Cardiovascular Physiology PDF - Summer 2024

CARDIOVASCULAR PHYSIOLOGY 8. Blood pressure Andre Azevedo, DVM, MSc Assistant Professor of Veterinary Physiology [email protected] ...

CARDIOVASCULAR PHYSIOLOGY 8. Blood pressure Andre Azevedo, DVM, MSc Assistant Professor of Veterinary Physiology [email protected]  I ftp.tffjff hiwgnestincenterotvesselvsnear edge Pressures in the cardiovascular system Blood pressures are not equal throughout the CVS If they were equal, blood would not flow PRESSURE DIFFERENCE IS THE DRIVING FORCE! min i cardiacoutput nowmymin.com co the votbloodflowinerwtincreasingflowlara.co reassigns i the ofbloodflowwill decreasewincreasing cross areaofblood sectional vessel  sonnow Pressures in the cardiovascular system With each beat of the heart a new surge of blood fills the arteries The amplitude of pressure pulsations in an artery is called the PULSE PRESSURE With each cardiac ejection, the great arteries become distended with blood, which causes the pressure to increase  theforcethefoodistryingtogenerate topushbloodoutofventriclesintomajor Pressures in the systemic circulation arteries stretchwallsofaorta recallaortais elastic i pressurein systolicpressure The pressure at the top of each pressure pulsation is the SYSTOLIC PRESSURE Is the highest arterial pressure measured during a cardiac cycle It is the pressure in the arteries after blood has been ejected from the left ventricle The pressure at the lowest point of each pulse is the DIASTOLIC PRESSURE Is the lowest arterial pressure measured during a cardiac cycle It is the pressure in the arteries during ventricular relaxation No blood is being ejected from the left ventricle er aorta isstretched duetoelasticity Incisura: closing of the aortic valve – brief period wants to recoiltonormal sizetheprocessin of retrograde flow whichtheaortareachesitsnormal sizeis shownas DiastolicPressure hence nobloodis beingejectedfrom the Lu Pressures in the systemic circulation The difference between these 2 pressures is the PULSE PRESSURE PRN 120 mmHg PRN80 mmHg PULSE PRESSURE = SYSTOLIC PRESSURE – DIASTOLIC PRESSURE 40mmHg Is an indicator of STROKE VOLUME because the magnitude of pulse pressure reflects the volume of blood ejected from the left ventricle on a single beat (when all factors are equal) pYf the granite COMPLIANCE = VOLUME/PRESSURE if the arterial compliance is constant, arterial pressure depends on the volume of blood the artery contains at any moment in time (systole/diastole)  5 Pressures in the systemic circulation The average pressure in a complete cardiac cycle is the MEAN ARTERIAL PRESSURE (MAP) 120340Hence the p ulse pressure MAP = DIASTOLIC PRESSURE + 1/3 PULSE PRESSURE Not a simple math average because a greater fraction of each cardiac cycle is spent in diastole than in systole From all the pressures described, MAP is the most significant! PRESSURE THAT CONTINUOUSLY DRIVES BLOOD INTO THE TISSUES OVER THE COURSE OF THE CARDIAC CYCLE MONITORED AND REGULATED BY BLOOD PRESSURE REFLEXES! Q = ΔP/R Q = Flow (mL/min) cardiac output ΔP = Pressure difference (mm Hg) R = Resistance (mm Hg/mL/min) Pressures in the systemic circulation The pressure pulses waves travel from high-compliance to high-resistance arteries rem in ELASTIC ARTERIES are high-compliance arteries Contain more elastin Important pulse-smoothing properties Ex: Aorta and carotid artery MUSCULAR ARTERIES are high-resistance arteries Contain more smooth muscle More capable to vasoconstriction and dilation Distribute blood according to tissue needs Ex: Femoral and mesenteric arteries