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ER Cardio
Cardiology
Acute/ Subacute Bacterial Endocarditis
 Infection of endothelium/ valves 2/2 colonization (i.e. during transient/ persistent bacteremia)
 Mitral valve MC (M> A> T> P) EXCEPT w/ IVDA, then it’s tricuspid valve
 Types
o Acute bacterial endocarditis- infection of normal valves w/ virulent organism (i.e. S. Aureus)
o Subacute bacterial endocarditis- indolent infection of abnormal valves w/ less virulent organisms (i.e. S. Viridans)
o Endocarditis in IVDA- MRSA, Pseudomonas Candida
o Prosthetic valve endocarditis
 Early (< 60 days): staph epidermis MC
 Late (> 60 days): resembles native valve endocarditis
 Microbiology
o Strep viridans- MC in subacute bacterial endocarditis, source- oral flora
o Staph aureus- MC in acute bacterial endocarditis & IVDA (esp MRSA) & patients w/ HIV
o Enterococci- MC in men 50 y/o w/ hx of GI/GU procedures
o HACEK organisms: Hemophilus, Actinobacillus, Cardiobacterium Eikenella, Klingella
 All are gram (-) that are associated w/ development of large vegetations (hard to culture)
 Signs/ Symptoms
o Fever (80-90%, including fever or unknown origin), anorexia, weight loss, fatigue, ECF conduction changes
o Janeway lesions- painless erythematous macules on the palms and soles (emboli/ immune)
o Roth spots- retinal hemorrhages w/ pale centers, petechiae on conjunctiva palate
o Osler’s nodes- tender nodes on the pads of digits
o Splinter hemorrhages of proximal nail bed, clubbing, hepatosplenomegaly, septic emboli (CNS, kidney, spleen)
 Diagnostic Studies
o Blood cultures- BEFORE abx, need 3 sets at least 1 hr apart Dressler Syndrome: pericarditis
o ECG- asses at regular intervals for changes post- MI
 Dx Criteria (Dukes)
o 2 Major OR 1 major + 3 minor OR 5 minor

Major Minor
 2 separate blood cultures  Predisposing heart condition OR IVDA
 Abnormal Echo  Temp > 38 degrees C
 Vascular phenom (major arterial emboli, septic pulm infarcts, mycotic aneurysm,
intracranial hemorrhage, conjunctival hemorrhage, janeways lesions)
 Immunological phenomena (Osler’s nodes, glomerulonephritis, Roth spots, rheumatoid
factor)
 Microbiological evidence (culture or active infection)

 Management
o Surgery indications- refractory CHF or infection. Invasive infection, prosthetic valve, recurrent emboli, fungal
o Empiric therapy 4-6 wks
 Acute (native valve) - Nafcillin + Genta OR Vanco + Genta
 Subacute (native valve)- PCN/ Amp + Genta, Vanc for IVDA
 Prosthetic valve- Vanc + Genta + Rifampin (for staph A)
 Fungal- Amphotericin B 6-8 weeks (surgery)
o Prophylaxis
 Congenital heart disease
 Dental/ Resp/ Skin procedures
 Rx Amoxi 2 g 30-60 min before
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Angina
 Def: substernal chest pain often brought on by exertion d/t decreased supply & increased demand
 Classification:
o I- unusually strenuous activity, still no limits
o II- more prolonged or rigorous activity, slight activity limits
o III- during usual daily activity, marked physical activity limits
o IV- angina at rest, often can’t do physical activity
 Signs/ symptoms:
o History (the most important aspect) - Physical Exam- often normal
 Chest pain- often substernal, poorly localized, nonpleuritic, & exertional
- Can radiate to arm, teeth, lower jaw and back
- Often 1-5 min but less than 30 by definition
- Levine’s sign- clenched fist over chest
- Relieved by rest or nitro, worse w/ exertion
 Associated symptoms- dyspnea, nausea, sweating, numb, fatigue
 Diagnosis
o Workup- ECG first, stress test second, angiography GOLD STANDARD
 ECG
- ST depression- CLASSIC
- Normal while at rest in 50% of patients w/ stable angina
- Left ventricular hypertrophy = increased adverse outcome
 Stress testing (most useful noninvasive screening tool)
- Stress
o Bruce protocol: standard increments in workload w/ monitoring of HR, BP, & ECG
o (+) = ST depressions, hypotension/ hypertension, arrhythmias, or symptoms
- Myocardial perfusion imaging stress (physical or pharm)
o Done for patients w/ odd ECG at baseline
o Agents- adenosine or dipyridamole
o Contraindications- asthma
- Echo
o Can locate ischemia
o Uses dobutamine- that increases myocardial O2 demand & provokes ischemia
 Angiography = Definitive, GOLD STANDARD
- Indications: confirm/ exclude CAD in patients +/- for sx or who may need revascularization
 Treatment
o Revascularization (definitive)
 Percutaneous Transluminal Coronary Angioplasty
- Ind- 1 or 2 vessel disease NOT involving left main coronary artery AND ventricular function is normal
- Worried about restenosis for ~ 3 mo after
- Restenosis reduced w/ stents (and have ASA/ Clopidogrel)
 Coronary Artery Bypass Graft
- Ind: Left main coronary artery disease, symptomatic or critical stenotic, 3 vessel disease, or ejection fraction < 40%
o Pharmacological
 Nitroglycerin (sublingual is best)
- Increase myocardial blood supply & decrease demand
- If need 3 doses  ACS
- SE: HA, flushing, tolerance, hypotension, edema, tachyphylaxis (after 24 hrs)
- CI: SBP < 90, RV MI, Sildenafil
 Beta Blockers (Metropolol, Atenolol, Propranolol, Nadolol)
- Increase supply (coronary vasodilation) & decrease demand (reduces O2 need during stress)
- Ind: first line for chronic management
 Calcium Channel Blockers (Diltiazem, Verapamin)
- Increase supply (coronary vasodilation), decreases demand (decreases contractility & HR)
- Ind: Prinzemetal angina (pain at rest)
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 Aspirin
- Stops platelet aggregation. -- Just stops chronic stable angina -> ACS
 Reduction in risk factors: smoking cessation, control HTN/ DM/ HL
 Chronic (stable) angina: d/t fixed plaque (coronary obstruction), relieved w/ nitro
 Prinzmetal (Variant) Angina
o Considered a coronary vasospasm disorder  transient ST elevations usually w/o MI
o Symptoms:
 Non-exertional chest pain
 In AM (may wake up)
 Hyperventilation, emotional stress, cold weather
o Diagnosis:
 ECG- transient ST elevations that resolve w/ CCB or nitro
o Treatment: CCB & nitrates as needed

