The document discusses regional circulations, focusing on coronary, cerebral, and cutaneous circulation. It provides details on the anatomy, blood supply, regulation, and clinical implications of each circulation. For coronary circulation, it describes the blood vessels that supply the heart muscle and how blood flow is regulated to meet myocardial oxygen demands. For cerebral circulation, it outlines the unique anatomical features of the brain's blood supply and factors that control blood flow. For cutaneous circulation, it explains the role of arteriovenous anastomoses and arterioles in regulating heat transfer and sympathetic nervous system control of cutaneous blood flow.
This document summarizes the circulation and key features of several vascular beds in the body. It discusses:
1. The cerebral circulation receives 14% of cardiac output and has good autoregulation over a wide range of blood pressures. Local factors like H+, K+, and adenosine cause vasodilation while endothelin causes vasoconstriction in pathological states.
2. The coronary circulation receives 4% of cardiac output. Flow parallels metabolism with greater metabolism resulting in greater flow. Local metabolites are a major influence on flow.
3. The skin circulation receives 4% of cardiac output at rest and is mainly involved in thermoregulation. Vasoconstrictors and vasodilators influence flow
The document summarizes several aspects of regional circulations, including the coronary, cutaneous, cerebral, skeletal muscle, splanchnic, and renal circulations. Specific details provided on the coronary circulation include its high blood flow even at rest, regulation of flow through metabolic and neural mechanisms, and implications for conditions like myocardial infarction and heart failure. Key aspects of the cutaneous circulation discussed are its role in temperature regulation through sympathetic nervous system control of arterioles and anastomoses, and local vasodilation or constriction in response to heating and cooling.
Effects of anaesthetic agents on the cardiovascular systemaratimohan
The document discusses the cardiovascular effects of various anesthetic agents. It notes that volatile agents like halothane and enflurane cause decreases in blood pressure mainly through effects on myocardial contractility, while isoflurane, desflurane and sevoflurane lower blood pressure primarily by decreasing systemic vascular resistance. These agents also attenuate the baroreceptor reflex. Intravenous induction agents can cause an initial drop in blood pressure due to vasodilation, which is compensated for by an increase in heart rate, but may lead to hypotension in vulnerable patients. Barbiturates, benzodiazepines and other intravenous agents have varying effects depending on their class.
Cardiac output is the volume of blood pumped by the heart per minute. It is calculated as stroke volume multiplied by heart rate. The document discusses various factors that affect cardiac output such as preload, afterload, contractility, and heart rate. It also describes direct and indirect methods for measuring cardiac output, with the oxygen Fick method and thermodilution method explained in detail. Conditions that cause cardiac output to increase or decrease are also outlined.
Cardiovascular physiology for anesthesiamarwa Mahrous
This document discusses cardiovascular physiology including the structure and function of the heart, regulation of the cardiovascular system, blood flow through the pulmonary and systemic circulations, factors that influence cardiac output and stroke volume, and regulation of the systemic vasculature. Key points include:
- The cardiovascular system consists of the heart, blood vessels, and mechanisms that regulate blood circulation and pressure.
- Cardiac output is determined by stroke volume and heart rate. Stroke volume depends on preload, afterload, and contractility.
- The pulmonary circulation has low pressure and resistance while the systemic circulation has higher pressure and resistance.
- Autonomic nervous system and chemical factors regulate heart rate and contractility. Venous return and vascular
This document discusses the physiology of coronary blood flow. It begins with an introduction and overview of topics to be covered, including the anatomy of the heart, coronary blood flow, control of coronary blood flow, and nervous control. It then provides details on the coronary arteries and veins, factors that influence coronary blood flow like oxygen demand and determinants of oxygen consumption, and mechanisms that control blood flow like metabolic regulation and reactive hyperemia. It concludes with a discussion of how autonomic nervous stimulation can affect coronary flow both directly through effects on blood vessels and indirectly by altering cardiac work and oxygen demand.
The document summarizes the cardiovascular system and regulation of blood pressure. It describes how the brain monitors and controls blood flow and pressure on a beat-to-beat basis to meet metabolic demands. Blood pressure is influenced by cardiac output, peripheral resistance, and blood volume. The document then discusses short term regulation of blood pressure by baroreceptor reflexes, chemoreceptor reflexes, and local mechanisms, as well as long term regulation by the renal-body fluid system including the renin-angiotensin-aldosterone mechanism.
This document summarizes the circulation and key features of several vascular beds in the body. It discusses:
1. The cerebral circulation receives 14% of cardiac output and has good autoregulation over a wide range of blood pressures. Local factors like H+, K+, and adenosine cause vasodilation while endothelin causes vasoconstriction in pathological states.
2. The coronary circulation receives 4% of cardiac output. Flow parallels metabolism with greater metabolism resulting in greater flow. Local metabolites are a major influence on flow.
3. The skin circulation receives 4% of cardiac output at rest and is mainly involved in thermoregulation. Vasoconstrictors and vasodilators influence flow
The document summarizes several aspects of regional circulations, including the coronary, cutaneous, cerebral, skeletal muscle, splanchnic, and renal circulations. Specific details provided on the coronary circulation include its high blood flow even at rest, regulation of flow through metabolic and neural mechanisms, and implications for conditions like myocardial infarction and heart failure. Key aspects of the cutaneous circulation discussed are its role in temperature regulation through sympathetic nervous system control of arterioles and anastomoses, and local vasodilation or constriction in response to heating and cooling.
Effects of anaesthetic agents on the cardiovascular systemaratimohan
The document discusses the cardiovascular effects of various anesthetic agents. It notes that volatile agents like halothane and enflurane cause decreases in blood pressure mainly through effects on myocardial contractility, while isoflurane, desflurane and sevoflurane lower blood pressure primarily by decreasing systemic vascular resistance. These agents also attenuate the baroreceptor reflex. Intravenous induction agents can cause an initial drop in blood pressure due to vasodilation, which is compensated for by an increase in heart rate, but may lead to hypotension in vulnerable patients. Barbiturates, benzodiazepines and other intravenous agents have varying effects depending on their class.
Cardiac output is the volume of blood pumped by the heart per minute. It is calculated as stroke volume multiplied by heart rate. The document discusses various factors that affect cardiac output such as preload, afterload, contractility, and heart rate. It also describes direct and indirect methods for measuring cardiac output, with the oxygen Fick method and thermodilution method explained in detail. Conditions that cause cardiac output to increase or decrease are also outlined.
Cardiovascular physiology for anesthesiamarwa Mahrous
This document discusses cardiovascular physiology including the structure and function of the heart, regulation of the cardiovascular system, blood flow through the pulmonary and systemic circulations, factors that influence cardiac output and stroke volume, and regulation of the systemic vasculature. Key points include:
- The cardiovascular system consists of the heart, blood vessels, and mechanisms that regulate blood circulation and pressure.
