Cardiovascular Flashcards
End organ damage in HTN (4)
Brain –> ischemic stroke, ICH, cerebral atrophy/dementia
Eyes –> HTN-retinopathy, retinal hemorrhages, vitreous hemorrhage, impaired vision, blindness
Kidneys –> CKD –> ESRD
Heart –> CAD, ischemic heart disease, LVH, HF, acute aortic dissection, arterial aneurysm, hypertensive emergency
**High levels of aldosterone & angiotensin II contribute to tissue modulation and end organ damage (fibrosis, endothelial dysfunction, inflammation –> CAD!)
Stages of hypertensive retinopathy
- Arteriolar narrowing
- AV nicking
- Hemorrhage, cotton wool spots, exudates
- Stage 3+ papilledema
Screening guidelines for HTN
18-39, no risk factors, & BP measurement <130/80 can measure every 3-5 years
> 40, +RF, or bp >130-139/85-89 measure ANNUALLY
Classification of HTN in adults
Normal: <120/80 Elevated: 120-129 AND <80 Stage 1: 130-139 or 80-89 Stage 2: >140 or >90 HTN crisis: >180 and/or >120
** ONLY prescribe meds for stage 1 HTN if pt has already had cardiovascular event or is at high risk of MI/CVA based on age, DM, CKD, or calculation of atherosclerotic disease
Diagnosing HTN
High BP readings on TWO separate office visits w/ TWO or more properly measured readings per visit
BFTP: Normal: <120/80 Elevated: 120-129 AND <80 Stage 1: 130-139 or 80-89 Stage 2: >140 or >90
Initial Evaluation of HTN - factors to consider in history
Ask about pt PMH (HTN, CVA, TIA, CAD, HF, PAD, DM, HLD)
Ask about family hx (HTN, DM, HLD)
Medications hx (NSAIDs, stimulants, TCAs, SSRIs, OCPs, cold remidies (pseudoephedrine), GC, OTC herbals)
Ask about social history (smoking, ETOH, cocaine, exercise, work/stress, sleep habits)
RF Primary HTN
Age (see elevated SBP AND DBP), obesity, family hx, race, high-sodium diet (>3g/day), excess ETOH, physical inactivity, DM/HLD, hostile/angry/depressed
PE person w/ HTN
BP, pulse, eyes (fundoscopic exam for end organ damage), neck/abd (bruits from CAD)
Can have xantholasma from HLD or displaced PMI 2/2 LVH 2/2 HTN etc
Selective testing to evaluate presentation of HTN
BMP - electrolytes, glucose
Lipids - HDL, LDL, TG
H/H
UA - protein? = indicator of microvascular disease
EKG - baseline & to look for prior MI (Q wave) or LVH
Treatment HTN
Non-pharmacologic: Weight reduction (dec BP 5-20), DASH eating plan (diet rich in fruits, vegetables, low fat dairy, dec BP 8-14) dietary sodium reduction (dec BP 2-8), physical activity (dec BP 4-9), dec ETOH intake (dec BP 2-4), smoking cessation → effects not all additive & time/dose dependent
Pharmacologic: Thiazide diuretics, CCB, ACE/ARB
Presribe meds for stage 1 if + CV risk or stage 2 w/o CV risk
How to choose diuretic vs CCB vs ACEi/ARB…..
Order of importance when choosing therapy → CKD > RACE > Comorbidities
If a person has CKD → ANY AGE OR RACE → ACE or ARB
African American (without CKD) → Thiazide or CCB
Follow up after dx HTN
Elevated HTN –> tx = non-pharmacologic, annual follow up
Stage I HTN –> tx = non-pharmacological management → q1-6 months **UNLESS HAVE CV RISK (prior event, elevated calculated CV risk) then stage I also gets drugs!!!
