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Arterial blood pressure
Blood pressure is the force exerted by blood against a vessel wall. It maintains blood flow through capillaries. It depends on blood volume & compliance (destinsibility) of blood vessels. Arterial BP is not constant, it rises during ventricular systole (contraction) & falls during ventricular diastole (relaxation).
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Systolic BP Is the peak (highest) BP measured during ventricular systole = 120 mmHg, in a young Person at rest. Diastolic BP Is the minimum B.P. at the end of ventricular diastole = 80 mmHg, in a young person at rest. Pulse pressure Is the difference between systolic and diastolic BP
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Mean BP Calculated by adding one-third of the pulse pressure to the diastolic BP. If BP = 120/90 mmHg. The mean BP = – 90 3 = = 100 mmHg. Mean arterial BP = C.O. x total peripheral resistance. C.O. determines systolic BP. Total peripheral resistance determines diastolic BP.
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Blood Pressure Must Be Regulated
Low Blood Pressure Blood will not reach all Tissues specifically those Where gravity is acting against flow. Most importantly the brain. High Blood Pressure Heart is placed under great stress Excess plasma leakage At the extreme, capillaries burst
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Physiological variations in BP
Age Sex Body mass index Meals Exercise Posture Anxiety ↓ Slightly during inspiration and ↑ Slightly during expiration
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Determinants of arterial BP
Total peripheral resistance (TPR) Cardiac output (CO) Blood viscosity. Blood volume. Arterial BP = CO X TPR
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Factors affecting diameter of arterioles (resistance)
Vasodilator agents: Adenosine Atrial natriuretic peptide (ANP) - ↑ potassium or Hydrogen ions. - ↓ Oxygen or ↑ CO2 Histamine Nitric oxide and lactic acid Prostacyclin Vasoconstrictor agents: Noradrenaline Sympathomimetic drugs. Vasopressin (ADH) Angiotensin II Endothelin-1
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Blood viscosity: Hematocrit
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Effect of hematocrit on blood viscosity
Effect of hematocrit on blood viscosity. Above-normal hematocrits produce a sharp increase in viscosity. Because increased viscosity raises vascular resistance, hemoglobin and oxygen delivery may fall when the hematocrit rises above the normal range.
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Blood Viscosity ↓ Plasma protein → ↓ blood viscosity Hypoalbumenimia: Burns. Malnutrition
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REGULATION OF ARTERIAL BLOOD PRESSURE
Regulation of Blood Pressure Nervous Mechanism Renal Mechanism Hormonal Mechanism Local Mechanism By Vasomotor Center and Impulses from Periphery By Regulation of ECF Volume and renin – angiotensin mechanism By Vasocons- -trictor and Vasodilator Hormones By Local Vasocons- -trictors and Vasodilators
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Effect of Blood Volume Changes in blood volume affect arterial pressure by changing cardiac output: An increase in blood volume increases end–diastolic volume → ↑ ventricular preload → ↑ ventricular stroke volume by the Frank-Starling mechanism. ↑ Stroke volume → ↑ cardiac output and ↑ arterial blood pressure.
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Hemodynamics Is the branch of physiology concerned with The physical principles governing: Pressure, Flow, Resistance, Volume, and Compliance as they relate to the CVS. Resistance to blood flow results from the inner friction & viscosity of blood.
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Pressure flow and resistance are related by: (Ohm’s Law), Q = ΔP/R
Pressure flow and resistance are related by: (Ohm’s Law), Q = ΔP/R . Q = blood flow. ΔP = the pressure difference between the two ends of the vessel. R = Resistance. Resistance depends on the radius & length of the blood vessel & the viscosity of blood (Poiseuilleʾs law).
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Q ~ ᷊4 R ~ 1 / ᷊4 Q = ΔP / R . R = V x L / ᷊4 Q = ΔP x ᷊4 / V x L .
Length does not change, and viscosity rarely changes enough to have a significant effect on resistance. There for small changes in arteriolar radius can cause large changes in blood flow. Q ~ ᷊4 R ~ 1 / ᷊4
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The influence of tube length and radius on flow
The influence of tube length and radius on flow. Because flow is determined by the fourth power of the radius, small changes in radius have a much greater effect than small changes in length. Furthermore, changes in blood vessel length do not occur over short periods of time and are not involved in the physiological control of blood flow. The pressure difference (P) driving flow is the result of the height of the column of fluid above the openings of tubes A and B.