- Cardiac output is determined by stroke volume and heart rate. Stroke volume depends on preload, afterload, and contractility.
- The pulmonary circulation has low pressure and resistance while the systemic circulation has higher pressure and resistance.
- Autonomic nervous system and chemical factors regulate heart rate and contractility. Venous return and vascular
This document discusses the physiology of coronary blood flow. It begins with an introduction and overview of topics to be covered, including the anatomy of the heart, coronary blood flow, control of coronary blood flow, and nervous control. It then provides details on the coronary arteries and veins, factors that influence coronary blood flow like oxygen demand and determinants of oxygen consumption, and mechanisms that control blood flow like metabolic regulation and reactive hyperemia. It concludes with a discussion of how autonomic nervous stimulation can affect coronary flow both directly through effects on blood vessels and indirectly by altering cardiac work and oxygen demand.
The document summarizes the cardiovascular system and regulation of blood pressure. It describes how the brain monitors and controls blood flow and pressure on a beat-to-beat basis to meet metabolic demands. Blood pressure is influenced by cardiac output, peripheral resistance, and blood volume. The document then discusses short term regulation of blood pressure by baroreceptor reflexes, chemoreceptor reflexes, and local mechanisms, as well as long term regulation by the renal-body fluid system including the renin-angiotensin-aldosterone mechanism.
Blood pressure is generated by ventricular contraction and measured in mmHg. It has two components: systolic (maximum pressure) and diastolic (minimum pressure). Blood pressure is regulated through both rapid nervous mechanisms like baroreceptor and chemoreceptor reflexes, and longer-term mechanisms involving blood volume control. Baroreceptors detect changes in blood pressure and stimulate the vasomotor center to increase or decrease sympathetic outflow and heart rate. Chemoreceptors detect chemical changes in blood and stimulate respiratory and cardiovascular responses during hypoxia or hemorrhage.
Normal blood pressure is regulated through control of cardiac output and peripheral vascular resistance. Cardiac output depends on stroke volume and heart rate, which are influenced by sodium homeostasis and beta-adrenergic systems. Peripheral resistance is determined by vascular tone, regulated by vasoconstrictors like angiotensin II and vasodilators like nitric oxide. The kidneys, through the renin-angiotensin system and natriuretic peptides, help regulate blood volume and pressure by controlling sodium balance and reabsorption. When blood pressure falls, renin is released to produce angiotensin II which causes vasoconstriction and sodium retention, raising blood pressure.
Control of blood pressure involves both immediate and long-term mechanisms. Immediate control is mediated by autonomic reflexes like the baroreceptor reflex which senses changes in blood pressure and regulates sympathetic outflow. Intermediate control involves the renin-angiotensin-aldosterone system and arginine vasopressin. Long-term control is regulated by the kidneys which alter sodium and water balance. Most tissues also autoregulate blood flow by dilating or constricting arterioles in response to pressure and metabolic changes.
This document discusses coronary blood flow and its control. It begins by introducing the unique nature of the coronary circulation and the importance of balancing oxygen supply and demand. It then covers several topics in depth: the control of coronary blood flow during different parts of the cardiac cycle; the determinants of myocardial oxygen consumption; coronary autoregulation and how it can become impaired; transmural variations in coronary blood flow; endothelium-dependent modulation of coronary tone through factors like nitric oxide, prostacyclin, and endothelin; and the components of coronary vascular resistance. The overall goal is to provide an in-depth overview of coronary circulation and the factors that influence blood flow to the heart.
This document discusses cardiac output and the factors that affect it. It provides details on:
- Normal cardiac output values at rest and during activity.
- How the Frank-Starling mechanism and venous return primarily control cardiac output.
- Factors like metabolism, exercise, age, and body size that directly impact cardiac output.
- Pathologically high or low cardiac outputs and their underlying causes, including reduced peripheral resistance or issues with heart function.
- How cardiac output is measured and its relationship to venous return under normal conditions.
This document discusses congestive heart failure (CHF), including its prevalence, mortality rates, causes, pathophysiology, clinical presentation, treatment, and management challenges. Some key points:
- CHF affects millions of Americans and hospitalization rates are high, with 5-year mortality rates around 50-60%. Common causes include coronary artery disease, hypertension, and valvular heart disease.
- Pathophysiology involves an imbalance in cardiac preload and afterload leading to inadequate cardiac output. Neurohormonal activation also occurs as a compensatory mechanism.
- Clinical presentation depends on whether left or right ventricular failure predominates. Left ventricular failure causes pulmonary edema while right ventricular failure causes peripheral edema.
This document discusses the coronary circulation and blood supply to the heart. It notes that the main coronary arteries lie on the heart's surface and penetrate into the cardiac muscle, supplying it with blood. The left coronary artery supplies the left side of the heart while the right coronary artery supplies the right side. Coronary blood flow increases during exercise to meet the heart's higher metabolic demands. Local muscle metabolism is the primary controller of coronary blood flow to match blood supply with nutrient needs. The autonomic nervous system can also affect coronary flow both directly through its effects on coronary vessels and indirectly by changing heart activity.
Short-term regulation of rising blood pressure involves increased parasympathetic activity and decreased sympathetic activity, which lowers heart rate and dilates blood vessels to reduce blood pressure. Long-term regulation increases blood volume through renin release, angiotensin conversion, aldosterone stimulation of sodium reabsorption in the kidneys, and subsequent water retention, restoring normal blood pressure. Dehydration triggers antidiuretic hormone to increase water conservation and thirst to promote fluid intake, again restoring normal blood volume and pressure.
The document discusses several regional circulations, focusing on coronary and cerebral circulation. For coronary circulation, it describes the anatomy of coronary blood vessels, factors regulating blood flow such as autoregulation, and clinical conditions like coronary artery disease. For cerebral circulation, it outlines the anatomy including the circle of Willis, characteristics like high blood flow and oxygen extraction, regulation of normal flow through intracranial pressure, and the cushioning function of cerebrospinal fluid.
Blood pressure is regulated through both short-term and long-term mechanisms. Short-term regulation involves neural mechanisms like the autonomic nervous system and baroreceptor reflexes which sense changes in blood pressure and heart rate. It also involves vascular mechanisms like changes in capillary fluid and stress relaxation as well as hormonal mechanisms like catecholamines and renin-angiotensin system. Long-term regulation is controlled by the kidneys and renal mechanisms as well as hormones like aldosterone, ADH, ANP and the renin-angiotensin-aldosterone system. Together these mechanisms tightly control blood pressure and ensure adequate perfusion to tissues.
This document provides an overview of the regulation of circulation and blood pressure. It discusses how blood pressure is controlled through nervous mechanisms like the sympathetic and parasympathetic nervous systems as well as renal-body fluid mechanisms involving the renin-angiotensin system, aldosterone, and ADH. The autonomic nervous system regulates blood pressure through reflexes like the baroreceptor reflex which senses changes in blood pressure and activates sympathetic or parasympathetic responses as needed to maintain normal pressure.
