Cardio

Question 1

Dilated Cardiomyopathy:

Pathophys, Etiology & Epidemiology

Answer 1

• Def: systolic dysfunction (S3 gallop) leading to a dilated, weak heart with EF <40%
• Pathophys:
  
  • increased heart size & weight, ventricular dilation, thinned ventricular walls (usually due to increased volume)
• Etiology:
  
  • Idiopathic = most common cause
  • alcohol (#2)
  • myocarditis (#3)
  • cocaine
  • doxorubicin
  • infection (viruses eg coxsackie, HSV 6, adenovirus)
• Epidem:
  
  • age 20-60
  • most COMMON type of cardiomyopathy

Question 2

Dilated Cardiomyopathy: S/sxs

Answer 2

• Sxs:
  
  • pulm congestion (Left HF): dyspnea, orthopnea, rales
  • systemic congestion (Right HF): peripheral edema, JVD, nausea, abdominal pain, nocturia, enlarged liver
  • Low CO: fatigue, weakness
• Other:
  
  • HTN or hypotension
  • tachycardia, tachypnea
  • S3 gallop
  • mitral/tricuspid regurg: papillary muscles stretches with dilation -→ valvular dysnfunction
  • PMI shifted laterally

Question 3

Dilated Cardiomyopathy: Dx

Answer 3

• Diagnostic Criteria:
  
  • inclusion: EF <40%
    
    • LVEDD >177% of predicted
• Labs to order:
  
  • BNP
  • Na, Mg, K
  • BUN, Cr (CMP)
  • Hemoglobin (CBC with diff)
• CXR:
  
  • cardiomegaly
  • pulmonary edema
  • pleural effusion
• EKG:
  
  • wide QRS
  • LBBB
• Echocardiogram:
  
  • L ventricular dilation
  • thin ventricle walls
  • decreased ejection fraction (<50%, but often <30%)

Question 4

Dilated Cardiomyopathy: Dx

Answer 4

• Diagnostic Criteria:
  
  • inclusion: EF <40%
    
    • LVEDD >117% of predicted
• Labs to order:
  
  • BNP
  • Na, Mg, K
  • BUN, Cr (CMP)
  • Hemoglobin (CBC with diff)
• CXR:
  
  • cardiomegaly
  • pulmonary edema
  • pleural effusion
• EKG:
  
  • wide QRS
  • LBBB
• Echocardiogram:
  
  • L ventricular dilation
  • thin ventricle walls
  • decreased ejection fraction (<50%, but often <30%)

Question 5

Dilated Cardiomyopathy: Tx

Answer 5

• tx just like systolic heart failure
  
  • beta-blockers (metoprolol, carvedilol) + [ACE-I (lisinopril, captopril, enalapril) =mainstay of tx] + Loop diuretic (furosemide)
  • Anticoag if EF <30%
• if you need increased contractility = digoxin (digitalis)
• Pt education:
  
  • limit activity
  • salt restriction <2g/day
  • fluid restriction <2L/day
• extreme cases = heart transplant or L ventricular assist device

Question 6

Canadian Cardiovascular Society Classification System: Angina

Answer 6

• Stage I: angina with strenuous activity
• Stage II: slight limitation of ordinary activity; angina walking 2 blocks, up stairs rapidly
• Stage III: marked limitation of ordinary activity; angina walking 1-2 blocks
• Stage IV: Angina at rest

Question 7

Major Risk Factors of Coronary Artery Disease (CAD)

Answer 7

• Diabetes Mellitus (Worst risk factor, considered a CAD equivalent)
• Smoking (Most important modifiable risk factor)
• Hyperlipidemia, HTN
• Men >45yo, Women >55yo
• Fam Hx of CAD: (first degree relative – father or brother before age 55, mother or sister before age 65)

Question 8

Etiology of Acute Coronary Syndrome

Answer 8

• Etiology:
  
  • atherosclerosis = most common cause -→ acute coronary artery thrombosis with platelet adhesion with fibrin formation
  • coronary artery vasospasm: prinzmetal variant angina, cocaine induced
• Silent MI:
  
  • 25% are atypical, more common in women, elderly, diabetics, obese patients; sxs include: dyspnea, epigastric pain, syncope, or sudden death

Question 9

NSTEMI: def, s/sxs, dx, & tx

Answer 9

• Definition: myocardial necrosis (evidenced by elevated troponins & cK-MB) without acute ST segment elevation; coronary artery not completely blocked, subendocardial infarct
• S/sxs:
  
  • Chest pain, SOB
• Dx:
  
  • EKG: ST-depression, T-wave inversion
  • Troponins: positive, usually need 2+ draws on this, troponins take up to 3 hours to become elevated
• Tx:
  
  • First line: oxygen of o2 <95%
    
    • sublingual nitroglycerin (1-2 sprays Q5 min, max of 3)
    • Aspirin (inhibits platelet activation)
  • either IV unfractionated heparin (inhibits factor IIa (thrombin, and factor Xa) OR SQ enoxaparin (low molecular weight heparin, only inhibits factor Xa)
  • clopidogrel 300mg
  • if going for PCI → high dose statin prior to angiography
  • Then eventually: BAAAS (b-blocker, ace-i or ARB, stain)
  • ***Do NOT use Thrombolytics***
  • “go to cath lab if not responding to treatment and still having chest pain, significant ST changes etc. Not all NSTEMI go to Cath emergently, many do not need to. Can cath semi-electively” -Dr Pearl

Question 10

STEMI: def, s/sxs, dx & Tx

Answer 10

• Definition: myocardial necrosis (evidenced by elevated troponin & CK-MB) with acute ST-segment elevation or Q-waves; coronary artery completely blocked; full thickness infarct
• S/sxs:
  
  • Chest pain
  • SOB
  • pain radiating to jaw and/or arm
• PE:
  
  • Inferior Wall MI:
    
    • bradycardia or heart block (R. coronary artery supplies the AV node)
    • epigastric pain
    • may have S4
  • Triad of R ventricle MI:
    
    1. JVD
    2. Clear lungs
    3. positive Kussmaul sign : paradoxical JVP that occurs during inspiration -→ heart cannot accommodate extra blood that returns via the venous system when the intrathoracic pressure becomes negative during inspiration
• Dx:
  
  • EKG: new ST-elevation in two contiguous leads of >1mm
    
    • reciprocal changes in opposite leads
    • **progression: hyperacute T-waves → ST elevations → Q waves
  • Troponin:
    
    • positive → returns to baseline in 7-10 days
    • **may be falsely positive in pts with renal failure, advanced heart failure, acute PE, or CVA**
• Tx: a) prevent further clot formation by inhibiting platelet function- Aspirin and Clopidogrel
  