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Flow rate as a function of resistance
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Arterioles & small arteries are
called (resistance vessels). They determine the mean arterial blood pressure.
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Types of blood flow Laminar (Streamline) flow : Smooth flow at a steady rate. The central portion of blood stays in the center of the vessel → Less friction. Turbulent flow : High flow rate in all directions (Mixing) → increase resistance & slow flow rate. In restricted blood flow or valvular lesions bruits or murmurs can be heard.
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Streamline and turbulent blood flow
Streamline and turbulent blood flow. Blood flow is streamlined until a critical flow velocity is reached. When flow is streamlined, concentric layers of fluid slip past each other with the slowest layers at the interface between blood and vessel wall. The fastest layers are in the center of the blood vessel. When the critical velocity is reached, turbulent flow results. In the presence of turbulent flow, flow does not increase as much for a given rise in pressure because energy is lost in the turbulence.
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Axial streamline and flow velocity
Axial streamline and flow velocity. The distribution of red blood cells in blood vessel depends on flow velocity. As flow velocity increases, red blood cells move toward the center of the blood vessel (axial streaming), where velocity is highest. Axial streaming of red blood cells lowers the apparent viscosity of blood
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Measurement of B.P.
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Systolic pressure can also be estimated by palpating the radial artery and noting the cuff pressure at which the first pulsation is felt.
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Hypertension in adults is a BP greater than 140/90
Hypertension in adults is a BP greater than 140/90. BP at or below 120/80 is normal. Values between 121/81 and 139/89 indicate a state of pre-hypertension. Hypertension increases the work load of the heart → enlargement of the left ventricle → ↑ muscle mass → ↑ oxygen demand. Insufficient coronary circulation → symptoms of ischemic heart disease.
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Dangers of hypertension
Silent killer: Patients are asymptomatic until substantial vascular damage occurs. Atherosclerosis increases afterload. Increase workload of the heart. Congestive heart failure. Damage cerebral blood vessels. Cerebral vascular accident (stroke) Chronic renal failure.
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Elastic rebound During systole the arterial walls expand to accommodate the extra amount of blood pumped by the ventricles. During diastole the BP falls, the arteries recoil to their original dimensions (Elastic rebound) → maintains blood flow in the arteries when the ventricle is in diastole.
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If the blood pressure drops suddenly
Two problems confronts the pressure control system: The first is survival, to return the arterial pressure immediately to near a normal level that the person can live trough the acute episode.
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The second is to return the blood volume eventually to its normal level
So that the circulatory system can re-establish full normality, Including return of the arterial pressure back to its normal value
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Three mechanisms in regulating the blood pressure
React rapidly, within seconds or minutes; Respond over an intermediate time period, minutes or hours Provide long-term pressure regulation, days, months, and years.
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Effects of Rapidly Acting Pressure Control Mechanisms
To cause constriction of the veins and provide transfer of blood into the heart. To cause increased heart rate and contractility of the heart and provide greater pumping capacity by the heart To cause constriction of the peripheral arterioles to impede the flow of the blood out of the arteries. All these effects occur almost instantly to raise the arterial pressure back into a survival range.
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Rapidly Acting Pressure Control Mechanisms
1- The baroreceptors: Stretch receptors in large systemic arteries (particularly the carotid artery and aorta). 2- Carotid and aortic chemoreceptors: Monitor changes of oxygen, carbon dioxide, and hydrogen ions. 3- CNS ischemic responses.
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Sudden increase in BP → ↑ activity of the baroreceptors which produces:
1- ↓ H.R. & ↓ C.O. due to ↓ sympathetic & ↑parasympathetic activity. 2- Widespread peripheral vasodilatation due to inhibition of the vasomotor center. Sudden decrease in BP → ↓ activity of the baroreceptors which produces: 1- ↑ H.R. & ↑ C.O. due to ↑ sympathetic & ↓ parasympathetic 2- Widespread peripheral vasoconstriction due to stimulation of the vasomotor center.
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Importance of the baroreceptor reflex
To keep the arterial pressure relatively constant in the rang of 70 mmHg to 150 mmHg, maintain the mean blood pressure at about 100 mmHg Pressure buffer system – reduce the blood fluctuation during the daily events, such as changing of the posture, respiration, excitement etc.
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Baroreceptor Resetting
Baroreceptor will adapt to the long term change of blood pressure. If the blood pressure is elevated for a long period of time, several days or years, the set point will transfer to the elevated mean blood pressure. That makes the baroreceptor system unimportant for long-term regulation of arterial pressure
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Denervation of the baroreceptors can lead to paroxysmal hypertension.
