The document discusses glomerular filtration rate (GFR) and the factors that determine it. GFR is determined by the balance of hydrostatic and colloid osmotic pressures across the glomerular capillary membrane as well as the capillary filtration coefficient. The average GFR in adults is about 125 mL/min. Increased glomerular capillary hydrostatic pressure or decreased colloid osmotic pressure will increase GFR, while increased colloid osmotic pressure or Bowman's capsule pressure will decrease GFR. GFR can be estimated by measuring creatinine or inulin clearance. Glomerular diseases can present as nephritic syndrome with hematuria and mild proteinuria or nephrotic syndrome with
This document discusses renal physiology, including renal blood flow, oxygen consumption, regulation of blood flow, glomerular filtration, and factors affecting glomerular filtration rate (GFR). Some key points:
- Renal blood flow is approximately 1/4 of cardiac output, or 1200 ml/min. Blood flow to the cortex is higher than to the medulla.
- Glomerular filtration is determined by the net filtration pressure and filtration coefficient. Forces increasing filtration are glomerular hydrostatic pressure and oncotic pressure in Bowman's space. Forces decreasing filtration are plasma oncotic pressure and hydrostatic pressure in Bowman's space.
- GFR is regulated through autoregulation mechanisms like tub
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.
1. Renal blood flow is tightly regulated to maintain a constant rate of around 1200 mL/min despite wide changes in blood pressure, through mechanisms like autoregulation and tubuloglomerular feedback.
2. The kidneys receive a high blood flow of around 20-30% of cardiac output despite their small size, and oxygen consumption in the kidneys is very high, second only to the heart.
3. Blood enters the kidneys through the renal artery and is distributed through a branching network of arteries before entering the glomerular capillaries and surrounding the nephron tubules, with the renal veins collecting the blood and returning it to circulation.
The document discusses the functions of the juxtaglomerular apparatus and hormonal control in the urinary system. It describes the juxtaglomerular apparatus as a specialized structure located where the distal tubule contacts the renal corpuscle. It regulates renal functions through the renin-angiotensin-aldosterone system and vasopressin response to osmolarity levels which control water retention and excretion. These systems work together to maintain fluid and electrolyte balance.
Renal blood flow (The Guyton and Hall physiology)Maryam Fida
In an average 70-kilogram man, the combined blood flow through both kidneys is about 1100 ml/min, or about 22 per cent of the cardiac output. Two kidneys makes about 0.4 % of total body weight but receive very high blood flow as compared with other body organ. The purpose of additional blood flow is to supply sufficient plasma for high rates of GF which is essential for regulating body fluid volumes & solute concentrations.
Characteristics of the renal blood flow:
1, High blood flow. 1100 ml/min, or 22 percent of the cardiac output. 94% to the cortex.
2, Two capillary beds
High hydrostatic pressure in glomerular capillary (about 60 mmHg) and low hydrostatic pressure in peritubular capillaries (about 13 mmHg)
Blood flow to renal medulla is supplied by vasa recta.
Blood flow in vasa recta of medulla is very low as compared to blood flow in cortex.
Blood flow in renal medulla is 1-2 % of total renal blood flow.
Vasa recta are important to form concentrated urine.
This document provides an overview of coronary circulation and coronary blood flow. It discusses the anatomy of the coronary blood vessels, characteristics of coronary blood flow such as rates at rest and during exercise. It describes phasic changes in coronary blood flow during the cardiac cycle. Methods for measuring coronary blood flow are presented. The regulation of coronary blood flow through local control mechanisms like autoregulation and metabolic factors as well as neural and hormonal influences are reviewed. Finally, factors that can affect coronary blood flow such as blood pressure, exercise, and hormones are outlined.
There are three main mechanisms that control arterial blood pressure:
1. Rapid mechanisms act within seconds to minutes through baroreceptor and chemoreceptor reflexes in the medulla to increase or decrease heart rate, cardiac contractility, and peripheral resistance.
2. Intermediate mechanisms act over hours to days through stress relaxation of blood vessels and capillary fluid shifts to regulate blood volume and pressure.
3. Long-term mechanisms act over days to weeks through regulation of extracellular fluid volume by atrial natriuretic peptide, ADH, and the renin-angiotensin system to control blood pressure by altering sodium and water reabsorption in the kidneys.
The document discusses the mechanism of urine concentration in the kidney through countercurrent flow. It explains how the loop of Henle acts as a countercurrent multiplier and the vasa recta acts as a countercurrent exchanger to generate and maintain an osmotic gradient in the renal medulla. This gradient allows water to be reabsorbed in the collecting ducts under the influence of ADH, resulting in concentrated urine when water intake is low. The kidney thus regulates urine concentration through countercurrent mechanisms to maintain water homeostasis.