Coronary Heart Disease

 Non-ST Acute MI (NSTEMI) and Unstable Angina Treatment
o Antithrombics
 ASA- prevent platelet aggregation (via COX inhibitor)
 ADP Inhibitors (Clopidogrel aka Plavix)
- For ASA allergy, inhibits ADP platelet aggregation, CI for CABG w/in 7 days, hepatic /renal impairment, bleeding
 GP IIb/ IIA Inhibitors (Eptifibatide, Tirofiban, Abciximab)
- For UA, NTEMI, or undergoing PCI, CI if bleeding w/in 30 days, major trauma/ surgery,
 Unfractionated heparin
- MOA: binds/ potentiates antithrombin III  inactivate factor Xa  inactivates Factor IIa (aka prevents new clots)
- IND: ACS patients w/ ECG changes/ (+) cardiac markers
 LMWH (Lovenox)
- MOA: binds & increases antithrombin III  inactivate factor IIa (less thrombin inhibition)
- IND: same as UFH but better (longer t ½, no need of IV/ PTT monitoring, less thrombocytopenia)
- SE: thrombocytopenia, dosed for renal impairment
o Adjunctive therapy
 BB (Metoprolol- lower O2 consumption w/ antiarrhythmic effects, titrate for HR < 70
- CI: HR < 50, SBP< 90, decompensated CHF, 2nd/ 3rd heart block, shock, cocaine
 Nitrates- for anginal symptoms
 Morphine- for pain  decreases anxiety, venodilation  decreases preload
 CCB (Verapamil, Diltiazem)- if pt can’t do BB, drug of choice for vasospastic disorders
 ST Segment Elevation MI (STEMI) management
o Reperfusion (most important)
 Do w/in 12 hrs via PCI or thrombolytics
- PCI: best w/in 3 hrs of sx onset, better than thrombolytics
o PTCA or CABG if > 3 vessels/ L main artery/ decreased L ventricle EF
- Thrombolytic
o Tissue plasminogen activators (Ateplase aka TPA Reteplase, Tenecteplase)
 MOA- activate tissue plasminogen to break down clots
 SE: higher rebleed risk
o Streptokinase
 MOA: binds to plasminogen, activating it into plasmin
 IND: less effective than TPA, less intracranial bleeding, cheap
 SE: tolerance develops
o Antithrombotic
 ASA- chew for faster metabolism
 UFH, Glycoprotein IIb/IIIa inhibits
o Adjunctive
 BB- decreases wall tension  preventing MI complications)
 ACE-I- decreases ventricular remodeling  slows progression of CHF during & after STEMI
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- CI: SBP < 100, renal failure
- SE: angioedema, cough
 Nitrates- IV for continuing discomfort
 Morphine- for pain  decreases anxiety, venodilation  decreases preload
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Arrhythmias/ Conduction Disorders
 Sinus tachy: rate > 100
 Sinus brady: < 60 bpm
o Etiology: excess vagal stimulation, BB, CCB, Digoxin, SA node ischemia
o Treatment: Atropine 1st! Epi & transcutaneous pacing second line
 Sick sinus syndrome (brady- tachy syndrome)
o Combo of sinus arrest w/ alternating bouts of tachy & brady
o Etiology: often d/t SA node disease & corrective cardiac surgery
o Treatment: PPM for sx, PPM + automatic cardioverter-defibrillator if brady  tachy
 AV conduction blocks = Interruption from SA to AV node (look at PR interval)
o 1st degree
 Constant prolonged PRI (> .20 sec)
 QRS after every P wave
 Tx: observe
o 2nd degree
 Not all atrial impulses are passed on  some QRS is dropped
 Mobitz I- Wneckebach
- Progressive PRI lengthening  dropped QRS (shorter R-R)
- Tx: Sx (atropine, Epi +/- PPM), Asx (observe, consult)