After pt reaches goal BP, follow up q3-6 mo, check SCr & K+ at all
Pharmacological intervention (indicated for stage 1 if +CV risk or stage 2 if no CV risk) → Increase dose or add drug at 2-4 week intervals until the pt reaches goal (on thiazides check potassium levels 3 weeks after each adjustment)
Resistant HTN
BP uncontrolled despite adequate adherence to 3 drugs dosed at >50% max
Consider why therapy might not be working: poor adherence to meds/lifestyle modifications, or inaccurate BP measurement, or suboptimal anti-hypertensive therapy, or white coat syndrome
At this point, the pt needs to be referred to hypertension specialist
Resistant HTN = more likely to have an identifiable cause (ie more likely to be secondary hypertension)
HTN etiology - PRESSURE
P - Pheochromocytoma;
Polycythemia,
Pre-eclampsia/Eclampsia
R - Renovascular (7%)
E - Endocrine: Hyperthyroid,
Cushing, Aldosteronism,
Hyperparathyroid
S - Substances: GC, OCPs, MAOIs, sympathomimetics, Estrogens (BSP), Caffeine, Cocaine, sympathomimetics, ETOH withdrawal
S - Structural - HEART/VESSEL: Coarctation of aorta, AI,
Arteriosclerosis
U - Upper Motor Neuron Problem: Elevated intracranial pressure, sleep apnea, acute stress
R - Renoparenchymal (0.5%):
Glomerulonephritis, Diabetic nephropathy
E - Essential: 90% of hypertension, Error in cuff size
Regulation of arterial pressure & mechanisms of HTN (4 main)
Arterial pressure (AP) = CO X PVR
CO = SV X HR
PVR - determined by vascular structure (anatomy) and vascular function)
Mechanisms of HTN:
1. Increased intravascular volume = increases PVR because to maintain constant blood flow across bed & blood flow = pressure across bed/vascular resistance
- Autonomic Nervous System - doesn’t cause HTN but v active in regulating blood pressure - therefore if it is out of whack can get HTN-
Adrenergic reflexes modulate BP over short term (INC AP = inc baroreceptor firing = decreased SANS outflow, DEC AP = dec baroreceptor firing = INC SANS outflow etc)
Alpha 1 - on smooth muscles in vessels - activation = vasoconstriction
Alpha 2 - Activation = decreased SANS (catecholamine) activity - blockade = increased SANS (catecholamine) activity
B1 (located on HEART and kidney) activation = inc renin release, increased cardiac conduction strength & rate = inc CO. Therefore can block B1 = dec CO = dec AP
B2 - located on vessels - activation = vasodilation
Therefore anti-HTN use alpha 1 blockers (terazosin) or alpha 2 agonists (methyl-dopa, clonidine), or beta-blockers
HTN often associated w/ increased SANS outflow - esp in the obese & those w/ OSA - therefore block w/ clonidine
- RAAS -
Renin prod in aferent arterioles = angio II = vasoconstrictor & aldosterone = hold onto sodium = intravascular volume inc - Vascular Mechanisms - - atherosclerotic disease = HTN
Vascular radius and compliance = v important determinants of arterial pressure.
