Final OSCE Flashcards
Dilated Cardiomyopathy:
Pathophys, Etiology & Epidemiology
- 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
Dilated Cardiomyopathy: S/sxs
-
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
Dilated Cardiomyopathy: Dx
-
Diagnostic Criteria:
- inclusion: EF <40%
- LVEDD >177% of predicted
- inclusion: EF <40%
-
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%)
Dilated Cardiomyopathy: Dx
-
Diagnostic Criteria:
- inclusion: EF <40%
- LVEDD >117% of predicted
- inclusion: EF <40%
-
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%)
Dilated Cardiomyopathy: Tx
- 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
Canadian Cardiovascular Society Classification System: Angina
- 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
Major Risk Factors of Coronary Artery Disease (CAD)
- 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)
Etiology of Acute Coronary Syndrome
-
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
NSTEMI: def, s/sxs, dx, & tx
- 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
-
First line: oxygen of o2 <95%
STEMI: def, s/sxs, dx & Tx
- 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:
- JVD
- Clear lungs
- 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
-
Inferior Wall MI:
-
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**
-
EKG: new ST-elevation in two contiguous leads of >1mm
-
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
Post MI Complications
- 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
Stable Angina
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
- provides a definitive dx → defines location and extent of CAD but only used if:
-
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)
- NBC (mnemonic to remember)
Unstable Angina
- 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
Stress Test (Exercise Testing)
- 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
Angina- Prinzmetal Variant
-
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
-
EKG: transient ST-elevation that resolves with symptom resolution
-
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
-
calcium channel blockers: first line monotherapy -→ given at NIGHT (Non-dihydropyridine: diltiazem, verapamil Qday)
Acute vs. Chronic Heart Failure
-
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
-
Chronic Heart Failure (compensated):
Systolic Heart Failure
-
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
Diastolic Heart Failure
-
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
Management goals of Heart Failure
- Afterload: make it easier for the heart to empty
- preload: appropriate stretch, get the heart back on the proper part of the Sterling curve
- 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
Tx of Heart Failure
- **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
Left-Sided Heart Failure: Pathophys, Etiology, S/sxs, PE
-
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
Right-Sided Heart Failure: Pathophys, Etiology, S/sxs, PE
-
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
-
inferior vena cava:
Hypercholesterolemia: primary vs secondary, etiology, risk factors
- 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
- sex, age, HTN, DM, smoking, family hx of coronary heart disease
Primary Prevention of ASCVD in age 0-19 years
- lifestyle to prevent or reduce ASCVD risk
- Diagnosis of familial hypercholesterolemia?
- statin
Primary Prevention of ASCVD in Age 20-39
- Estimate lifetime risk to encourage lifestyle to reduce ASCVD risk
- Consider statin if family hx, premature ASCVD and LDL-C ≥ 160mg/dL
Primary Prevention of ASCVD in Age 40-75 and LDL-C ≥ 70 to <190 mg/dL without diabetes mellitus
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
- Risk discussion:
-
≥ 20%: “high risk”:
- initiate statin to reduce LDL-C ≥ 50%
At what LDL-C level do you initiate high intensity statin with no risk assessment?
LDL-C ≥ 190 mg/dL
What population do you initiate a moderate-intensity statin regardless of risk factors?