The intensity of pulsations become progressively less in smaller arteries, arterioles and especially capillaries  n Pulsatile characteristic of large arteries PULMONARY CIRCULATION IS A LOW- PRESSURE CIRCULATION SYSTEMIC CIRCULATION IS A HIGH-PRESSURE CIRCULATION PALPATION OF THE PULSE PRESSURE IN THE FEMORAL ARTERY NORMAL PULSE PRESSURE WEAK PULSE PRESSURE STRONG PULSE PRESURE  Pressures in the systemic circulation The COMPLIANCE AND RESISTANCE of the arterial system is important in reducing the PRESSURE PULSATIONS This is called DAMPING OF THE PRESSURE PULSES Blood doesn’t need to flow immediately to peripheral vessels only during cardiac systole Blood flows mainly continuous and reach capillaries with almost no pulsation  Pressures in the systemic circulation The resistance of the systemic circulation is also called TOTAL PERIPHERAL RESISTANCE (TPR) TPR is defined as a pressure difference (aortic – vena cava) divided by a flow (total amount of blood that flows in the systemic circuit = cardiac output) Q = ΔP/R R = ΔP/Q ΔP = Q x R TPR = MEAN ARTERIAL PRESSURE (MAP) – MEAN VENOUS PRESSURE Q = Flow (mL/min ΔP = Pressure difference (mm Hg) CARDIAC OUTPUT (CO) R = Resistance (mm Hg/mL/min) Because the pressure in vena cava is usually close to zero, it is ignored Rearranging the equation: TPR = MAP / CO If the mean arterial pressure is increased, it must be because the cardiac output increased, the TPR MAP = CO X TPR increased, or both  whatarefactorsthatcanaffectResistance ofblood viscosity Pressures in the systemic circulation ofbloodvesselexincrbodyweight incrinlength length was VENOUS PRESSURES in the systemic circulation are much lower than arterial pressure By the time the blood reaches the venules and veins the pressure is very low (less than 10 mm Hg in humans) and will decrease even further in the vena cava and right atrium (close to zero). The resistance and compliance provided by the blood vessels at each level of the systemic vasculature causes the fall in pressure ofallvesselsasthat thestructure member thineffects I haIn If  Pressures in the systemic circulation Vena Cava / Right atrial pressure is considered the CENTRAL VENOUS PRESSURE (CVP) Blood from all the systemic veins flows into the right atrium The central venous pressure is regulated by: The ability of the heart to pump blood out of the right atrium and ventricle into the lungs If the right heart is pumping strongly  right atrium pressure decreases Weakness of the heart  right atrium pressure increases The tendency for blood to flow from the peripheral veins into the right atrium (VENOUS RETURN) Increase in blood volume Increase in large vessel tone throughout the body  increase peripheral venous pressure Dilation of the arterioles  decreases the TPR  allows flow from the arteries into the veins Pressures in the pulmonary circulation Pressure in the PULMONARY CIRCULATION is lower than the systemic circulation Pulmonary vascular resistance is lower Only 1/12 the resistance of the systemic circulation in a dog Pulmonary blood vessels are quite compliant, and they readily distend to accept an increase in blood flow Blood flow through the lungs are designed to match to the amount of fresh air that is being delivered to the alveoli (ventilation-perfusion matching) PVR = MEAN PULMONARY ARTERY PRESSURE – MEAN PULMONARY VENOUS PRESSURE CARDIAC OUTPUT PVR = PULMONARY VASCULAR RESISTANCE  β Regulation of mean arterial pressure MAP is regulated by: 1. BARORECEPTOR REFLEX Is a fast (seconds), neural mediated reflex that attempt to keep arterial pressure constant