VOLUME: Resistance to flow varies inversely to the 4th power with radius. Remodeling of vessels 2/2 athero = hypertrophic changes = dec lumen size = increased resistance in arterioles
ELASTICITY: Also elastic vessels can accommodate inc in volume w/o inc in pressure but in semi-rigid vessels, sm inc in volume = large inc in pressure
Also, in normal pt, vascular endothelial system = release NO = vasodilation, this system = impaired in pt w/ HTN
Hypertensive Encephalopathy
Normally, cerebral pressure remains same over widely varying mean arterial pressures via system called autoregulation. Autoregulation failure = HTN encephalopahy
Si/sx: HA, N/V (projectile), focal neurological sign, AMS - left untreated = coma, seizures
Note: You MUST distinguish HTN-encephalopathy from other neurological conditions that present w/ HTN: Cerebral ischemia, CVA, seizure disorder, mass lesion, pseudotumor cerebri, delirium tremens, meningitis, acute intermittent porphyria, and acute uremic encephalopathy
HTN & Neurological SX - differential dx - PLACES to look …
P - pseudotumor cerebri L - lesion - mass in brain, meningitis A - acute uremic syndrome, acute porphyria, alcohol withdrawal (Delirium tremens) C - cerebral ischemia, CVA E - encephalopathy - hypertensive S - Seizure disorder
Clues specific to secondary HTN
History → Onset < 30 YO, stage II severity unresponsive to tx, episodic/HA/palpitations (→ indicates pheo, thyroid dys), morbid obesity w/ hx snoring/daytime sleepiness (sleep d/o)
Exam → pallor/edema (→ sign of renal dz), abd diastolic bruit (→ sign of renovascular HTN), truncal obesity/purple striae/buffalo hump (→sign of hyper-cortisolism)
New onset at younger age, patients presenting w/ stage II HTN, abrupt onset HTN in previously normal, HTN resistant to treatment, clinical clues (listed above), & hypokalemia
Suspected culprit - test to order:
Cushings - do dexmeth suppression test. CKD - get eGFR. Coarctation - get CT angio. Pheo - 24 hr urine metanephrine test. renovascular - Doppler flow or MR angiography. Sleep apnea - sleep study w/ O2 sat. Thyroid/PTH disease - TSH, serum PTH.
Pheochromocytoma Sx
Triad: Palpitations, diaphoresis, headache, also: resistant or paradoxical HTN
Tx - surgical resection of tumor. Pretreat 2 wks w/ alpha blocker (phenoxybenazamine)
DO NOT use beta-blockade to treat pheo sx -unopposed beta block (aka beta block w/o alpha block) = severe refractory HTN
HTN urgency
> 180 SDP or >120 DBP, asymptomatic, NO evidence of acute end-organ damage,
Treatment → slow reduction over SEVERAL HOURS→DAYS (NO benefit in rapid reduction)
Reduce too fast → hypoperfusion, stroke, or MI
Goal < 160/100mmHg or no more than 25-30% baseline BP
Medications used → furosemide (if not volume depleted), oral clonidine, oral catopril (if not volume overloaded)
Do make sure you manage so the person doesn’t go into hypertensive emergency
HTN Emergency
HYPERTENSIVE EMERGENCY→ >200/100
Immediate but careful reduction in blood pressure is indicated
Excessive hypotension may lead to ischemic complications (hypoperfusion → stroke)
Parenteral agents → nitroprusside, nitroglycerin, nicardipine, labetalol, esmolol, hydralazine
ACEi - Uses, ADRs
Use in HTN for blood pressure reduction: Decreasing angiotensin II = Reduce TPR = Reduce BP& inc vessel compliance = less work for heart
Used to decrease protein in urine and stabilize renal function in DM/CKD (“renal protective” effect)
Evidence for use in heart failure and post-MI
Therefore used in HTN, post-MI, left ventricular systolic dysfunction (dec afterload), systolic heart failure, diabetic nephropathy (dec glomerular injury by dec capillary pressure), CKD
ADRs:
Acute renal failure (short term kidneys sense the dec in perfusion = kidneys work go into overdrive w/ renin = AKI/ARF - norally seen w/ initiation or dose increases)
Dry cough
Hyperkalemia (no ald = no retention of Na+ w/ excretion of K+), angioedema, TERATOGENIC - affects fetus’ kidney fxn = BAD, not as effective on AA b/c their HTN not due to RAAS system overdrive
Angiotensin Receptor Blockers (ARBs)
MOA: Binds directly to AT1 receptors and blocks endogenous angiotensin’s effects
Losartan also great for gout (decreases uric acid levels)
Indications: HTN, post-MI, CKD etc same as an ACEi
ADRs: Hyperkalemia, AKI/ARF, angioedema, hypotension, teratogenic etc
4 specific populations w/ indication for statin therapy
- Those with clinically evident ASCVD (CVA, MI, TIA)
- > 21 YO w/ LDL > 190
- 40 -75 YO w/ DM & LDL 70-189
- Those w/ 10-year ASCVD risk >7.5% who are 45-75 YO w/ LDL 70-189