Diabetes Mellitus age 40-75yo
Risk assessment to consider high-intensity statin
CAC
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
Best meds to lower elevated LDL
-
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
Best Meds to Lower Triglycerides
- Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
- Niacin
Best Meds to Increase HDL
- Niacin
- Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
Treatment of Secondary Hypercholesterolemia without high-risk (clinically stable)
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
Treatment of Secondary Hypercholesterolemia with High Risk (unstable)
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
Abnormal Lipid Values
- 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
Hypertriglyceridemia
- 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
Essential HTN: definition, PE, and diagnosis
-
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**
- resting systolic ≥ 130 or diastolic ≥ 80 on at least 2 readings on at least 2 separate visits with no identifiable cause
-
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
Essential HTN: Tx
-
ACC/AHA:
- goals: <130/80
- AntiHTN therapy initiated in the following populations:
- all pts with stage 2 HTN (baseline ≥140/90)
-
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
- recommendation is
- 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
- for non-black pts, including DM give either:
ACC/AHA Classification of BP
Hypertensive Emergency: definition, Dx, & Tx
- 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
Hypertensive Urgency: Definition, Dx, & Tx
- 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
Secondary HTN Definition and Causes
- 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
Secondary HTN Red Flags, Dx, & Tx
-
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
- when HTN is newly diagnosed consider ordering:
-
Tx:
- tx the underlying condition and aim for BP <130/80
Mixed Venous O2 vs A-VO2 difference
-
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
- Normal:
- amount of oxygen that is in the venous blood upon return to the heart
-
A-VO2 difference:
- arterial O2 (~98%) - venous O2 saturation
- normal <30%
- higher the difference = the WORSE the situation
- arterial O2 (~98%) - venous O2 saturation
- As mixed venous O2 drops, AVO2 difference will increase (inverse relationship)
Delivery of oxygen is affected by
DO2 = CO x CaCO2
delivery of oxygen is affected by cardiac output and arterial oxygen content
Hypovolemic Shock: Definition, Etiologies, Pathophys, S/sxs
-
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
Features of Hypovolemic Shock
- 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)
Normal Blood Volume
-
Adults: 7% IBW (75ml/kg)
- → 70kg adult = 5.5 Liters or approx 15 units
- Children: 9% IBW (90 ml/kg)
IBW = ideal body weight
Phases of Hypovolemic Shock
-
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
Tx of Hypovolemic Shock
- 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
- usually 3-4 liters:
- control the source of hemorrhage +/- packed RBCs if severe
- maintain body temp (prevent hypothermia)
Distributive Shock: Definition, Pathophys, & Etiologies
- 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
Distributive Shock: S/sxs of Sepsis, Anaphylaxis, and Neurogenic Shock
-
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
Features of Septic Shock
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
Features of Neurogenic Shock
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
Tx of Distributive Shocks
-
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
Obstructive Shock: Definition, Etiology & Tx
- 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)
Cardiogenic Shock: Definition, Etiology, & S/sxs
- 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
-
Pump Failure:
-
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
Features of Cardiogenic Shock
- 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)
Tx of Cardiogenic Shock
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])
Hypertrophic obstructive Cardiomyopathy: Pathophys & Risk Factors
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
Hypertrophic Cardiomyopathy: S/sxs & PE
-
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
- Echo:
Tx of Hypertrophic Cardiomyopathy
-
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
Restrictive Cardiomyopathy: Definition, Etiology, & S/sxs
-
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
- R & L HF:
Restrictive Cardiomyopathy: Dx & Tx
-
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
- Echo:
-
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
HEART Score
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
Acute Bacterial Endocarditis Definition and organism
- Definition: infection of a normal valve with a virulent organism (usually S. Aureus).
- Rapidly destructive (fatal < 6 weeks if untreated)
Subacute Bacterial Endocarditis: Definition & Organism
- 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)
Bacterial Endocarditis: General Definition, Risk factors, & Sxs
-
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
Types of Endocarditis
- Native Valve Endocarditis: **majority of cases**, infx of mitral & aortic valves with streptococci, enterococci (GI/GU), staphylococci, or normal mouth organisms
- .Prosthetic valve endocarditis: 10-20% of cases, S. epidermidis = most common
- .IV Drug Associated endocarditis: infx of right-sided valves (tricuspid, pulmonic) with S. aureus (acute bacterial endocarditis) (or fungi, gram -)
