SEMINAR ON BLOOD PRESSURE REGULATION, Determinants of Arterial BP
Functions Of Blood Pressure
Physiological Variations In Bp
Blood Pressure Regulation
Applied Physiology
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REGULATION OF BLOOD PRESSURE
Content Introduction Determinants of Arterial BP Functions Of Blood Pressure Physiological Variations In Bp Blood Pressure Regulation Applied Physiology Conclusion
Arterial blood pressure is defined as the lateral pressure exerted by the column of blood on the wall of arteries. Arterial blood pressure is expressed in four different terms: 1. Systolic blood pressure 2. Diastolic blood pressure 3. Pulse pressure 4. Mean arterial blood pressure.
Systolic blood pressure : measures the pressure in blood vessels when heart beats. Diastolic pressure : measures the pressure in blood vessel when heart rests between beats. Normal value --- 120/80 mm Hg At risk ( pre hypertension) --- 120-139 / 80-89 mm Hg High – higher than 140 /90 mm Hg
Determinants of Arterial BP Central Factors Cardiac output: systolic pressure is directly proportional to cardiac output. Hear t Rate : marked alteration in heart rate effects BP by altering the cardiac output. Peripheral factors: Peripheral Resistance : Diastolic pressure is directly proportional to peripheral resistance
Blood Volume: BP is directly proportional to blood volume. Venous Return: blood pressure is directly proportional to venous return. Elasticity of blood vessels: BP is inversely proportional to the elasticity of blood vessels. Velocity of Blood Flow: BP is directly proportional to the velocity of blood flow. Diameter of Blood Vessels: BP is inversely proportional to the diameter of blood vessel. Viscosity of Blood: BP is directly proportional to the viscosity of blood.
FUNCTIONS OF BLOOD PRESSURE Intra-ventricular BP for ejection of blood (stroke volume). Systemic arterial BP for blood flow to tissues (tissue perfusion) Capillary hydrostatic BP for filtration (tissue fluid formation). Systemic venous BP for blood flow back to heart (venous return) Systemic arterial blood pressure = cardiac output * total peripheral resistance
PHYSIOLOGICAL VARIATIONS IN BP AGE SBP AND DBP gradually rise with age (>30) SEX Rise in BP is more in males with age CIRCADIAN VARIATON ( DIURAL VARIATION) Lowest during sleep and highest in the mornings after waking up. Increased transient during physical stress, mental stress, emotion excitement. EFFECT OF GRAVITY When erect BP in any vessel varies in relation to the vertical distance from the heart level.
BLOOD PRESSURE REGULATION SHORT TERM REGULATION BARORECEPTOR MECHANISM / SINOAORTIC MECH CHEMORECEPTOR MECHANISM VASOMOTOR CENTER MECHANISM INTERMEDIATE TERM REGULATION STRESS RELAXATION FLUID SHIFT MECHANISM RENIN ANGIOTENSIN MECHANISM LONG TERM REGULATION RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM
NERVOUS MECHANISM SHORT-TERM REGULATION The nervous regulation is rapid among all the mechanisms involved in the regulation of arterial blood pressure nervous system brings the pressure back to normal within few minutes quick in action, but it operates only for a short period and then it adapts to the new pressure.
SHORT TERM REGULATION Works for few seconds Baroreceptor mechanism Baroreceptors are stretch receptors located in the walls of heart and blood vessels. Whenever BP increases, BR present in carotid sinus (bifurcation of carotid artery) and arch of aorta are stimulated. Inhibits the Vasomotor Center (VMC) and stimulates Vagal nucleus. IX and X cranial nerves, called Buffer Nerves.
Posture and Baroreceptors Change of posture lying down to sitting / standing reduces arterial blood pressure and blood flow to the upper parts of the body. Discharge of impulse decreases from baroreceptors triggering spontaneous discharge from VMC. This restores blood pressure by an increases in heart rate and peripheral resistance.
Chemoreceptor Mechanism Decrease in BP reduces blood flow to chemoreceptors present in the carotid body and arch of aorta. Reduced oxygen supply stimulates the chemoreceptor. Stimulate VMC increasing the heart rate and peripheral resistance by vaso constriction Increase of blood pressure.
Vasomotor Center Mechanism Reduced blood flow to VMC causes its ischemia. Stimulate VMC causing increase in heart rate and peripheral resistance. Net effect, changes the increase in BP
INTERMEDIATE TERM REGULATION Few minutes to few hours. Stress relaxation Increased BP exerts greater force on the walls of blood vessels. Stretch of blood vessel causes initial contraction of smooth muscle in its walls followed by relaxation. Relaxation of the vessel wall brings down BP.
