INTERNAL MED EOR EXAM STUDY GUIDE: CHF

Scientific Concepts





SYMPTOM COMPLEX, NOT DX
Condition from any functional or structural cardiac disorder that impairs the ability of the heart to fill
or pump a sufficient amount of blood through the body. (or a combo of both)

Systolic- depressed ejection fraction (this is more common dysfunction, dilation)
Diastolic- preserved ejection fraction. Not enough blood volume. Passive stiffness
Causes:
o CAD (with or without MI)
o Ischemic Cardiomyopathy (CMO)- Most Common ( ischemic event that caused an
exacerbation acutely
o Non-Ischemic CMO (rare- sarcoid/amyloid)
o Systemic Hypertension
Stages of Heart
Failure

CHF Prognosis Risk increases with diastolic dysfunction and worsening prognosis (because the pulmonary system is
getting worse- affecting everything behind it)
Improving with use of ACEI and Beta blockers
CHF History and
Physical
Symps
o Dyspnea (at rest and exertional)
o Orthopnea
o Paroxysmal Nocturnal Dyspnea (PND)
o Chronic cough (non-productive) vascular congestion
o Nocturia
o Fatigue
o With RV Failure: RUQ Pain, Nausea, Loss of appetite, Peripheral edema, Ascites
PE
o Vitals: can be normal, may have Tachycardia, Hypotension , Decreased pulse pressure,
Diaphoresis, Cool extremities
o WEIGHT! Follow very closely
o JVD
o Thyromegaly
o Carotid pulse- Aortic Stenosis (AS)
o Lungs: Crackles, Wheezes, Rhonchi, Pleural effusions
o LV lift or sustained pulsation
o Diminished first sound: annulus around the valves change, not getting closing snap
o S3 gallop
o Murmurs
o RV failure: hepatomegaly
CHF Lab Eval and
Workup
CBC Anemia
BMP- Renal insufficiency (BUN and Cr increased, but still making urine)/Renal Failure Electrolytes (K,
Mg), Decreased Na, Hypokalemia in Afib
Thyroid
BNP (BRAIN NATRIURETIC PEPTIDE)
o Major source is the cardiac ventricles
o direct proportion to ventricular volume expansion and pressure overload.
CHF Workup: EKG Hypertrophy
Arrhythmia : ie A-fib
MI
Non-specific
*Compare priors
CHF Workup: CXR Cardiomegaly silhouette should not be more than one half the size of the chest
Pulmonary venous hypertension
Perivascular edema (haziness of vessel outlines)
Interstitial edema
Pleural effusions (transudate)
CHF Treatment Underlying
o Valvular disease
o MI : Stent, Angioplasty, CABG
o HTN
o Arrhythmias
o Alcohol
o Drugs: CA++ channel blockers
o Pericardial disease
Diuretics
o Most effective for symptoms
o Careful for excessive use
o Electrolyte abnormalities (K+ )
o Thiazide diuretics
HCTZ 25mg Daily
Metolazone 2.5-5 mg Daily
Chlorthalidone 50 mg Daily
Works on distal loop, prevention of absorbtion of Na+
Worsening HF (adding more diuretics want to assess by symptomology)
o Furosemide (Lasix) 20-40 mg Daily, titrate
o Bumetinide (Bumex) 0.5-2 mg Daily
o Torsemide
o BID preferred
o Watch electrolytes
K+ sparing drugs (aldosterone antagonists)
o Spironolactone (Aldactone) 25-50 mg Daily
o Triamterene, Amiloride, Eplerenone (Inspra)
o Along with ACE and diuretics, reduction in mortality and improve symps
ACEI
o Prevents hospitalizations
o Increased exercise tolerance
o Decreases symptoms
o Enalapril, Ramipril, Benazepril, Avoid if Renal artery stenosis
o ACEI First line tx in pts with EF < 40%
o Used in combo with diuretics: Potential side effects are hypotension and hyponatremia.
o Cough, angioedema, hypotension
ARBs
o Not to be used with ACEI
o Chronic Failure: Candesartan or valsartan can benefit as alone or in addition to diuretic
o Losartan (Cozaar)
Beta Blockers (Carvedilol, Metoprolol)
o Decreased HR allows more time for the heart to fill.
o Clinical effects: improve long term symps; reduce hospitalizations, sudden death; improve
survival; reduce remodling/progression
Caution: Could worsen LV function
Detrimental to use a pure beta blocker for HF
Digoxin/Digitalis
o Only oral positive inotrope
o Used in conjunction with patients with atrial fibrillation
o Enhances sympathetic tone which delays AV conduction
o Can be given with other meds
o Amiodarone (CORDARONE)
o Quinidine
o Propafenone (RYTHMOL)
o Verapamil
Vasodilators/Nitrates
o Reduction of AV afterload
o Need an agent or a combination of agents to improve both factors
o NTG, Sodium Nitroprusside, Isosorbide 20-80 mg TID, NTG paste
o Hydralazine
Potent arterial vasodilator
Markedly increased CO
Stand alone does not perform well to improve symptoms or exercise tolerance
Combination of nitrate and hydralazine has greater hemodynamic effects (BiDil:
Hydralazine + Isosorbide)
Frequently limited by side effects
GI, HA,Hypotension
Dobutamine/Milrinone: positive inotropes, role is limited to pts with hypoperfusion and
deteriorating kidney function, or pts awaiting transplant. Continuous therapy increases mortality.
CHF Tx: CCBs May accelerate progression of HF
Exception is Amlodipine (NORVASC)
General rule is to avoid use unless treating HTN associated angina
Anticoagulation LV failure and reduced EF can give risk of intra-cardiac thrombus formation and systemic embolus
Antiarrhythmic
Therapy
Moderate to severe failure can have increased incidence of arrhythmia
Tx: Implantable
Defibrillators
Reduction of sudden death from heart failure related arrhythmia (EF <30%, risk of sudden cardiac
death increases significantly)
INDICATED IN CLASS III HF for primary prevention of sudden death
Non-Pharm Tx Diet, exercise management
o Reduction in weight, sodium intake
o Exercise training to reverse deconditioning
Biventricular Pacing For use in widened QRS complex situations
Can improve EF and exercise tolerance
Reduction in death and hospitalizations
Cardiac
Transplantation
Last ends of care