  • b) Prevent thrombus formation by blocking Fibrin with Heparin
  • c) Decrease Myocardial Oxygen demand (while working to improve supply)- Beta Blockers
  • d) Vasodilate coronaries (spasm may occur as well with ischemia) and decreases preload as well by vasodilation- NTG
  • e) Oxygen- only if sats below about 95%
  • f) Morphine-used less frequent now- need a good BP, avoid in right ventricular infarction
  • g) ACE inhibitor may be added later for remodeling and for afterload reduction, can use sooner if hypertensive
• Definitive care:
  
  • If < 3-5 hours and having STEMI go emergently to Cath lab for PTCA ( Balloon and Stent). Goal is 90 minutes door to reperfusion.
  • IF > 3 hours before one can get to a cath lab then use Thrombolytic Therapy TPA or TKI etc. for STEMI

Question 11

Post MI Complications

Answer 11

• Pericarditis: 1-3 weeks post MI (Dressler Syndrome)
• VSD (ventricular septal defect: 1-5 days post MI: shock, new murmur, pulmonary edema
• Acute Mitral Regurg: shock, apical murmur, pulmonary edema
• new or recurrent MI: chest pain, new ECG changes possible, new bump in troponins

Question 12

Stable Angina

Answer 12

Coronary Artery Disease

• predictable and occuring with exertion → typically same distance each time
• relieved with rest or NTG
• Workup:
  
  • EKG: Normal, q-waves (if prior MI)
  • Cardiac Stress Test: pt should be able to walk 6 min on treadmill or else unreliable, goal is 85% of max predicted HR
    
    • bruce protocol (increase by 2% grade & 0.8mph q 3 minutes)
    • monitor: BP, EKG, Echo, sxs (CP, SOB)
  • coronary angiography:
    
    • provides a definitive dx → defines location and extent of CAD but only used if:
      
      • pt is severely symptomatic despite medical therapy and being considered for PCI
      • pt with sxs difficult to dx
      • angina sxs in pts who have survived cardiac death event and ots with ischemia on non-invasive testing
• Tx:
  
  • NBC (mnemonic to remember)
    
    • beta blockers: decrease HR, contractility, blood pressure → decreased demand (metoprolol, carvedilol)
    • nitroglycerin: sublingual or IV: decrease preload/afterload, vasodilate coronary arteries
    • Calcium channel blockers: decrease afterload/blood pressure (velocity) , may dilate coronary arteries (non-dihydropyridine CCBs → diltiazem, verapamil)
    • Statins: improve endothelial function
    • aspirin: prevent thrombus formation (anti-platelet activation)

Question 13

Unstable Angina

Answer 13

• Definition: occurs at rest (Canadian Angina Classification Level 4), or not relieved by rest or NTG. Some include exertional angina that is occurring more frequently, with lesser exertion, more intense, lasting longer (Crescendo Angina
• Dx:
  
  • EKG = ST segment depression >1 mm
  • Troponins: Negative (no cell death)
  • angiography = gold standard for diagnosing CAD but only used when revascularization is being considered
• Tx:
  
  • antiplatelet drugs (aspirin and/or clopidogrel (plavix) ticagrelor)
  • beta-blockers (metoprolol, carvedilol)
  • nitroglycerin & Ca channel blockers for symptom control
  • Revascularization if sxs persist despite medical therapy
  • ACE-I + statins

Question 14

Stress Test (Exercise Testing)

Answer 14

• Pt must be able to walk 6 min on a treadmill: goal is 85% of max predicted HR
• initial test in pts who are stable and able to exercise
  
  • Bruce Protocol: increase grade by 2% and speed by 0.8mph q 3 minutes
  • Monitor: BP, EKG, symptoms (CP, SOB)
  • Duke Treadmill Score: (duration of exercise in min) - (ST segment depression in mm)x (5) - (angina score)x(4)
• if patient cannot exercise:
  
  • can use adenosine for myocardial perfusion imaging
  • can use dobutamine for a stress echo

Question 15

Angina- Prinzmetal Variant

Answer 15

• Definition:
  
  • Coronary artery vasospasm causing transient ST-segment elevations, not associated with clot. Usually happens at night or early morning
  • risks: COCAINE ABUSE, female >50yo, hx of vasospastic disorders
  • triggers: cold weather, exercise, alpha-agonists, hyperventilation
• S/sxs:
  
  • chest pain at rest (usually midnight to early morning, non-exertional & not relieved with rest)
  • Preserved exercise capacity
• Dx:
  
  • EKG: transient ST-elevation that resolves with symptom resolution
    
    • inverted U-waves
• Tx:
  
  • calcium channel blockers: first line monotherapy -→ given at NIGHT (Non-dihydropyridine: diltiazem, verapamil Qday)
    
    • → can add long acting nitrate (Isosorbide mononitrate ER 30-60mg QAM: SEs: Methemoglobinemia, severe hypotension)
  • Nitroglycerin IR for sx relief (1-2 sprays sublingual Q5 min PRN, max of 3 doses)
  • AVOID BETA-Blockers! → may cause unopposed vasospasm

Question 16

Acute vs. Chronic Heart Failure

Answer 16

• S/sxs:
  
  • Chronic Heart Failure (compensated):
    
    • congestion
    • laterally displaced apical impulse
  • Acute Heart Failure:
    
    • breathlessness
    • rapid weight gain
    • fluid build-up in the lungs and around the body
    • inadequate time for compensation: largely systolic (HTN crisis, acute MI, papillary muscle rupture); often fatal

Question 17

Systolic Heart Failure

Answer 17

• Definition: heart failure with decreased ejection fraction
  
  • impaired contractility
  • thin ventricular walls (DILATED)
  • S3 gallop (sys-tol-ic)
• Etiology:
  
  • ischemic heart disease, rapid HTN, dilated cardiomyopathy (LEADING CAUSE), myocarditis, congenital, post-surgical, PE, sepsis

Question 18

Diastolic Heart Failure

Answer 18

• Definition: Heart failure with preserved ejection fraction
  
  • impaired filling/relaxation
  • thick ventricular walls (**Hypertrophied**)
  • S4 gallop (Di-a-stol-ic)
• Etiology:
  
  • HTN, aortic stenosis, restrictive & hypertrophic cardiomyopathy, fibrosis, amyloidosis, sarcoidosis, constrictive pericarditis, normal aging, CAD scarring

Question 19

Management goals of Heart Failure

Answer 19

1. Afterload: make it easier for the heart to empty
2. preload: appropriate stretch, get the heart back on the proper part of the Sterling curve
3. contractility: help the heart function better (pump, squeeze, relaxation, rate & rhythm)

**Uncompensated heart failure: diuretics, afterload reduction, inotropes, mechanical support, transplantation

**Compensated heart failure: diuretics, afterload reduction, beta-blockers

Question 20

Tx of Heart Failure

Answer 20

• **initial management usually consists of an ACEI & (maybe a beta blocker) + diuretic (for sxs)**
• Long Term Tx (Afterload reduction:
  
