifting the Starling curve down and right, include: 1. Volume contraction e.g bleeding 2. Increases in the intrathoracic pressure (from positive pressure ventilation or tension pneumothorax) or increases in the pericardial pressure (from tamponade ) 3. Decreases in venous tone and venous return to the heart.  2.Autonomic Innervation Role of the Autonomic Nervous System - Although heart rate is established by the SA nodal cells, it can be affected by the autonomic nervous system. Changing heart rate is the body’s principal short-term mechanism of controlling cardiac output and blood pressure. When stroke volume decreases, the body attempts to maintain adequate cardiac output by increasing the rate and strength of cardiac contraction. The most important control of heart rate and strength of contraction is autonomic innervation  Cardio-acceleratory center The medulla oblongata, located in the brain, includes a cluster of neurons that make up the cardio-acceleratory center (CAC). Sympathetic fibers that begin in the CAC innervate the SA node, the AV node, and parts of the myocardium. CAC stimulation causes these fibers to release norepinephrine, thereby increasing heart rate and contraction strength.  Cardio-inhibitory Center The medulla oblongata also contains an opposing cardioinhibitory center (CIC). Parasympathetic fibers that begin in the CIC also innervate the SA node and AV node. CIC stimulation results in the transmission of nerve impulses along the parasympathetic fibers and the release of acetylcholine, which decreases heart rate. Baroreceptors 1. Baroreceptor Reflex - stimulated by increase in arterial pressure (stretch) - Effect: negative chronotropic and inotropic - regulate the heart when BP increases or drops - involved in short term regulation of BP 2. Chemoreceptor Reflex- stimulated by low oxygen, low pH, or high CO2 - overall effect: positive choronotropic and inotropic. - less important in regulating cardiac function 3.Hormones When norepinephrine, epinephrine, and acetylcholine are released, the force of myocardial contraction is altered, thus affecting stroke volume. Norepinephrine and Epinephrine In response to sympathetic stimulation, norepinephrine is released in the myocardium, and norepinephrine and epinephrine are released by the adrenal medullae. Norepinephrine increases heart rate and myocardial contractility. Epinephrine excites the SA node, thereby increasing the rate and strength of myocardial contraction  Acetylcholine Parasympathetic stimulation results in the release of acetylcholine, which inhibits heart activity by decreasing the force of cardiac contractions Secondary Factors - ECF Ion Concentration : Elevated levels of extracellular potassium or sodium ions can decrease heart rate and stroke volume. - Calcium Ion Concentrations : Abnormal calcium ion concentrations affect the strength and duration of cardiac contractions, which then affects stroke volume. High calcium levels cause strong and lengthy contractions. Low calcium levels weaken contraction strength Temperature and Emotions Other Factors Changes in body temperature can also affect heart rate and contractility. Increased body temperature results in increased heart rate. Decreased body temperature slows heart rate and results in less powerful contractions. Strong emotions, such as anger, fear, and anxiety, tend to increase heart rate. Other mental states, such as depression and grief, probably stimulate the cardio-inhibitory center, resulting in a slower heart rate Sex and Age Sex and age also affect heart rate. The heartbeat of females is generally faster than that of males. Finally, heart rate is fastest at birth and decreases throughout life. STROKE VOLUME AND CARDIAC OUTPUT  Table No. 1 : Example values in healthy 70 kg man End - diastolic volume ( EDV ): 120 ml 65 - 240 ml End - systolic volume ( ESV ): 50 ml 16 - 143 ml Stroke volume ( SV ): 70 ml 55 - 100 ml Ejection fraction ( Ef ): 65 % 55 to 70 % Heart rate ( HR ): 75 bpm 60 to 100 bpm Cardiac output ( CO ): 5 L / minute 4.0 - 8.0 L / min  Time for questions… 2020.06.20 Dr.Brisik Hayder Rashad 40  Thanks