via changes in the output of the sympathetic and parasympathetic systems 2. RENIN-ANGIOTENSIN-ALDOSTERONE-SYSTEM Is a hormonal system that regulates MAP primarily by regulating blood volume  I short Baroreceptor reflex Is a reflex arc composed by: RECEPTORS FOR BLOOD PRESSURE Baroreceptors AFFERENT NEURONS Carry the information to the medulla oblongata BRAIN STEM CENTERS (medulla) Process the information and coordinate an appropriate response EFFERENT NEURONS Direct changes in the heart and blood vessels EFFECTOR ORGAN Heart and blood vessels  is Baroreceptor reflex BARORECEPTORS are located within the walls of the carotid sinus and the aortic arch Mechanoreceptors sensitive to pressure or stretch Relay information about blood pressure to cardiovascular vasomotor centers in the medulla oblongata Increase arterial pressure, increase stretch and firing rate in afferent nerves and vice-versa Information is carried to the medulla on the: Carotid sinus nerve (joins the glossopharyngeal nerve – CN IX) Sensory division of the Vagus nerve (CN X)  µ Baroreceptor reflex There are 3 cardiovascular centers located in the medulla: 1. VASOCONSTRICTOR CENTER Efferent neurons from this vasomotor center are part of the sympathetic nervous system and synapse in the spinal cord, then in the sympathetic ganglia, and finally on the target organ CAUSES VASOCONSTRICTION IN THE ARTERIOLES AND VENULES 2. CARDIAC ACCELERATOR CENTER incrite B2receptors Efferent neurons from this center are part of the sympathetic nervous system and synapse in the spinal cord, then in the sympathetic ganglia and finally in the heart CAUSES INCREASE FIRE RATE OF THE SA NODE (INCREASE HR); INCREASE CONDUCTION VELOCITY THROUGH THE AV NODE AND INCREASE CONTRACTILITY 3. CARDIAC DECELERATOR CENTER M2 M3 Efferent neurons from this center are part of the parasympathetic nervous system, travel in the motor division of the vagus nerve and synapse in the SA NODE CAUSES DECREASE IN HEART RATE  n Baroreceptor reflex baro this detecting receptors change The strongest stimulus for the baroreceptors is a rapid change in MAP 1. An increase in MAP is detected by the baroreceptors and increase firing rate of afferent nerves 2. The afferent nerves synapse at the medulla, where they transmit information. The coordinated responses comes from the medullary cardiovascular centers 3. Increase in parasympathetic activity to the SA node decrease HR 4. The decrease in sympathetic activity to SA node complements the decrease in HR and also decreases cardiac contractility Together this actions lead to a decrease in CO 5. The decrease in sympathetic activity also dilate arterioles (α receptor) and decrease TPR Barg 6. All these actions lead to the decrease in MAP resistance peripheral MAP = CO X TPR  18 Baroreceptor reflex RESPONSE OF BARORECEPTOR REFLEX TO PRESSURE DROP (i.e. HEMORRAGE) MAP = CO X TPR  so Baroreceptor reflex RECEPTOR ACCOMODATION The sensitivity of baroreceptors can be altered by disease The receptor becomes less sensitive to a sustained stimulus over time If blood pressure rises slowly or remains stable at an abnormally high level, the receptors gradually adjust their response to accept the new pressure as normal I.e. in chronic hypertension, hypertension will be maintained, rather than corrected by the baroreceptor reflex! Renin-angiotensin-aldosterone system The RAAS regulates MAP primarily by regulating blood volume Much slower than Baroreceptor reflex because is hormonally, rather than neurally mediated Activated in response to a decrease in MAP flowofbloodtorest decrease