  • ACE Inhibitors (Captopril, Enalapril, Lisinopril): reduce afterload by vasodilation & BP reduction, useful in pts with EF <35%,mainstay of tx, (adverse effects: hyperkalemia, cough, angioedema, & elevated creatinine)
  • Angiotensin II Receptor Blockers (Losartan, Valsartan): blocks effects of angiotensin II, indicated in pts who cannot tolerate ACEI (cough)
  • Angiotensin Receptor Neprilysin Inhibitor (Sacubitril/Valsartan): inhibits breakdown of BNP so BNP no longer becomes a reliable marker in pts taking this
  • Beta-Blockers (Carvedilol, Metoprolol, Bisprolol): usually added after ACEI or AR
• Long Term Tx (Preload Reduction)
  
  • Loop Diuretics (furosemide, bumetanide, torsemide): inhibit water transport across the Loop of Henle, effective for sx tx.
  • potassium sparing diuretics (spironolactone, eplerenone): aldosterone antagonist, decreased mortality
  • Thiazides (hydrochlorothiazide, Metolazone): inhibits DCT reabsorption of Na+
• Long Term Tx (Positive Inotropes):
  
  • Digoxin: positive inotrope; 2nd line for pts in CHF with sinus rhythm, 1st line for pts with afib + CHF

Question 21

Left-Sided Heart Failure: Pathophys, Etiology, S/sxs, PE

Answer 21

• Pathophys: leads to increased pulmonary venous pressure from fluid backing up into the lungs. Increased hydrostatic pressure drives protein-poor fluid into alveoli through an intact barrier
  
  • → resolution depends on Na+ reabsorption and lymphatic drainage
• Etiology:
  
  • Coronary artery disease, HTN = most common
• S/sxs:
  
  • dyspnea: exertional, paroxysmal nocturnal dyspnea, orthopnea
  • fatigue
  • cough with frothy sputum
  • activity intolerance
• PE:
  
  • pulmonary edema & congestion → crackles, rhonchi, wheezing, tachypnea
  • cheyne-stokes breathing: deep, fast breathing with gradual decrease in episodes of apnea
  • cyanosis
  • S3 or S4 gallop

Question 22

Right-Sided Heart Failure: Pathophys, Etiology, S/sxs, PE

Answer 22

• Pathophys:
  
  • leads to increased systemic venous pressure from fluid backing up into the IVC, SVC, and hepatic circulation
• Etiology:
  
  • left sided heart failure = most common
  • pulmonary disease (COPD, pulmonary HTN), mitral stenosis
• S/sxs/Pe:
  
  • inferior vena cava:
    
    • peripheral edema
  • Superior Vena Cava:
    
    • jugular vein distention
  • hepatic: anorexia, weight loss, n/v, hepatojugular reflex
  • hepatosplenomegaly

Question 23

Hypercholesterolemia: primary vs secondary, etiology, risk factors

Answer 23

• primary: WITHOUT known CV disease (carotid, heart, arteries)
• Secondary: with known clinical CV disease
• Etiology:
  
  • hypothyroidism, pregnancy, kidney failure
• Risk Factors:
  
  • sex, age, HTN, DM, smoking, family hx of coronary heart disease
    
    • 1st degree male relative with CHD before age 55
    • 1st degree female relative with CHD before age 65

Question 24

Primary Prevention of ASCVD in age 0-19 years

Answer 24

• lifestyle to prevent or reduce ASCVD risk
• Diagnosis of familial hypercholesterolemia?
  
  • statin

Question 25

Primary Prevention of ASCVD in Age 20-39

Answer 25

• Estimate lifetime risk to encourage lifestyle to reduce ASCVD risk
• Consider statin if family hx, premature ASCVD and LDL-C ≥ 160mg/dL

Question 26

Primary Prevention of ASCVD in Age 40-75 and LDL-C ≥ 70 to <190 mg/dL without diabetes mellitus

Answer 26

10-year ASCVD risk percent begins risk discussion:

• <5%: “low risk”
  
  • emphasize lifestyle to reduce risk factors
• 5-<7.5%: “borderline risk”:
  
  • If risk enhancers present then risk discussion regarding moderate-intensity statin therapy
• ≥7.5-<20%: “Intermediate Risk”
  
  • Risk discussion:
    
    • if risk estimate + risk enhancers favor statin, initiate moderate-intensity statin to reduce LDL-C by 30-49%
    • if unsure, can use CAC score
• ≥ 20%: “high risk”:
  
  • initiate statin to reduce LDL-C ≥ 50%

Question 27

At what LDL-C level do you initiate high intensity statin with no risk assessment?

Answer 27

LDL-C ≥ 190 mg/dL

Question 28

What population do you initiate a moderate-intensity statin regardless of risk factors?

Answer 28

Diabetes Mellitus age 40-75yo

Risk assessment to consider high-intensity statin

Question 29

CAC

Answer 29

Coronary Artery Calcium Score

• if risk decision is uncertain in age 40-75yo with intermediate risk (≥7-<20%)
• CAC = zero
  
  • (lower risk; consider no statin unless diabetes, family hx of premature CHD, or cigarette smoking are present)
• CAC = 1-99
  
  • favors statin (esp. after age 55)
• CAC = 100+ and/or ≥75th percentile:
  
  • initiate statin therapy
• Calculate MESA score with CAC, will give you a percentage by which to evaluate whether to initiate statin

Question 30

Best meds to lower elevated LDL

Answer 30

• Statins (Rosuvastatin, atorvastatin, etc) → inhibit HMG Co-A reductase
  
  • impair production of cholesterol in the liver → upregulation of LDL receptors
• Bile Acid Sequestrants (Cholestyramine, colesevelam, colestipol) & Cholesterol absorption inhibitors (Ezetimibe)
  
  • impair enterohepatic recirculation and gut absorption → less hepatic cholesterol → upregulation of LDL receptors

Question 31

Best Meds to Lower Triglycerides

Answer 31

• Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
• Niacin

Question 32

Best Meds to Increase HDL

Answer 32

• Niacin
• Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins

Question 33

Treatment of Secondary Hypercholesterolemia without high-risk (clinically stable)

Answer 33

secondary hypercholesterolemia = WITH known clinical CV disease

• high-intensity statin
• can add ezetimibe if inadequate response (<50% LDL reduction); goal is LDL <70 mg/dL

Question 34

Treatment of Secondary Hypercholesterolemia with High Risk (unstable)

Answer 34

secondary hypercholesterolemia = WITH known clinical CV disease

• high-intensity statin
• can add ezetimibe
• can also add PCSK9 monoclonal antibody (Alirocumab, Evolocumab) : blocks PCSK9 binding to LDL receptor → direct upregulation of LDL receptors → lowers LDL 30-60%; injections Q2-3 weeks
• goal is LDL <55 mg/dL

Question 35

Abnormal Lipid Values

Answer 35

• Low HDL <40 mg/dL
• High LDL > 190 mg/dL
  
  • high LDL in diabetic >70 mg/dL
• high total cholesterol >250 mg/dL
• high fasting triglyceride >150 mg/dL