Short-term regulation of blood pressure involves nervous and chemical mechanisms that act within seconds or minutes to control blood pressure. The nervous system regulates blood pressure by changing blood vessel diameter and heart rate through the sympathetic and parasympathetic nervous systems. Baroreceptors in the carotid sinus and aortic arch detect changes in blood pressure and stimulate reflex responses to return blood pressure to normal levels. Chemoreceptors sense oxygen and carbon dioxide levels and stimulate responses to maintain proper gas exchange in the lungs and tissues. If blood pressure drops severely, the brain triggers a central nervous system ischemic response to rapidly constrict blood vessels and raise blood pressure.
Cardiac output is the volume of blood pumped by the heart each minute. It is calculated as stroke volume multiplied by heart rate. Stroke volume is the volume of blood pumped from the left ventricle with each beat. Factors that affect cardiac output include body metabolism, exercise level, age, and body size. Cardiac output increases with exercise and decreases with age. It is tightly regulated to meet the metabolic demands of the body's tissues.
1) The heart has four chambers and uses electrical signals to coordinate contractions that pump blood through two circuits.
2) The sinoatrial node initiates electrical impulses that spread through the heart, causing atria to contract before ventricles.
3) Cardiac output depends on heart rate, preload, afterload and contractility and is regulated by nervous and hormonal factors.
There are four main mechanisms that regulate blood pressure: nervous, renal, hormonal, and local. The nervous mechanism acts the fastest via the vasomotor system to control heart rate and vasoconstriction/vasodilation in response to baroreceptors and chemoreceptors. The renal mechanism regulates blood pressure long-term by controlling extracellular fluid volume and through the renin-angiotensin system. Hormonal and local factors also contribute to blood pressure regulation.
This document discusses the concepts of blood pressure including systolic, diastolic, and mean arterial pressure. It defines normal blood pressure ranges and factors that can influence blood pressure such as age, sex, body size, emotions, exercise, meals, sleep, and gravity. The relationship between cardiac output, total peripheral resistance, and blood pressure is explained. Mechanisms for short-term blood pressure regulation including baroreceptor reflex, chemoreceptor reflex, and central nervous system ischemic response are outlined. Long-term regulation involves the kidneys, renin-angiotensin system, and pressure natriuresis.
HEART RATE
REGULATION OF HEART RATE
VASOMOTOR CENTER – CARDIAC CENTER
MOTOR (EFFERENT) NERVE FIBERS TO HEART
FACTORS AFFECTING VASOMOTOR CENTER
for all medical & health care students
The cardiac cycle begins with an electrical impulse from the sinoatrial node that causes atrial contraction. This is followed by a delayed impulse from the atrioventricular node that causes ventricular contraction. The cycle involves electrical and mechanical events represented by the ECG. Cardiac function is controlled by the autonomic nervous system and hormones. Parasympathetic stimulation decreases heart rate while sympathetic stimulation increases it. Important cardiac reflexes maintain homeostasis by regulating heart rate and contractility in response to pressure and chemical sensors.
This document discusses the pathophysiology of heart failure. It begins by describing the essential functions of the heart in providing adequate blood supply and receiving blood returning from tissues. Heart failure occurs when the heart can no longer meet the metabolic demands of tissues despite normal or increased blood return. The key mechanisms involved in heart failure development include disorders of preload, contractility, and afterload. Chronic neurohormonal abnormalities also contribute to the progression of heart failure over time.
11.03.08(b): Regulation of Arterial Blood PressureOpen.Michigan
Slideshow is from the University of Michigan Medical School's M1 Cardiovascular / Respiratory sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M1Cardio
The document summarizes blood flow to different parts of the body, including the brain, heart, skeletal muscles, skin, lungs, and gastrointestinal system. It describes how blood flow is controlled and changes in each area, such as increasing during exercise in muscles or decreasing to conserve heat in the skin. Blood flow to the brain remains constant across a wide range of conditions through autoregulation and is sensitive to carbon dioxide levels.
This document discusses cerebral blood flow, intracranial pressure, and their regulation. It describes how blood flows to and drains from the brain through various arteries and veins. Factors like carbon dioxide levels, oxygen levels, metabolism and autoregulation help control cerebral blood flow. Intracranial pressure is maintained by a balance of brain tissue, blood and cerebrospinal fluid, and can increase due to masses, swelling or fluid accumulation. Signs of elevated intracranial pressure include headache, vomiting and altered consciousness. Treatments aim to reduce pressure through drainage, medication and other interventions to preserve adequate cerebral perfusion.
Blood pressure is generated by ventricular contraction and measured in mmHg. It has two components: systolic (maximum pressure) and diastolic (minimum pressure). Blood pressure is regulated through both rapid nervous mechanisms like baroreceptor and chemoreceptor reflexes, and longer-term mechanisms involving blood volume control. Baroreceptors detect changes in blood pressure and stimulate the vasomotor center to increase or decrease sympathetic outflow and heart rate. Chemoreceptors detect chemical changes in blood and stimulate respiratory and cardiovascular responses during hypoxia or hemorrhage.
Normal blood pressure is regulated through control of cardiac output and peripheral vascular resistance. Cardiac output depends on stroke volume and heart rate, which are influenced by sodium homeostasis and beta-adrenergic systems. Peripheral resistance is determined by vascular tone, regulated by vasoconstrictors like angiotensin II and vasodilators like nitric oxide. The kidneys, through the renin-angiotensin system and natriuretic peptides, help regulate blood volume and pressure by controlling sodium balance and reabsorption. When blood pressure falls, renin is released to produce angiotensin II which causes vasoconstriction and sodium retention, raising blood pressure.
Control of blood pressure involves both immediate and long-term mechanisms. Immediate control is mediated by autonomic reflexes like the baroreceptor reflex which senses changes in blood pressure and regulates sympathetic outflow. Intermediate control involves the renin-angiotensin-aldosterone system and arginine vasopressin. Long-term control is regulated by the kidneys which alter sodium and water balance. Most tissues also autoregulate blood flow by dilating or constricting arterioles in response to pressure and metabolic changes.
This document discusses coronary blood flow and its control. It begins by introducing the unique nature of the coronary circulation and the importance of balancing oxygen supply and demand. It then covers several topics in depth: the control of coronary blood flow during different parts of the cardiac cycle; the determinants of myocardial oxygen consumption; coronary autoregulation and how it can become impaired; transmural variations in coronary blood flow; endothelium-dependent modulation of coronary tone through factors like nitric oxide, prostacyclin, and endothelin; and the components of coronary vascular resistance. The overall goal is to provide an in-depth overview of coronary circulation and the factors that influence blood flow to the heart.
This document discusses cardiac output and the factors that affect it. It provides details on:
- Normal cardiac output values at rest and during activity.
