Professional Documents
Culture Documents
Types
1. Primary or Essential hypertension
No known etiology
2. secondary hypertension
occurs as a result of other disorders
renal stenosis
renal parenchymal diseases (pheochromocytoma)
hyperaldosteronism
medications
coarctation of aorta (congenital)
Pathophysiology
Multifactorial
Increased SNS stimulation
Increased reabsorption of Na, Cl, and water
Increased in RAAS activity
Decreased vasodilation of arteriole related to dysfunction of endothelium
Resistance to insulin action
Elderly: increased atherosclerotic plaque and decreased elasticity of blood
vessel
Clinical manifestations
History and PE
Lad test
ECG
Chest XRAY
2D Echo
Medical management:
goal: prevent death and complication by maintaining a normal BP
o lifestyle modification
o pharmacologic therapy
lifestyle modification
o loose weight if overweight
o limit alcohol intake
o increase aerobic physical activity
o reduce sodium intake to 2-4 grams/day
o maintain adequate intake of K, Ca, Mg
o stop smoking
pharmacologic therapy
diuretics
o Thiazide diuretics
Hydrochlorothiazide
o Loop diuretics
Furosemide, Bumetanide
o Potassium sparing diuretics
Spironolactone, Amelioride, Triamterene
Adrenergic agents
o Peripheral agents: Reserpine
o Central antagonist: Methyldopa (Aldomet), Clonidine (Catapres)
Clinical Manifestation
Diastolic pressure above 120mmHg
Headache, drowsiness, confusion, change in neurologic status
Tachycardia, tachypnea, dyspnea
Cyanosis
Seizure
Intervention
inability of the heart to pump sufficient blood to meet the needs of the
tissues for oxygen and nutrients
Etiology
1. CAD
2. cardiomyopathy
a. dilated cardiomyopathy
– causes systolic failure
- diffused necrosis results in decreased contractility
causative factors
↓↓
myocardial damage
↓↓
CHF
↓ CO
↑ Left ventricle,
↑ afterload diastolic pressure
↑ preload
compensatory mechanism
↑RAAS
↑ SNS
↑ vasoconstriction
Classification
Class I – ordinary physical activity does not cause symptoms
- no limitation of activity (climbs ≥2 flight of stairs with ease)
- good prognosis
Class II – no symptoms at rest but increase physical activity elicits Ssx
-slight limitation of activity (climbs stairs but with difficulty)
-good prognosis
Class III – comfortable at rest but less than ordinary activities cause ssx
-marked limitation of activity ( ≤1 flight of stairs)
- fair prognosis
Class IV – symptoms even at rest
- poor prognosis
Pathophysiology
1. ↓↓ ventricular contraction
↓↓ Ventricular filling
↓↓
2. Stimulation of the SNS
(supports myocardium - ↑↑↑ CO, HR, BP, contractility, vasoconstriction)
↓↓
3. Down regulation or loss of beta 1-adrenergic receptor sites
(= further myocardial damage)
↓↓
4. ↑↑ renin level -- ↑↑angiotensin II and aldosterone --vasoconstriction, ↑BP
↓↓
5. ↑↑ preload, afterload = ↑↑↑ cardiac workload
↓↓
6. ↓↓ cardiac contractility --- ventricular dilation
↓↓
7. ↑↑↑ stress on the ventricular walls – hypertrophy
↓↓
8. ↑↑↑ O2 demand and coronary blood flow – ischemia/infarction
↓↓
9. SNS promotes coronary vasoconstriction – myocardial ischemia
Diastolic failure
Cardiac hypertrophy and ↓↓ contractility
↓↓
↓↓ ventricular filling
↓↓
↓↓CO
Assessment
Immediate management
1.place the client on high fowler with thelegs in the dependent position
2.administer O2 in high concentration
3.prepare for intubation and ventilator support
4.suction as needed
5.assess level of consciousness, VS
6.monitor progression of edema (weight, abdominal girth, pulses)
7.monitor I&O, insert foley catheter
8.avoid unnecessary IVF
9.administer medications as prescribed
morphine SO4 for sedation and vasodilation
diuretics to reduce preload and pulmonary congestion
digitalis to increase cardiac contractility increasing CO
inotropic meds to facilitate contractility
vasodilators to decrease afterload
10. ABG and electrolyte analysis
Following the acute episode
Medical Management
1. ACE inhibitors
`Vasodilation --- ↓↓ afterload
`Causes diuresis -- ↓↓ afterload
3. Beta blockers
`Metoprolol, Propranolol
`S/E dizziniess, hypotension, bradycardia
`C/I asthma, bradycardia, congestion
4. Diuretics
` increase UO, decrease edema, decrease preload
`Thiazide, loop and K+ sparing diuretics
5. Digitalis: Digoxin
`↑myocardial contraction and ↓↓conduction = ↑↑ CO and diuresis
`Digitalis toxicity: enhanced by hypokalemia
Fatigue, depression, malaise, anorexia, n/v,
headache, altered visual perception
changes in the rhthym
`N/I assess apical HR before administration (assess bradycardia)
monitor serum potassium
6. Angiotensin II blockers
`Losartan, Telmisartan, Valsartan
7. Ca-channel blockers
` vasodilation for improvement of symptoms
` indicated for diastolic dysfunction
`Amlodipine, Felodipine
`Verapamil, Diltiazem and Nifedipne are C/I in HF
8. Anticoagulants
` Ibuprofen and decongestants are avoided
Nutritional therapy
Low Na diet
Avoid excessive fluid intake