INTERNAL MED EOR STUDY GUIDE: HYPERTENSION
JNC7 Classification

Diagnosis Serial blood pressure measurements on at least 3 separate occasions
Major exceptions to single elevated BP measurement
o Unequivocal evidence of life-threatening end-organ damage (hypertensive emergency)
o BP is >220/125 mm Hg, but life-threatening end-organ damage is absent (hypertensive
urgency)
Patient Evaluation 1. Assess CV risk factors and comorbidities
2. Reveal identifiable causes of HTN
3. Assess presence of target organ damage and CVD
Risk Factors and
Comorbidities

Identifiable Causes
HTN

Target Organ Damage
and CVD

Scientific Concepts:
Primary Essential HTN
**95% of hypertensive patients, onset between ages 25 and 50
Genetic and Environmental Factors
Sympathetic NS hyperactivity: Younger persons with tachycardia and elevated CO
RAAS: High Renin Activity, Caucasian and younger
Elevated intracellular sodium and calcium levels
Exacerbating factors: Obesity, Sleep apnea, Increased salt, ETOH, Cigarettes, Polycythemia, NSAIDs, Low
potassium intake
History and Physical Symptoms
o Asymptomatic : Silent killer
o Nonspecific: HA, Blurred vision, Dizziness, Facial flushing
o Severe Symps: N/V, Irregular HR, Tinnitus, Dyspnea
PE
o BMI
o Verify contralat arm
o Funduscopic exam
o Palpate peripheral pulses
o Bruits (carotid, renal, femoral)
o Thyroid gland enlargement or masses
o Cardiac (LVH)
o Kidney enlargement
o Abdominal masses and AAA pulsation
o BLE edema and pulses
o Neurological assessment (cerebrovascular dz)
Diagnostic Studies Labs
UA
FBG or HgA1c, K+, creatinine, GFR, Ca++
Fasting lipid panel
Hematocrit
Target organ damage
Labs, radiologic studies, EKG- but echo better
Complications of
Longstanding
Hypertension
CV: LVH, CAD, CHF, Afib
Cerebrovascular Disease: Stroke, hemorrhage, encephalopathy
Renal: Nephrosclerosis, accelerates DM Nephropathy
Aortic Dissection: HTN contributing factor
Hypertensive
Emergencies
Require substantial reduction of BP within 1 hour to avoid risk of serious morbidity or death
Includes:
o Hypertensive encephalopathy (HA, irritability, confusion, AMS)
o Hypertensive nephropathy (hematuria, proteinuria, progressive kidney dysfunction)
o Intracranial hemorrhage, aortic dissection, preeclampsia-eclampsia, pulmonary edema,
unstable angina, MI
Malignant Hypertension
o Elevated BP results in target organ damage (CNS, CV, renal system)
o Characterized by encephalopathy or nephropathy with accompanying papilledema (must
be present)
o Progressive kidney disease results if treatment not provided
o Same treatment as other hypertensive emergencies, table 11-12 CMDT. Depends on
organ affected, includes: Nicardipine, Ntg + Labetalol or Esmelol, Fenoldopam,
Clevidipine, Labetalol
Health Maintenance&
Treatment Goals
Primary focus is reaching SBP goal, most reach DBP goal once SBP goal is reached
Treating to <140/90 is associated with decrease in CVD complications
Goal is <130/80 for patients with HTN and DM or renal dz
Lifestyle: sodium recommended 1500 mg, no more than 2300 mg/day or 1 TSP
F/U monthly intervals for adjustment of medications until BP goal is reached and assess for
adverse reactions
More frequent visits for stage 2 HTN or if complicating comorbid conditions
Labs: Serum potassium and creatinine 1-2 times/year and other labs as indicated
BP to goal and stable: 3 to 6 months intervals
Clinical Therapeutics Multidrug treatment
o 2 drugs at lower doses avoid adverse effects that may occur with higher doses of single
agent