Community Associated vs Healthcare Associated Endocarditis
-
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)
Bacterial Endocarditis: PE and tests to order
-
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
- Labs:
Diagnosis of Bacterial Endocarditis
DUKE CRITERIA
-
Duke Criteria-Major:
- Sustained bacteremia: 2 positive blood cultures by organism known to cause endocarditis
- Echocardiogram showing vegetation, dehiscence, or abscess
- New valvular regurgitation
-
Duke Criteria Minor:
- Predisposition (heart condition or IVDA)
- Fever >38C (100.4F)
- Vascular: emboli to organs/brain hemorrhages
- Immunologic: glomerulonephritis, Osler’s nodes, Roth spots, RF
- Positive blood culture not meeting major criteria (1 positive)
- 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
Prophylaxis of Bacterial Endocarditis: Indicated cardiac conditions, Procedures, & Regimen
**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
- dental:
-
Regimen:
- 2g amoxicillin PO 1H before procedure (if allergic: 500mg Azithro, 2g cephalexin, 600mg clinda)
Indications for Surgery in Bacterial Endocarditis
- 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
Tx of Bacterial Endocarditis
- 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
Acute Pericarditis: Definition, Etiology, Classification, & Types
-
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
Acute Pericarditis: S/sxs & PE
-
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
-
Pericardial friction rub:
Acute Pericarditis: Diagnosis
-
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
Acute Pericarditis: Tx & Admit factors
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)
Myocarditis: Definition, Pathophys, Etiology, Epidemiology, Classifications
- 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
Myocarditis: S/sxs, PE, and Profiles
-
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:
-
Acute Coronary Syndrome-Like:
- 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
-
New onset or worsening HF:
- new onset or progressive HF over 2weeks - 3months with symptoms, impaired LV +/- RV systolic function
-
Life-threatening Condition:
- life threatening arrhythmias or aborted sudden death, cardiogenic shock
-
Acute Coronary Syndrome-Like:
Myocarditis: Dx & DDx
-
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
Myocarditis: When to suspect & Tx
-
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
Pericardial Effusion: Definition & Etiology
- 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
Pericardial Effusion: S/sxs, PE, & Dx
- 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
- EKG: electrical alternans (alternating amplitudes of the QRS complexes)
Pericardial Effusion: When to suspect & Tx
-
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
Cardiac Tamponade: Definition, Etiology, S/sxs, & PE
-
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
- EKG:
Cardiac Tamponade: Tx
- immediate: oxygen, IV fluids, type & culture
- Don’t give pain meds, sedate, or intubate (causes vasodilation which will lower BP even further)
- Pericardiocentesis
“water bottle” appearance
associated with pericardial effusion/ cardiac tamponade
Beck’s Triad
Associated with Cardiac Tamponade
- elevated JVP
- muffled heart sounds
- systemic hypotension
Mnemonic to Remember Medical Tx of STEMI
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
Dressler’s Syndrome
Post-MI pericarditis
tx = aspirin or colchicine
Triad of R Ventricular Infarction
- JVD
- Clear Lungs
-
Positive Kussmaul Sign
- paradoxical rise of JVP with inspiration (blood backs up into vein during inspiration due to failure of R ventricle)
3 populations with atypical sxs for acute MI
elderly, women, diabetics
Which cardio biomarker peaks the fastest?
Myoglobin
My O My you are fast
Aortic Stenosis
CRESCENDO- DECRESCENDO murmur R 2nd intercostal space
- increased murmur when leaning forward (ERBs) and increased venous return (squatting, supine, leg raise)
- pulsus parvus et tardus (weak, delayed carotid pulse)
-
Etiology:
- degenerative: calcifications > 70 yo
- congenital & bicuspid valve <70 yo
-
S/sxs: ASH
- angina
- syncope
- heart failure
-
Dx:
- ECHO = best test
- ECG = L ventricular Hypertrophy
- Tx: aortic valve replacement = ONLY effective treatment
Aortic Regurgitation
Diastolic high-pitched blowing DECRESCENDO murmur along LSB +/- apex
- murmur LOUDER when sitting up and leaning forward
-
Etiology:
- acute → MI, aortic dissection, endocarditis
- chronic → aortic dilation, rheumatic fever, HTN
-
Physical Exam:
- Water hammer pulse: swift upstroked and rapid fall of radial pulse accentuated with wrist elevation
- De-Musset’s Sign: head-bobbing with heart beat
- Hill’s Sign: popliteal artery systolic pressure > brachial artery by 60 mmHg (most sensitive)
- Quincke’s Pulses: visible pulsations in the fingernail bed
- Muller’s Sign: visible systolic pulsations of the uvula
-
Dx:
- Echocardiogram → regurgitant jet
- L ventricular dilation as compensation
-
Tx:
- decrease the afterload improves the forward flow (e.g. ACE-I, ARBs, nifedipine, hydralazine)
- surgery = definitive tx
*
Mitral Stenosis
- Diastolic murmur heard best at the apex
-
LOUD S1 (forceful closure of mitral valve) with OPENING SNAP (forceful opening of mitral valve →early diastolic sound followed by a mid-diastolic rumbling murmur.
- → initial rumble during passive filling of ventricle, followed by active rapid filling during atrial “kick”
- Etiology: rheumatic heart disease = most common cause!