Question 36

Hypertriglyceridemia

Answer 36

• Definition: fasting blood triglyceride level of >150 mg/dL
• Etiology:
  
  • diabetes mellitus, EtOH, obesity, steroids, estrogen
• S/sxs:
  
  • pancreatitis, eruptive xanthomas, lipemia retinalis (creamy white discoloration of the retinal vessels), corneal arcus (grey arc of deposit on outer iris)
• Dx:
  
  • fasting lipid panel
  • Severity:
    
    • 150-499: mild
    • 500-886: moderate
    • >886: severe
• Tx:
  
  • Best meds to lower elevated triglycerides → Fibrates (fenofibrate, gemfibrozil), niacin
  • Best meds to lower elevated LDL → Statins, bile acid sequestration
  • Best meds to increase HDL → Niacin (Nicotinic Acid), fibrates
  • Type II DM → statins, fibrates
  • Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
  • Nicotinic Acid (Niacin): increases HDL levels, causes flushing
    
    • fish oil supplements
  • Lifestyle modification: avoid alcohol & refined sugars, lower caloric intake, exercise

Question 37

Essential HTN: definition, PE, and diagnosis

Answer 37

• Definition:
  
  • resting systolic ≥ 130 or diastolic ≥ 80 on at least 2 readings on at least 2 separate visits with no identifiable cause
    
    • **need to measure BP in Both Arms**
• PE:
  
  • fundoscopic exam: hypertensive retinopathy → AV nicking
• Diagnosis:
  
  • see above definition
  • BP>15 mmHg higher in one arm than the other is associated with a higher mortality → eval of upper vasculature is required!!
  • Other tests you can order: -urinalysis and spot urine albumin: creatinine ratio
  • blood tests (creatinine, K, Na, fasting plasma glucose, lipid profile, and TSH
  • ECG

Question 38

Essential HTN: Tx

Answer 38

• ACC/AHA:
  
  • goals: <130/80
• AntiHTN therapy initiated in the following populations:
  
  1. all pts with stage 2 HTN (baseline ≥140/90)
  2. pts with stage 1 HTN (130-139/80-89 mmHg) who have 1+ of the following:
     
     • ASCVD
     • Type II DM
     • CKD
     • 10-year calculated ASCVD risk ≥ 10%
• Lifestyle Modifications:
  
  • DASH diet, increase fruits and veggies
  • Sodium reduction <2.3grams/day (1 tsp)
  • reduce alcohol intake:
    
    • → Men: 1-2 drinks daily max
    • → Women: 1 drink daily max
  • Exercise goals:
    
    • → >150 minutes of moderate intensity/week
    • → >75 minutes of vigorous intensity/week
• ONE drug given initially:
  
  • for non-black pts, including DM give either:
    
    • → ACE-I or ARB
    • → long acting CCB (often a dihydropyridine like amlodipine)
    • → or a thiazide-like diuretic (chlorthalidone, or indapamide)
  • for stage 2 HTN or a black adults:
    
    • recommendation is
      
      • → 2 BP-lowering meds from different classes
  • If Target BP is not achieved in 1 month, dose of drug can be increased or a second drug added → BP should be checked monthly until the target is met

Question 39

ACC/AHA Classification of BP

Answer 39

Question 40

Hypertensive Emergency: definition, Dx, & Tx

Answer 40

• Definition: >180 systolic and/or >120 diastolic WITH signs of damage to target organs (except papilledema = hypertensive retinopathy) → encephalopathy, nephropathy, intracranial hemorrhage, aortic dissection, pulmonary edema, unstable angina or MI
• Diagnosis:
  
  • BP measurement
  • ECG
  • urinalysis
  • ophthalmic exam
  • serum BUN
  • serum creatinine
• Tx:
  
  • sodium nitroprusside = drug of choice
  • pt should be admitted to ICU
  • If pt has: Aortic dissection, severe pre-eclampsia or eclampsia or pheochromocytoma crisis
    
    • → reduce SBP to <140mmHg during first hour and then to <120 mmHg in aortic dissection
  • If pt does NOT have any of the above:
    
    • Reduce BP by (10-20%) max 25% over first hour, then to 160/100-110 mm/Hg over next 2-6 hours, then to normal over next 24-48 hours

Question 41

Hypertensive Urgency: Definition, Dx, & Tx

Answer 41

• Definition: SBP >180 and/or DBP >120 without target-end organ damage
• Dx:
  
  • BP measurement
  • ECG
  • urinalysis
  • ophthalmic exam
  • serum BUN, serum creatinine
• Tx:
  
  • immediate BP reduction is NOT required
  • Clonidine = drug of choice

Question 42

Secondary HTN Definition and Causes

Answer 42

• Definition: SBP ≥130 and/or DBP ≥80 WITH identifiable cause
• Causes:
  
  • Primary aldosteronism = MOST COMMON
  • renal vascular disease
  • pheochromocytoma
    
    • adrenal tumor that secretes catecholamines (ie norepi and epi)
  • Cushing’s Syndrome
    
    • activation of the renin-angiotensin system
  • Congenital Adrenal Hyperplasia
  • Hyperthyroidism
  • Myxedema
    
    • associated with hypothyroidism
  • Coarctation of the Aorta
  • Excessive alcohol intake
  • Use of Oral Contraceptives

Question 43

Secondary HTN Red Flags, Dx, & Tx

Answer 43

• Red Flags:
  
  • HTN at an early age <25 without a family hx
  • HTN first develops >50 yo
  • previously controlled now refractor
  • Pt is refractory on antihypertensive medications or has severe BP
• Dx:
  
  • when HTN is newly diagnosed consider ordering:
    
    • urinalysis
    • spot urine albumin: creatinine ratio → albuminuria ratio = >30mg/day
      
      • indicative of CKD
    • Blood tests
      
      • creatinine, K, Na, fasting glucose = BMP
      • lipid panel
      • TSH
    • EKG
• Tx:
  
  • tx the underlying condition and aim for BP <130/80

Question 44

Mixed Venous O2 vs A-VO2 difference

Answer 44

• Mixed Venous O2:
  
  • amount of oxygen that is in the venous blood upon return to the heart
    
    • Normal:
      
      • Superior Vena Cava = 65% (brain uses most oxygen)
      • Inferior Vena Cava = 75%
    • Abnormal: <65%
      
      • <50% = danger zone
• A-VO2 difference:
  
  • arterial O2 (~98%) - venous O2 saturation
    
    • normal <30%
    • higher the difference = the WORSE the situation
• As mixed venous O2 drops, AVO2 difference will increase (inverse relationship)

Question 45

Delivery of oxygen is affected by

Answer 45

DO2 = CO x CaCO2

delivery of oxygen is affected by cardiac output and arterial oxygen content

Question 46

Hypovolemic Shock: Definition, Etiologies, Pathophys, S/sxs

Answer 46

• Definition:
  
  • reduction in intravascular volume/preload → decreased CO → insufficient perfusion
• Etiologies:
  
