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
