B4-041 Hypertension Flashcards
laterally displaced PMI may indicate
left ventricular hypertrophy
high QRS voltage
ST depressions in lateral leads
left ventricular hypertrophy
LVH is compensatory to overcome
increased afterload
LVH leads to
- distolic heart failure
- perfusion mismatch
what does an abdominal bruit 5 cm left of umbilicus signify?
renal artery stenosis
how does renal artery stenosis cause hypertension?
- fibromuscular dysplasia and atherosclerotic plaque build up cause decreased renal perfusion
- kidney increases arterial pressure through RAAS
if patient has dyslipidemia, assess […] risk
ASCVD
hypertensive emergency
greater than 200/120
or end organ damage
hypertensive urgency
SBP > 180 or DBP > 120
without end organ damage
symptoms of end organ damage
- headache
- papilledema
- renal failure
- dyspnea
- chest pain
- encephalopathy
stage 1 hypertension
130-139/80-89
stage 2 hypertension
greater than 140/90
hypertension is diagnosed by
2 readings on at least 2 occasions
every 20 mmHg of SBP or 10mmHg of DBP
doubles risk of death from stroke or CVD
systolic BP correlates with
SV and arterial compliance
diastolic BP correlates with
TPR and HR
95% of cases are […] hypertension
primary
[…] hypertension has no defineable cause
primary
if a patient is <40,
likely CO issue
if patient is older,
TPR issue
causes of secondary hypertension
- renal parenchyma damage
- renovascular disease
- pheochromocytoma
- endothelial cell dysfunction
- hyperaldosteronism
damage impairs ability to excrete Na+ and H20
renal parenchyma damage
renal parenchyma damage results in
increased blood volume
increased preload, SV, CO, and MAP
elderly patient, historically well controlled BP worsening, escalating medications
renovascular htn
triggers RAAS system
renovascular htn
- headaches
- sustained vs. paroxysmal meteoric BP
- diaphoretic
pheochromocytoma
release of NE and EPI causes HTN from increased CO and TPR
pheochromocytoma
HTN + spontaenous or easily provoked hypokalemia with diuretic
hyperaldosteronism
if you have a patient with:
HTN with OSA
HTN with a fib
think…
hyperaldosteronism
how does baroreceptor dysfunction impact HTN treatment?
baroreceptors will perceive hypotension, when in reality patient is normotensive due to chronic baseline elevation of MAP
very first treatment strategy for HTN
lifestyle changes
- decrease TPR via relaxation of arteriolar vascular smooth muscle
- decrease CO by reducing venous return through relaxation of veins
alpha 1 antagonists
reduce CO by decreasing HR and inotropic state
beta blockers
end in -pril
ACE inhibitors
end in -sartan
ARBs
preferred treatment of primary aldosteronism
- spironolactone
- eplerenone
preferred in HFrEF
carvedilol
not first line therapy, except in CAD and HFrEF
beta blockers
associated with orthostatic hypotension
alpha-1 blockers
increase risk of hyperkalemia in CKD
ACE inhibitors and ARBs
cause edema
dihydropyridine CCBs
amlodopine
treatment: stage 1 HTN
monotherapy
treatment: stage 2 HTN
2 first line agents
DOC without contraindication
- thiazides
- ACE inhibitors
- ARB
- CCB
- beta blocker
DOC if patient has DM or CHF
- ACE inhibitor
- ARB
DOC patient with BPH
alpha blocker
DOC patient with osteoporosis
thiazide
hypercalcemia
DOC if pregnant
- labetalol
- CCB
- hydralazine (co-admin beta blocker for reflex tachy)
if ASCVD is greater than 7.5%…
statin
initial first line therapy for stage 1 hypertension
- thiazide
- CCBs
- ACE/ARBs
function of endothelin-1
increase TPR
can cause hypertension
hypertension drug classes contraindicated in pregnancy
- aliskiren
- ACE
- ARBs
can cause injury and death to developing fetus in 2nd and 3rd trimesters
ACE inhibitors
hypertension due to adrenal tumor which is releasing high levels of aldosterone
conn’s syndrome
plasma renin markedly elevated
renovascular hypertension
low amplitude, long duration T wave
hypokalemia
high levels of aldosterone promote
sodium reabsorption and potassium excretion
causing hypokalemia
elevated plasma aldosterone will increase
blood volume –> increased venous return –> increased CO –>hypertension
left ventricular hypertrophy suggests MAP
has been chronically elevated
abdominal bruit
renovascular hypertension
caused by plaque in renal artery
renovascular hypertension
decreased renal blood flow causes
renin release –> angiotensin 2–> increased TPR
causes increased renin, angiotensin, and aldosteron
decreased renal blood flow
how does left ventricular hypertrophy affect the pressure volume curve?
shift up and to the left