- How the Frank-Starling mechanism and venous return primarily control cardiac output.
- Factors like metabolism, exercise, age, and body size that directly impact cardiac output.
- Pathologically high or low cardiac outputs and their underlying causes, including reduced peripheral resistance or issues with heart function.
- How cardiac output is measured and its relationship to venous return under normal conditions.
This document discusses congestive heart failure (CHF), including its prevalence, mortality rates, causes, pathophysiology, clinical presentation, treatment, and management challenges. Some key points:
- CHF affects millions of Americans and hospitalization rates are high, with 5-year mortality rates around 50-60%. Common causes include coronary artery disease, hypertension, and valvular heart disease.
- Pathophysiology involves an imbalance in cardiac preload and afterload leading to inadequate cardiac output. Neurohormonal activation also occurs as a compensatory mechanism.
- Clinical presentation depends on whether left or right ventricular failure predominates. Left ventricular failure causes pulmonary edema while right ventricular failure causes peripheral edema.
This document discusses the coronary circulation and blood supply to the heart. It notes that the main coronary arteries lie on the heart's surface and penetrate into the cardiac muscle, supplying it with blood. The left coronary artery supplies the left side of the heart while the right coronary artery supplies the right side. Coronary blood flow increases during exercise to meet the heart's higher metabolic demands. Local muscle metabolism is the primary controller of coronary blood flow to match blood supply with nutrient needs. The autonomic nervous system can also affect coronary flow both directly through its effects on coronary vessels and indirectly by changing heart activity.
Short-term regulation of rising blood pressure involves increased parasympathetic activity and decreased sympathetic activity, which lowers heart rate and dilates blood vessels to reduce blood pressure. Long-term regulation increases blood volume through renin release, angiotensin conversion, aldosterone stimulation of sodium reabsorption in the kidneys, and subsequent water retention, restoring normal blood pressure. Dehydration triggers antidiuretic hormone to increase water conservation and thirst to promote fluid intake, again restoring normal blood volume and pressure.
The document discusses several regional circulations, focusing on coronary and cerebral circulation. For coronary circulation, it describes the anatomy of coronary blood vessels, factors regulating blood flow such as autoregulation, and clinical conditions like coronary artery disease. For cerebral circulation, it outlines the anatomy including the circle of Willis, characteristics like high blood flow and oxygen extraction, regulation of normal flow through intracranial pressure, and the cushioning function of cerebrospinal fluid.
Blood pressure is regulated through both short-term and long-term mechanisms. Short-term regulation involves neural mechanisms like the autonomic nervous system and baroreceptor reflexes which sense changes in blood pressure and heart rate. It also involves vascular mechanisms like changes in capillary fluid and stress relaxation as well as hormonal mechanisms like catecholamines and renin-angiotensin system. Long-term regulation is controlled by the kidneys and renal mechanisms as well as hormones like aldosterone, ADH, ANP and the renin-angiotensin-aldosterone system. Together these mechanisms tightly control blood pressure and ensure adequate perfusion to tissues.
This document provides an overview of the regulation of circulation and blood pressure. It discusses how blood pressure is controlled through nervous mechanisms like the sympathetic and parasympathetic nervous systems as well as renal-body fluid mechanisms involving the renin-angiotensin system, aldosterone, and ADH. The autonomic nervous system regulates blood pressure through reflexes like the baroreceptor reflex which senses changes in blood pressure and activates sympathetic or parasympathetic responses as needed to maintain normal pressure.
Short-term regulation of blood pressure involves nervous and chemical mechanisms that act within seconds or minutes to control blood pressure. The nervous system regulates blood pressure by changing blood vessel diameter and heart rate through the sympathetic and parasympathetic nervous systems. Baroreceptors in the carotid sinus and aortic arch detect changes in blood pressure and stimulate reflex responses to return blood pressure to normal levels. Chemoreceptors sense oxygen and carbon dioxide levels and stimulate responses to maintain proper gas exchange in the lungs and tissues. If blood pressure drops severely, the brain triggers a central nervous system ischemic response to rapidly constrict blood vessels and raise blood pressure.
Cardiac output is the volume of blood pumped by the heart each minute. It is calculated as stroke volume multiplied by heart rate. Stroke volume is the volume of blood pumped from the left ventricle with each beat. Factors that affect cardiac output include body metabolism, exercise level, age, and body size. Cardiac output increases with exercise and decreases with age. It is tightly regulated to meet the metabolic demands of the body's tissues.
1) The heart has four chambers and uses electrical signals to coordinate contractions that pump blood through two circuits.
2) The sinoatrial node initiates electrical impulses that spread through the heart, causing atria to contract before ventricles.
3) Cardiac output depends on heart rate, preload, afterload and contractility and is regulated by nervous and hormonal factors.
There are four main mechanisms that regulate blood pressure: nervous, renal, hormonal, and local. The nervous mechanism acts the fastest via the vasomotor system to control heart rate and vasoconstriction/vasodilation in response to baroreceptors and chemoreceptors. The renal mechanism regulates blood pressure long-term by controlling extracellular fluid volume and through the renin-angiotensin system. Hormonal and local factors also contribute to blood pressure regulation.
This document discusses the concepts of blood pressure including systolic, diastolic, and mean arterial pressure. It defines normal blood pressure ranges and factors that can influence blood pressure such as age, sex, body size, emotions, exercise, meals, sleep, and gravity. The relationship between cardiac output, total peripheral resistance, and blood pressure is explained. Mechanisms for short-term blood pressure regulation including baroreceptor reflex, chemoreceptor reflex, and central nervous system ischemic response are outlined. Long-term regulation involves the kidneys, renin-angiotensin system, and pressure natriuresis.
HEART RATE
REGULATION OF HEART RATE
VASOMOTOR CENTER – CARDIAC CENTER
MOTOR (EFFERENT) NERVE FIBERS TO HEART
FACTORS AFFECTING VASOMOTOR CENTER
for all medical & health care students
The cardiac cycle begins with an electrical impulse from the sinoatrial node that causes atrial contraction. This is followed by a delayed impulse from the atrioventricular node that causes ventricular contraction. The cycle involves electrical and mechanical events represented by the ECG. Cardiac function is controlled by the autonomic nervous system and hormones. Parasympathetic stimulation decreases heart rate while sympathetic stimulation increases it. Important cardiac reflexes maintain homeostasis by regulating heart rate and contractility in response to pressure and chemical sensors.
This document discusses the pathophysiology of heart failure. It begins by describing the essential functions of the heart in providing adequate blood supply and receiving blood returning from tissues. Heart failure occurs when the heart can no longer meet the metabolic demands of tissues despite normal or increased blood return. The key mechanisms involved in heart failure development include disorders of preload, contractility, and afterload. Chronic neurohormonal abnormalities also contribute to the progression of heart failure over time.