Fluid shift mechanism Increased BP increases hydrostatic pressure This pushes fluid out of blood vessel into interstitial space Loss of fluid from blood vessel reduces blood volume Reduced venous return and hence decrease in BP
Renin Angiotensin Mechanism Reduced BP decreases blood flow to kidney. Causes juxta glomerular apparatus of kidney to produce Renin. Renin acts on plasma substrate, angiotensinogen, to form angiotensin I
Angiotensin I converted to angiotensin II by angiotensin converting enzyme (ACE) present in lungs. ACE inhibitors prevent conversion of angiotensin I to angiotensin II angiotensin II causes peripheral vaso constriction and increases peripheral resistance. Restore the blood pressure
LONG TERM REGULATION Renin-Angiotensin- Aldosterone Mechanism Angiotensin II produced during intermediate term regulation stimulates adrenal cortex to produce aldosterone as a delayed effect. Aldosterone increases sodium reabsorption Water retained along with sodium Helps to increase fluid volume
Increased fluid volume increase venous return to heart and blood pressure increases Stimulate hypothalamus and posterior pituitary to release anti diuretic hormone (ADH) ADH helps in water retention Mechanism activates thirst, enhancing fluid intake. Retention of salt and water increases systemic arterial pressure
In turn will increase hydro static pressure facilitating formation of larger volume of filtrate Increased salt and water promoting formation of a larger volume of filtrate rich in salt is termed PRESSURE NATRIURESIS AND DIURESIS.
PULMONARY HYPERTENSION Type of blood pressure affecting arteries in lungs and right side of heart. Arteries and capillaries become narrowed, blocked or destroyed. Thus harder for blood to flow through lungs, raises pressure within lung arteries. Lower chamber of heart has to work harder, causing heart muscle to weaken and fails.
Pul . Arterial circulation is high flow and low pressure sys with lower blood pressure than systemic BP. Doesn’t exceed 30/15mmHg even in exercise. Normal value btw 3-8mmHg in pulmonary vein.
Pulmonary hypertension is defined as a systolic BP in the pulmonary arterial circulation above 30mmHg. Types Pulmonary Idiopathic Secondary
Idiopathic Pul . Hypertension Uncommon condition of unknown cause. Young females between 20-40years, children around 5 years. Etiology Neurohumoral vasoconstrictor mechanism Unrecognized thromboemboli / amniotic fluid emboli Collagen vascular disease Ingestion of substance like bush tea, oral contraceptive, appetite depressant agents like amniorex Familial occurrence
Secondary pulmonary Hypertension Occurs secondary to recognized lesion in heart or lungs. Any age it can occur, more in above 50 years. Etiopathogensis Passive: 1) mitral stenosis 2) chronic left ventricular failure Hyperkinetic pulmonary hypertension
The lethal effects of hypertension are caused mainly in three ways: 1 . Excess workload on the heart leads to early heart failure and coronary heart disease, often causing death as a result of a heart attack. 2. The high pressure frequently damages a major blood vessel in the brain, followed by death of major portions of the brain; this is a cerebral infarct. Clinically it is called a “stroke.” Depending on which part of the brain is involved, a stroke can cause paralysis, dementia, blindness, or multiple other serious brain disorders. 3. High pressure almost always causes injury in the kidneys, producing many areas of renal destruction and, eventually, kidney failure, uremia, and death.
HYPERTENSION It is the persistent high blood pressure. Clinically when systolic pressure remains elevated above 150mmHg, and diastolic pressure remains elevated above 90mmHg, it is considered as hypertension. Types Primary hypertension Benign hypertension Malignant hypertension
Primary (Essential) Hypertension Elevated blood pressure in the absence of any underlying diseases. It is increases because of increased peripheral resistance, which occurs due to some unknown cause. About 90 to 95 per cent of all people who have hypertension are said to have “primary hypertension,” also widely known as “essential hypertension” In most patients, excess weight gain and sedentary lifestyle appear to play a major role in causing hypertension.
Benign hypertension historical terms that are considered misleading, as hypertension is never benign, and consequently they have fallen out of use The terminology persisted in the International Classification of Disease (ICD9), but is not included in the current ICD10
Malignant Hypertension Extremely high blood pressure that develops rapidly Typically above 180/120 mmHg Treated as a medical emergency Cause high blood pressure is the main cause of malignant hypertension. Missing doses of blood pressure medications can also cause it. Collagen vascular disease, such as scleroderma
Kidney disease Spinal cord injuries Tumor of the adrenal gland Use of certain medications, including birth control pills and MAOIs Use of illegal drugs, such as cocaine
Rare case About 1% of people who have a history of high blood pressure develop this life-threatening condition. Symptoms Damage happens to the kidneys or the eyes Blurred vision Chest pain (angina) Difficulty breathing Dizziness Numbness in the arms, legs, and face Severe headache Shortness of breath
Malignant hypertension can cause brain swelling, which leads to a dangerous condition called hypertensive encephalopathy. Symptoms include: Blindness Changes in mental status Coma Confusion Drowsiness Headache that continues to get worse Nausea and vomiting Seizures
Diagnosis A diagnosis of malignant hypertension is based on blood pressure readings and signs of acute organ damage. Recheck blood pressure and listen to heart and lungs for abnormal sounds Examine eyes to check for damage to the blood vessels of the retina and swelling of the optic nerve
Blood And Urine Tests that may include: Blood urea nitrogen (BUN) and creatinine levels, which increase in kidney damage Blood clotting tests Blood sugar (glucose) level Complete blood count Sodium and potassium levels Urinalysis to check for blood, protein, or abnormal hormone levels related to kidney problems
Echocardiogram to check heart function and blood flow through the heart Electrocardiogram (ECG) to check the heart’s electrical function Chest X-ray to look at the shape and size of the heart structures and to detect fluid in the lungs
Treatment Malignant hypertension is a medical emergency, treated in a hospital, often in an intensive care unit. The goal of treatment is to carefully lower blood pressure within a matter of minutes. Blood pressure medicines through an IV, Once blood pressure is at a safe level, the medications may be switched to oral forms. If pat develops kidney failure, need to do kidney dialysis.