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
Cardiac output is the volume of blood pumped by each ventricle per minute. It is calculated as stroke volume multiplied by heart rate. Normal cardiac output is 5 liters per minute. Cardiac output is regulated by factors that influence stroke volume and heart rate. Stroke volume depends on end diastolic volume and end systolic volume. Heart rate is controlled by the autonomic nervous system, including the parasympathetic and sympathetic nerves, as well as the vasomotor center in the medulla. Parasympathetic stimulation decreases heart rate while sympathetic stimulation increases it.
This document discusses the regulation of arterial blood pressure. It defines terms related to blood pressure and lists factors that can cause physiological variations. The determinants of arterial blood pressure are cardiac output and total peripheral resistance. Blood pressure is regulated through short, intermediate, and long-term control mechanisms involving the nervous system, kidneys, hormones, and local factors. The baroreceptor and renin-angiotensin systems help maintain normal blood pressure levels.
This document discusses cardiovascular regulation through humoral, neuronal, and local control systems. It provides details on various vasodilators and vasoconstrictors that regulate blood flow and pressure through humoral mechanisms. Key neuronal control centers in the medulla are described, including the vasomotor center, nucleus ambiguus, and nucleus tractus solitarius. The roles of the sympathetic and parasympathetic nervous systems in regulating heart rate and blood vessel tone are also outlined.
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.
This document discusses the anatomy and physiology of cutaneous blood flow regulation. It notes that cutaneous blood flow at rest is 10-15 ml/min/100g of skin, falling to 1 ml/min/100g with cold exposure and increasing tenfold with heat exposure. Blood flow is primarily regulated by the sympathetic nervous system. Exposure to heat causes arteriole dilation, cutaneous vessel dilation, sweating, and bradykinin-induced dilation. Exposure to cold triggers vasoconstriction. Various reflexes and cortical mechanisms also influence blood flow regulation and skin color changes.
Regulation of arterial blood pressure (The Guyton and Hall Physiology)Maryam Fida
BLOOD PRESSURE
The pressure exerted by the blood on vessel wall is known as blood pressure.
SYSTOLIC BLOOD PRESSURE
The maximum pressure exerted in the arteries during systole of heart.
Normal systolic pressure: 120 mm Hg.
DIASTOLIC BLOOD PRESSURE
The minimum pressure exerted in the arteries during diastole of heart.
Normal diastolic pressure: 80 mm Hg.
PULSE PRESSURE
The difference between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).
MEAN ARTERIAL BLOOD PRESSURE
The average pressure existing in the arteries.
Mean Arterial Blood Pressure = Diastolic Pressure + 1/3 Pulse Pressure
Pulse Pressure = (Systolic – Diastolic)
Mean Arterial Blood Pressure =Diastolic Pressure+1/3(Systolic – Diastolic)
Cardiac output by Dr. Amruta Nitin Kumbhar Assistant Professor, Dept. of Phys...Physiology Dept
Definition of cardiac output and related terms
Measurement of cardiac output
Variations in cardiac output
Regulation of cardiac output
Cardiac output control mechanisms
Role of heart rate in control of cardiac output
Integrated control of cardiac output
Heart–lung preparation
A comprehensive presentation on glomerular filtration rate (GFR) & renal blood flow and how these entities are impacted by intrinsic and extrinsic regulation.
This was presented by the author in the finals of the physiology seminar presentation in medical school.
Autoregulation of glomerular filtration rate and renal bloodDeepa Devkota
The document summarizes the autoregulation of glomerular filtration rate (GFR) and renal blood flow. It describes two main mechanisms - tubuloglomerular feedback and myogenic autoregulation. Tubuloglomerular feedback senses sodium chloride concentration at the macula densa and controls afferent and efferent arteriole diameter to maintain GFR. Myogenic autoregulation involves the vascular smooth muscle sensing changes in arterial pressure to resist vessel stretching and regulate resistance. These mechanisms help keep GFR and renal blood flow relatively constant despite changes in blood pressure, preventing extreme fluctuations in renal excretion.
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.
This document discusses cardiac output and the factors that regulate it. Cardiac output is the amount of blood pumped by the heart each minute and is determined by heart rate and stroke volume. Stroke volume is influenced by three main factors: preload, contractility, and afterload. Preload refers to the stretching of the heart before contraction and is represented by end-diastolic volume; increased preload results in increased stroke volume according to the Frank-Starling law. Contractility is the strength of ventricular contraction independent of preload; increased contractility also increases stroke volume. Afterload is the resistance against which the heart must pump during contraction; increased afterload decreases stroke volume. The relationship between cardiac output and these factors can
“Cardiac output refers to the volume of blood pumped out per ventricle per minute.”
Cardiac output is the function of heart rate and stroke volume.
STROKE VOLUME:
The amount of blood pumped by the left ventricle in one compression is called the stroke volume.
Heart Rate
The cardiac output increases with the increase in heart rate.