11.03.08(b): Regulation of Arterial Blood PressureOpen.Michigan
Slideshow is from the University of Michigan Medical School's M1 Cardiovascular / Respiratory sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M1Cardio
The document summarizes blood flow to different parts of the body, including the brain, heart, skeletal muscles, skin, lungs, and gastrointestinal system. It describes how blood flow is controlled and changes in each area, such as increasing during exercise in muscles or decreasing to conserve heat in the skin. Blood flow to the brain remains constant across a wide range of conditions through autoregulation and is sensitive to carbon dioxide levels.
This document discusses cerebral blood flow, intracranial pressure, and their regulation. It describes how blood flows to and drains from the brain through various arteries and veins. Factors like carbon dioxide levels, oxygen levels, metabolism and autoregulation help control cerebral blood flow. Intracranial pressure is maintained by a balance of brain tissue, blood and cerebrospinal fluid, and can increase due to masses, swelling or fluid accumulation. Signs of elevated intracranial pressure include headache, vomiting and altered consciousness. Treatments aim to reduce pressure through drainage, medication and other interventions to preserve adequate cerebral perfusion.
The document discusses the physiology of the cardiovascular system, specifically arterial blood pressure. It defines blood pressure and its components, including systolic, diastolic, mean arterial pressure, and pulse pressure. It describes the functions of arterial blood pressure in maintaining tissue perfusion and capillary hydrostatic pressure. It also discusses various physiological variations in arterial blood pressure related to factors like age, sex, body region, meals, exercise, sleep, emotions, temperature, position, and respiration. Finally, it outlines the rapid mechanisms that regulate arterial blood pressure, including the baroreceptor feedback mechanism, chemoreceptor mechanism, central nervous system ischemic mechanism, adrenal medulla hormones, and antidiuretic hormone.
Short-term control of blood pressure is mediated by the nervous system and chemicals that regulate peripheral resistance within seconds or minutes. The baroreceptor reflex detects changes in blood pressure and regulates heart rate, stroke volume, and vascular tone to maintain pressure. Chemoreceptors sense oxygen and carbon dioxide levels and stimulate the vasomotor center. If blood flow to the brain decreases severely, the CNS ischemic response triggers powerful vasoconstriction to increase pressure.
This document discusses cardiac output and the factors that affect it. It defines key terms like stroke volume, minute volume, cardiac index and cardiac reserve. It describes physiological factors like age, gender, exercise and posture as well as pathological factors like fever, anemia and heart failure that can impact cardiac output. The document also covers methods of measuring cardiac output like Fick's principle, dye dilution and thermodilution techniques.
1. Several substances act as vasoconstrictors or vasodilators to regulate blood flow, including norepinephrine, epinephrine, angiotensin II, vasopressin, histamine, bradykinin, ions like calcium and potassium.
2. During exercise, sympathetic nervous system discharge causes widespread vasoconstriction except in active muscles, along with increased heart rate, arterial pressure and cardiac output to elevate blood flow to muscles.
3. Coronary blood flow supplies the heart and increases during exercise to meet heightened cardiac demand, with the left coronary artery mainly supplying the left ventricle and right coronary artery mainly supplying the right ventricle.
1. Several substances act as vasoconstrictors or vasodilators to regulate blood flow, including norepinephrine, epinephrine, angiotensin II, vasopressin, histamine, bradykinin, ions like calcium, potassium, magnesium, and hydrogen ions.
2. During exercise, sympathetic nervous system discharge causes widespread vasoconstriction except in active muscles, along with increased heart rate, arterial pressure and cardiac output to elevate blood flow to working muscles.
3. The coronary circulation normally supplies the heart muscle with blood, and collateral circulation ensures delivery even if major vessels are occluded. Blood flow increases during diastole and decreases during systole in a
This document provides an overview of topics to be covered in NURS 216 Spring 2013 related to cardiovascular anatomy, physiology, and disorders. Key points include:
- Review of cardiovascular anatomy, physiology, and mechanical functions of the heart.
- Discussion of disorders such as atherosclerosis, hypertension, coronary heart disease, myocardial infarction, and venous disorders.
- Objectives are to review cardiovascular concepts and discuss various cardiovascular disorders, including their causes, signs and symptoms, diagnosis, and treatment.
This document provides an overview of topics to be covered in NURS 216 Spring 2013 related to the cardiovascular system. It includes:
1) A reading assignment from the textbook and objectives to review cardiovascular anatomy, physiology, and disorders.
2) An outline of topics such as the heart's mechanical functions, layers of the heart, blood pressure regulation, arterial and venous systems, electrocardiograms, and cardiac output.
3) Details on specific cardiovascular conditions like atherosclerosis, hypertension, peripheral arterial disease, aneurysms, and orthostatic hypotension.
This document discusses cerebral blood flow and its regulation. It begins by outlining the clinical importance of abnormalities in blood flow, metabolism, fluids, composition, pressure and how they profoundly affect brain function. It then covers the vascular anatomy of the brain, control of cerebral blood flow, determinants of cerebral perfusion pressure, local and neurohumoral regulation of cerebral blood flow. Specific topics discussed in more detail include autoregulation of cerebral blood flow, effects of intracranial pressure, humoral control including catecholamines and neuropeptides, neural innervation, cerebrospinal fluid system, brain barriers, and circumventricular organs.
1. Coronary blood flow is regulated locally by the heart muscle in response to metabolic demand and oxygen needs. When the heart works harder, blood flow increases to supply more oxygen and nutrients.
2. Atherosclerosis occurs when cholesterol builds up in artery walls, forming plaques that block coronary blood flow. This reduced flow can cause myocardial infarction (heart attack) if the flow is cut off to part of the heart muscle.
3. Cerebral blood flow is tightly regulated to maintain adequate oxygen and remove waste. It increases with higher carbon dioxide and hydrogen ion levels but is relatively unaffected by oxygen levels within normal ranges. Blood flow autoregulation keeps flow stable during changes in blood pressure.
1. Coronary blood flow is regulated locally by the heart muscle in response to metabolic demand and oxygen needs. When the heart works harder, blood flow increases to supply more oxygen and nutrients.
2. Atherosclerosis occurs when cholesterol builds up in artery walls, forming plaques that block coronary blood flow. This reduced flow can cause myocardial infarction (heart attack) if the flow is cut off to part of the heart muscle.
3. Cerebral blood flow is tightly regulated to maintain adequate oxygen and remove waste. It increases with higher carbon dioxide and hydrogen ion levels but is relatively unaffected by oxygen levels within normal ranges. Blood flow autoregulation keeps cerebral flow stable during changes in blood pressure.
This document summarizes several key aspects of cerebral circulation:
1) The brain has the highest blood flow of any organ and is least tolerant of ischemia, relying on a dual internal carotid and vertebral arterial supply forming the Circle of Willis to maintain constant blood flow.
2) Cerebral circulation has unique features like being enclosed in the rigid skull, maintaining a constant volume through autoregulation of blood flow in response to pressure changes.