ofbody affect severely bioneedalotoblood kidneys f Produces a series of responses that attempt to restore arterial pressure to normal  wallhasbaroreceptors arterial afferent here Renin-angiotensin-aldosterone system STEP 1: A decrease in MAP causes a decrease in renal perfusion pressure, which is sensed by mechanoreceptors in the kidney Baroreceptors are present in the walls of the afferent arterioles of the kidney They detect changes in blood pressure The message is sent to the juxtaglomerular cells (granular cells) of made smooth muscle NEPHRON = THE FUNCTIONAL UNIT OF THE KIDNEY  un undergo Renin-angiotensin-aldosterone system reninany iffy liver in STEP 2: Juxtaglomerular cells secrete RENIN made y STEP 3: This enzyme catalyzes the conversion of ANGIOTENSINOGEN to ANGIOTENSIN I Decrease in blood pressure (hypotension) stimulates the release of renin Renin secretion is also increased by sympathetic activation and decrease in sodium levels STEP 4: In the lungs and kidneys ANGIOTENSIN I is converted to ANGIOTENSIN II Reaction catalyzed by an ANGIOTENSIN-CONVERTING ENZYME (ACE) STIMULI FOR RENIN SECRETION Decrease in filtrate sodium concentration (detected by cells of macula densa) Reduced perfusion pressure in the kidney (detected by baroreceptors area main in the afferent arteriole) Sympathetic stimulation of the juxtaglomerular apparatus via β1 adrenoreceptors  Renin-angiotensin-aldosterone system STEP 5: ANGIOTENSIN II is a peptide with biologic actions in several places ADRENAL CORTEX VASCULAR SMOOTH MUSCLE KIDNEYS BRAIN HEART Ang II BINDS TO AT1 RECEPTOR TO PROMOTE THESE EFFECTS  Goodman's Basic Medical Endocrinology (Fifth Edition)  angiotensin callsfor backup Renin-angiotensin-aldosterone system STEP 6: ANGIOTENSIN II acts on the ZONA GLOMERULOSA CELLS of the adrenal cortex STIMULATES THE PRODUCTION AND SECRETION OF ALDOSTERONE remembermineralcorticoide The major mineralocorticoid Requires gene transcription and new protein synthesis Takes hours to days to occur Act on the principal cells of the renal distal tubule and collecting duct http://liu.diva-portal.org/smash/record.jsf?pid=diva2%3A1376727&dswid=-8938 Increases sodium, chloride and water absorption and the excretion of potassium Increases blood volume c  we Renin-angiotensin-aldosterone system ANGIOTENSIN II also has its own direct effect on the KIDNEY STIMULATES SODIUM AND HYDROGEN ION EXCHANGE IN THE RENAL PROXIMAL TUBULE INCREASES REABSORPTION OF SODIUM AND BICARBONATE  n Renin-angiotensin-aldosterone system ANGIOTENSIN II also acts directly on the ARTERIOLES by binding to AT1R Activates IP3/Calcium second messenger system to cause VASOCONSTRICTION Increase total peripheral resistance and increase MAP PLC = PHOSPHOLIPASE C PIP2 = PHOSPHATIDYLINOSITOL 4,5-BIPHOSPHATE RECALL MLCK = MYOSIN LIGHT CHAIN KINASE SMOOTH MLC = MYOSIN LIGHT CHAIN (PHOSPHATASE) VSMC = VASCULAR SMOOTH MUSCLE CELLS MUSCLE CONTRACTION LECTURES  is Renin-angiotensin-aldosterone system ANGIOTENSIN II acts on HYPOTHALAMUS to increase thirst and water intake HYPOTHALAMUS IS THE BODY’S “THRIST CENTER” Has OSMORECEPTORS that sense changes in ECF OSMOLALITY (ammount of solutes in the blood/osmotic pressure) Both cerebral and peripheral osmoreceptors contribute to water balance Decrease in blood volume or increase [Na] stimulates water ingestion RECALL OSMOTIC PRESSURE: Pressure of solutes in water trying to equalize their concentrations across a semipermeable membrane  a recallposterior onlysecretesoxytocin ADH pituitary toreceptoroncollecting thin Renin-angiotensin-aldosterone system