 Mobitz II
- Block in bundle of HIS, constant prolonged PRI  dropped QRS
- Tx: Atropine or temporary pacing Can lead to 3rd degree, PPM is definitive
o 3rd degree
 AV dissociated (P don’t give a shit about Q)
 All P waves are not followed by DRS  decreased CO
 Tx: temporary pacing  PPM (definitive)
 Atrial Dysrhythmias
o Atrial flutter
 “saw tooth” waves 25—350 bmp (no p waves)
 Tx: stable (vagal, BB, CCB), unstable (synced cardiovert), definitive (ablation)
 Atrial Fibrillation
o Irregularly irregular w/ narrow QRS, NO P waves
o Asherman’s phenomenon: occasional aberrant QRS after short R-R cycles
o Types
 Paroxysmal: self-terminate w/in 7 days (often 24 hrs)
 Persistent: lasts > 7 days, need medical/ electric termination
 Permanent: > 1 year, refractory to cardioversion
 Lone: one of the above 3 without evidence of heart disease
o Treatment
 Stable
- Rate control (preferred initial management over rhythm control)
o BB: Metoprolol (could  reactive airway disease) CHF
o CCB: Diltiazem HTN
o Digoxin: elderly, preferred in hypotension or CHF Age > 75 (2 pts)
- Rhythm control (think younger patients w/ lone a fib) DM
o Direct synced cardioversion (preferred over pharm) Stroke (2 pts)
 If AF < 48 hrs OR after 3-4 wks of anticoag & TEE shows no thrombi Vascular disease
o Pharm- Ibutilide, Flecainide, Sotalol, Amiodarone Age (65-74)
o Radiofrequency ablation Sex (female)
 Unstable: direct current (synched) cardioversion
 Anticoagulation
- Assess risk of embolization (CHA2DS2VASc)
o 0 pts= no anticaog needed 1 pt= based on clinical judgement > 2 pts= anticoagulate
- Determine benefits vs/ risks of anticoag
o Non vit K antagonist PO anticoagulants: Now preferred over Warfarin!
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 Ex: Dabigatran (Thrombin inhibitor) Rivaroxaban, Apixoban, Edoxaban (Antithrombin II inhibitior)
o Warfarin [INR goal 2-3]
 Ind: chronic kidney disease, less expensive
 Long QT Syndrome
o Congenital or acquired
o Signs/ symptoms- recurrent syncope, ventricular arrhythmias, sudden cardiac death
o Treatment: d/c offending drug, correct e-, AICD for congenital or recurrent

 Paroxysmal Supraventrical Tachycardia (PVST)

o HR > 100, rhythm usuallt regular, narrow QRS, hard to see P waves
o Has sudden onset and termination (MC after atrial contraction)
o 2 types
 AV nodal reentry tachycardia (MC): 2 paths within AV node
 AV reciprocating tachycardia: 1 path w/in AV node & 2nd path OUTSIDE (WPW & LGL)
- Wolf Parkinson White
o Accessory path (bundle of Kent) pre-excites the ventricles: slurred, wide QRS
o ECG- delta wave (the slur), wide QRS, short PR interval
o Avoid AV node blockers (Adenosine, BB, CCB, Digoxin)
- Lown-Ganong-Levine Syndrome
o Short PR interval w/ normal QRS complex
o Accessor path (bundle of James) connects to HIS (QRS is narrow)
o Conduction patterns
 Orthdromic (MC): impulse goes down normal AV node & returns via accessory path (NARROW complex)
 Antidromic: goes down accessory first & returns via normal path (WIDE complex)
o Treatment
 Stable (narrow): vagal maneuvers, Adenosine 1st line med, AV node blockers (BB, CCB)
 Stable (wide): antiarrhythmics (amiodarone, Procainamide for WPW)
 Unstable: synced cardiovert
 Definitive: ablation