Dr. Nilesh Kate's document discusses oxygen transport. It begins by outlining the objectives of oxygen uptake in the lungs, transport in blood, and release in tissues. It then covers the introduction, uptake of oxygen by pulmonary blood due to the concentration gradient between the alveoli and arteries. Oxygen is transported in arterial blood both dissolved and bound to hemoglobin. The sigmoid shaped oxygen-hemoglobin dissociation curve allows for efficient loading and unloading of oxygen in tissues. Shifts in this curve are also discussed. Myoglobin assists with oxygen storage in muscle tissue.
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 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 the regulation of blood flow to tissues and organs. It describes acute control which occurs rapidly through vasoconstriction or vasodilation and long term control which involves changes to blood vessel structure over days or weeks. Key mechanisms of acute control include autoregulation to maintain constant blood flow despite pressure changes, active hyperemia to increase flow during increased activity, and reactive hyperemia providing a temporary surge in flow after ischemia. Long term control involves angiogenesis and developing collateral blood vessels. Regulation also occurs through vasoactive hormones, ions, and other chemicals that cause vasoconstriction or vasodilation.
This document discusses the general principles of circulation, including:
1. It describes the functional organization and structures of the vascular system, including the different types of blood vessels like windkessel vessels, resistance vessels, and exchange vessels.
2. It discusses pressure and blood flow in different segments of the circulatory system, providing tables of typical pressure values in structures of the systemic and pulmonary circulations.
3. It covers hemodynamics, explaining concepts like blood flow, cardiac output, laminar versus turbulent flow, and how blood flow is determined by factors like pressure difference and vascular resistance according to Poiseuille's law.
The document discusses coronary circulation and coronary artery disease. It begins by describing the anatomy of the coronary blood vessels and the blood supply to the heart. It then discusses characteristics of coronary blood flow such as autoregulation and factors that regulate it like metabolites and nervous control. Measurement techniques for coronary blood flow are also outlined. The document concludes by describing coronary artery disease conditions like angina and myocardial infarction as well as treatments.
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.
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.
The cardiac cycle describes the sequence of events in one heartbeat. It begins with atrial systole which pushes additional blood into the ventricles. This is followed by ventricular systole where the ventricles contract to pump blood out. Isovolumic contraction occurs as ventricular pressure rises, closing the AV valves before ejection. Ejection then proceeds rapidly initially and more slowly later. Isovolumic relaxation happens as ventricular pressure falls, opening the AV valves before rapid ventricular filling from the atria. The cycle then repeats with atrial systole.
The document discusses the mechanism of urine concentration in the kidney through countercurrent flow. It explains how the loop of Henle acts as a countercurrent multiplier and the vasa recta acts as a countercurrent exchanger to generate and maintain an osmotic gradient in the renal medulla. This gradient allows water to be reabsorbed in the collecting ducts under the influence of ADH, resulting in concentrated urine when water intake is low. The kidney thus regulates urine concentration through countercurrent mechanisms to maintain water homeostasis.
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
Cardiac output is the volume of blood pumped by each ventricle per minute. It is calculated as stroke volume multiplied by heart rate. Normal cardiac output is 5 liters per minute. Cardiac output is regulated by factors that influence stroke volume and heart rate. Stroke volume depends on end diastolic volume and end systolic volume. Heart rate is controlled by the autonomic nervous system, including the parasympathetic and sympathetic nerves, as well as the vasomotor center in the medulla. Parasympathetic stimulation decreases heart rate while sympathetic stimulation increases it.
This document discusses the regulation of arterial blood pressure. It defines terms related to blood pressure and lists factors that can cause physiological variations. The determinants of arterial blood pressure are cardiac output and total peripheral resistance. Blood pressure is regulated through short, intermediate, and long-term control mechanisms involving the nervous system, kidneys, hormones, and local factors. The baroreceptor and renin-angiotensin systems help maintain normal blood pressure levels.
This document discusses cardiovascular regulation through humoral, neuronal, and local control systems. It provides details on various vasodilators and vasoconstrictors that regulate blood flow and pressure through humoral mechanisms. Key neuronal control centers in the medulla are described, including the vasomotor center, nucleus ambiguus, and nucleus tractus solitarius. The roles of the sympathetic and parasympathetic nervous systems in regulating heart rate and blood vessel tone are also outlined.
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.
This document discusses the anatomy and physiology of cutaneous blood flow regulation. It notes that cutaneous blood flow at rest is 10-15 ml/min/100g of skin, falling to 1 ml/min/100g with cold exposure and increasing tenfold with heat exposure. Blood flow is primarily regulated by the sympathetic nervous system. Exposure to heat causes arteriole dilation, cutaneous vessel dilation, sweating, and bradykinin-induced dilation. Exposure to cold triggers vasoconstriction. Various reflexes and cortical mechanisms also influence blood flow regulation and skin color changes.
Regulation of arterial blood pressure (The Guyton and Hall Physiology)Maryam Fida
BLOOD PRESSURE
The pressure exerted by the blood on vessel wall is known as blood pressure.
SYSTOLIC BLOOD PRESSURE
The maximum pressure exerted in the arteries during systole of heart.