- S/sxs: increased L atrial pressure/volume overload → pulm congestion → pulm HTN → CHF
-
Dx:
- ECG = L atrial enlargement, A fib, pulmonary HTN (RVH, R axis deviation)
- ECHO = most useful non-invasive tool
- Cardiac Cath = most accurate but rarely done
-
Tx:
- percutaneous balloon valvuloplasty
Mitral Regurgitation
Systolic murmur Blowing Holosystolic murmur heard best at the APEX → murmur radiates to the axilla, can be heard well in the LLD position
-
Etiology: Mitral Valve prolapse = most common cause in the US
- rheumatic fever = most common in developing countries
- MI/ischemia → papillary muscle dysfunction
- dilated cardiomyopathy → ruptured chordae tendineae
-
S/sxs:
- dyspnea = most common, blood backs up into L atrium then lungs
-
Dx:
- ECHO = most useful non-invasive test
-
Tx: sx control by reducing afterload (ACE-I, ARBs)
- surgery = repair > replacement
Mitral Valve Prolapse
Mid-late systolic ejection click best heard at the apex
- → any maneuver that makes the LV smaller (decreases preload) results in an earlier click & longer murmur duration (e.g. valsalva, standing) due to increased prolapse
- MVP = MOST common cause of mitral regurgitation
-
Population:
- Most common in young women
-
Dx:
- ECHO → posterior bulging leaflets
-
Tx:
- MVP is associated with good prognosis → reassurance
- beta-blockers for pts with autonomic dysfunction
- mitral valve repair only for severe regurg and CHF
Pulmonary Stenosis
harsh mid-systolic crescendo-decrescendo murmur
- murmur increases with inspiration (bigger preload)
-
Pathophys:
- Right ventricle encounters more resistance → hypertrophy → less preload→ blood backs up
-
epidemiology:
- almost always congenital and in the young
- Tx: balloon valvuloplasty
Pulmonary Regurgitation
Diastolic decrescendo murmur best heart at the L upper sternal border
- murmur increases with inspiration and venous return
-
Pathophys:
- retrograde blood flow from the pulmonary artery into the Right Ventricle causing R-sided volume overload
-
Etiology:
- almost always congenital
Tricuspid Stenosis
mid-diastolic rumbling murmur at the lower left sternal border
- blood backs up into the R atrium causing R atrial enlargement which may lead to R-sided heart failure
-
Tx:
- decrease R atrial volume overload with diuretics and Na restriction
- surgery
Tricuspid Regurgitation
Holocystolic murmur at 4th ICS left midsternal border
- may radiate to liver
-
Pathophys:
- blood flows back into the R atrium
-
Etiology:
- functional overload (pulm HTN, RV dilation)
- dirty needles (staph etc often up on tricuspid valve)
-
PE:
-
Carvallo’s Sign:
- holosystolic murmur that becomes louder during inspiration
-
Carvallo’s Sign:
-
Tx:
- tx the underlying condition
- valve replacement
S3
Sys-tol-ic Murmur
can be normal in young and athletic hearts
associated with a dilated ventricle (more compliant ventricle)
S4
di-a-stol-ic
atrial kick against a stiff wall, associated with hypertrophy or scar
NEVER normal
What can accentuate mitral murmurs
Left lateral decubitus position with the bell
What can accentuate aortic murmurs
sitting up and leaning forward
What does increasing venous return do?
increases intensity of all murmurs EXCEPT hypertrophic cardiomyopathy, mitral valve prolapse
“the MVP Hates Conforming to the rules”
Pneumonic to remember which murmurs are diastolic
MS. PRARTS DIED
MS = mitral stenosis
PR = pulmonary regurg
AR = aortic regurg
TS = tricuspid stenosis
DIED = diastolic, everything else is a systolic murmur
Maneuvers to increase venous return
lying supine
squatting
lifting legs
Maneuvers to decrease venous return
standing
valsalva maneuver
Inspiration increases venous return to which side of the heart
Right Side: RINSPIRATION
→ increases the sound of murmurs on the R side
Expiration increases venous return to which side of the heart
Left side → increases sound of all murmurs on the L side
Increased Total Peripheral Resistance & Murmurs
How to: handgrip, phenylephrine
- increased resistance decreases forward flow & increases backward flow → increases aortic regurg, mitral regurg (regurgitant murmurs)
- decreases AS, MVP, hypertrophic cardiomyopathy
Decreased Total Peripheral Resistance & Murmurs
How to: Amyl Nitrate
- direct arteriolar vasodilator increases forward flow through the aortic valve
- increases AS, MVP, hypertrophic cardiomyopathy
- decreases AR, MR (regurgitant murmurs)
What does the pitch tell you about the murmur?