 Wondering Atrial Pacemaker (WAP) & Multifocal Atrial Tachycardia (MAT)

o WAP- HR < 100 bpm, > 3 P wave morphologies
o MAT- HR > 100 BPM, > 3 P wave morphologies, associated w/ COPD

 AV Junctional Dysrhythmias
o AV node becomes dominant pacemaker
o Etiologies: sinus disease, CAD, MC rhythm for digoxin toxicity
o ECG: P waves inverted or not seen (I, II, aVF), often narrow QRS
 Junctional rhythm- HR 40-60
 Accelerated- HR 60-100
 Tachycardia- > 100 bpm

 Premature Ventricular Complex (PVC)

o Premature beating of ventricle  wide, odd, early QRS, T wave in opposite direction of QRS, compensation pause
o Treatment: NONE

 Ventricular tachycardia
o > 3 consecutive PVCs > 100 BPM (sustained is > 30 seconds)
o Torsades De Pointes- MC d/t hypomagnesium or hypokalemia
o Treatment
 Stable, sustained: antiarrhythmics (Amiodarone, Lidocaine, Procainamide)
 Unstable w/ pulse: Synced Cardiovert
 VT (no pulse): Unsynced cardiovert + CPR
 Torsades de pointes- IV Magnesium!
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 Ventricular fibrillation- unsynced cardiovert

 Pulseless Electric Activity/ Asystole - CPR + Epi + Check for shockable rhythm
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Cardiac Tamponade
 Tamponade: pericardial effusion causing significant pressure on the heart  restricts filling  decreased output
o If acute, it can only take 10 cc to cause distress, if a chronic malignant illness, can hold up to 1 L of fluid

 Signs/ Symptoms
o Beck’s triad- 1. Distant/ muffled heart sounds 2. Increased JVP 3. Hypotension
o Pulsus paradoxus
 Exaggerated > 10mmHg decrease in systolic BP w/ inspiration & decreases pulses w/ inspiration. Increased filling of the
right side of the heart during inspiration decreases left sided ventricular filling  pulsus paradoxus.
o Dyspnea, fatigue, peripheral edema, shock (hypotension, tachycardia, cool extremities)
o Electrical Alternans: alternating QRS amplitude changes

 Diagnosis
o Echo- shows effusion & diastolic collapse of cardiac chambers (d/t pericardial pressure being greater than chamber
pressure)

 Management
o Pericardiocentesis immediately (pericardial window drainage if recurrent)

Myocarditis
 Inflammation of the heart muscle: complication of heart failure MC in kids

 Etiologies
o Infections
 Viral: Enterovirus (Esp Coxsackie) MCC
 Bacterial: Rickettsial (Lyme disease, RMSF, Q fever), Chagas disease (rare in US, think South America)
 Fungal
 Parasitic
o Toxic- scorpion venom, diphtheria toxins
o Autoimmune- SLE, rheumatic fever, RA, Kawasaki, Ulcerative Colitis
o Systemic- Uremia, Hypothyroidism
o Medications- Clozapine, Tetracycline, Amphotericin-B, Penicillin

 Patho
o Myocellular damage  myocardial necrosis & dysfunction  heart failure (d/t systolic dysfunction, cardiac enlargement &
myocardial fibrosis)

 Signs/ Symptoms
o Viral prodrome- fever, myalgia, malaise for several days  Heart failure
o Heart failure
 Dyspnea at rest, exercise intolerance, syncope, tachypnea/ cardia, hepatomegaly
 Impaired systolic function: S3 +/- S4, Severe (hypotension, poor pulses/ perfusion, AMS)
 +/- Concurrent perdicaditis

