B p control mechanism

mauryaramgopal 1,286 views 18 slides Oct 31, 2018
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About This Presentation

blood pressure regulation


Slide Content

MECHANISMS TO CONTROL BLOOD PRESSURE PRESENTER :- DR RAVE RANJAN KUMAR MODERATOR :- DR ZIA ARSHAD

ARTERIAL BLOOD PRESSURE MAP is proportionate to the product of SVR × CO. This relationship is based on an analogy to Ohm’s law, as applied to the circulation: MAP − CVP ≈ SVR × CO Because CVP is normally very small compared with MAP the former can usually be ignored. Hypotension is the result of a decrease in SVR, CO, or both. The largest pressure drop, nearly 50%, is across the arterioles, and the arterioles account for the majority of SVR.

MAP may be estimated by the following formula: MAP = Diastolic pressure + Pulse pressure/3 Pulse pressure is the difference between systolic and diastolic blood pressure. Arterial pulse pressure is directly related to stroke volume, but is inversely proportional to the compliance of the arterial tree. Thus, decreases in pulse pressure may be due to a decrease in stroke volume, an increase in SVR, or both.

CONTROL OF THE SYSTEMIC VASCULATURE AUTONOMIC CONTROL is primarily sympathetic. passes out  of the spinal cord at all thoracic and first two lumbar segments. innervate all parts of the vasculature except for capillaries. regulate vascular tone which serve to regulate blood pressure and the distribution of blood flow to the various organs.

The vasculature has sympathetic vasoconstrictor and vasodilator fibers . Sympathetic-induced vasoconstriction (via α1 adrenergic receptors) -- in skeletal muscles, kidneys, gut and skin. Vasodilatory fibers -- in skeletal muscles, mediates increased blood flow (via β-2- adrenergic receptors) in response to exercise.

Vasomotor Centers Controls vascular tone and autonomic influences on the heart. located in the reticular formation of the medulla and lower pons . Vasoconstriction is mediated by the antero -lateral areas of the lower pons and upper medulla, responsible for adrenal secretion of catecholamines , as well as the enhancement of cardiac automaticity and contractility. Vasodilatory areas, are located in the lower medulla, are also adrenergic, but function by projecting inhibitory fibers upward to the vasoconstrictor areas. Areas in the postero -lateral medulla receive input from both the vagal and the glossopharyngeal nerves, important role in mediating a variety of circulatory reflexes.

ENDOTHELIUM-DERIVED FACTORS vasodilators (nitric oxide, prostacyclin [PGI2]), Nitric oxide synthesized from arginine by nitric oxide synthetase , binds to guanylate cyclase , increases c-GMP levels and produces vasodilation . vasoconstrictors ( endothelins,thromboxane A -2), Endothelins are released in response to thrombin and epinephrine.

Control of Arterial Blood Pressure Immediate Control Minute-to-minute control Mediated by autonomic nervous system reflexes :- Baroreceptor Reflexes Chemoreceptor Reflexes Bezold-Jarisch Reflex Atrial Reflexes Central Nervous System Ischemic Reflex

Baroreceptor Reflex Peripheral baroreceptors are located at the bifurcation of common carotid arteries (carotid sinus) and the aortic arch. Elevations in blood pressure increase baroreceptor discharge. Carotid baroreceptors send afferent signals to the depressor portion of the vasomotor center via Hering’s nerve (a branch of the glossopharyngeal nerve), whereas aortic baroreceptor via the vagus nerve. leading to decrease in vasoconstrictive impulses causing vasodilation throughout the peripheral circulation, decreased heart rate, and decreased myocardial contractility.

Responsible for minimizing changes in blood pressure that are caused by acute events, such as a change in posture,blood loss and shock. Carotid baroreceptors sense MAP most effectively between pressures of 80 and 160 mm Hg. Adaptation to acute changes in blood pressure occurs over the course of 1–2 days, rendering this reflex ineffective for longer term blood pressure control. All volatile anesthetics depress the normal baroreceptor response. Patients with chronic hypertension have a decreased baroreceptor reflex response.

Chemoreceptor Reflex located in the carotid bodies and aortic body responds to hypotension (SBP < 80 mmHg), acidosis and hypoxia (Pao 2 < 60 mm Hg ) Impulses from the chemoreceptors are transmitted to the vasomotor center leading to increased sympathetic activity which increases blood pressure towards normal.

Atrial Reflexes The right atrial wall and cavoatrial junction contains low-pressure atrial stretch receptors. An increase intravascular volume causes an increase in atrial pressure stimulating these receptors. They send their impulses through vagal afferents to inhibit parasympathetic activity which leads to increase in heart rate (Bainbridge reflex). The increase in heart prevents accumulation of blood in the atria, veins, or pulmonary circulation.

Bezold-Jarisch Reflex A decrease in left ventricular volume activates chemoreceptors and mechanoreceptors present in the LV wall which sends impulses through vagal afferents leading to bradycardia . This compensatory decrease in heart rate allows for increased ventricular filling, but this also exacerbate hypotension. The bradycardia and hypotension that can occur during spinal or epidural anesthesia and during reperfusion of ischemic myocardium have been attributed to this reflex.

Central Nervous System Ischemic Reflex The Cushing reflex is a central nervous system ischemic reflex response that results from increased intracranial pressure. The initial reflex is a direct CNS sympathetic stimulation leading to increased heart rate, contractility and blood pressure in an effort to increase cerebral perfusion. This is followed by reflex bradycardia mediated by baroreceptors reflex as a result of increased peripheral vascular tone.

Intermediate Control In the course of a few minutes Sustained decreases in arterial pressure, together with enhanced sympathetic outflow, activate the renin–angiotensin–aldosterone system, increases secretion of arginine vasopressin (AVP), and alter normal capillary fluid exchange. Both angiotensin II and AVP are potent arteriolar vasoconstrictor. Angiotensin constricts arterioles via AT 1 receptors. AVP mediates vasoconstriction via V 1 receptors and exerts its antidiuretic effect via V 2 receptors.

Long-Term Control Apparent within hours of sustained changes in arterial pressure. The kidneys alter total body sodium and water balance to restore blood pressure to normal. Hypertension increases sodium and water excretion. The resultant decrease in blood volume leads to decreases in cardiac output and systemic blood pressure. Contrasts with rapid-acting to moderately rapid-acting mechanisms, which cannot return systemic blood pressure entirely back to normal.

AUTOREGULATION Most tissue beds regulate their own blood flow ( autoregulation ). Arterioles generally dilate in response to reduced perfusion pressure or increased tissue demands and vice-versa. Due to both an intrinsic response of vascular smooth muscle to stretch and the accumulation of vasodilatory metabolic by-products like K + , H + , CO 2 , adenosine, and lactate.
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