Hypertension Flashcards
what is blood pressure
*measure of adequacy of circulation
*balance between: blood volume ejected by LV & peripheral resistance to blood flow
*adequate BP is vital to perfusion of body tissues
complications of elevated BP
*intracranial hemorrhage
*stroke
*vascular disease
*kidney damage
*hypertensive heart disease
*retinopathy
complications of low BP
*shock
*kidney failure
*anoxic encephalopathy
*lactic acidosis
BP measurement technique: in-office
*2 readings, 5 minutes apart, sitting in chair
*confirm elevated readings in the contralateral arm
BP measurement technique: ambulatory BP monitoring
*indicated for evaluation of “white-coat” HTN
*absence of 10-20% BP decrease during sleep may indicate increased CVD risk
BP measurement technique: self-measurement
*provides information on response to therapy
*may help improve adherence to therapy and evaluate “white coat” HTN
changes in systolic & diastolic BP with age
*systolic BP continues to rise throughout life
*diastolic BP starts to DECREASE around age 50
*this phenomenon is due to stiffening of blood vessels
cardiovascular disease risk based on BP
*each increment of 20/10 mmHg doubles the risk of CVD across the entire BP range, starting from 115/75 mmHg
*the BP relationship to risk of CVD is continuous, consistent, and independent of other risk factors
ACC/AHA blood pressure classifications
*normal: SBP < 120 mmHg AND DPB < 80
*elevated: SBP 120-129 OR DBP <80
*stage 1 HTN: SBP 130-139 OR DBP 80-89
*stage 2 HTN: SBP 140+ OR DBP 90+
note: whichever value is the higher stage is what HTN you have
epidemiology of HTN
*CVA & SVD are the most common causes of death and disability in developed countries
*HTN is a key modifiable risk factor
*HTN affects nearly 50% of adult population in the world
*primary HTN accounts for 90% of cases
causes of primary HTN
*multifactorial: obesity, insulin resistnace, age, sodium retention, sympathetic activation, etc
target organ damage resulting from long-standing HTN
1) heart:
-left ventricular hypertrophy
-angina or myocardial infarction
-heart failure
2) brain: stroke or TIA
3) chronic kidney disease
4) peripheral arterial disease
5) retinopathy
6) aortic aneurysms and dissections
pathophysiology of LV hypertrophy as a result of long-standing HTN
*according to law of Laplace (wall stress law), INCREASING THE THICKNESS OF THE LV WALL actually DECREASES the wall stress
*hence, an increase in wall thickness in response to increased pressure maintains/decreases wall stress
heart failure and HTN
*people in heart failure are extremely sensitive to small changes in blood pressure (compared to people without heart failure)
*therefore, we need to maintain their BP even lower than normal because it does not take much afterload to compromise their stroke volume
HTN complication: higher wall thickness:lumen ratio in the arteries
*law of Laplace applies to arteries too (increasing the wall thickness helps to decrease the wall stress)
*therefore, arteries and arterioles become hyperplastic/hypertrophied in the setting of longstanding HTN, which can lead to more complications down the line
HTN and retinopathy
*long-standing HTN can cause retinopathy, characterized by:
-cotton wool spots
-AV nicking
-thin arteries
-papilledema
identifiable causes of secondary HTN
*sleep apnea
*drug-induced or related causes
*chronic kidney disease
*primary aldosteronism
*renovascular disease
*chronic steroid therapy & Cushing’s syndrome
*pheochromocytoma
*coarctation of the aorta
*thyroid or parathyroid disease
*renal channelopathy
pheochromocytoma - overview
*rare cause of secondary HTN
*tumor containing chromaffin cells which secrete catecholamines (esp. EPINEPHRINE)
*young-middle aged with female predominance
pheochromocytoma - clinical features
*intermittent HTN, palpitations, sweating, anxiety “spells”
*may be provoked by triggers such as tyramine-containing foods (beer, cheese, wine), pain, trauma, drugs (clonidine, TCA, opiates)
pheochromocytoma - screening
*best detected during or immediately after episodes
*3 options, looking for excess breakdown products of epinephrine:
1) plasma free metanephrine
2) 24h urine metanephrine
3) 24h urine VMA
pheochromocytoma - diagnosis
*imaging for localization of tumor:
-MIBG scintigraphy
-CT
-MRI
pheochromocytoma - treatment
*surgical removal of tumor:
-anesthesia must avoid certain triggers
*caution with beta blockers!!! (can cause unopposed alpha stimulation → Pheo crisis)
*must start BP control with alpha blockers (phenoxybenzamine) and then start beta blocker once the irreversible alpha blocker is on board
pheochromocytoma “pheo crisis” with beta blockers
*Pheo crisis: beta blockers can cause unopposed alpha stimulation:
-by blocking the beta receptors, all the catecholamines (epi and NE) will go to alpha-1 receptors → significant vasoconstriction
medication timeline for preparing a pheochromocytoma patient for surgery
- epinephrine from the tumor → BP to increase
- give phenoxybenzamine first (an irreversible alpha blocker) → BP goes LOWER THAN ORIGINAL BASELINE b/c the catecholamines are going to beta 2, causing vasodilation
- give non-selective beta blocker
coarctation of the aorta
aortic narrowing near the insertion of the ductus arteriosus
*defined by location of coarctation relative to ligamentum arteriosum (preductal. ductal, or postductal)
*commonly presents as HTN in upper extremities, but lower extremities are cold with weak, delayed pulses
*high association with BICUSPID AORTIC VALVE, other heart defects, and Turner Syndrome
*if symptomatic, angioplasty vs. surgery
*even with repair, have a lower than expected life expectancy
*collateral blood supply typically forms to maintain perfusion of the abdomen
*complications: HF, increased risk of cerebral hemorrhage (berry anuerysms)
characteristic CXR finding of aortic coarctation
*rib-notching of ribs on CXR
*this is evidence of collateralization of blood flow through the intercostal arteries to help supply blood beyond the coarctation
*the bone adapts to having a large vessel running by it
behaviors associated with HTN risk
*excessive alcohol
*sodium consumption
*obesity/dietary excess
*lack of aerobic exercise
lifestyle modifications to manage HTN
*weight reduction
*DASH eating plan
*dietary sodium reduction
*physical activity
*moderation of alcohol consumption
HTN tx based on ACC/AHA BP classifications
*normal: encourage lifestyle modifications, no meds
*elevated: encourage lifestyle modifications, no meds
*stage 1 HTN: emphasize lifestyle modifications, START 1 MEDICATION
*stage 2 HTN: emphasize lifestyle modifications, START 2 MEDICATIONS
first-line antihypertensive drug therapies
*thiazide diuretics
*dihydropyridine (amlodipine, nifedipine) calcium channel blockers (vasodilation is good for tx HTN)
*ACE inhibitors
*angiotensin receptor blockers (ARB)
compelling indications for individual antihypertensive drug classes in HEART FAILURE patients
*ACE inhibitors or angiotensin receptor blockers (ARB)
*beta blockers
*aldosterone antagonist (ALDO ANT)
compelling indications for individual antihypertensive drug classes in POST-MYOCARDIAL INFARCTION PATIENTS
*beta blockers
*ACE inhibitors or angiotensin receptor blockers (ARB)
*aldosterone antagonist (ALDO ANT)
compelling indications for individual antihypertensive drug classes for DIABETES PATIENTS
*ACE inhibitors or angiotensin receptor blockers (ARB)
compelling indications for individual antihypertensive drug classes for CHRONIC KIDNEY DISEASE patients
*ACE inhibitors or angiotensin receptor blockers (ARB)