 Diagnostic Studies

 Management
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Heart Failure
 Dilated (95%)
o Patho- decreased contractility (systolic dysfunction, ventricular dilation)… a dilated weak heart
o Etiologies
 Idiopathic (50%)- postviral MCC of idiopathic (not proven)
 Viral Myocarditis- Entervirus MC (i.e. Coxsackie B, Echovirus), Lyme disease, Chagas, PB19, HIV
 Toxic- ETOH abuse, cocaine, anthracyclines (Doxorubicin), radiation
 Other- preggo, infiltrative, AI, Metabolic (thyroid disorders)
o Signs/ Symptoms
 Viral prodrome weeks before => + cardiac enzymes, ST-T changes
 L CHF sx- rales, tachycardia, cough, pleural effusion
 R CHF sx- peripheral edema, increased JVP, hepatic congestion
o Diagnosis-
 Echo shows dilation w/ decreased EF
 CXR- Cardiomegaly
o Treatment-
 Like CHF: BB, ACE-I, diuretic, digoxin, Na restriction
- Implantable defibrillator (AICD) if EF < 35%
 Avoid ETOH/ stop chem
o Differential
 Takotsubo cardiomyopathy
- Apical left ventricular ballooning s/p catecholamine surge (broken heart syndrome)
- EKG- ST elevations + cardiac enzymes, NO thrombosis on catheterization
 Hypertrophic Obstructive Cardiomyopathy
o Diastolic dysfunction
o Patho- genetics  obstructed aortic outflow 2/2 hypertrophied septum & systolic anterior wall motion (SAM), diastolic
dysfunction
o SX: Murmur = aortic stenosis, (harsh crescendo- decrescendo at IJSB)
 increases intensity w/ decreased venous return (valsalva or standing),
 decreases intensity w/ increased venous return (squatting, supine)
o Diagnosis-
 Echo = asymmetric wall thickness
 EKG- Left ventricle hypertrophy
o Tx: avoid dehydration, avoid exercise (BB 1st line!) = CCB, ETOH ablation, myectomy
 Concentric Hypertrophic Cardiomyopathy
o Patho- HTN
o Patient- Diastolic CHF
o Diagnosis- echo= concentric
o Treatment- DIA CHF= avoid dehydration, CCB = BB, control BP, transplant as last resort
 Restrictive Cardiomyopathy
o Impaired diastolic filling w/ relatively preserved contractility
o Ventricular rigidity stops ventricular filling or increases the effort needed(decreased compliance)
o Patho-
 Infiltrative- Amyloid (MCC), sarcoid, CA, Fibrosis
 Noninfiltrative- familial, idiopathic
o Patient- DIA, CHF (R MC)
 Amyloid neuropathy
 Sarcoid  Pulm disease
 Hema  Cirrhosis, DM, CHF
o Physical-
 Kussmaul’s sign: JVP increases w/ inspiration (stiff inelastic RV  impaired filling  increased blood flow back up in
venous system
 HF signs: S3, JVD, Rales, Hepatomegaly, LE Swelling
o Diagnosis- echo = restrictive, ventricles not dilated or are thickened w/ dilation of atria
 Amyloid  fat pad bx
 Sarcoid  Cardiac MRI  Bx
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 Hema  Ferritin  Genetics
o Treatment- DIA CHF  BB = CCB, gentle diuresis

Heart Failure (PPP organization)

 MCC is coronary artery disease
 Forms:
o Left sided vs. Right sided
 Right MCC- Left sided heart failure/ pulm diseases
- Increased system venous pressure  overall fluid retention (peripheral edema)
- JVD, GI/ Hepatic congestion: anorexia, N/V, hepatosplenomegaly, RUQ TTP
 Left sided (MCC is CAD/ HTN)
- Increased pulm pressue (fluid backup into lungs)  pulm congestion, ronchi/ rales, cough, pink/ frothy
- Dyspnea (MC), nocturnal dyspnea, HTN, tachypnea (Cheyne-strokes)
- Increased adrengic activation  dusky/ pale skin, sweating, sinus tachy, cool extremities
o Systolic vs. Diastolic
 Systolic (MC form)
- Decreased EF, thin ventricles, + S3
- Eti: post MI, dilated cardiomyopathy
 Diastolic
- Normal EF, forced contraction into stiff ventricle, thick ventricles, +S4
- Eti: HTN, left ventricular hypertrophy, elderly
 Diagnosis-
o Echo is the most useful (EF < 35%)
o CXR- cardiomegaly, Kerly B lines, Butterfly pattern, Pulm edema
o BNP- ID CHF as cause of dyspnea (> 100 = CHF likely)
 Treatment: ACE-I > BB
o Meds that decrease mortality: ACE-I, ARB, BB, Nitrate + Hydralazine, Spironolactone
o Outpt: ACE-I + diuretic  + BB
 Implantable defibrillator if EF 35%
 Use ARBS and ACE-I is no go, Use Hydralazine + Nitrates if ACE-I/ ARBS are no go (AA/ Preggo)
 Diuretics best for mild- mod CHF sx

Examples MOA Side Effects Contraindications

ACE-I “pril” Decrease pre/after load 1st dose hypoTN Hypotension
Vasodilate Renal insufficiency Preggo
Hyperkalemia
Cough/ angioedema
ARBs “artan” Blocks angiotensin II
BB Carvedilol Carvedilol- dizzy, Decompensated CHF
Metoprolol hypotension
Hydralazine + Nitrates Hyd- decreases afterload Dizzy, HA,
NTG- decreases preload tachyphylaxis
Loop diuretics Furosemide (Lasix) Increase H2O excretion Hypo (K, Ca, Na, Cl)
CHF, HTN, severe edema Bumetanide Hyper (BG, uricemia)
mild renal disease
Torsemide Sulfa allergy
K Sparing Diuretics Spironolactone Aldosterone antag Hyperkalemia Renal failure
Severe CHF Eplerenone Gynecomastia Hyponatremia
HCTZ Hypo (K, Na)
Combo w/ loop Hyper (BG, uricemia)
Sympathomimetics Digoxin (only chronic) Prolong contraction Narrow TI
Short term, severe CHF, Afib Dobutamin Decrease conduction CNS (seizures, dizzy)
Dopamine speed & HR GI
Vasodilation (Dob) Visual
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ECG (down sloping ST)
Hypokalemia worsens
toxicity