Normal systolic pressure: 120 mm Hg.
DIASTOLIC BLOOD PRESSURE
The minimum pressure exerted in the arteries during diastole of heart.
Normal diastolic pressure: 80 mm Hg.
PULSE PRESSURE
The difference between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).
MEAN ARTERIAL BLOOD PRESSURE
The average pressure existing in the arteries.
Mean Arterial Blood Pressure = Diastolic Pressure + 1/3 Pulse Pressure
Pulse Pressure = (Systolic – Diastolic)
Mean Arterial Blood Pressure =Diastolic Pressure+1/3(Systolic – Diastolic)
Cardiac output by Dr. Amruta Nitin Kumbhar Assistant Professor, Dept. of Phys...Physiology Dept
Definition of cardiac output and related terms
Measurement of cardiac output
Variations in cardiac output
Regulation of cardiac output
Cardiac output control mechanisms
Role of heart rate in control of cardiac output
Integrated control of cardiac output
Heart–lung preparation
A comprehensive presentation on glomerular filtration rate (GFR) & renal blood flow and how these entities are impacted by intrinsic and extrinsic regulation.
This was presented by the author in the finals of the physiology seminar presentation in medical school.
Autoregulation of glomerular filtration rate and renal bloodDeepa Devkota
The document summarizes the autoregulation of glomerular filtration rate (GFR) and renal blood flow. It describes two main mechanisms - tubuloglomerular feedback and myogenic autoregulation. Tubuloglomerular feedback senses sodium chloride concentration at the macula densa and controls afferent and efferent arteriole diameter to maintain GFR. Myogenic autoregulation involves the vascular smooth muscle sensing changes in arterial pressure to resist vessel stretching and regulate resistance. These mechanisms help keep GFR and renal blood flow relatively constant despite changes in blood pressure, preventing extreme fluctuations in renal excretion.
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.
This document discusses cardiac output and the factors that regulate it. Cardiac output is the amount of blood pumped by the heart each minute and is determined by heart rate and stroke volume. Stroke volume is influenced by three main factors: preload, contractility, and afterload. Preload refers to the stretching of the heart before contraction and is represented by end-diastolic volume; increased preload results in increased stroke volume according to the Frank-Starling law. Contractility is the strength of ventricular contraction independent of preload; increased contractility also increases stroke volume. Afterload is the resistance against which the heart must pump during contraction; increased afterload decreases stroke volume. The relationship between cardiac output and these factors can
“Cardiac output refers to the volume of blood pumped out per ventricle per minute.”
Cardiac output is the function of heart rate and stroke volume.
STROKE VOLUME:
The amount of blood pumped by the left ventricle in one compression is called the stroke volume.
Heart Rate
The cardiac output increases with the increase in heart rate.
Dr. Nilesh Kate's document discusses oxygen transport. It begins by outlining the objectives of oxygen uptake in the lungs, transport in blood, and release in tissues. It then covers the introduction, uptake of oxygen by pulmonary blood due to the concentration gradient between the alveoli and arteries. Oxygen is transported in arterial blood both dissolved and bound to hemoglobin. The sigmoid shaped oxygen-hemoglobin dissociation curve allows for efficient loading and unloading of oxygen in tissues. Shifts in this curve are also discussed. Myoglobin assists with oxygen storage in muscle tissue.
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 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 the regulation of blood flow to tissues and organs. It describes acute control which occurs rapidly through vasoconstriction or vasodilation and long term control which involves changes to blood vessel structure over days or weeks. Key mechanisms of acute control include autoregulation to maintain constant blood flow despite pressure changes, active hyperemia to increase flow during increased activity, and reactive hyperemia providing a temporary surge in flow after ischemia. Long term control involves angiogenesis and developing collateral blood vessels. Regulation also occurs through vasoactive hormones, ions, and other chemicals that cause vasoconstriction or vasodilation.
This document discusses the general principles of circulation, including:
1. It describes the functional organization and structures of the vascular system, including the different types of blood vessels like windkessel vessels, resistance vessels, and exchange vessels.
2. It discusses pressure and blood flow in different segments of the circulatory system, providing tables of typical pressure values in structures of the systemic and pulmonary circulations.
3. It covers hemodynamics, explaining concepts like blood flow, cardiac output, laminar versus turbulent flow, and how blood flow is determined by factors like pressure difference and vascular resistance according to Poiseuille's law.
The document discusses coronary circulation and coronary artery disease. It begins by describing the anatomy of the coronary blood vessels and the blood supply to the heart. It then discusses characteristics of coronary blood flow such as autoregulation and factors that regulate it like metabolites and nervous control. Measurement techniques for coronary blood flow are also outlined. The document concludes by describing coronary artery disease conditions like angina and myocardial infarction as well as treatments.
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.
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.