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Stimulation of chemoreceptors leads to a reflex increase in vasomotor tone,
which causes generalized vasoconstriction and hence a rise in blood pressure. Chemoreceptor mechanism is important in regulation of blood pressure when it fall below the range in which baroreceptors act (70 mmHg).
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CNS ischemic response Chemoreceptor reflex is useful in regulation of blood pressure when it falls to a level between 40 and 70 mmHg. But if the blood pressure below 40 mmHg, the last ray of hope for survival is the central nervous system (CNS) ischemia response. So it sometimes called the “last ditch stand” pressure control mechanism.
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Pressure Control Mechanisms That Act After Many Minutes (Intermediate-control mechanism)
The renin-angiotensin vasoconstrictor mechanism Stress-relaxation of the vasculature Shift of fluid through the tissue capillary wall in and out of the circulation to adjust the blood volume as needed.
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REGULATION OF BLOOD PRESSURE BY RENIN-ANGIOTENSIN MECHANISM
Decrease in Blood Pressure Normal Blood Pressure Stimulation Juxtaglomerular apparatus Renin Angiotensinogen Angiotensin I Converting enzyme Angiotensin II Vasoconstriction
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Stress-relaxation of the vasculature
When the pressure in the blood vessels becomes too high, they become stretched and keep on stretching more and more for minutes or hours. As a result, the pressure in the vessels falls toward normal. This continuing stretch of the vessels, called stress-relaxation, can serve as an intermediate-term pressure control.
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Shift of fluid through the tissue capillary wall in and out of the circulation
Any time the capillary pressure falls too low,. Fluid is absorbed by capillary osmosis from the tissue into the circulation. Thus increasing the blood volume and the pressure in the circulation.
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Long-term Regulation of Arterial Pressure by the Kidneys
The kidneys control the level of H2O and NaCl in the body, thus controlling the volume of the extracellular fluid and blood by: 1- Renal fluid shift through Antidiuretic hormone (ADH) 2- Renin- angiotensin- aldosterone mechanism. Importance It takes a few hours to show significant response for these mechanisms. Return the arterial pressure back to normal.
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Renin-Angiotensin-Aldosterone System
NaCl / Extracellular fluid volume / Arterial blood pressure Helps correct + H2O conserved Na+ (and Cl¯) osmotically hold more H2O in ECF + + Angiotensin-converting enzyme Renin Na+ (and Cl¯) conserved Angiotensinogen Angiotensin I Angiotensin II Aldosterone Na+ reabsorption by renal tubules ( Cl¯ reabsorption follows passively) Circulation + + + ADH Thirst Arteriolar vasoconstriction H2O reabsorption by kidney tubules Fluid intake Renin-Angiotensin-Aldosterone System
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Renal Urinary Output Curve
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Atrial baroreceptors (low pressure receptors)
Respond to stretch of the wall of the right atrium. ↑ atrial pressure → stimulate CV center → ↑ H.R.& ↑ C.O (Bainbridge reflex) → prevent damming of blood in veins, atria & pulmonary Circulation. Atrial stretch also → dilate afferent arterioles → ↑ GFR → ↓ ADH & ↑ ANP hormone secretion → ↑ urine output. → ↓ B.P.
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Hormonal regulation of CVS
The endocrine system provides both short-term and long term regulation of CVS. Epinephrine, and Norepinephrine, stimulate C.O. and vasoconstriction. Other hormones for long-term regulation of arterial BP include: 1- Antidiuretic hormone (ADH). 2- Angiotensin II- Aldosterone system 3- Erythropoietin. 4- Atrial natriuretic peptides (ANP).
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High BP Leads to: Low BP Leads to:
1- ↓ Antidiuretic hormone (ADH) secretion. 2- ↓ Angiotensin II hormone secretion 3- ↓ Aldosterone hormone secretion 4- ↓ Erythropoietin hormone secretion. 5- ↑ Atrial natriuretic peptides (ANP) hormone secretion. Low BP Leads to: 1- ↑ Antidiuretic hormone (ADH) secretion. 2- ↑ Aldosterone hormone secretion 3- ↑ Angiotensin II hormone secretion . 4- ↓ Natriuretic peptides (ANP) hormone secretion 5- ↑ Erythropoietin hormone secretion → ↑ RBCS, take few days.
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