  • hemorrhagic: trauma, GI bleed, ruptured aneurysm, post-operative, open central line
  • non-blood fluid loss: vomiting, diarrhea, 3rd spacing, burns, dehydration, DKA, over-diuresis
• Pathophys:
  
  • loss of blood/fluid volume → increased HR & vasoconstriction, increased epi, vasopressin, & angiotensin
• S/sxs:
  
  • tachycardia/tachypnea
  • narrowed pulse pressure (d/t vasoconstriction)
  • oliguria (d/t decreased CO)
  • hypotension
  • pale, cool dry skin and extremities
  • cap refill >3 sec
  • decreased skin turgor
  • dry mucous membranes
  • AMS

Question 47

Features of Hypovolemic Shock

Answer 47

• Preload: decreased (volume depletion)
• Cardiac Output: decreased
• Afterload: increased (vasoconstriction)
• BP: low
• Organ perfusion: decreased
• AVO2 Difference: high (b/c heart is delivering less blood so tissues are using more O2 from the available blood)

Question 48

Normal Blood Volume

Answer 48

• Adults: 7% IBW (75ml/kg)
  
  • → 70kg adult = 5.5 Liters or approx 15 units
• Children: 9% IBW (90 ml/kg)

IBW = ideal body weight

Question 49

Phases of Hypovolemic Shock

Answer 49

• Compensated: 0-24.9% blood loss (500-1250cc)
  
  • normal SBP/pulse pressure/ pulse, alert
• Uncompensated: 25-40% (1250-2000cc)
  
  • decreased SBP/ pulse pressure, tachycardic, anxious
• Irreversible: >40% blood loss
  
  • decreased SBP/ pulse pressure, very tachycardic, lethargic

Question 50

Tx of Hypovolemic Shock

Answer 50

• ABCs
• Volume resuscitation: Crystalloids (LR or NS)
  
  • usually 3-4 liters:
    
    • initially 1-2 NS boluses to restore tissue perfusion and continued at rapid rate until clinical signs of hypovolemia improve
• control the source of hemorrhage +/- packed RBCs if severe
• maintain body temp (prevent hypothermia)

Question 51

Distributive Shock: Definition, Pathophys, & Etiologies

Answer 51

• Definition: excessive vasodilation in small vessels & altered distribution of blood flow with shunting from vital organs to non-vital tissues
• Pathophys:
  
  • dilation of all blood vessels so the “tank” becomes too big
• Etiologies:
  
  • Septic: overwhelming infx → systemic inflammatory response → systemic vasodilation
  • Anaphylactic: severe rxn to allergen → systemic histamine release → widespread vasodilation
  • Neurogenic: acute spinal injury that results in loss of sympathetic tone that normally keeps vessels constricted → vessel walls veno/vasodilate
  • Endocrine: adrenal insufficiency

Question 52

Distributive Shock: S/sxs of Sepsis, Anaphylaxis, and Neurogenic Shock

Answer 52

• Sepsis: “Warm shock” “warm shock”
  
  • warm, flushed extremities (d/t systemic vasodilation of capillaries)
  • wide pulse pressure
  • bounding pulses
  • hypotension
• Anaphylactic Shock:
  
  • pruritus, urticaria
  • angioedema
  • hoarseness
• Neurogenic:
  
  • warm skin
  • bradycardia or normal HR
  • wide pulse pressure

Question 53

Features of Septic Shock

Answer 53

Type of Distributive Shock

• Preload: decreased
• Afterload: decreased
• Cardiac Output: decreased
• BP: low
• Organ perfusion: decreased
• Mixed venous O2: HIGH (oxygen is not reaching tissues and is not getting used due to loss of vascular tone)
• AVO2 difference: LOW (oxygen is not reaching tissues and is not getting used due to loss of vascular tone)
  
  • so mixed venous o2 is high and arterial o2 is also high

Question 54

Features of Neurogenic Shock

Answer 54

Type of Distributive Shock

• Preload: decreased
• Afterload: decreased
• Cardiac Output: increased
• BP: low
• Organ Perfusion: normal (b/c of good cardiac output so normal organ perfusion)
• AVO2 difference: normal

Question 55

Tx of Distributive Shocks

Answer 55

• Septic Shock:
  
  • broad spectrum IV abx
  • IV fluid resuscitation, then a vasopressor (vasoconstrictor: epinephrine, norepi/phenylephrine)
• Anaphylactic Shock:
  
  • -Epi
  • -Airway management
  • -antihistamines
• Neurogenic Shock:
  
  • IV fluid resuscitation
  • vasopressors +/- corticosteroids
• Endocrine Shock:
  
  • hydrocortisone

Question 56

Obstructive Shock: Definition, Etiology & Tx

Answer 56

• Definition: mechanical block to heart’s outflow or inflow
• Etiology:
  
  • very large PE
  • pericardial tamponade
  • tension pneumo
  • aortic dissection
• Tx: Tx the underlying cause
  
  • PE: heparin, thrombolytics (TPA, TKI)
  • Tamponade: pericardiocentesis
  • Tension Pneumo: needle decompression
  • oxygen, isotonic fluids, inotropic support (dobutamine, epi, milrinone)

Question 57

Cardiogenic Shock: Definition, Etiology, & S/sxs

Answer 57

• Definition: primary myocardial dysfunction (pump failure) → low cardiac output → inadequate tissue perfusion
• Etiology:
  
  • Pump Failure:
    
    • ischemia (CAD), acute MI, myocarditis, valve dysfunction (mitral regurg secondary to papillary rupture), cardiomyopathy, post-operative, myocardial contusion, acute ventricular septal or L ventricular rupture
  • Arrhythmia, toxic/metabolic
• S/sxs:
  
  • Acute hypotension (you can only compensate with increasing afterload [vasoconstriction) BP <90/60
  • tachycardia, tachypnea
  • weak pulses
  • mottled skin
  • diaphoretic
  • AMS
  • anxiety/restlessness
  • Elevated JVP
  • oliguria

Question 58

Features of Cardiogenic Shock

Answer 58

• Preload: increased (due to decreased stroke volume)
• Afterload: increased
• Cardiac Output: decreased
• BP: low
• Organ Perfusion: decreased
• AVO2 difference: high (b/c heart is delivering less blood, so tissues are using more O2 from the blood available)

Question 59

Tx of Cardiogenic Shock

Answer 59

Tx the underlying cause

• if acute MI: revascularize
• inotropic Support(dobutamine, epinephrine, milrinone)
• can use a vasodilator if BP is okay (dobutamine, milrinone)
• if hypotensive then use vasopressor (Epi, norepi/phenylephrine)
• intra-aortic balloon counterpulsation
• oxygen
• isotonic fluids: AVOID large amounts of fluid
  
  • if you use fluids, will eventually need to diurese (Lasix [furosemide])

Question 60

Hypertrophic obstructive Cardiomyopathy: Pathophys & Risk Factors

Answer 60

autosomal dominant

• Pathophys:
  
