HEMODYNAMIC DETERMINANTS Blood Pressure - P° generated when the heart contracts against the resistance of the BV MAP = CO * SVR MAP = DBP + (SBP – DBP)/3 DBP)/3 CO – CO – Cardiac Cardiac Output MAP – MAP – Mean Mean Arterial Pressure SVR – SVR – Systemic Systemic Vascular Resistance CO = SV * HR SV – SV – Stroke Stroke Volume HR – HR – Heart Heart Rate Causes of HTN - ↑ SVR rather than ↑ CO MODULATORS OF CARDIAC OUTPUT Extracellular Fluid - Total body sodium content not plasma sodium concentration - Regulated by sodium handling by the kidney Contractility/Heart Rate - Sympathetic tone - Inotropic effectors (cathecholamines: NorE, E) *↑ Natriuresis P°, ↑ Sodium Content MODULATORS OF SVR Humoral Factors - Sensors – baroreceptors, JG apparatus (Kidney), Atrium - Mediators – BP, BP, distal tubule chloride delivery, atrial stretch - Effectors o Vasoconstrictors – Angiotensin II, NorE, Thromboxane, Endothelin
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Vasodilators – – Prostaglandins, Bradykinin, Atrial Natriuretic Peptide Other Effects – altered sodium excretion by the kidney & manipulation of ECF
*Hypotension – *Hypotension – less less supply to other organs Local Factors - Mediators – endothelial cells, vascular smooth muscle cell - Signals – BP, shear stress(blood flow/viscosity, flow/viscosity, vessel diameter), humoral factors - Effectors (produced in BV) o Vasoconstrictors – Myogenic Response (depends on muscle contraction), Prostaglandins, Leukotrienes, Endothelin, Endothelium-derived Constricting Factor (EDCF), Angiotensin Vasodilators – Endothelium-derived Relaxing Factor o (EDRF), Prostaglandins - Local Mechanisms o Allow for autoregulation of blood flow and capillary pressure to various organs (brain, kidney - most prominently) o Allow for modulation of hemodynamics in an individual vascular bed with lesser changes in systemic hemodynamics *↑ BP activates sensors chain of rxn will happen *↑ volume of heart trigger baroreceptors PRIMARY HTN - AKA Essential HTN - Etiology unknown - Accounts for 90% of hypertensive pts th th - Onset: 5 -6 decade of life - Strong Family Hx – Hx – 70%-80% 70%-80% o HTN in both parents – parents – risk is ↑ 250%
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BP correlations are stronger among parent and child than between spouses, suggesting that environmental factors < genetic factors Certain races (African-Americans) - ↑ risk
*↑cholesterol will not really lead to HTN SECONDARY HTN – pag natreat, wala ng HTN - Kidney Dse - Renal Artery Stenosis - Hyperaldosteronism - Pheochromocytoma - Represents 10% of all HTN - Has specific therapy - Potentially curable *↑ sodium – water retention (↑ECF) *↑ sodium stimulates aldosterone (vasoconstrictor) *↑ aldosterone stimulates renin production stimulates angiotensin I production stimulates angiotensin II production vasoconstriction ↑ BP ROLE OF KIDNEY - With progressive loss of kidney fxn, virtually 10% of pts become hypertensive - Chronic kidney dse – MC form of 2° HTN - BP frequently improved with hemodialysis - Theories: o Kidney failure impaired sodium excretion expansion of ECF, volume overload & subsequent systemic HTN o Impaired kidney sodium excretion – necessary to sustain all forms of HTN o Persistent HTN necessitates abnormal pressure natriuresis phenomena *↑ Natriuretic P°, iihi ng iihin to correct BP
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ROLE OF RENIN-ANGIOTENSION SYSTEM - All infusion/overproduction causes HTN - Mechanism of Hypertensive Effects: o Angiotensin II directly induces vascular smooth muscle contraction o Angiotensin enhances sodium reabsorption ROLE OF ALDOSTERONE - Infusion of mineralocorticoids produces HTN - Aldosterone stimulates sodium retention & hypervolemia *Chronic Steroid Use HTN RENAL ARTERY STENOSIS AND HTN - Usually severe HTN - Clinical Clues: o Old, white male, smokers in wheelchair after amputation o High BP with low potassium o Presence of bruit (palpate jugular vein, mabilis yung flow) *Flow to kidney is impaired ↓ perfusion low volume activates renin-angiotensin system ROLE OF SYMPATHETIC NERVOUS SYSTEM (SNS) - Persistent increased SNS tone HTN - NorE modulates sympathetic tone - Increased levels HTN (Pheochromocytoma, Emotional Stress) - Mechanisms: o NorE directly stimulates vascular smooth muscle contraction and SVR through receptor mediated binding o NorE induces kidney sodium retention o NorE stimulates renin release *Predominant tone in the body: Parasympathetic *Pheochromocytoma – NorE-secreting tumor
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*Type A personality – agitated, closed to changes; may have 1° HTN PHEOCHROMOCYTOMA - Tumor that secretes NorE or NorE/Epinephrine - Rare condition - Usually produces severe HTN - Assoc. c other signs of increased cathecholamines (sweating and palpitation) JNC VII BP Classification Normal PreHTN Stage 1 HTN Stage 2 HTN Examples: 120/70 – Normal 130/90 – PreHTN 130/100 – Stage 2 160/90 – Stage 2 FOLLOW-UP RECOMMENDATION Initial BP Normal PreHTN Stage 1 HTN Stage 2 HTN