a murmur will be high-pitched if there is a large pressure gradient across the pathologic lesion and low pitched if the pressure gradient is low (Ex. aortic stenosis is high pitched d/t t the large pressure gradient b/w aorta and ventricle
Pulsus parvus et tardus
weak, delayed carotid pulse
often seen in Aortic Stenosis
Patent Ductus Arteriosus: Definition, Pathophys, & Risks
- Definition: persistent communication between the descending thoracic aorta and the main pulmonary artery after birth → L to R Shunt
-
Pathophys:
- continued Prostaglandin E1 production & low arterial oxygen content promotes patency. → Enlarged R atrium, R Ventricle, & L Ventricle
-
Risks:
- Prematurity, female, fetal hypoxia
Patent Ductus Arteriosus: S/sxs, PE
-
S/sxs:
- Most are asymptomatic:
- but some have → poor feeding, weight loss, frequent URIs
- if they experience Eisenmenger Syndrome → left-to-right shunt switches to a right-to-left shunt → Cyanosis
- Most are asymptomatic:
-
PE:
- Continuous Machinery Murmur loudest at the Left upper sternal border (PDA → personal digital assistant = machine)
- wide pulse pressure (bounding pulses)
Patent Ductus Arteriosus: Dx & Tx
- Dx: ECHO = best initial test
-
Tx:Indomethacin, ibuprofen (inhibits prostaglandin)
- surgical: left thoracotomy
- clip the premature babies
- ligate the neonates & infants
- divide and oversew the toddlers & infants
- Catheter based:
- coil device → for older infants & children
- surgical: left thoracotomy
Eisenmenger Syndrome
- Pulmonary HTN & Cyanotic heart disease occuring when a left-to-right shunt shunt switches to a right-to-left shunt → Cyanosis
Tetralogy of Fallot: 4 components
Most common cyanotic congenital heart disease (right-to-left shunt)
-
4 components’
- RV outflow obstruction (sometimes call pulm stenosis)
- R ventricular hypertrophy
- Overriding Aorta (shifted to the R; sits right over the VSD)
- Ventricular Septal Defect
Tetralogy of Fallot: S/sxs & PE
-
S/sxs:
- infants: Cyanosis
-
Older Children: TET spells: paroxysms of cyanosis relieved with squatting or pulling legs up
- (increased peripheral vascular resistance causes the shunt to switch to left-to-right shunt )
-
PE:
- Harsh systolic murmur at left mid-to-upper sternal border changes similar to HOCM (louder with decrease in ventricular volume- blue, softer with increase in ventricular volume -pink) → children will squat or pull legs to chest to increase peripheral vascular resistance
- R. ventricular heave
- digital clubbing
- cyanosis
- *Often dynamic (TOF spells) & progressive
Tetralogy of Fallot: Dx, Tx, and Mnemonic
-
Dx: Echo = test of choice
- CXR: Boot shaped heart (prominent R ventricle)
- EKG: RVH, R. Atrial Enlargement
-
Tx:
- DO NOT LET THEM GET DEHYDRATED → TOF spells (need to treat gastroenteritis aggressively)
- surgical repair by 3-6 months or sooner if blue
Boot Shaped Heart
Associated with Tetralogy of Fallot
demonstrates prominent R ventricle due to RV outflow obstruction
Ventricular Septal Defect: Definition & Types
-
Definition:
- abnormal opening in the ventricular septum, associated with a left-to-right shunt. Most common type of congenital heart defect!!