  • subaortic outflow obstruction d/t asymmetrical septal hypertrophy & systolic anterior motion of the mitral valve
  • **Hypercontractile**
  • can have myocardial ischemia d/t increased muscle mass and increased demand for O2
• Risk Factors:
  
  • young age, fam hx of sudden death, gene mutations prone to SCD, sustained VT or SVT, recurrent syncope, brady arrhythmias
• #1 cause of sudden death in competitive athletes <35 yo

Question 61

Hypertrophic Cardiomyopathy: S/sxs & PE

Answer 61

• S/sxs:
  
  • dyspnea, syncope
  • angina
  • palpitations
  • dizziness
  • fatigue
  • sudden cardiac death
• PE:
  
  • Hypertrophic Obstructive Cardiomyopathy Murmur: Crescendo-decrescendo systolic murmur (best heard at R sternal border)
  • increased with decreased venous return (valsalva or standing)
    
    • → d/t less volume in L ventricle meaning that the obstruction from the septum is more severe, (vs when it has more volume it pushes the septum to its “normal” place making the murmur less severe)
  • loud S4 (di-a-stol-ic)
  • mitral regurg
• Dx:
  
  • Echo:
    
    • asymmetrical ventricular wall thickness
    • systolic anterior motion of the mitral valve
    • small LV chamber
  • EKG:
    
    • Left ventricular hypertrophy
    • Septal Q-waves
    • R. atrial enlargement

Question 62

Tx of Hypertrophic Cardiomyopathy

Answer 62

• Tx:
  
  • Beta-blockers = 1st line, or CCB
  • Diuretics if CHF symptoms
  • surgery (if gradient >50 mmHg at rest or class III-IV heart murmur)
  • alcohol septal ablation
  • dual chamber pacing
  • cardiac transplant
  • Pt should avoid dehydration, extreme activity, & competitive sports (low-risk older pts can speak with a cardiologist)
• Complications:
  
  • can progress to dilated cardiomyopathy
  • a.fib, stroke
  • clinical deterioration is slow

Question 63

Restrictive Cardiomyopathy: Definition, Etiology, & S/sxs

Answer 63

• Definition:
  
  • rigid ventricular wall with impaired ventricular filling & reduced diastolic fnx in a non-dilated ventricle. No change in contractility
• Least common form of cardiomyopathy
• Etiology:
  
  • amyloidosis = most common
  • Sarcoidosis
  • Scleroderma
  • Hemochromatosis
• S/sxs:
  
  • R & L HF:
    
    • R: peripheral edema, JVD, hepatomegaly, ascites, GI sxs
    • L: dyspnea, fatigue
  • Other: Kussmaul sign, S4

Question 64

Restrictive Cardiomyopathy: Dx & Tx

Answer 64

• Dx:
  
  • Echo:
    
    • non-dilated ventricles with normal thickness
    • marked dilation of both atria
    • abnormal mitral flow (LA to LV)
  • **Endomyocardial biopsy = definitive diagnosis**
    
    • amyloid on biopsy may be d/t primary amyloidosis or secondary to multiple myeloma & hypergammaglobulinemia
• Tx:
  
  • Tx the underlying disorder
  • use drugs with caution: diuretics, vasodilators, CCB
  • DO NOT USE DIGITALIS (DIGOXIN) & other inotropic agents
  • Tx of hemochromatosis: phlebotomy & chelation therapy → cardiac fnx may normalize

Question 65

HEART Score

Answer 65

For Acute Coronary syndrome to tell you if the patient is low, medium, or high risk

• H: History
• E: EKG
• A: Age
• R: Risk factors (DM, dyslipidemia, HTN, smoking, CKD, prior CAD or PAD)
• T: Troponin

Question 66

Acute Bacterial Endocarditis Definition and organism

Answer 66

• Definition: infection of a normal valve with a virulent organism (usually S. Aureus).
• Rapidly destructive (fatal < 6 weeks if untreated)

Question 67

Subacute Bacterial Endocarditis: Definition & Organism

Answer 67

• Definition: indolent infection (causing little or no pain) of abnormal valves with less virulent organisms (S. Viridians = normal oral flora)
• slower onset, longer duration (may continue for weeks-months before fatal)

Question 68

Bacterial Endocarditis: General Definition, Risk factors, & Sxs

Answer 68

• General Definition:
  
  • infx of the endocardium (usually the valve) secondary to colonization. Mitral valve = most common valve involved (M> A> T >P)
• Risk Factors:
  
  • >60 yo, males, IV drug abusers, poor dentition
  • pre-existing structural cardiac abnormality, prosthetic heart valve, prior episode, intravascular device (indwelling catheter), congenital heart disease, hemodialysis, HIV, co-morbidities
• S/sxs:
  
  • Fever
  • Chills/sweats
  • Anorexia & weight loss
  • Malaise, fatigue
  • Arthralgias & myalgias

Question 69

Types of Endocarditis

Answer 69

1. Native Valve Endocarditis: **majority of cases**, infx of mitral & aortic valves with streptococci, enterococci (GI/GU), staphylococci, or normal mouth organisms
2. .Prosthetic valve endocarditis: 10-20% of cases, S. epidermidis = most common
3. .IV Drug Associated endocarditis: infx of right-sided valves (tricuspid, pulmonic) with S. aureus (acute bacterial endocarditis) (or fungi, gram -)

Question 70

Community Associated vs Healthcare Associated Endocarditis

Answer 70

• Community associated:
  
  • if diagnosed within 48 hours of hospital admission
• Healthcare Associated:
  
  • if recent contact with healthcare setting with onset of symptoms > 48 hours after hospitalization (25-30% of cases)

Question 71

Bacterial Endocarditis: PE and tests to order

Answer 71

• PE:
  
  • murmur → new or worse regurg murmur
  • splenomegaly
  • arterial emboli
  • petechiae (appear in crops then disappear in 2-3 days)
  • neurological features, clubbing, arrhythmia, scleral hemorrhage
  • Osler’s nodes (small, painful, purple-red SQ nodules on digits and palms)
  • Roth’s spots (oval retinal hemorrhages with pale center)
  • Janeway Lesions (small, non-tender hemorrhagic macules or nodules on palms & soles)
  • Splinter hemorrhages (linear reddish brown lesions under the nail bed)
• Tests to Order:
  
  • Labs:
    
    • BLOOD CXs : 3 sets > 1 hour apart
    • ESR or CROP: elevated
    • Rheumatoid factor: positive
    • Leukocytosis
    • Anemia
    • Proteinuria, microscopic hematuria
  • Transesophageal Echocardiogram:
    
    • more sensitive than TTE but obtain TTE first → looking for endocardial vegetations

Question 72

Diagnosis of Bacterial Endocarditis

Answer 72

DUKE CRITERIA

• Duke Criteria-Major:
  
