327 Exam 1 Pathophysiology of HTN

PP

pulse pressure

PP Equation

PP = SBP - DBP

Mean BP equation

Mean BP = 1/3PP + DBP

Essential Hypertension

Has no identifiable cause

Secondary Hypertension

Caused by an underlying medical condition

Causes of HTN

Sleep apnea, kidney disease, steroid treatment, thyroid disease, drug related, or drug induced, renovascular disease

Checklist for Accurate Measurment of BP

Properly prepare the patient, use proper technique for BP measurement, take the proper measurements needed for diagnosis, properly document accurate BP readings, average the readings, provide BP readings to patient

Patient BP Measurment Requirements

1. The patient should avoid caffeine, exercise, and smoking for at least 30 minutes before measurement. Ensure the patient has emptied their bladder.

2. Use a blood pressure device that has been validated for accuracy.

3. Use the correct cuff size on a bare arm

4. The patient’s arm should be supported at heart level

5. Have the patient relax, sitting in a chain, feet on floor, legs uncrossed, and back supported for more than 5 minutes

6. Neither the patient nor the clinician should talk during the rest period or during the measurement. Pt. should not be using their phone

7. BP measurements should be taken in a temperature-controlled room

8. Take 2 or more blood pressure measurements at least 1 minute apart. Average the readings and provide pt. with their BP

PVR

peripheral vascular resistance

Low BP

decreased organ perfusion

high BP

areolar damage

Arterial baroreceptors

detects pressure changes in arteries. Ex: drop in perfusion pressure to kidney increases adrenergic activity. When perfusion is high arterials constrict

Primary target of Heart Failure Therapy

Reduce LV Wall Stress

Target-Organ Damage

Brain, eyes, heart, kidney, peripheral vasculature

Risk Factors for CVD

Hypertension, Age, Diabetes mellitus, elevated LDL, low HDL, Low GFR, history, macroalbuminuria, obesity, physical inactivity, sleep apnea, tobacco use, too much work

Renin-angiotensin-aldosterone

hypoperfusion stimulates JG apparatus to synthesize renin

Renal artery stenosis

caused by atherosclerotic vascular disease and fibromuscular dysplasia. Decreased effective renal flow leads to increased renin and angiotensin II and aldosterone

Renal Vascular Hypertension

Decreased renal perfusion —> increased renin release —> angiotensinogen —> angiotensin I + ACE —> Angiotensin II —→ Vasoconstriction and aldosterone release

Hyperaldosteroneism

Caused by adrenal adenoma, bilateral adrenal hyperplasia, adrenal carcinoma, increased glucocorticoid effects. MOA: increased release or action of aldosterone which increases renal tubular Na+ reabsorption and plasma volume

Screening Resistant Hypertension Patients

Screen for secondary hypertension, screening for primary aldosteronism is recommended, if positive continue with antihypertensive agents

Chronic renal disease

Stage 1: >90 ml/min

Stage 2: 60-90 ml/min

Stage 3: 30-60 ml/min

Stage 4: 15-30 ml/min

Stage 5: <15 ml/min

Expansion of volume

Renal Failure: Decreased filtration of Na+ leads to decreased Na+ excretion and increased Na+ retention

Hallmark of Hypertension

Increased PVR, altered cardiac function also probably contributes. Large elastic arteries are important in damping the pulsatile flow created by the heart

Vascular remodeling

helps to normalize left ventricular and arterial wall stress and may compensate for a reduction in myocardial fiber function to preserve cardiac output

Medications that can increase hypertension

Alcohol, caffeine, decongestants, black licorice, amphetamines, antidepressants

Essential Hypertension Characteristics

Low Renin: Sodium dependent, primary increase in plasma volume/primary increase in renal tubular sodium reabsorption

High Renin: sodium independent, primary increase in PVR

Sodium Sensitive Hypertensive

Lower sodium excretion after an IV sodium load compared to Non hypertensives. Lower aldosterone levels and lower aldosterone urinary excretion in children or hypertensives

Acute Complications of Hypertension

BP >180/20, LV dysfunction, acute CV accidents, acute renal failure, acute visual dysfunction/blindness 

Chronic Complications of Hypertension

Cerebrovascular disease, congestive HF, myocardial infarction/ischemia, PVD, chronic kidney failure

Masked Hypertension

Normal BP in the clinic or office but an elevated BP out of the clinic

Rule out secondary causes

Pheochromocytoma: high plasma and urine catecholamine

Renal vascular disease: high renin, high aldosterone, metabolic alkalosis, hypokalemia, abnormal renal perfusion studies (renal scan, MRA, arteriogram)

Hyperaldosteronism: high aldosterone, low renin, metabolic alkalosis hypokalemia, enlarged or abnormal adrenal glands on CT or MRI

Chronic Renal Failure: elevated BUN, creatinine, decreased creatinine clearance