The cardiac cycle describes the sequence of events in one heartbeat. It begins with atrial systole which pushes additional blood into the ventricles. This is followed by ventricular systole where the ventricles contract to pump blood out. Isovolumic contraction occurs as ventricular pressure rises, closing the AV valves before ejection. Ejection then proceeds rapidly initially and more slowly later. Isovolumic relaxation happens as ventricular pressure falls, opening the AV valves before rapid ventricular filling from the atria. The cycle then repeats with atrial systole.
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.
This document provides an overview of electrocardiography (ECG), including how an ECG works, the basics of recording an ECG, ECG leads, normal ECG waveforms and intervals, interpreting an ECG, common abnormalities, and how to report an ECG. It discusses topics such as the cardiac conduction system, Einthoven's triangle, the 12-lead ECG, determining heart rate and axis, normal sinus rhythm, P waves, QRS complex, ST segment, T waves, and the QT interval.
This document summarizes blood pressure, including defining it as the lateral pressure exerted by flowing blood on artery walls. It discusses types of blood pressure depending on the blood vessel, normal ranges, measurement methods, factors that affect blood pressure both physiologically and pathologically, complications of hypertension, and mechanisms that regulate arterial blood pressure over rapid, intermediate, and long term timescales.
This document provides a summary of basics of electrocardiography (ECG/EKG). It discusses the history and development of ECG technology. It describes the components of a normal ECG waveform including the P, QRS, and T waves. It explains how to determine heart rate from an ECG and identify different arrhythmias based on the waveform. Key anatomical structures involved in heart's electrical conduction system are also outlined.
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.
This document discusses blood pressure, including its definition, normal values, measurement methods, short-term and long-term regulation, and related conditions like hypertension and hypotension. It defines systolic and diastolic blood pressure and other terms. It describes the nervous, hormonal, local, renal, and baroreceptor mechanisms that regulate blood pressure in the short-term and long-term. It provides details on hypertension types and treatment approaches, as well as causes of hypotension. The overall aim is to educate students on blood pressure, its determinants, regulation, and clinical implications.
The document discusses arterial blood pressure including definitions of systolic and diastolic blood pressure and their normal ranges. It describes factors that affect blood pressure both physiologically like age, hormones, and exercise, as well as anatomically like blood volume, vessel elasticity, and diameter. Methods of measuring blood pressure directly via arterial catheter or indirectly with a sphygmomanometer and stethoscope are provided. Potential complications of hypertension include headache, dizziness, chest pain, and visual issues.
Arterial blood pressure is the force exerted by blood on the walls of arteries. It is normally measured in millimeters of mercury (mmHg). Systolic pressure occurs when the heart contracts, while diastolic pressure occurs when the heart relaxes. Average normal pressures are 90-120 mmHg systolic and 60-80 mmHg diastolic. Blood pressure varies based on factors like age, hormones, exercise and stress level. It is highest in the arteries near the heart and decreases further from the heart. Hypertension can lead to complications like headaches, chest pain and visual issues if left untreated.
Maintaining homeostatic mean arterial blood pressuredwp_18
This document discusses mechanisms that regulate mean arterial blood pressure in the body. It describes that blood pressure needs to be regulated to maintain homeostasis. Short term mechanisms include baroreceptor and chemoreceptor reflexes which sense pressure changes and regulate heart rate and vessels. The renin-angiotensin-aldosterone system is a long term mechanism that helps regulate blood pressure and fluid balance. Hormones like atrial natriuretic peptide, epinephrine, norepinephrine, and vasopressin also affect blood pressure. The cardiovascular regulatory center integrates input from sensors and coordinates the autonomic nervous system response.
This document discusses arterial blood pressure, including its definition, normal ranges, components, determinants, regulation, and methods of measurement. It defines arterial blood pressure as the lateral pressure exerted by the column of blood on the walls of arteries. The main components discussed are systolic pressure, diastolic pressure, pulse pressure, and mean arterial pressure. Regulation of arterial blood pressure involves short-term, intermediate, and long-term mechanisms, including chemical, neural, renal, and renin-angiotensin-aldosterone system responses. Methods of measurement include palpatory, auscultatory, and oscillatory techniques using a sphygmomanometer.
Cardiac output is the volume of blood pumped by the heart per minute. It is calculated as heart rate multiplied by stroke volume. Cardiac output can vary depending on the body's activity level and is regulated by factors that influence heart rate and stroke volume. The Frank-Starling law of the heart states that increased venous return leads to increased stretch of the heart muscle and increased force of contraction, resulting in higher stroke volume and cardiac output.
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 cardiovascular physiology, including definitions of cardiac output and its determinants like heart rate, contractility, preload, and afterload. It describes the Frank-Starling relationship and how contractility, preload, and the anatomy and physiology of the coronary circulation impact cardiac output. Autoregulation and the control of arterial blood pressure through immediate, intermediate, and long-term mechanisms are examined. Various cardiac reflexes involving the baroreceptor, chemoreceptor, and other reflexes are also outlined.