  1. Sustained bacteremia: 2 positive blood cultures by organism known to cause endocarditis
  2. Echocardiogram showing vegetation, dehiscence, or abscess
  3. New valvular regurgitation
• Duke Criteria Minor:
  
  1. Predisposition (heart condition or IVDA)
  2. Fever >38C (100.4F)
  3. Vascular: emboli to organs/brain hemorrhages
  4. Immunologic: glomerulonephritis, Osler’s nodes, Roth spots, RF
  5. Positive blood culture not meeting major criteria (1 positive)
  6. Echocardiogram not meeting major criteria
• *Definitive Endocarditis: 2 major criteria; 1 major + 3 minor criteria; 5 minor criteria or histological findings
• *Possible Endocarditis: 1 major + 1-2 minor, 3 minor
• *Rejected Endocarditis: resolution within <4 days of abx, alternate dx made, no evidence of IE at surgery or autopsy, definite or possible criteria not met

Question 73

Prophylaxis of Bacterial Endocarditis: Indicated cardiac conditions, Procedures, & Regimen

Answer 73

**Recommended prior to procedures which may introduce bacteria into the bloodstream of patients who are at high risk of developing bacterial endocarditis**

• Indicated Cardiac Conditions:
  
  • Prosthetic Cardiac Valve, heart repairs with prosthetic material, prior endocarditis, Cyanotic congenital heart disease, cardiac transplant
• Procedures:
  
  • dental:
    
    • (manipulation of gums, roots of teeth, oral mucosa perforation)
  • respiratory:
    
    • respiratory mucosa manipulation, rigid bronchoscopy
  • Skin/MSK tissue procedures
    
    • including abscess I&D
  • GI/GU → NO longer recommended
• Regimen:
  
  • 2g amoxicillin PO 1H before procedure (if allergic: 500mg Azithro, 2g cephalexin, 600mg clinda)

Question 74

Indications for Surgery in Bacterial Endocarditis

Answer 74

• Refractory CHF
• persistent/ uncontrolled infx (sepsis)
• recurrent emboli
• endocarditis-associated valve dysfunction causing HF
• invasive infection (causing development of abscess, fistula, heart block)
• fungal infx
• pedunculated vegetation >1-2cm in size

Question 75

Tx of Bacterial Endocarditis

Answer 75

• Duration: 4-6 weeks of high dose therapy (indwelling catheter often used)
• Native:
  
  • anti-staph penicillin (nafcillin, oxacillin) + ceftriaxone or gentamicin
• Prosthetic:
  
  • vancomycin + gentamicin + rifampin
• Fungal:
  
  • Amphotericin B

Question 76

Acute Pericarditis: Definition, Etiology, Classification, & Types

Answer 76

• Definition:
  
  • inflammation or infection of the pericardium (outer layer of the heart)
  • Pericardium has 3 layers: fibrous pericardium, parietal pericardium (lines fibrous pericardium), and visceral pericardium (lines the epicardium)
• Etiology:
  
  • infectious: viral, bacterial (TB), fungal
  • noninfectious: secondary to MI (DRESSLER SYNDROME), neoplastic, uremic, traumatic
  • Hypersensitivity/autoimmune: rheumatic fever, SLE, RA, scleroderma, drug-induced (phenytoin, INH, procainamide, hydralazine)
• Classification:
  
  • Acute pericarditis: <6 weeks
  • subacute pericarditis: 6wks -6months
  • Chronic pericarditis: > 6 months
• Types:
  
  • serous: surface of heart look rough
  • fibrinous: “junk” stuck between layers
  • adhesive
  • hemorrhagic
  • purulent
  • constrictive

Question 77

Acute Pericarditis: S/sxs & PE

Answer 77

• S/sxs:
  
  • chest pain: sudden onset of pleuritic, persistent, postural CP (**Worse when supine, relieved by sitting up & leaning forward)
  • aggravated with cough, breathing
  • may radiate to back, shoulder, or neck
• PE:
  
  • Pericardial friction rub:
    
    • heard during both systole & diastole, high-pitched scratching/grating, loudest during inspiration, 2-3 components, may come and go

Question 78

Acute Pericarditis: Diagnosis

Answer 78

• EKG:
  
  • diffuse ST segment elevation (concave) in most limb leads & precordial v2-v6
  • ST depression in aVR +/- V1
  • sinus tach common d/t pain or infx
  • Stage 1: widespread ST elevation with reciprocal changes in aVR
  • Stage 2: Normalization of ST changes, T wave flattening
  • Stage 3: flattened T-waves or inverted
  • Stage 4: EKG returns to normal
• Echo:
  
  • useful for showing pericardial effusion +/- tamponade → can be performed at bedside
• Diagnosis (2 criteria must be met for diagnosis):
  
  • typical CP
  • pericardial friction rub
  • typical EKG changes
  • new/worse pericardial effusion
  • elevated CRP
• **no biomarkers for pericarditis → BUT 30% of pats have troponin elevation d/t myopericarditis

Question 79

Acute Pericarditis: Tx & Admit factors

Answer 79

tx the underlying disorder

• Tx:
  
  • Anti-inflammatory: NSAIDs x 2 weeks: aspirin 600-900mg QID, or indomethacin
  • Colchicine x 3 months
  • possibly steroids
  • AVOID anticoags (system is irritated so it is likely to bleed) & activity
• Admission Factors:
  
  • fever > 38C
  • subacute course
  • large pericardial effusion (>20mm)
  • immunosuppressed pts
  • use of anticoags
  • acute trauma
  • failure to improve after 7 days of NSAIDs + Colchicine
  • elevated cardiac troponin (suggest myopericarditis)

Question 80

Myocarditis: Definition, Pathophys, Etiology, Epidemiology, Classifications

Answer 80

• Definition: inflammation of the myocardium caused by infectious & noninfectious conditions. Focal or diffuse involvement
• Pathophys: myocellular damage leads to myocardial necrosis & dysfunction → heart failure
• Etiology:
  
  • 1st world = parvovirus B19, herpes virus 6, coxsackie B (enterovirus)– used to be the most cause, adenovirus, hepatitis C, COVID-19, lymphocytic, giant cell
  • 3rd world: HIV, chagas disease, rheumatic fever
• Epidemiology:
  
  • most common in 20-50yo with ***hx of recent viral infx***
• Classifications:
  
  • acute < 3 months
  • chronic > 3 months

Question 81

Myocarditis: S/sxs, PE, and Profiles

Answer 81

• S/sxs:
  
  • *many cases go undetected due to subclinical signs
  • chest pain, myalgia, fever, fatigue
  • CHF: dyspnea, fatigue
  • arrhythmia, sudden death
  • megacolon
• PE:
  
  • S3 or S4
  • mitral/tricuspid regurg
  • edema (hepatic & peripheral)
  • low cardiac output (shock)
  • tachycardia
• Profiles:
  
  1. Acute Coronary Syndrome-Like:
     
     1. severe, recurrent acute CP 1-4 weeks after viral illness, ST elevation or depression, T-wave inversion, global or regional LV +/- RV dysfunction, +/- troponin elevated
  2. New onset or worsening HF:
     