- Most common defect in Trisomy 21 (Down Syndrome)
-
Types:
- Membranous = most common type, hole in the LV outflow tract near tricuspid valve (higher up on the septum)
- Muscular: multiple holes in “swiss cheese” pattern → these may resolve on their own
Ventricular Septal Defect: S/sxs & PE
-
S/sxs:
- Small VSDs: may be asymptomatic
-
Large VSDs: symptoms manifest within 6 months of age:
- Failure to thrive (have to pump more blood, breath harder → higher caloric demand, and decreased ability to feed)
- Poor growth
- Tachypnea
-
GERD
- (liver enlarges due to heart failure and pushes on stomach)
-
Frequent URIs
- (due to wet lungs)
-
PE:
- high pitched holosystolic murmur best heard at the LLSB
- smaller VSDs are louder with more palpable thrills
- normal pulses
- high pitched holosystolic murmur best heard at the LLSB
Ventricular Septal Defect: Dx, Tx, & Mnemonic
-
Dx:
- Echo = determines size & location of VSD
- CXR: cardiomegaly &/or congestion
-
Tx:
- Diuretics, ACEI +/- Digoxin
- some may close or get smaller on their own
-
Indications for Surgery:
- unmanageable heart failure
- failure of medication management
- shunt greater than 1.5-2x with or without sxs (babies hearts can accommodate 1.5-2x the volume often before symptoms)
- **Want to try to get them to 3-6 months of age before surgery, but not necessary if FTT or other issues**
- Diuretics, ACEI +/- Digoxin
Coarctation of the Aorta: Definition & Pathophys
-
Definition:
- congenital narrowing of the aortic lumen at the juxtaductal area (insertion of ductus arteriosus distal to left subclavian artery)
- Often associated with Turner syndrome and bicuspid aortic valve
-
Pathophys:
- narrowing of the aorta most commonly → HTN in the arteries proximal to the lesion with hypotension in the lower extremities
- overtime, the body develops collaterals around the coarctation
- narrowing of the aorta most commonly → HTN in the arteries proximal to the lesion with hypotension in the lower extremities
Coarctation of the Aorta: S/sxs & PE
-
S/sxs:
-
Neonates: Failure to thrive
- poor feeding
- tachypnea, irritability
- CHF
- **Severe Coarctation: LV failure & Shock after birth when the ductus closes*
-
Older children/Teens:
- headache
- nosebleeds
- absent or diminished femoral pulses
- Unexplained HTN***
-
Neonates: Failure to thrive
-
PE:
- upper extremity systolic HTN with lower extremity hypotension
- Diminished or delayed lower extremity pulses (vs. VSD that has normal pulses
- Systolic murmur at LUSB with radiation to the scapula (back)
-
Dx:
- CT-angiography = Gold standard
- CXR: cardiomegaly
- posterior rib notching (due to increased intercostal artery collateral flow) after several years
- 3 sign (narrowed aorta looks like the notch of the number 3)
- ECG: LVH
- Echo: useful but difficult to visualize coarctation
Coarctation of the Aorta: Dx & Tx
-
Dx:
- CXR: cardiomegaly
- posterior rib notching (due to increased intercostal artery collateral flow) after several years
- 3 sign (narrowed aorta looks like the notch of the number 3)
- ECG: LVH
- Echo: useful but difficult to visualize coarctation
- CXR: cardiomegaly
-
Tx:
- surgical: left thoracotomy with extended end-to-end anastomosis; stents reserved for recurrent coarctations
- Prostaglandin E1 (Alprostadil) can be used to open the ductus arteriosus and relax the narrowed aortic segment
- Early referral saves lives!
3 Sign
associated with Coarctation of the Aorta
narrowed aorta looks like the notch of the number 3
Coarctation-Rib Notching
Associated with Coarctation of the Aorta
due to increased intercostal artery collateral flow after several years
How do you distinguish hypoxia from pulmonary disorders from cardiac disease?
Hyperoxia test
Truncus Arteriosus
- truncus did not separate into aorta and pulmonary artery
- Large VSD → R-L shunt
- repair: VSD closure, RV-PA conduit, usually operate in first 2 weeks of life
- associated with DiGeorge Syndrome 22q11
Still’s Murmur
Benign Murmur
- SYSTOLIC, grade 1-2/6
- best heard at APEX of heart & LL sternal border
- best heard with BELL of stethoscope
- represents the normal sound of blood gushing out into the aorta during contraction
- healthy 3-7 year old children
Murmurs that are never normal
- anything DIASTOLIC
- anything >II/VI
- → get an echo
3 problems with developmental heart processes that leads to congenital heart disease
-
Rotation:
- tetralogy of fallot
- transposition of the great arteries (TGA)
-
Septation:
- ventricular septal defects
- atrial septal defects
- truncus arteriosus
-
Migration:
- total anomalous pulmonary venous drainage (TAPVR)
Total Anomalous Pulmonary Venous Drainage (TAPVR)