Determinants of cardiac output for captivateleslielally
This document discusses determinants of cardiac output and factors that influence heart function. Cardiac output is determined by heart rate and stroke volume. Stroke volume depends on preload, afterload and contractility. Preload refers to ventricular filling, afterload is the resistance against which the heart pumps, and contractility is the heart's inherent ability to contract. Conditions such as heart failure, shock and arrhythmias can decrease cardiac output by impacting these determinants. Understanding hemodynamics helps evaluate a patient's cardiac function and guide treatment.
Blood pressure is regulated through multiple mechanisms:
1) Baroreceptors in the carotid sinus and aortic arch detect changes in blood pressure and stimulate the vasomotor center to increase or decrease sympathetic outflow and regulate cardiac output and peripheral resistance.
2) Low pressure receptors in the heart and lungs help regulate blood volume and pressure in response to changes.
3) The renin-angiotensin system and vasopressin help regulate fluid balance and vascular tone over the long-term to influence blood pressure.
4) Chemoreceptors sense oxygen levels and stimulate increases in blood pressure during hypoxia.
Normal arterial blood pressure ranges from 90-140/60-90 mmHg. Systolic pressure is the maximum pressure when blood is ejected from the heart, while diastolic is the minimum pressure when the heart is resting between beats. Mean arterial pressure, which averages 93 mmHg, is the main driving force for blood flow. Blood pressure is regulated through short term mechanisms like baroreceptor and chemoreceptor reflexes which control heart rate and vascular tone, and long term factors like blood volume and vessel elasticity. Strict control of blood pressure is important to ensure adequate blood flow to vital organs.
This document discusses veins, central venous pressure (CVP), microcirculation, lymphatics, local control of blood flow, arterial blood pressure control, cardiac output, and the relationship between the cardiovascular and lymphatic systems. Key points include that 60% of blood is in veins, CVP is measured invasively or noninvasively, capillary filtration is determined by Starling forces, blood flow is regulated locally and through neural and hormonal mechanisms, and cardiac output is determined by stroke volume and heart rate.
This document discusses veins, venous pressure, microcirculation, lymphatics, local blood flow control, arterial blood pressure control, cardiac output regulation, and the coupling of cardiac and vascular function. Key points include that veins act as reservoirs and return 60% of blood to the heart, central venous pressure measures right atrial pressure, the Starling forces that govern capillary filtration, and mechanisms like autoregulation, reactive hyperemia, and baroreceptor reflexes that control local blood flow and arterial pressure.
Cardiac output, blood flow, and blood pressureChy Yong
This document discusses cardiac output, blood flow, and blood pressure. It defines cardiac output as the volume of blood pumped per minute by each ventricle, which is determined by heart rate and stroke volume. Stroke volume depends on factors like preload, contractility, and afterload. The document also discusses regulation of heart rate and contractility by the autonomic nervous system as well as intrinsic properties like the Frank-Starling law. Additional topics covered include blood volume, factors influencing blood flow, vascular resistance, blood pressure regulation via baroreceptors, and measurement of blood pressure.
BLOOD PRESSURE
BY: SAIYED FALAKAARA
ASSISTANT PROFESSOR
DEPARTMENT OF PHARMACY
SUMANDEEP VIDYAPEETH
Definition
Arterial blood pressure can be defined as the lateral pressure exerted by moving the column of blood on the walls of the arteries.
Significance
To ensure the blood flow to various organs
Plays an important role in exchange of nutrients and gases across the capillaries
Required to form urine
Required for the formation of lymph
Normal values
Normal adult range can fluctuate within a wide range and still be normal
Systolic/diastolic
100/60 – 140/80
Unit - mmHg
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2. What is B.P.?
Pressure = force/unit area
Blood pressure =
pressure exerted by blood
on the walls of the
heart or
blood vessels
2
3. Container vs. Content example
same container;
same capacity;
less content
same content;
greater capacity
as the container
expands
PRESSURE falls
PRESSURE falls
e.g. haemorrhage
e.g. generalized
vasodilation
3
7. Functions of BP
• Intraventricular BP ejection of blood (stroke volume)
• Systemic arterial BP blood flow to tissues (tissue
perfusion)
• Capillary hydrostatic pressure filtration (tissue fluid
formation)
• Systemic venous BP blood flow back to the heart
(venous return)
The unconditional term
BLOOD PRESSURE
refers to
SYSTEMIC ARTERIAL
BLOOD PRESSURE
7
10. Systemic arterial blood pressure
= Cardiac output x Total peripheral
resistance (TPR)
or
Systemic vascular
reistance (SVR)
The 2 Major Determinants of Arterial B.P.
The other Determinants of Arterial B.P.?
10
11. Ventricular contraction
Ventricular relaxation
Aorta is the most
elastic artery
When aortic elasticity
decreases (ageing or
disease):
Less expansion during
systole Incr. SBP
Less elastic recoil
during diastole decr.