Complications Untreated, malignant hypertension causes death. Aortic dissection, which is a sudden rupture of the main blood vessel leaving the heart Coma Fluid in the lungs, called pulmonary edema Heart attack Heart failure Stroke Sudden kidney failure
Reno Vascular Hypertension condition in which high blood pressure is caused by the kidneys' hormonal response to narrowing of the arteries supplying the kidneys. When functioning properly this hormonal axis regulates blood pressure. Due to low local blood flow, the kidneys mistakenly increase blood pressure of the entire circulatory system. It is a form of secondary hypertension - a form of hypertension whose cause is identifiable.
Signs and symptoms High blood pressure (early age) Kidney dysfunction Narrowing of arteries elsewhere in the body Pulmonary edema
Cause Any narrowing/blockage of blood supply to the renal organ (renal artery stenosis). As a consequence of this action the renal organs release hormones that indicate to the body to maintain a higher amount of sodium and water, which in turn causes blood pressure to rise. Factors that may contribute are: Diabetes High cholesterol Advanced age Unilateral condition is sufficient to cause renovascular hypertension.
Diagnosis Blood test (for renal function) Urinary test (tests for microalbuminuria) Serology (to exclude systemic lupus erythematosus ) Lipid profile Urinalysis (to exclude presence of red blood cells)
Treatment Surgical revascularization versus medical therapy for atherosclerosis, it is not clear if one option is better than the other according to a 2014 cochrane review; balloon angioplasty did show a small improvement in blood pressure. Surgery can include Percutaneous surgical revascularization
Nephrectomy or autotransplantation Individual may be given beta-adrenergic blockers. Early therapeutic intervention is important if ischemic nephropathy is to be prevented. Inpatient care is necessary for the management of hypertensive urgencies, quick intervention is required to prevent further damage to the kidneys.
Pregnancy hypertension Few women of childbearing age have high blood pressure, up to 11% develop hypertension of pregnancy. While generally benign, it may herald three complications of pregnancy: Pre- Eclampsia a disorder of pregnancy characterized by the onset of high blood pressure and often a significant amount of protein in the urine
HELLP syndrome complication of pregnancy characterized by h emolysis, e levated l iver enzymes, and a l ow p latelet count. Eclampsia onset of seizures (convulsions) in a woman with pre- Eclampsia Follow-up and control with medication is therefore often necessary.
Chronic Hypertension (High blood pressure) is caused by impaired renal fluid excretion Diastolic blood pressure is greater than about 90 mm hg and the systolic pressure is greater than about 135 mm hg. In severe hypertension, the mean arterial pressure can rise to 150 to 170 mm Hg, with diastolic pressure as high as 130 mm Hg and systolic pressure occasionally as high as 250 mm Hg. At severely high pressures—mean arterial pressures 50 per cent or more above normal—a person can expect to live no more than a few more years unless appropriately treated.
Neurogenic hypertension Excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction resulting from chronic high activity of the sympathoadrenal system, the sympathetic nervous system and the adrenal gland. The specific mechanism involved is increased release of the "stress hormones", epinephrine (adrenaline) and norepinephrine which increase blood output from heart and constrict arteries
Isolated systolic hypertension Diastolic number less than 80mmHg and systolic higher or equal to 130 mm Hg is called as ISP Caused by underlying conditions like artery stiffness an overactive thyroid (hyperthyroidism) Diabetes
Isolated systolic hypertension can lead to serious health problems, such as: Stroke Heart disease Chronic kidney disease
HYPOTENSION SYSTOLIC PRESSURE LESS THEN THAT OF 90mm Hg BP below 100/60mmHg in females and less than 110/70mmHg in men. Ortho static hypotension, blood rushes into the lower parts of the body when sitting down or standing up fast.
Causes Diseases Severe hemorrhage Heart diseases Addison’s diseases Drug Anti hypertensive drug Diuretics Vasodilators
Treatment If cerebral, renal and cardiac perfusion is maintained, hypotension itself doesn’t need any vigorous direct treatment. Sympathomimetic agents used in in emergency Nor epinephrine Phenylephrine
Conclusion Blood pressure in the body is regulated through different mechanism which helps the body to maintain normal physiological functions. Mild to severe variation in it, can alter normal physiological function and even damage of organs which can even lead to death. Thus it is important to have regular checkups to maintain the normal blood pressure .
Reference Essentials of physiology for dental students by K Sembulingam Januszewicz A,et al, Malignant hypertension: new aspect of an old clinical entity, Pol Arch Med Wewn.2016;126(1-2):86-93.