3) Local cerebral blood flow is tightly regulated by a combination of myogenic and metabolic mechanisms to ensure adequate oxygen and nutrient delivery to brain tissue.
Ppt cvs phsiology a small review for anaesthetistdrriyas03
The document discusses the cardiovascular system and heart function. It describes the heart as a pump that circulates blood through vessels to distribute essential substances and remove waste. The cardiovascular system transports 5 liters of blood per minute through a network of arteries, veins, and capillaries. Precise regulation of the cardiovascular system is achieved through neural, hormonal, and local control mechanisms.
This document defines and describes the different types of shock:
1) Hypovolemic shock occurs when there is severe bleeding, fluid loss, or reduced circulating blood volume leading to decreased cardiac output and blood flow.
2) Cardiogenic shock results from heart failure or damage that prevents the heart from pumping effectively.
3) Septic shock is caused by an overwhelming systemic infection where toxic substances impair blood flow.
4) Anaphylactic shock involves an allergic reaction that causes blood vessel dilation and low blood pressure through histamine release.
The document discusses the neural regulation of circulation. It covers:
1. Neural control shifts blood flow between different parts of the body as needed, such as more to muscles during exercise.
2. The circulatory system has cardiac and vascular innervation from both the sympathetic and parasympathetic nervous systems which control heart rate, contraction force, and vessel diameter.
3. The brain monitors blood flow and pressure through signals and controls them by altering cardiac output, peripheral resistance, and blood volume through short, intermediate, and long-term mechanisms like baroreceptor reflexes, the renin-angiotensin system, and kidney functions.
This document summarizes key concepts in cardiovascular physiology including:
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The document discusses the mechanisms that regulate blood pressure in the short term, including the nervous system and chemicals. It explains that the nervous system, including the baroreceptor reflex and chemoreceptors, controls blood pressure by changing peripheral resistance within seconds or minutes in response to changes in blood pressure. The document also outlines the roles of the vasomotor center, sympathetic and parasympathetic activity, and adrenal glands in short term blood pressure regulation.
The thalamus is a paired structure located in the brain that serves as a relay center and integrator for sensory and motor signals. It receives input from various areas of the body and brain and relays this information to the appropriate regions of the cerebral cortex. The thalamus is divided into several nuclei that serve functions like relaying sensory information, regulating states of consciousness, and participating in memory and emotion. Damage to certain thalamic nuclei can cause syndromes with loss of sensory abilities and motor impairments on the opposite side of the body.
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Attitude, ethics & communication (AETCOM)2 competenciesDRRAJNEE
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• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
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These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
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- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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4. Coronary blood vessels
Heart receives blood supply from two coronary
arteries
– Left coronary artery
Anterior descending branch
Circumflex branch
– Right coronary artery
Dominance
– Right in 50%
– Left in 20%
– Equal in 30%
5. Coronary circulation
4% of Cardiac Output
high resting blood flow of 70-80 ml/min/100g
– At maximal cardiac work: 300-400 ml/min/100 g
Has a high capillary density (3000-5000 mm2, about
one capillary per myocyte)
large surface area
short diffusion distances (≤9µm)
6. Coronary blood flow
Coronary blood flow occurs
during diastole
Why
– During systole, contraction of
heart musculature squeezes
the coronary vessels
– This effect is more in deeper
layers (subendocardial vessels)
than superficial layers
(epicardial vessels)
– This effect is maximal in the
left ventricle
7.
8. Coronary circulation
myocardial blood flow is characterized by
almost complete oxygen extraction (70-80%)
from the blood across the coronary capillaries
therefore, blood flow must increase to increase
oxygen delivery to the heart
myocardial oxygen delivery is FLOW LIMITED
aortic pressure provides driving force for
coronary blood flow
10. Metabolic (Functional) Hyperemia
primary determinant of coronary blood flow is
myocardial oxygen consumption
– which is dependent on metabolic activity
myocardial oxygen consumption is influenced by
– cardiac pressure development
– wall tension
– heart rate
– cardiac output
– inotropic state
– Afterload
– preload
11.
12. Mechanism
The exact means by which increased oxygen
consumption causes coronary circulation not known
Possible mechanism
– Hypoxia -> vasodilator substances to be released from
cardiac muscle cells
– Adenosine is the main vasodilator substance
– adenosine produced in myocytes from the metabolism of
ATP
– stimulates nitric oxide release from endothelium
– nitric oxide is a potent vasodilator
13. Other factors
K+ ions
H+ ions
CO2
Bradykinin
Prostaglandins
Lactate
14. Reactive hyperemia
brief occlusion of coronary vessel is followed by
a transient increase in coronary blood flow
occlusion results in the accumulation of
vasodilator metabolites in the interstitium
magnitude and duration of extra flow
dependent on the duration of the occlusion
15.