Hypertension
 Urgency
o Increased BP but no apparent organ damage
o Treatment- decrease BP by 25% in 24-48 hrs w/ PO Rx
 Clonidine- short term only, rebound HTN
 Captopril- CI w/ AKI
 Furosemide
 Labetolol- CI w/ CHF
 Nicardipine
 Emergency
o Increased BP  acute END organ damage
 SBP > 180 OR DBP > 120
o W/u: neuro exam, EKG, Trop, CXR (AAA, Pulm Edema) , UA (AKI- proteinuria, hematuria), retinal damage (papilledema)
o Treatment
 IV Rx: no more than 25% the first 24 hrs
- Except w/ ischemic stroke & aortic dissection
 Emergencies & Treatments
- HTN encephalopathy- Nicardipine, Clevidipine, Labetolol (R/o stroke)
o Symptoms: AMS, HA, N/V
- Hemorrhagic stroke- Nicardipine or Labetolol
- Ischemic stroke- Nicardipine or Labetolol
o ONLY BP >220/ 120 (can’t use thrombolytics) or > 185/110 (can use thrombolyics)
- Aortic Dissection- Esmolol, Labetolol
- ACS- Nitroglycerin, BB
- Acute heart failure- Nitro, Furosemide
o Avoid hydralazine/ BB
- Renal- Fenoldopam

Hypotension
– Orthostatic
o Patho: impaired autonomic reflexes & or reduced blood volume
 Meds
 Neuro- DM autonomic neuropathy, Parkinson’s, Guillain-Barre
o Symptoms: weak pulses, cool extremities, tachycardia, tachypnea
o Diagnosis: W/in 2 minutes of stand after 5 min of lying down
 SBP falls > 20 mmHg & OR
 DBP falls > 10 mmHg
o W/u: BMP, CBC, ECG
o Treatment
 Remove problem Rx, increase Na & fluids
 Pharm- Fludrocortisone, Midodrine (vasopressor)

– Cardiogenic Shock
o Cardio dysfunction  bad tissue perfusion  decreased CO  increased system vascular resisitance
o Eti: often systolic in nature, cardio disease (MI, congenital, etc)
o Patho: decreased CO & tissue hypoxia w/ adequate volume w/ increased pulm capillary wedge pressure
o Tx: O2, small fluid repletion (only shock w/ little fluids), Inotropic support (Dobutamine, Epi), tx cause

Pericardial Effusion
– Increased fluid in pericardial space
– Etiology: pericarditis
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– PE: distant, muffles heart sounds
– Diagnosis:
o EKG: low voltage QRS (large effusion/ tamponade) OR electric alternans
o Echo
o CXR: cardiomegaly
– Treatment: observe if no evidence of tamponade & tx underlying cause

Peripheral Vascular Disease

– Arterial Disease
o AS disease of lower extremities
o Signs/ symptoms
 Intermittent claudication (MC sx)- pain in legs during walking, relieved by rest
 If at rest = advanced disease (limb ischemia risk)
 6 P’s- paresthesia, pain, paralysis, pallor, pulseless, poikilothermia (cold)
 Gangrene- wet (ulces), dry (digit mummification)
 PE: skin changes (atrophy, hairless, thick nails, usually no edema), pale on elevation, dusky red when standing/ lower
than heart, LATERAL malleolar ulcers & more ulcers on toes/ bony prominences

o Diagnosis
 ABI:
- <0.85 = can’t heal ulcers
- < 0.9 = (+) PAD dx
- 1-1.2 = normal
- > 1.2 = possible calcified vessels
 Arteriography (GOLD STANDARD)- usually only done if revascularization is planned
 Hand held doppler- assesses distal blood flow & pulses

o Treatment
 Plt inhibitors: Cilostazol (#1- vasodilator, ADP-I), ASA, Clopidogrel
 Revascularization: PTA, bypass graft, endarterectomy
 Supportive: exercise (stop w/ sx & resume when gone 1 hr / day), foot care

– Venous Disease
o Virchow’s- intimal damage + stasis + hypercoagulability (Factor V mutation)
o Signs/ symptoms
 Worse w/ leg elevation (i.e. at night)
 PE: MEDIAL/ lower calf ulcers
o Treatment: surgery/ leg stockings