     1. new onset or progressive HF over 2weeks - 3months with symptoms, impaired LV +/- RV systolic function
  3. Life-threatening Condition:
     
     1. life threatening arrhythmias or aborted sudden death, cardiogenic shock

Question 82

Myocarditis: Dx & DDx

Answer 82

• Dx:
  
  • Labs: CBC, BMP, acute phase reactants (CRP, sed rate), troponin (may be elevated), BNP (increased)
• CXR:
  
  • congestion (not usually cardiomegaly yet)
• EKG: nonspecific ST changes, PACs/PVCs
• Echo:
  
  • LV dilation, wall motion abnormalities, decreased systolic dysfunction
• MRI:
  
  • inflammatory hyperemia, edema, wall motion abnormalities, global function, size/geometry
• Endomyocardial Biopsy: definitive diagnosis
  
  • infiltration of lymphocytes with necrosis of myocardial tissue
• Nasal swab: PCR for viruses
• DDx:
  
  • ischemic heart disease, valvular heart disease, other causes of cardiomyopathy, congenital heart disease, pulmonary disease, takotsubo, pericarditis

Question 83

Myocarditis: When to suspect & Tx

Answer 83

• When to suspect:
  
  • onset of otherwise unexplained cardiac abnormality such as CHF, shock, arrhythmia, in a 20-50 yo with a hx of viral illness
  • LV dysfunction without apparent etiology
  • pericarditis with accompanying troponin elevation
  • Acute Mi presentation without hx of CAD & negative angiogram
  • ECG changes
• Management:
  
  • supportive care: oxygen, inotropes, diuretics, antiarrhythmics, afterload reduction (ACEI), anticoag, mechanism support
  • Steroids: anti-inflammatory but suppresses the immune system
  • IVIG
  • Antivirals (if documented)
  • plasmapheresis: takes out immunoglobulins that are attacking the heart
  • immunosuppression

Question 84

Pericardial Effusion: Definition & Etiology

Answer 84

• Definition: Accumulation of fluid in the pericardial space (normal pericardial space has about 5-50cc)
• Etiology:
  
  • Acute pericarditis (viral, bacterial, TB, idiopathic) serous or purulent
  • autoimmune disease
  • Post Mi or cardiac surgery → serous or hemorrhagic
  • blunt or sharp chest trauma → hemorrhagic
  • Mediastinal radiation (d/t Hodgkin’s or breast cancer)
  • Renal failure with uremia
  • Myxedema (hyperthyroidism)
  • aortic dissection extending into the pericarium
  • Drugs

Question 85

Pericardial Effusion: S/sxs, PE, & Dx

Answer 85

• S/sxs: chest pain, dyspnea, fatigue
• PE:
  
  • decreased (muffled) heart sounds d/t fluid → as fluid increases friction rub may disappear & heart sounds may become faint
• Dx:
  
  • EKG: electrical alternans (alternating amplitudes of the QRS complexes)
    
    • low QRS voltage (something b/w the heart & EKG leads → fluid)
  • Echo: Diagnostic test of choice
    
    • increased fluid in the pericardial space
  • CXR: “water bottle appearance”
  • Labs: gram stain & bacterial/fungal culture, cytology, AFB stain, PCR

Question 86

Pericardial Effusion: When to suspect & Tx

Answer 86

• When to suspect:
  
  • in all cases of acute pericarditis
  • unexplained new radiographic cardiomegaly without pulmonary congestion
  • presence of isolated left pleural effusion
  • fever of hemodynamic deterioration in a pt with another disease process involving the pericadium
• Tx:
  
  • if minimal (<20mm) or no evidence of hemodynamic compromise: no immediate intervention needed but may treat conservatively with therapy aimed at underlying cause & hemodynamic monitoring
  • if progressively enlarging or symptoms suggest cardiac tamponade then pericardiocentesis is indicated
  • if related to pericarditis treat with NSAIDS (2weeks) & Colchicine (x3mo)
  • if chronic consider surgery: pericardial window

Question 87

Cardiac Tamponade: Definition, Etiology, S/sxs, & PE

Answer 87

• Definition:
  
  • pericardial effusion causing significant pressure on the heart, impeding cardiac filling, leading to decreased cardiac output and shock. The Rate of accumulation of fluid is more critical than volume. (slow accumulation of large volume is OKAY if pericardium is compliant)
• Etiology:
  
  • Malignancy, idiopathic pericarditis, & uremia (renal failure) are the most common causes
• S/sxs:
  
  • Dyspnea
  • Fatigue
  • peripheral Edema
  • BECK’s Triad:
    
    • distant (muffled) heart sounds
    • increased JVP
    • systemic hypotension
• PE:
  
  • EKG:
    
    • Electrical Alternans (alternating amplitudes of the QRS complexes)
    • low QRS voltage
  • Echo:
    
    • pericardial effusion & diastolic collapse of teh cardiac champers
  • CXR:
    
    • “water bottle” appearance

Question 88

Cardiac Tamponade: Tx

Answer 88

• immediate: oxygen, IV fluids, type & culture
• Don’t give pain meds, sedate, or intubate (causes vasodilation which will lower BP even further)
• Pericardiocentesis

Question 89

Answer 89

“water bottle” appearance

associated with pericardial effusion/ cardiac tamponade

Question 90

Beck’s Triad

Answer 90

Associated with Cardiac Tamponade

1. elevated JVP
2. muffled heart sounds
3. systemic hypotension

Question 91

Mnemonic to Remember Medical Tx of STEMI

Answer 91

MOAN & BASH

Morphine, oxygen if O2 <90%, Aspirin 162 mg, Nitro q 5 min (don’t give to pts with systolic <90, or to inferior MI with R ventricular involvement → dependent on preload and nitro decreases preload)

Beta blockers (Decrease remodeling, decrease oxygen demand of heart, decreases HR, improve L ventricular hemodynamic funx, reduce incidence of ventricular arrhythmias; Contraindication in Heart block, high risk for cardiogenic shock) , ACE-I/ARB (more for long term use → improve L ventricular EF, mortality rate), Statin, Heparin (antithrombotic therapy → impede progression of thrombus in coronary artery)

TPA if pt cannot have reperfusion from cath lab in <90minutes from door to lab

Question 92

Dressler’s Syndrome

Answer 92

Post-MI pericarditis

tx = aspirin or colchicine

Question 93

Triad of R Ventricular Infarction

Answer 93

1. JVD
2. Clear Lungs
3. Positive Kussmaul Sign
   
   1. paradoxical rise of JVP with inspiration (blood backs up into vein during inspiration due to failure of R ventricle)

Question 94

3 populations with atypical sxs for acute MI

Answer 94

elderly, women, diabetics

Question 95

Which cardio biomarker peaks the fastest?

Answer 95

Myoglobin

My O My you are fast