DBP
Pulse pressure ?
11
12. The Determinants of Arterial B.P.
SBP
DBP
• SBP
• Aortic distensibility
(elasticity)
• TPR
• Stroke volume
• Aortic distensibility
(elasticity)
SBP = CO x TPR
DBP = CO x TPR
12
13. Physiological Variations in BP
• Age:
– SBP and DBP gradually rise with age (after about 30 years), the
SBP more so and more sustained than the DBP
• Sex:
– the rise in BP with age is greater in males
• Circadian variation (diurnal variation):
– lowest during sleep (nocturnal dip) and highest in the mornings after
waking up
• Increased transiently during physical stress (e.g. muscular
exercise), mental stress(anger, apprehension, resentment, mental
concentration), emotional excitement
• The effect of Gravity: When erect, BP in any vessel
varies in relation to the vertical distance from the heart
level
14. Physiological Variations in BP
• Gravity
– In an upright position, BP
in the arteries below the
heart level is increased,
and that in the arteries
above the heart level is
decreased by 0.77 mm Hg
for each cm of vertical
distance below or above
the heart.
– Thus, routine
measurement of BP
should be performed with
the artery at the heart
level.
15. Effect of Gravity
• Pressure in large artery in the
foot 105 cm below the heart =
[0.77 mmHg/cm x 105 cm = 80
mm Hg)] +
• 100 mm Hg (Mean ABP at heart
level)
• = 180 mm Hg
• Pressure in vein in the foot 105
cm below the heart = [0.77
mmHg/cm x 105 cm = 80 mm
Hg)] +
• 4 mm Hg (right atrial pressure)
• = 84 mm Hg
16. REGULATION OF SYSTEMIC ARTERIAL B.P.
– MAINTENANCE OF RESTING B.P.
B.P. HOMEOSTASIS
• SITUATIONAL ADJUSTMENT OF B.P.
e.g. changes in B.P. during muscular exercise
16
18. Systemic arterial blood pressure
Total peripheral
= Cardiac output x resistance
(arteriolar tone)
More immediate
More efficient:
RESISTANCE =
1
Radius 4
More economical
18
19. BP REGULATORY MECHANISMS
NEURAL: CARDIOVASCULAR REFLEXES
Baroreceptor reflexes
Chemoreceptor reflexes
Brain(CNS) ischaemic response
Short term:
Rapid
Short term:
HORMONAL
Intermediate
Catecholamines
Renin-angiotensin-aldosterone(RAA) system
Vasopressin
Long term
RENAL-BODY FLUID CONTROL SYSTEM
19
20. Integrating centres
Afferents
Efferents
Hypothalamus
Vasopressin
Brain stem: Medulla
X
IX, X
(Parasym)
(Parasym)
Spinal cord:
SYMPATHETIC
NERVOUS
SYSTEM
Receptors
• Baroreceptors
• Chemoreceptors
Sym .outflow
Effectors
• Heart, Blood vessels
• Adrenal medulla: Catecholamines
20
• Kidney: activation of RAA system
21. Sympathetic Nervous System
•
•
•
•
Major effector system for BP control
Increased sympathetic tone incr. BP
decreased sympathetic tone decr. BP
Sym.N.S. is under the control of vasomotor
centre (VMC) in the medulla
• Descending tracts from the VMC excites the
sympathetic nervous system
• Inputs from the broreceptors and other receptors
go to the VMC (the integrating centre)
21
22. How does sympathetic N.S. activity
increase BP?