– Venous insufficiency disease

o Most often after superficial thrombophlebitis/ DVT/ trauma
o Leg pain:
 Worse w/ standing/ sitting a long time
 Better w/ elevation/ walking
o Hyperpigmentation (brownish), stasis dermatitis (itching/ scaling/ weeping)
o Ulcers on MEDIAL malleoulos (vs. lateral w/ arterial disease)
o Diagnosis: Trendelenburg test (elevate leg at 90 degrees  Stand  if ankle fills ins 20 sec = (+))
o Treatment: compression & ulcer management

Syncope
 Ddx: seizures, cardiac arrhythmias, MI, vasovagal (MCC) Ortho Hypotn
 Eval: Hx, PE, EKG, CBC, CMP, Tilt table test
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Valvular Disease
– All made worse w/ increased blood flow & better w/ less (less blood = more murmur)
o i.e. Get louder w/ squat/ leg raise & softer w/ Valsalva
– All dx w/ echo
– Mitral Stenosis
o Patho- Rheumatic heart disease (MCC), stenosis of valve, decreased forward flow during diastole
 Atrial stretch  pulm congestion/ HTN  CHF
o Patient- Afib w/ CHF sx
 OPENING SNAP, loud S1. MID/EARLY DIASTOLIC rumble decrescendo Murmur @ LLD
 More intensity (volume) w/ more blood (squatting)
 Pulm sx (dyspnea, hemoptysis)
 Mitral facies (flushed cheeks w/ facial pallor)
o Diagnosis: EKG w/ left atrial enlargement
o Treatment- balloon valvotomy, valve replacement
Diastolic: ARMS
REST
– Mitral Regurg
o Patho- Backflow into LA from LV  LA dilation  Blood in pulm circulation  less CO
 Acute: infection, infarction, ruptured papillary muscle, chordae tendinea
 Chronic: prolapse (leaflet abnormality (MCC)), ischemia
o Patient
 Acute: fulminant CHF, hypoxemia, hypotension
 Chronic: Afib, exertional dyspnea, pulm HTN
 SYSTOLIC. Blowing HOLOSYSTOLIC murmur at apex  AXILLA
 More intensity w/ more blood (squatting)
o Diagnosis: echo (hyperdynamic LV, EF < 60%)
o Treatment- valve replacement (preferred over repair
o Also consider Mitral Valve prolapse
 Sounds like mitral regurge BUT doesn’t change w/ blood flow like you would expect
- More blood = less murmur (standing= quiet murmur)
 Patient- congenital defect, women (esp preggo)
 Treatment- valve replacement

– Aortic Regurg
o Patho- ischemia, infection, dissection, rheumatic disease, aortic root dilation (Marfan or HTN)
 Incomplete closure  LV overload  LV dilation  CHF
o Patient- often sick, hypotension, CHF
 DIASTOLIC DECRESCENDO murmur at aortic valve  LUSB
 Wide pulse pressure, Water- hammer pulses (bounding), Quickne’s Pulse (nail bed)
 Head bobbing
 More intensity w/ more blood (squatting)
o Diagnosis- echo, catheter is definitive
o Treatment- valve replacement, intra-aortic balloon pump Murmur Grading:
 Meds- afterloade reduction w/ vasodilators (ACE-I, ARBS) I- S1, S2 > Murmur
II- S1, S2 = Murmur
– Aortic Stenosis (MC valve disease) III- S1, S2 < Murmur
o Patho- calcifications, sclerosis of outflow from ventricle, rheumatic disease IV- palpable thrill
 Stenosis  increased afterload  LVH V- ½ stethoscope off chest
o Patient- old man w/ atherosclerosis VI- no stethoscope needed
 SOB (MC sx), Syncope, chest pain, CHF
 SYSTOLIC ejection click CRESCENDO-DECRESCENDO murmur
 2ND RUSB  CAROTID
 More intensity w/ more blood (squatting)
o Treatment- valve replacement ONLY, balloon doesn’t work
 F/u b/c may need CABG if replacing valve d/t coronary perfusion
o Differential
 Hypertrophic Obstructive Cardiomyopahty
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- Sounds like AS BUT doesn’t respond to blood change like you would expect
o More blood = less murmur (standing = quiet murmur)
Vascular Disease
– Aortic Aneurysm
o > 3.0 cm  aneurysmal  MC occurs infrarenally
o RF- Atherosclerosis (MC), smoking, > 60 y/o, Males, Marfan’s syndrome, Smoking
o Patho
 Laplace Law- larger aneurysms expand faster
 Ascending  medial degeneration
 Descending  atherosclerosis
 Average dilation  0.25- 0.5 cm/ yr
 > 5 cm  increases risk of rupture
o Signs/ Symptoms
 Most asx until they rupture
 Triad: 1. Abd pain 2. Hypotension 3. Pulsatile abd mass
 Acute leaky ruptures- classic presentation (older male w/ severe abd/ back pain)
- Presents w/ syncope/ hypotension + tender, pulsatile abd mass
- +/- Flank bruising
- May complain of unilateral groin/ hip pain
 Chronic contained rupture- uncommon, may be tamponaded by surrounding peritoneum
 Aortoenteric fistula- presents as acute GI bleed in pts who underwent aortic grafting
o Diagnosis
 U/S (INITIAL STUDY) to determine size/ extent & progression
 CT (TEST OF CHOICE) for further eval
 Angiography (GOLD STANDARD)
 Thoracic XR- widened mediastinum shadow, displaced trachea
 Abd XR- classifications
o Treatment
 Surgical Management based on size:
- > 5.5 cm OR > 0.5 cm growth in 6 mo: surgery NOW (even if asx)
- > 4.5 cm: vascular surgeon referral
- 4-4.5 cm: monitor w/ US q 6 mo
- 3-4 cm: monitor w/ US q 1 yr
 BB to reduce shearing forces