ANGIOTENSIN II also stimulates secretion of ANTIDIURETIC HORMONE (ADH or VASOPRESSIN or ARGININE VASOPRESSINE or AVP) ADH is produced by NEURO-HYPOPHYSIS and increases water reabsorption in the kidney ADH also causes VASOCONSTRICTION By increasing total body water and causing vasoconstriction, these effects complement aldosterone effects Increase ECF volume, blood volume and blood pressure  a Renin-angiotensin-aldosterone system ANGIOTENSIN II increases contractility Also causes vascular and cardiac hypertrophy and myocardial fibrosis (remodeling)  33 DECREASE IN INCREASE IN BLOOD BLOOD PRESSURE PRESSURE ACTIVATE RAAS AND STIMULATES Na AND H2O MAP = CO X TPR REABSORPTION; WATER (BOTH INCREASE) INTAKE AND VASOCONSTRICTION INCREASE ECF INCREASE IN FRANK-STARLIN AND BLOOD VENOUS LAW = INCREASE IN VOLUME RETURN CARDIAC OUTPUT (PRELOAD)  34 Ienn Yghn n'totbloodvolume pressure Other mechanisms regulating MAP 1. ANTIDIURETIC HORMONE from released pit posterior 2. ATRIAL NATRIURETIC PEPTIDE 3. CHEMORECEPTORS FOR O2 4. CHEMORECEPTORS FOR CO2  rememberbaro receptor isa Mechanoreceptor atrialreceptor onaorta carotidsinu Other mechanisms regulating MAP CARDIOPULMONARY LOW PRESSURE BARORECEPTORS are located in the VEINS, ATRIA and pulmonary arteries They are called CARDIOPULMONARY VOLUME RECEPTORS Sense changes in blood volume (the fullness of vascular system) Are located in the VENOUS SIDE of the circulation Because is where most of the blood volume is held  has ANP effects opposite wehave too much cirsodecreasehaveinhibition bloodinvenous onRAAS Other mechanisms regulating MAP When blood volume increases, the resulting increase in CVP is detected The cardiopulmonary volume receptors coordinate to return volume to normal Primarily by increasing excretion of sodium and water The response to an increase in blood volume includes several actions: 1. INCREASED SECRETION OF ATRIAL NATRIURETIC PEPTIDE (ANP) 2. DECREASED SECRETION OF ADH 3. RENAL VASODILATION 4. INCREASED HEART RATE  38 Other mechanisms regulating MAP PERIPHERAL RECEPTORS for O2 are located in the carotid and aortic bodies Carotid and aortic bodies have high blood flow Their CHEMORECEPTORS are sensitive to: thisfrompreviouslecture recall Highly sensitive to decrease in partial pressure of O2 (PO2) Increase in partial pressure of CO2 (PCO2) Decrease in PH (increase in hydrogen ion concentration) acidity is related with H+ concentration THEY ARE PRIMARILY INVOLVED WITH CONTROL OF BREATHING Activate respiratory centers in the Brainstem Increase or decrease pulmonary ventilation  m DECREASE INCREASE IN LUNG ARTERIAL PO2 VENTILATION INCREASE IN FIRING RATE OF DECREASE CO2 AFFERENT NERVES FROM THE CAROTID AND AORTIC BODIES INCREASE O2 INCREASE SYMPATHETIC DECREASE PARASYMPATHETIC OUTFLOW TONE TO THE HEART ACTIVATION OF SYMPATHETIC VASOCONSTRICTOR CENTER INCREASE HEART RATE CO = SV X HR ARTERIOLAR VASOCONSTRICTION IN SKELETAL MUSCLE, RENAL AND INCREASE BLOOD INCREASE CARDIAC SPLANCHNIC VASCULAR BEDS PRESSURE OUTPUT MAP = CO X TPR  40 Other mechanisms regulating MAP CENTRAL CHEMORECEPTORS are also located in the brainstem The brain is intolerant to decreases in blood flow Highly sensitive to increase in partial pressure of CO2 (PCO2) Decrease in partial pressure of O2 (PO2) Decrease in pH (increase in hydrogen ion)  41 INCREASE INCREASE IN LUNG PCO2 VENTILATION INCREASE SYMPATHETIC OUTFLOW ACTIVATION OF SYMPATHETIC VASOCONSTRICTOR CENTER BLOOD FLOW INCREASED TO THE BRAIN ARTERIOLAR VASOCONSTRICTION IN MANY VASCULAR BEDS WITH INCREASE BLOOD INCREASE IN TPR MAP = CO X TPR PRESSURE