HTN/Hypotension Flashcards
elevated BP
stage 1 hypertension
treat if
stage 2 htn
SBP 120-129 and DBP <80 mm Hg
SBP 130-139 mm Hg or DBP 80-89 mm, lifestyle chngs (high potassium foods)
clinical ASCVD or 10-yr ASCVD risk score ≥10%,1 med
≥140/90, start 2 meds+reassess in 1 month
HTN in AA without HF or CKD tx
thiazide-type diuretic or calcium channel blocker
cardiogenic shock in STEMI
Right sided pulmonary edema in cardiogenic shock
LV infarction
papillary muscle rupture, ventricular septal rupture, free-wall rupture with tamponade, and (RV) infarction.
acute MR from lateral papillary muscle rupture (the regurgitant jet is directed towards the R pulm veins)
acute stent thrombosis
recurrent or new ST elevations
mixed venous o2 sat in cardiogenic shock vs septic
decreased
orthostatic vital signs
normal
autonomic dysfunction
POTS
cardiodepressor syncope
5-10 drop in SBP, 5-10 increase in DBP, 10-25 increase in HR
brief rise in HR ff by >20+ >10 fall in SBP and DBP, HR doesn’t change much
modest drop in BP + extreme rise in HR
marked drop in HR, ff by drop in BP
Newly diagnosed HTN
EKG to assess for LVH, arrhythmia, MI
Also get fasting glucose, CBC, BMP, TSH, u/a
resistant HTN, early onset, abrupt onset or worsening or increasingly difficult to control, flash pulmonary edema, abdominal systolic-diastolic bruit
difficult to control HTN
suspect renovascular disease, -> renal doppler u/s
get sleep study
MI c/b cardiogenic shock
IABP, start with NE for inotropy/vasopressor
*avoid phenylephrine and vasopressin-> vasoconstrict-> increase afterload-> may decrease CO
use dobutamine for inotropy
milrinone
low CO but preserved BP
It can worsen hypotension by dilating peripheral arts
also causes hypotension, avoid in renal failure, induces arrhythmias
HTN, already on 3 agents including diuretic
add spironolactone
reduces SBP by 24 mm Hg at 6 months
hctz dosing
not much benefit beyond 25 mg daily if normal renal function
HTN treatment target
<130/80
can start two agents at once if needed (CAD). Most patients need 2
hypertensive emergency vs urgency treatment
inpatient, IV meds vs outpatient, PO meds (DBP> 120 in both)
lower SBP by no more than 25% in the first hour, then to approximately 160/100 mm Hg over the next 2-6 hours, and then eventually to normal over the next 24-48 hours.
lower SBP <140 in pheo/pre eclampsia, <120 in aortic dissection
meds which cause orthostatic hypotension
alpha blockers like terazosin (schedule at bedtime)
tamsulosin, tizanidine, trazodone (and other antipsychotic/antidepressant medications), and carvedilol (with its alpha-blocking properties)
HTN in DM/CKD/albuminuria
ACEI/ARB
normal bump in creatinine after ACEI/ARB initiation
cause serum creatinine to increase ≤30% because of concurrent reduction in glomerular filtration rate (GFR).
Further GFR decline should be investigated and may be related to other factors, including volume contraction, use of nephrotoxic agents, or renovascular disease
LVH with normal BP
ambulatory monitoring (masked hypertension)
question in-office elevated BP if
pseudoresistant HTN
no LVH on ECG/echo, h/o dizziness
elevated in office, not elevated at home
resistant htn in CKD tx
loop diuretics
refractory htn
not controlled by 5 meds including diuretic and MRA
white coat effect vs white coat HTN
hypertensive vs nonhypertensive
cold, low BP, renal dysfunction
HF exac GDMT
poor perfusion, wet and cold HF-> perishock
continue unless hemodynamically unstable/ CI
HTN from RAS due to fibromuscular dysplasia tx
HTN from RAS due to athero (elderly)
antihypertensives (ACEI/ARB)-> balloon angioplasty
same, meds-> revasc
hemodynamic changes in aging
increased SBP decreased DBP Increased pulse pressure Increased pulse wave velocity Increased arteriolar resistance, decreased NO
causes of essential htn
increased sympathetic nerve activity
increased concentrations of vasoactive and salt-retaining hormones
endothelial dysfunction, increased vascular reactivity, arterial stiffness, and remodeling.
HFpEF risk factors
hypertension, DM, obesity, h/o CAD
Hypertensive emergency choice of treatment agent
NO LABETALOL OR ESMOLOL (decrease contractility) OR HYDRALAZINE (rebound tachycardia)
Use
nitroglycerin (if ACS/pulmonary edema, not if recent viagra)
nitroprusside (not if recent viagra)
nicardipine (not in AS)
phentolamine (pheo, cocaine, MAOI, meth, clonidine withdrawal)
STEMI + cardiogenic shock
revascularize regardless of timing from onset of MI
CULPRIT-SHOCK: only treat culprit vessel with PCI
NSAIDs (including aspirin) increase BP by
inhibition of cyclooxygenase 2 in the kidney, which results in reduced sodium excretion and an increase in intravascular volume.
HTN diagnosis
2 readings on two or more occasions
relationship between HTN and cardiovascular risk
log-linear
increase of 20/10= double risk
exponential relationship
bimodal
deterministic
single point increase= double risk
different responses in different categories
certain regardless of severity/measure
difficult to control htn+ hypokalemia
diagnosis
treatment
primary hyperaldosteronism
A plasma aldosterone concentration/plasma renin activity (PAC/PRA) ratio ≥20 with a PAC of ≥12 ng/d
MRA
orthostatic hypotension on diuretic
decrease dose, may need to have permissive mild hypervolemia
cardiac index formula
causes of cardiogenic shock
O2 consumption / arteriovenous O2 difference
MI, acute valvular insufficiency, or an acute intracardiac shunt.
ARNI indicated in
(NYHA) functional class II-IV and an LVEF ≤40%.