– Aortic Dissection
o Tear in the innermost later of the aorta (intima)
o MC site- ascending (near aortic arch or subclavian)
o Ascending= high mortality
o RF: HTN IS THE MOST IMPORTANT, bimodal age RF, vasculitis, turners, collagen disorders, cocaine
o Signs/ Symptoms
 Abrupt/ severe chest pain that radiates to SCAPULA
- Aortic arch- Neck/ jaw pain
- Type A- Anterior chest pain
- Type B- Abd pain
 Feeling of impending doom (tearing/ ripping pain)
 HTN, Aortic insufficiency, pulse deficit in radial/ femoral arteries (> 20
mmHg)
o Diagnosis
 EKG to r/o ACS
 CXR: wide mediastinum
 CT w/ & w/o contrast (TEST OF CHOICE)
 MRI angiography (GOLD STANDARD)
 TEE- accurate, portable, may be initial test
o Treatment
 Surgical- acute proximal (Stanford AND Debakey I & II) OR acute distal (Type III) w/ complications
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 Medical- descending if no complications (Stanford B/ Debakey III)
- BB First line! Esmolol, Labetalol
- Goal BP: SBP 100-120 & pulse < 60 in 20 min
- Na Nitroprusside + if needed +/- Nicardipine
– Superficial Thrombophlebitis
o Inflammation & thrombus of superficial vein MC w/ IVs/ trauma/ preggos/ varicose veins
o Trousseau’s sign: migratory thrombophlebitis d/t malignancy elsewhere
o Symptoms: local (tender, induration, red, edema, +/- palpable cord)
o Diagnosis: US w/ noncompressible vein
o W/u: Hypercoaguability (factor V leiden MCC) or Malignancy w/u for specific CA
o Tx: supportive is mainstay- warm compress, NSAIDs, elevation
– Deep Venous Thrombosis
o RF: Virchow’s (venous stasis + hypercoagulability + endothelial damage) Homan’s sign- pain w/
 Most start in calf & important consequence is PE dorsiflexion & flexed
o Signs/ Symptoms knee, not reliable
 Unilateral leg swelling/ edema of lower extremity
 Calf pain/ tenderness (phlebitis/ Homans sign)
o Diagnosis:
 Venous US (FIRST LINE)- noncompressible & echogenic
 D-Dimer- if (-) can r/o DVT, (+) doesn’t mean shit
 Venography (GOLD STANDARD)
o Treatment
 Anticoag- LMWH or UFH  Warfarin
- LMWH:
o SQ lasts 12 hrs, don’t need to check PTT
o CI w/ thrombocytopenia
- UFH: prevents further emboli
o Want PTT 1.5-2.5
o SE- thrombocytopenia
- Warfarin: stops Vit K pathway
o Overlap w/ heparin for 5 days until INR > 2-3 for > 24 hrs
 IVC filter for patients w/ contraindications

Shit that isn’t on the list but seems important

Acute Coronary Syndrome
 Def: sx of acute myocardial ischemia 2/2 to acute plaque rupture & varying degrees of coronary artery thrombosis
 Includes: Unstable angina, NSTEMI, & STEMI

Constrictive Peridcarditis
 Def: fibrotic, calcified pericardium limits ventricular diastolic filling
 Eti: Post viral (enterovirus, coxsackie, echovirus)
 Signs/ Symptoms:
o R sided heart failure sx (peripheral edema, increased JVP, hepatic congestion, N/V
o Pericardial knock- 3rd heart sound
o Pulsus paradoxus
o Kussmaul’s sign- increased JVP w/ insp
 Dx: echo
 Tx: Pericardiectomy

Cardiac Markers
Appears Returns to baseline
CK/ CK-MB 4-6 hrs 3-4 days
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Troponin (best one) 4-8 hrs 7-10 days