• Direct cardiovascular effects
• Neuroendocrine effects: activation of
– adrenal medulla
– renin-angiotensin-aldosterone (RAA) system
22
26. RENIN- ANGIOTENSIN-ALDOSTERONE SYSTEM
BLOOD
VOLUME/PRESSURE
Baroreceptor reflex
Sympathetic tone
Renal perfusion pressure
LIVER
Juxtaglomerular(JG) cells in
afferent arteriolar muscle coat in KIDNEY
Angiotensin-
Angiotensinogen
RENIN
Angiotensin I
Converting
Enzyme
ANGIOTENSIN II
VASCULAR and VOLUME EFFECTS
Endothelial cells of
pulmonary circulation
26
27. ANGIOTENSIN II
VASOCONTRICTION
Vascular smooth muscle
Sympathetic nerve endings
Brain: Hypothalamus
TPR
Facilitates release of
NORADRENALINE
Release of VASOPRESSIN
Stimulation
of THIRST
Adrenal cortex
Water intake
Secretion of ALDOSTERONE
Renal reabsorption of Sodium
BLOOD VOLUME
27
Renal reabsorption of Water
28. THE BARORECEPTOR REFLEX
operates within seconds
for moment to moment, day to day control
of BP
for BP homeostasis in the face of
challenges such as blood loss
Afferents: Parasympathetic
Efferents: Sympathetic noradrenergic
28
29. Baroreceptors = stretch receptors in the walls of
• Heart
Atria
Volume receptors
Low pressure baroreceptors
• Arteries (arterial baroreceptors)
Aortic arch
High pressure baroreceptors
Carotid sinus
Stimulation of Stretch
receptors in the wall
Stretch on
the wall
BP
Wall
29
32. Incr. baroreceptor discharge
• Stimulates the Parasympathetic centres
(Dorsal motor nucleus of vagus) in the
medulla
• Inhibits the vasomotor centre (VMC) in the
medulla (through inhibitory interneurones)
– Decr. excitatory discharge from the VMC to
the Sympathetic Nervous System in the spinal
cord
– decr. sympathetic noradrenergic discharge
32
33. Carotid sinus, aortic arch
Parasym. fibres in IX and
X cranial nerves
Inhibits VMC
stimulates motor vagal
nuclei
33
36. Note
• BP may not fall with minor haemorrhage
• Fall in venous return is detected by low
pressure baroreceptors increase in
TPR compensates for fall in CO BP
unchnaged
• When blood loss is >20% of circulating
blood volume, the fall in CO is great
enough to cause a fall in BP
• BP = CO x TPR
36
41. BP
BLOOD FLOW STAGNATION
O2 delivery to tissues (stagnant hypoxia)
CO2 uptake from tissues
O2
CO2
(in tissues)
Stimulation of chemoreceptors
IX, X
nerves
•Stimulation of medullary respiratory centre
•Stimulation of medullary VMC
sympathetic discharge
BP
42. The CNS ischaemic response
Medulla oblongata
CEREBRAL
BLOOD FLOW
CNS ISCHAEMIA
PO2
BLOOD
PRESSURE
VASOMOTOR
PCO2
Stagnant
hypoxia
CENTRE
Spinal Cord
(+)
(+)
SYMPATHETIC
OUTFLOW
Sympathetic tone
42
43. CUSHING’S
REFLEX
HEAD INJURY
Increased intracranial pressure
Pressure on cerebral arteries
CNS ISCHAEMIA
CEREBRAL
BLOOD FLOW
BLOOD
PRESSURE
Normal
BARORECEPTOR REFLEX
PO2
VMC
PCO2
Stagnant
hypoxia
VAGAL TONE
HEART RATE
(+)
(+)
SYMPATHETIC
OUTFLOW
Sympathetic tone
43
44. Head injury CNS ischaemia The rise in BP
• Baroreceptor reflex
– stimulation of vagus fall in HR (since
parasympathetic control of HR is dominant
over sympathetic control)
– but baroreflex-mediated inhibition of VMC
is counterbalanced by direct stimulation of
VMC by CNS ischaemia
– sympathetic-mediated generalized
vasoconstriction maintained Incr. in BP
Slow, full and bounding pulse
CUSHING’S REFLEX
44
45. Cushing's reflex
• Because the skull is rigid
after infancy, intracranial
masses or swelling may
increase intracranial
pressure. When intracranial
pressure is increased
sufficiently, regardless of the
cause, Cushing's reflex and
other autonomic
abnormalities can occur.
• Cushing's reflex includes
systolic hypertension,
increased pulse pressure,
and bradycardia.
45
46. Renal regulation of B.P.
I. Physical : by variation of Glomerular
filtration pressure variation in urine
formation
II. Hormonal : by secretion of renin
• Renin-Angiotensin (AGII)Aldosterone system (RAAS)
46
47. Renal regulation of B.P.
When blood volume and BP is increased,
KIDNEYS excrete excess fluid by
• Pressure diuresis
increased urine formation as a result of increased
glomerular filtration due to raised renal perfusion
pressure
• Pressure natriuresis
increased urinary excretion of sodium as a
result of increased glomerular filtration of
sodium due to raised renal perfusion pressure
47
48. Renal regulation of B.P.
When blood volume and BP is decreased:
decr. glomerular capillary H.P. decr.GFR
• Oliguria (deceased urine formation)
• Anuria (renal shutdown – no urine formation)
Thus KIDNEYS conserve ECF Volume
48
50. Summary :Systemic Arterial
Blood Pressure
• Varies with the amount of blood in the systemic
arterial system (begins at the aorta, ends at
arterioles in various tissues)
• This is because the systemic arteries are not
very distensible
• The greater the cardiac output, the greater the
inflow of blood into the systemic arterial system,
the higher is the BP
• The greater the TPR, the lesser the outflow of
blood out of the systemic arterial system, the
50
higher is the BP
51. Systemic Arterial Blood
Pressure
• Sympathetic nervous system and the RAA
system are powerful systems that can increase
BP
• Moment to moment control is by baroreceptor
reflex.
• What is the use of increasing the BP when blood
supply to almost all tissues are shut down by
arteriolar constriction?
• Ans. Local vasodilatory mechanisms in the vital
organs- the brain and the heart, will overcome
the systemic vasoconstrictor effect– diverting
blood flow to them at the expense of other
organs and tissues
End
51