16. Autoregulation
blood flow is relatively constant at perfusion
pressures from 60 mmHg → 150 mmHg
metabolic and myogenic mechanisms involved
curve resets upward at elevated O2 such as
during exercise
autoregulatory capacity is important in
maintaining coronary flow when vessels are
partially obstructed
DR. RAJNEE
18. Neural control
sympathetic vasoconstrictor fibers - tonic
activity
– direct effect of SNS stimulation is vasoconstriction
via α1-adrenergic receptors
– net effect of sympathetic stimulation of the heart is
to increase coronary blood flow due to increase in
the production of metabolic vasodilators with
increased oxygen consumption
DR. RAJNEE
19. Neural control
parasympathetic cholinergic fibers
– → direct effect to vasodilate coronary resistance
vessels via endothelial release of NO
– net effect of parasympathetic stimulation of the
heart may actually be reduced coronary blood flow
resulting from decreased heart rate and oxygen
consumption
DR. RAJNEE
20. When the systemic BP falls
The overall effect of increase in noradrenergic
discharge is increased coronary blood flow due
to
– Metabolic changes
– On the contrary cutaneous, renal and splanchnic
vessels are constricted
– Protecting the heart
DR. RAJNEE
22. Clinical conditions
CAD (Coronary artery disease)
– Coronary artery disease (CAD) (or atherosclerotic
heart disease) is the end result of the accumulation
of atheromatous plaques within the walls of the
coronary arteries that supply the myocardium
– Is the leading cause of death worldwide
WHO Data
DR. RAJNEE
24. Clinical conditions
CAD causes
– Angina pectoris, commonly
known as angina
is severe chest pain due to
ischemia (a lack of blood and
hence oxygen supply) of the
heart muscle, generally due to
obstruction of the coronary
arteries
– Myocardial infarction (MI)
commonly known as a heart
attack
is the interruption of blood
supply to part of the heart,
causing some heart cells to die
DR. RAJNEE
26. General Characteristics
brain least tolerant of organs to ischemia
-↓blood flow for 5 seconds →loss of
consciousness
-↓blood flow for a few minutes →irreversible
damage
DR. RAJNEE
27. Anatomical details
Two internal carotids
Two vertebral arteries
– Basilar artery
Circle of Willis
No crossing over from R to L (because of equal
pressure)
Occlusion of vessel produces ischaemia and
infarction
DR. RAJNEE
28. General Characteristics
Rest: blood flow
– of 50-60 ml/min/100 g (750 ml/min)
(in contrast Coronary: 70-80 ml/min/100g; 250ml/min)
15% of cardiac output
– (in contrast Coronary: 4% of CO)
Exercise: blood flow of 750 ml/min
greatest flow goes to grey matter (100
ml/min/100 g)
35% O2 extraction at rest
DR. RAJNEE
29. Notable Anatomic Characteristics
circulation is enclosed in a rigid skull →
constant volume
brain tissue is incompressible
brain “floats” in a water bath of cerebrospinal
fluid
high capillary density (3000 - 4000/mm2)
→large surface area, short diffusion distances
blood-brain barrier - tight junctions between
endothelial cells →prevents circulating
vasoactive substances from affecting cerebral
blood flow
DR. RAJNEE
31. Normal Flow
Constant cerebral blood flow is maintained
under varying conditions
Factors affecting the total cerebral blood flow
– Arterial pressure at brain level
– Venous pressure at brain level
– The intracranial pressure
– The viscosity of blood
– The degree of active contraction/dilatation of
cerebral arterioles
This is controlled by local vasodilator metabolites
DR. RAJNEE
32. Role of intracranial pressure
Since the brain is enclosed within the skull the volume
of blood, brain and CSF should remain constant
(Monro-Kellie hypothesis)
ICP is normally 0-10 mmHg
Whenever ICP increases, cerebral vessels are
compressed
Change in venous pressure cause a similar change in
ICP
Rise in venous pressure decreases CBF by
compressing the vessels thereby decreasing perfusion
pressure
DR. RAJNEE
33. Autoregulation
pronounced autoregulatory capacity from 50 -
170 mmHg
both myogenic and metabolic mechanisms
involved
sympathetic nervous system activity can shift
the curve to the right
DR. RAJNEE
37. Arterial pH (acidosis)
– has little effect
– H+ does not cross the BBB
Arterial PO2 (normal, 80-100 mmHg)
– diffuses easily from blood to cerebral ECF
– hypoxia (PO2<40-50 mmHg) →dilatation
– PO2 > 100 mmHg →little effect
– dilatation adenosine mediated (?)
DR. RAJNEE
38. Neural control
Sympathetic nervous system
– rich innervation from superior cervical ganglion
– maximum sympathetic nervous system activity
causes only small vasoconstrictor response
– baroreceptor reflexes have little influence on
cerebral blood flow
– ↑sympathetic nervous system activity may prevent
hyperperfusion during acute ↑ in MAP
DR. RAJNEE
39. Neural control
Parasympathetic nervous system
– innervation via facial and superficial petrosal nerves
– stimulation of nerves cause vasodilatation (ACh stimulates
NO release)
– cut nerves → no effect
– physiological importance is unknown
Other
– ↑nerve activity → ↑NO release → local vasodilatation
– Perivascular neurons also contain 5HT (serotonin) a
powerful vasoconstrictor - may cause vasospasm
eg. in migraine
DR. RAJNEE
40. Metabolic
Potassium
– ↑K+ (i.e., seizures, hypoxia) → vasodilatation
– ↑K+ → stimulation of Na+/K+ATPase → hyperpolarize membrane
– stable concentration in autoregulatory range
Adenosine
– ↑ interstitial adenosine concentration with hypoxia, ischemia, ↓ perfusion
pressure, ↑metabolic activity, ↓supply/demand
– vasodilatation occurs
Nitric Oxide
– NO synthase active under basal conditions
– tonic vasodilator effect
– glial-derived (astrocytes) - NOS stimulated by NE, bradykinin, glutamate
→ Role?
DR. RAJNEE
41. Central Nervous System Ischemic
Response
When the blood flow to the brain has been sufficiently
interrupted to cause ischemia of the vasomotor center
these vasomotor neurons become strongly excited
causing massive vasoconstriction as a means of
raising the blood pressure to levels as high as the
heart can pump against
This response can raise the blood pressure to levels as
high as 270 mm Hg for as long as 10 minutes
DR. RAJNEE
42. Central Nervous System Ischemic
Response
This response is a last ditch stand to preserve the
blood flow to vital brain centers
it does not become activated until blood pressure has
fallen to at least 60 mm Hg, and it is most effective in
the range of 15 to 20 mm Hg
If the cerebral circulation is not reestablished within 3
to 10 minutes, the neurons of the vasomotor center
cease to function
↑sympathetic nervous system vasoconstrictor activity
to systemic resistance vessels →↑TPR → ↑MAP → ↑∆P
→ ↑cerebral blood flow
DR. RAJNEE
43. Cushing’s Reflex
The Cushing reflex is a special type of CNS reflex resulting from
an increase in intracranial pressure
space-occupying lesion (i.e., tumor, hemorrhage) will ↑ICP
forces brainstem down into the foramen magnum
brainstem becomes compressed → ischemia
↑sympathetic nervous system vasomotor drive to systemic
resistance vessels → vasoconstriction →↑TPR →↑MAP →↑∆P →
↑cerebral blood flow
baroreceptor-mediated reflex bradycardia
Main features: hypertension, bradycardia, respiratory
depression
The Cushing reflex is usually seen in the terminal stages of
acute head injury
DR. RAJNEE
47. Stroke
rapidly developing loss of brain function due to
disturbance in the blood supply to the brain,
caused by a blocked or burst blood vessel
This can be due to ischemia caused by
thrombosis or embolism
or due to a hemorrhage
DR. RAJNEE
50. CUTANEOUS CIRCULATION
primary role is regulation of internal
temperature
protection against the environment
blood pressure control
6% of the CO at rest (10-20 ml/min/100g)→
↓50% to retain heat, ↑7-fold to lose heat
DR. RAJNEE
52. Arteriovenous anastomoses
coiled, thick-walled vessels
direct connections between dermal arterioles and veins
provide low resistance shunt pathways → feed dermal venous
plexus
little basal tone (myogenic)
little metabolic control - no autoregulation or reactive
hyperemia
sympathetic nervous system vasoconstrictor innervation has
almost exclusive control
→tonic activity
located in “acral skin”: areas of high SA/vol. - fingers, toes,
palms, soles, lips, nose, ears
passive vasodilation due to ↓sympathetic nervous system
activity
DR. RAJNEE
53. Arterioles
located in non-acral skin - limbs, trunk, scalp
high density of α-adrenergic receptors
lack of β2-adrenergic receptors
sympathetic nervous system vasoconstrictor
innervation - little activity at normal core temperature
sympathetic nervous system cholinergic (vasodilator)
innervation is prominent to sweat glands →
BRADYKININ
bradykinin mediates “active” vasodilation
arterioles exhibit autoregulation, reactive hyperemia
and basal tone (myogenic)
DR. RAJNEE
54. Venous Plexus
contains greatest cutaneous blood volume -
acts as a reservoir
important for heat transfer
sympathetic nervous system vasoconstrictor
innervation
DR. RAJNEE
55. Control of Cutaneous Blood Flow
Sympathetic Nervous System
– to conserve heat SNS activity increases causing
vasoconstriction and reducing heat transfer to the
environment
– to lose heat SNS activity is reduced causing
vasodilation and enhanced heat transfer to the
environment
DR. RAJNEE
56. Local Skin Reflexes
local warming will produce local vasodilation
and sweating
local cooling will produce local vasoconstriction
due to increased affinity of α2-adrenergic
receptors for norepinephrine
intensity controlled by central brain
temperature centers
cutting spinal cord results in extremely poor
temperature regulation
DR. RAJNEE
58. Cold-Induced Vasodilation
– when temperature falls, smooth muscle becomes
paralyzed and vasodilatation occurs
Physical compression (e.g. sitting)
– ischemia →accumulation of metabolites →
stimulates nociceptors → pain → shift weight
– → reactive hyperemia (substance P/CGRP?)
