Module 9 Hypertension NSG 320 PDF
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This document provides an overview of hypertension, focusing on the circulatory system and blood pressure regulation. It discusses cardiac output, stroke volume, and the determinants of systemic blood pressure, along with blood pressure measurements and related mechanisms.
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Module 9 Hypertension NSG 320 OVERVIEW OF THE CIRCULATORY SYSTEM Distribution of blood 9% in the pulmonary circulation 7% in the heart 84% in the systemic circulation What makes blood flow? Force that drives flow is greater than resistance 2 Arteria...
Module 9 Hypertension NSG 320 OVERVIEW OF THE CIRCULATORY SYSTEM Distribution of blood 9% in the pulmonary circulation 7% in the heart 84% in the systemic circulation What makes blood flow? Force that drives flow is greater than resistance 2 Arterial Blood Pressure Desired BP is systolic 120 or Systolic: The maximum less and diastolic 80 or less pressure in the arteries when the heart contracts Pressure differences between the left and right sides of the heart that produce systemic movement of blood Diastolic: The minimum pressure in the arteries Arterial blood pressure is when the heart relaxes produced by the force of left between beat ventricular contraction overcoming the resistance of the aorta to open the aortic valve Arterial Blood Pressure Key points about cardiac output and stroke volume: Cardiac output: Stroke volume: Represents the total Represents the amount of volume of blood pumped blood ejected from the by the heart per minute. heart with each contraction. Measured in liters per Measured in milliliters per minute. beat. Can be calculated by Affected by factors like multiplying the heart rate preload (ventricular filling), (beats per minute) by the contractility (force of stroke volume (volume contraction), and afterload per beat). (resistance to blood flow). Arterial Blood Pressure Determinants of Systemic Blood Pressure Cardiac output (CO) and the resistance to the ejection of blood from the heart CO = SV (stroke volume) x HR (heart rate) End-diastolic volume is the preload Ø Amount of blood returned to the heart Systemic vascular resistance (SVR, afterload) is determined by the radius of arteries and degree of vessel compliance BP=CO x SVR Arterial Blood Pressure Systemic Arterial Blood Pressure Arterial Blood Pressure Measurement of Blood Pressure Components of blood pressure measurement Ø Systolic blood pressure—peak pressure during cardiac systole Ø Diastolic blood pressure—lowest pressure during cardiac diastole Ø SV (Stroke volume) is the primary factor influencing systolic pressure Ø SVR (Systemic Vascular Resistance) is the major determinant of diastolic pressure Ø Pulse pressure = Systolic - diastolic Arterial Blood Pressure Measurement of Blood Pressure Components of blood pressure measurement Ø Mean arterial pressure (MAP) is the calculated average pressure within the circulatory system throughout the cardiac cycle Ø MAP = (2 x diastolic pressure) + systolic pressure 3 Arterial Blood Pressure Direct Measurement of Blood Pressure- ART LINE Requires intra-arterial catheter and specialized equipment to transduce arterial fluid pulsations into electrical signals (waveforms) Catheter commonly placed in radial artery Most accurate method of measuring blood pressure Arterial Blood Pressure Indirect Measurement of Blood Pressure Commonly measured via the brachial artery using a stethoscope and sphygmomanometer or automated oscillometric system Requires careful technique to ensure accuracy Auscultation of Korotkoff sounds Ø Systolic pressure: onset of Korotkoff sounds Ø Diastolic pressure: disappearance of Korotkoff sounds White coat effect Elderly: auscultatory gap Mechanisms of Blood Pressure Regulation Short-Term Regulation of Systemic Blood Pressure Changes in BP are mediated through activation of the sympathetic nervous system Results in release of neurotransmitters epinephrine and norepinephrine Parasympathetic nervous system: slows heart Mechanisms of Blood Pressure Regulation Short-Term Regulation of Systemic Blood Pressure Vasomotor center directly activated by various stimuli or indirectly via baroreceptors which monitor MAP variations Ø Activates α1 (Alpha1) receptors in smooth muscle of arterioles, causing vasoconstriction (Increase SVR) Ø Activates β1 (Beta1) receptors of the heart (Increase heart rate) Chemoreceptors stimulate the medullary vasomotor center to increase SNS activity Ø Located in carotid and aortic arterials Ø Activated only when BP extremely low Mechanisms of Blood Pressure Regulation Long-Term Regulation of Systemic Blood Pressure Regulated by neural, hormonal, renal Connected to fluid volume Increase in extracellular fluid volume = increased CO and SVR = elevated BP Ø Causes kidneys to excrete excess sodium and fluid Increased serum sodium level = increased osmolality (particle concentration) = increased ADH secretion Ø Causes kidneys to reabsorb water Mechanisms of Blood Pressure Regulation Long-Term Regulation of Systemic Blood Pressure Renin–angiotensin–aldosterone system (RAAS) important regulator of BP Ø Juxtaglomerular cells when stimulated by low arterial pressure release renin activates angiotensinogen to angiotensin I Ø Angiotensin I when in contact with ACE activates angiotensin II, a potent vasoconstrictor