Hypertension & Afib Flashcards
Hypertension
As BP increases, so does the risk of
MI
Heart failure
Stroke
Renal disease
BPs
Normal: less than 120/ less than 80
Elevated: 120-129/ less than 80
HTN stage 1: 130-139/ 80-89
HTN stage 2: 140+/ 90+
HTN crisis: 180+/ 120+
Primary HTN
no identified cause
Secondary HTN
Specific cause can be identified and corrected
Suspect with: Unexplained hypokalemia, Abdominal bruit over renal arteries, Variable B/P with history of tachycardia, sweating, tremor, Family Hx of renal disease
Risk Factors for Primary Hypertension
Age
Alcohol
Tobacco use
Diabetes mellitus
Elevated serum lipids
Excess dietary sodium
Gender
Family history
Obesity
Ethnicity
Sedentary lifestyle
Socioeconomic status
Stress
Pathophysiology of Primary Hypertension
Genetic Links
Water and sodium retention
Stress and increase sympathetic nervous system activity
Altered renin-angiotensin-aldosterone system (RAAS)
Insulin resistance and hyperinsulinemia
Endothelial dysfunction
Clinical Manifestations HTN
“silent killer”
Symptoms of severe hypertension
Fatigue
Dizziness
Palpitations
Angina
Dyspnea
Target Organ Diseases
Heart
-Coronary artery disease (CAD)
-Left ventricular hypertrophy (LVH)
-Congestive heart failure (CHF)
Peripheral vascular disease (PVD)
Kidneys (Nephrosclerosis)
Eyes (Retinal damage)
Goals HTN
Goal:
< 140 / 90 mm Hg
< 130 / 80 mm Hg for those at high risk for / with CAD
Medications
Decrease circulating blood volume
Reduce SVR – systemic vascular resistance (“After-load”)
Medication Therapy
Diuretics
Adrenergic inhibitors
Vasodilators
Angiotensin & renin inhibitors
Ca+ channel blockers
Drug Therapy action
Decrease the volume of circulating blood
Reduce systemic vascular resistance
Diuretics
promote sodium and water excretion, reduce plasma volume, and reduce the vascular response to catecholamines
Adrenergic-inhibiting agents (Beta blockers)
act by diminishing the SNS effects that increase BP. Adrenergic inhibitors include drugs that act centrally on the vasomotor center and peripherally to inhibit norepinephrine release or to block the adrenergic receptors on blood vessels.
Direct vasodilators
decrease the BP by relaxing vascular smooth muscle and reducing SVR
Calcium channel blockers
increase sodium excretion and cause arteriolar vasodilation by preventing the movement of extracellular calcium into cells.