DR. RAJNEE
59. Hormones
– epinephrine → constriction
– angiotensin II → constriction
– vasopressin → constriction
Role in Blood Pressure Control
– Hypotension → ↑sympathetic nervous system →AVA,
arteriole and venous constriction
– → ↑TPR and mobilization of blood to support venous
pressure
– During exercise enhanced blood flow to the cutaneous
circulation is necessary for
– dissipating heat → reduces venous return to the heart →
arterial pressure falls
DR. RAJNEE
60. White reaction
When a pointed object is drawn across the skin
Stroke lines becomes pale
Called white reaction
Due to mechanical stimulus initiating
precapillary sphincter contraction
DR. RAJNEE
61. Triple response
When the skin is stroked more strongly
Triple response
– 1. Red reaction
Capillary dilatation
– 2. Wheal (swelling)
Increased capillary permeability
– 3. Flare (redness spreading out from injury)
Arteriolar dilatation
Due to axon reflex
DR. RAJNEE
62. Axon reflex
A response in which impulses initiated in
sensory nerves by the injury are relayed
antidromically down other branches of the
sensory nerve fibres
Skin
Arteriole
DR. RAJNEE
65. enormous range of blood flow in skeletal
muscle: 3.0 ml/min/100 g at rest (20% of CO)
exercise: 100 ml/min/100g (80-85% of CO)
resistance vessels have high resting tone
(myogenic)
DR. RAJNEE
66. Regulation of Skeletal Muscle Blood
Flow
Neural
– neural control dominates at rest
– tonic sympathetic nervous system vasoconstrictor
activity (1 Hz) - α1-adrenergic receptor mediated
– an increase in sympathetic nervous system activity
(4-5 Hz) can decrease flow by 70%
– vasodilatation at rest is passive due to withdrawal
of sympathetic nervous system activity
– sympathetic-cholinergic fibers are anatomically
present - physiological role is uncertain
DR. RAJNEE
68. Hormonal
– circulating epinephrine vasodilates at low
concentration (β2-adrenergic receptor),
– constricts at high concentration (α1/α2-adrenergic
receptors)
– vasopressin → constricts
– angiotensin II → constricts
DR. RAJNEE
69. Metabolism (functional hyperemia)
with increased activity there is an increase in
the production of vasodilator metabolites
vasodilator metabolites are dominant during
exercise although sympathetic nervous system
activity to the working muscle is also enhanced
DR. RAJNEE
71. Physical Factors
cyclical contraction and relaxation of active
skeletal muscle vessels
vessels are compressed during the contraction
phase → blood flow becomes intermittent
muscle perfusion is enhanced by the muscle
pump
during activity muscle pump lowers the venous
pressure which increases the pressure gradient
driving flow
DR. RAJNEE
73. Autoregulation
– blood flow is relatively constant from 60 → 120
mmHg (mainly myogenic)
Reactive Hyperemia
– brief occlusion of blood flow is followed by a
transient increase in flow
74. Role of Skeletal Muscle Circulation in Blood
Pressure Control
– large mass of tissue: 40 - 45% of body weight
– major site of resistance vessels
– Peripheral resistance regulated by controlling
muscle resistance
– resistance influenced by
tonic vasoconstrictor activity
metabolic vasodilators
regulation by reflex mechanisms (baroreceptors,
cardiopulmonary receptors, etc.)
76. blood flow 25% of resting CO - can increase by
30 -100% after a meal
blood flow is closely coupled to absorption of
water, electrolytes and nutrients
Series/parallel configuration: the venous
drainage from the capillary bed of the
gastrointestinal tract, spleen and pancreas
flows into the portal vein, which provides most
of the blood flow to the hepatic circulation
77.
78. the hepatic artery provides the remainder of
the blood flow into the liver
high compliance venous system (25
ml/mmHg/kg) → acts as a reservoir (especially
the liver)
contains 20% of the blood volume at rest
DR. RAJNEE
79. Neural
Sympathetic nervous system
– innervation of arterioles, precapillary sphincters and
venous capacitance vessels
– little or no basal sympathetic nervous system tone
– ↑sympathetic nervous system activity → strong
vaso- and venoconstriction →
– redistributes BF, and increases functional circulating
blood volume (“mobilization”)
80. Parasympathetic nervous system
no innervation of blood vessels
↑activity → ↑motility, ↑metabolism→
functional hyperemia due to local vasodilator
metabolites (NO?)
DR. RAJNEE
83. Autoregulation
– poorly developed → metabolic mechanism
dominates
Autoregulatory escape
– ↑sympathetic nervous system activity → transient ↓
in BF
– after 2 -4 minutes blood flow returns towards
normal due to accumulation of metabolites
(adenosine) and vasodilation of arterioles
– veins remain constricted
DR. RAJNEE
84. Role in Blood Pressure Control
Hypotension
– vasoconstriction due to ↑sympathetic nervous
system, AII and VP→ ↑TPR
– venoconstriction →displaces blood centrally →
↑CVP → ↑SV
87. Renal circulation
At rest 25% CO, 1.2-1.3 l/min
Pressure drop across the glomerulus is only 1-3 mmHg
Further drop at the efferent arteriole
Regulation
– Norepinephrine, Angiotensin II - vasoconstriction
– Dopamine – vasodilatation
– Sympathetic activity (alpha receptor) – vasoconstriction
– Stimulation of renal nerves - increases renin secretion
Autoregulation is present
– Myogenic effect, NO may be involved
Renal cortex high blood flow poor O2 extraction but in medulla
low blood flow but high O2 extraction