and stimulates release of aldosterone Ø Aldosterone, a hormone, causes reabsorption of sodium and water passively follows Mechanisms of Blood Pressure Regulation RAAS https://youtube.com/shorts/1F mrkC_KBso?si=xyN8wyfMlElU Y9aB Mechanisms of Blood Pressure Regulation Long-Term Regulation of Systemic Blood Pressure Angiotensin II produces an increase in SVR Atrial natriuretic peptides cause kidneys to increase sodium and water excretion by increasing the glomerular filtration rate Endothelin-1: important in BP control Mechanisms of Blood Pressure Regulation Normal Fluctuations in Systemic Blood Pressure Suprachiasmatic nuclei (body’s internal clock) in the brain govern daily variations in bodily functions Ø Rises before awaking (morning surge) Ø Highest in the middle of the morning Ø Lowest at night (nocturnal dip) Neural, hormonal regulation, external environmental factors influence BP Lifestyle, cognitive activity and emotional state can affect BP Hypertension Most common primary diagnosis in the United States Increases morbidity and mortality associated with heart disease, kidney disease, peripheral vascular disease, and stroke Responsible for an annual worldwide death rate of 7 million Hypertension Role of the sympathetic nervous system Copyright © 2019, Elsevier Inc. All rights reserved. 21 Hypertension Pathophysiology of hypertension 22 Hypertension Definition and Classification Determined by the Joint National Committee (JNC) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure Pre-hypertension is a range of pressures between normal and Stage 1 hypertension in an effort to initiate interventions early enough to prevent or deter progression of the disease process Primary Hypertension Also called essential hypertension Idiopathic disorder Most common form of hypertension Rare prior to the age of 10 Systolic BP: major risk factor for cardiovascular disease Primary Hypertension Subtypes Ø Isolated systolic hypertension: systolic BP is ≥140 mm Hg while diastolic pressure remains 90 mmHg 130-139 mmHg Stage 1 80-89 mmHg 120-129 mm Hg Elevated 20 mm Hg or >10 mm Hg within 3 minutes) when moving to an upright position Low Blood Pressure (Hypotension) Orthostatic (Postural) Hypotension Excessive increase in heart rate (by 20-30 beats/minute) may also be diagnostic Results in dizziness, blurred vision, confusion, and possible syncope Associated with cardiovascular disease and is a risk factor for stroke, cognitive impairment, and death Low Blood Pressure (Hypotension) Orthostatic (Postural) Hypotension May be a result of: Ø Problem with vasomotor or baroreceptor response Ø Adverse effect of drug therapy Ø Arterial stiffness Ø Volume depletion Ø Secondary disease process Ø Vasovagal reaction Ø Cardiac dysrhythmias Low Blood Pressure (Hypotension) Orthostatic (Postural) Hypotension Treatment Ø Review medication history Ø Slow positional changes Ø Avoid hot environments Ø Avoid large or carbohydrate-heavy meals Ø When symptoms begin, squatting/bending forward or crossing legs may reduce effects Ø Elastic compression stockings, abdominal binders, elevate head of bed Ø Increase salt and fluid intake if not contraindicated Pharmacology 41 Pharmacologic Therapy Review of blood pressure control Ø Principal determinants of blood pressure Arterial pressure = Cardiac output × Peripheral resistance Cardiac output Heart rate Myocardial contractility Blood volume Venous return Ø Systems that help regulate blood pressure Sympathetic baroreceptor reflex Renin-angiotensin-aldosterone system Renal regulation of blood pressure 42 Pharmacologic Therapy Classes of antihypertensive drugs Ø Diuretics Thiazide diuretics Loop diuretics Potassium-sparing diuretics Ø Sympatholytics (antiadrenergic drugs) Beta-adrenergic blockers Alpha1 blockers Alpha/beta blockers: Carvedilol and labetalol Centrally acting alpha1 agonists Adrenergic neuron blockers 43 Pharmacologic Therapy More Sympatholytics (anti-adrenergic drugs, continued) Ø These quiet the sympathetic response) Direct-acting vasodilators: Hydralazine and minoxidil Calcium channel blockers Drugs that suppress RAAS ACE inhibitors Angiotensin II receptor blockers Aldosterone antagonists Direct renin inhibitors: The Diuretics Mechanism of action: promote "diuresis"-movement of fluids and electrolytes out of body. Two major uses: Ø Hypertension Ø Edema Classification: Ø Loop diuretics Ø Thiazide diuretics Ø Osmotic diuretics (will not review) Ø Potassium-sparing diuretics Thiazide and Thiazide Type Diuretics Example: hydrochlorothiazide "HCTZ" (HydroDIURIL®) and chlorothiazide (Diuril®) Much less diuresis compared to "Loops": and so are used extensively for uncomplicated hypertension cases. Mechanism of action: similar to "loop" diuretics except site is distal convoluted tubule of kidney Major uses: Ø Hypertension Ø Edema due to mild to moderate congestive heart failure ADR's: dehydration, hypotension, hypokalemia, increase uric acid to increase gout, increases lipids. Thiazide and Thiazide Type Diuretics Allergy: derived from sulfonamides, so avoid if history of sulfa allergy Important drug interactions: Ø digoxin since low K+ increase digoxin Ø Other blood pressure meds with thiazides may further decrease BP Ø Diuretics increase lithium levels resulting in toxicity Ø NSAIDS decrease blood flow to kidneys, thus decreased diuretic effect Thiazides Do NOT work well in renal impairment when CrCl