SBP <120 120-130 140-159
DBP & <80 Or 80-90 Or 90-99
≥ 160
Or ≥100
If c DM, kidney dse, lifestyle modification trial to reduce BP to 130/80 or less; if not, may give medication
ISOLATED SYSTOLIC HTN - SBP more important cardiovascular risk factor p age of 50 - DBP more important before age of 50 HYPERTENSIVE URGENCIES - Severely elevated BP - Without progressive end-organ dysfunction - Example: highly elevated BP s severe headache, SOB or chest pain - Usually d/t uncontrolled HTN - Lower BP within days HYPERTENSIVE EMERGENCIES - Severely elevated BP - With progressive target organ dysfunction - Require emergent lowering of BP *slurry speech, vomiting, seizures, blurry vision, etc
Follow-up Recheck in 2 yrs Recheck in 1 yr Confirm within 2 mos Evaluate or refer within 1 mo If c very high BP (>180/110mmHg) evaluate & treat within 1 wk
PREHYPERTENSION - Not a dse category - Designation for individuals at high risk for developing HTN - Not candidate for drug therapy - Advised lifestyle modification, targeting risk factors
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HYPERTENSION IN WOMEN - Oral contraceptives may increase BP - Risk of HTN increases c duration of use - Women c HTN who become pregnant should be followed up regularly o Increased risk to mother & fetus o Recommended drugs: methyldopa, Betablockers, Vasodilators o ACEI & ARB – Contraindicated d/t potential fetal defects - Preeclampsia o HTN + Pregnancy th o Occurs p the 20 wk of pregnancy o New-onset or worsening HTN, albuminuria & hyperuricemia *High risk; followed up every wk or 2wks
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HYPERTENSION IN CHILDREN & ADOLESCENT - BP (on repeated measurement) at the 95 percentile or greater adjusted for age, height & gender (may map); common in obese pts - Lifestyle modifications strongly recommended - Identify possible causes of HTN - Uncomplicated HTN not reason to restrict children from participating in physical activities o Long term exercise may lower BP RESISTANT HYPERTENSION - Failure to reach goal BP in pts who are adhering to full doses of an appropriate 3-drug regimen that includes diuretic COMPLICATION OF PROLONGED UNCONTROLLED HYPERTENSION - Changes in vessel wall vessel trauma & arteriosclerosis throughout the vasculature - Complications arise d/t the “target organ” dysfunction & ultimately failure - Damage to the BV can be seen on fundoscopy *Hemorrhagic Stroke – HTN EFFECTS ON CARDIOVASCULAR SYSTEM - Ventricular Hypertrophy, Dysfunction & Failure - Arrhythmias - Coronary Artery Disease, Acute MI - Arterial Aneurysm, Dissection & Rupture EFFECTS ON KIDNEYS - Glomerular sclerosis impaired kidney fxn & end stage kidney dse - Ischemic kidney dse especially when renal artery stenosis – cause of HTN EFFECTS ON CENTRAL NERVOUS SYSTEM
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Stroke Cerebral Atrophy ((-) substance ng brain) and Dementia (early onset)
EFFECTS ON EYES - Retinopathy - Vitreous Hemorrhage, Retinal Detachment - Neuropathy extraocular muscle paralysis & dysfunction BP Lifestyle Initial Drug Initial Drug Classification Modification Therapy Therapy Without With Compelling Compelling Indication Indication Normal Encourage No Anti-HTN drug Drugs for indicated compelling indications PreHTN Yes Stage 1 HTN Yes Thiazide type Drugs for diuretics for most; compelling may consider ACEI, indications ARB, BB, CCB or combination Stage 2 Yes 2-drug combination for most (thiazidetype diuretics + ACEI or BB or CCB) LIFESTYLE MODIFICATION Modification Recommendation WEIGHT REDUCTION
Maintain normal body wt (BMI: 2 18.5 -24.9kg/m )
ADOPT DASH EATING PLAN
Consume a diet rich in fruits, vegetables & low fat dairy
Approx. SBP Reduction 5-20mmHg /10kg wt loss 8-14mmHg
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DIETARY SODIUM RESTRICTION PHYSICAL ACTIVITY
MODERATE ALCOHOL INTAKE
products c a ↓ content of saturated & total fat ↓ dietary sodium intake to no more than 100mmol/day (2.4g sodium or 6g NaCl) Engage in regular aerobic physical activity (at least 30min/day, most days of the wk) Limit intake to no more than 2 drinks (1oz or 30ml ethanol, 24oz beer, 10oz wine, 3oz/80proof whiskey)/day in men and to no more than 1 drink per day in women
2-8mmHg
4-9mmHg
2-4mmHg
GENERAL STRATEGIES IN MX OF HTN - Increase Sodium Excretion (Diuretics) - Inhibits Aldosterone Production (Spironolactone) - BV smooth muscle relaxation/vasodilation (Vasodilators, CCB, BB) - Inhibits angiotensin II production and a ction (ACEI, ARB) RECOMMENDED DRUGS
COMPELLING INDICATIONS HEART FAILURE
DIU
BB
ACEI
ARB
(+)
(+)
(+)
(+)
(+)
(+)
POST-MI
(+)
(+)
(+)
DIABETES
(+)
(+)
(+)
(+)
(+)
(+)
RECURRENT STROKE PREVENTION
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(+)
AA
(+) (+)
HIGH CORONARY DISEASE RISK
CHRONIC KIDNEY DISEASE
CCB
(+) (+)
(+)
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