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
MOA Statin & ADRs/CI, & pleiotropic effects
HMG-CoA Reductase inhibitors (block synthesis of cholesterol)
ADR: Myalgia (no CK inc), myopathy (>10x CK inc), rhabdo (> 10-100x CK inc), increased LFTs, HA, constipation
DO NOT GIVE IN CHRONIC LIVER DISEASE OR PREGNANCY
Pleiotropic effects: Decrease endothelial dysfunction, increase plaque stability, decrease platelet activation/aggregation, decrease vascular inflammation
RF for statin-induced myopathies & management
Advanced age, woman, CKD (inc statin level b/c filtered thru kidneys), DDIs, impaired liver function, alcohol abuse
Rule out secondary causes (DDIs causing supratherapeutic statin serum level, injury), switch to more hydrophilic statin (fluva, prava, rosuva), try QOD dosing w/ longer-acitng statins
Fluva metab via 2C9 = interactions w/ omeprazole, azole antifungals etc)
Lova, simva, atorva = 3A4 = DDIs w/ azoles, verapamil, dilt, protease inhibitors, macrolides, cyclosporines, cimetidine = all = INC statin serum levels
Bile Acid Sequesterants
Indication: Statin-intolerant pt who needs LDL lowered
MOA: Prevent reabsorption of BA, therefore liver has to breakdown more cholesterol to make more bile
ADRs: POORLY tolerated - GI upset - also INCREASE TG, dec ab of fat-soluble vitamins (ADEK)…
SAFE IN PREGGERS! but last line due to tolerability issues…
Niacin (indication, MOA, ADR)
Indication: 2nd line LDL lowering therapy but primary target = TG lowering
MOA: reduces VLDL synthesis in liver & dec FFA release from adipose tissue
ADRs: Flushing, increases uric acid & blood sugar (all use OAT for excretion)
CONTRAINDICATED IN PREGGERS
Ezetimibe (Indication, MOA, ADR)
Indication: Third-line agent (behind statin, niacin) for LDL-lowering. In pt w/ ACS may be added to reduce risk mortality.
MOA: Prevents dietary ab of cholesterol @ brush border of GIT. No effects on TG.
ADRs: Fairly-well tolerated. HA, sinusitis
NOT SAFE W/ BAS
NOT SAFE IN PREGNANCY
Gemfibrozil, Fenofibrate (indication, MOA, ADR)
Indication: Patients w/ TG > 500 despite implantation of lifestyle modifications
MOA: PPAR-alpha R-agonist = dec VLDL synthesis, increased lipolysis, increased clearance of TG-rich lipoproteins
ADRs: MYOPATHIES - when used w/ statins, risk of myopathies is ADDITIVE, increased LFTs, Nausea, GI upset
NOT SAFE IN PREGNANCY
Lovaza (indication, MOA, ADR)
Lovaza = prescription formulation of omega 3 - need 15 gm/day to see effect.
Indication: To lower TG
MOA: Inhibits hepatic secretion of TB & promotes metabolism of TG
ADR: FIshy-tase, burping, anti-plt effects at high doses
Alirocumab
Evolocumab
Bococizumab
MOA:
PSCK-Inhibitors - PSCK-9 normally eats up LDL-R, less LDL-R = less LDL removed from blood. PSCK-9-Inhibitors are monoclonal ab that bind & block PSCK-9 so it can’t eat up the LDL-R - increased LDL-R = increased clearance of LDL
Indications:
When added to statin = > 60% additional reduction!!! BUT very expensive, so reserved for those w/ familial hypercholesterolemia not responding to statins, those w/ statin intolerance, or those w/ multiple risk factors (DM, previous CVD event)
ADR: Injection site reactions
Pericarditis Etiology
P - Post Traumatic
E - Endocrine - severe hypothyroidism
R - Renal Failure - end stage
I - Idiopathic/infectious: post-URI = (VIRAL - COXSACKIE & FLU = MC), also Fungal, bacterial, others (LYME PERICARDITIS)
C - complications = cardiac tamponade 2/2 large pericardial effusion
A - Aneurysm
R - Rheumatic Fever, RA
D - Drugs: Hydralazine, Minoxidil, Procainamide
I - Infarction - AMI - peri after = DRESSLERS SYNDROME
TI - Tumor invasion, Cancers - lung/breast, HL
S - SLE, syphilis, Scleroderma, Serum Sickness
Diagnostics to order pericardial effusion
EKG = MOST USEFUL DIAGNOSTIC - ST elevations across the board!!!
CBC (WBC inc), cardiac enzymes (troponin), inflammatory markers (sed rate, CRP), echo (check for effusion), +/- CXR
Symptoms pericarditis
Pleuritic chest pain - sharp, worse w/ inspiration (95% of pt w/ pericarditis have cp)
Pt sitting up & LEANING FORWARD - relieves pressure from pericardial fluid (pt also leaning forward in pancreatitis)
Diagnostic criteria pericarditis
> 2 following:
Pericardial chest pain (pleuritic, sharp)
Pericardial friction rub
Changes on EKG (ST elevations across board)
New or worsening pericardial effusion
Management pericarditis
NSAIDS or aspirin x 2-3 wk
+/- colchicine
+ PPI (prevent gastritis)
Refractory pericarditis (add GC therapy w/ taper)
Dressler’s - use ASA + colch
Pericarditis disposition (when to hospitalize)
Fever > 100.4
Evidence of tamponade (tamp becks on HEAD = heart sounds muffled, elevated JVP w/ no BP, large pericardial effusion, immunosuppressed state, acute trauma, coumadin/antiplatelet therapy, failure to respond to NSAID as an outpatient, elevated cardiac troponin
Peripheral arterial disease - CP & PE
Clinical presentation Intermittent claudication (<0.9 = >50% stenosis) progressing to rest pain (ABI < 0.4 = SEVERE stenosis)
Physical Exam
Cool shiny limb w/ decreased hair
Normal ABI = >0.9-1.3
PAD:
P - pain w/ walking, relieved by rest
A - alopecia - no hair on legs, shiny
D - diminished pulses, decrease in ABI < 0.9
Rheumatic fever diagnosis
Add picture in phone - jones
- Arthritis moves from joint to joint in an asymmetrical pattern
- Antistreptolysin O (ASO) often positive
- Requires long term prophylaxis against strep
What is the role of ACEi in heart failure?
ACEi are used in HF because they reduce ventricular hypertrophy and produce a more hemodynamic state by restoring arterial compliance
Remember AGII acts on vessels to increase PVR which puts more strain on the heart (more afterload) - also more venous dilation is decreased filling pressure = decreased preload