Thiazide Diuretics Chlorthaizide, Chlorthalidone, HCTZ, Polythiazide, Indapamide, Metolazone
Initial therapy for most patients with HTN
Enhance the antihypertensive effects of multi-drug regimens (ACEI, BB)
Adverse: Decrease K, Mg, Ca, Na; Increase uric acid, glucose, lipid
Hypotension, HA, weakness, muscle cramps, photosensitivity, rash, ED
ACE Inhibitors Benazepril, Captopril, Enalapril, Fosinopril, Lisinopril, Moexipril, Perindopril, Quinapril, Ramipril,
Trandolapril
More effective in Caucasians and younger patients
Less effective in African Americans and older patients
Benefits
o Slow progression of loss of kidney function (diabetic nephropathy and CKD)
o Reduce LVH and indicated for CHF
Adverse Effects
o Increase K, uric acid; elevated BUN/Cr
o Hypotension,** cough **angioedema (severe rxn)
o If cough, switch to ARB

Angiotensin II
Receptor Blockers
Candesartan, Eprosartan, Irbesartan, Losartan, Olmesartan, Telmisartan, Valsartan
Benefits
o Less side effects than ACEI (cough and angioedema)
o Effectiveness and enhanced interaction with diuretics is similar to ACEIs
o Prevention of stroke,
o Possibly diminish progression of Alzheimers
ADEs similar to ACEI
Calcium Channel
Blockers
Benefits: Effective in treating arrhythmias
Adverse reactions: HA, peripheral edema, bradycardia, heartburn, constipation

Beta Blockers Atenolol, Betaxolol, Bisoprolol, Metoprolol, Nadolol, Propranolol, Timolol
Cardioselective primarily beta-1 receptors (heart)
Nonselective beta-1 and beta-2 (lungs, blood vessels, tissues
Benefits
o Cardioprotective
o Useful in patients with angina, prior MI, stable CHF
o Treatment for migraines and anxiety
Adverse reactions
o Worsen chronic lung disorders
o Possibly worsen heart failure and peripheral vascular disease
o Abrupt withdrawal may trigger angina or MI in patients with heart disease
o Dizziness, fatigue, insomnia, depression, erectile dysfunction, Raynauds, increase TG
Treatment: Compelling
Indications














INTERNAL MED EOR EXAM STUDY GUIDE: HEART MURMURS
Aortic Stenosis Harsh systolic ejection murmur heard best at right upper sternal border (RUSB)
o Mid to late peak
o Reduced intensity of second heart sound
o Radiates to carotids
o Pulses-parvus et tardus (slow and late)
o Narrow pulse pressure
o Begins after S1, ends before A2
Aortic Insufficiency (aka
regurgitation)
High pitched diastolic decrescendo murmur
o Louder along left sternal border in third to fourth intercostal space
Widened pulse pressure, Water hammer/Corrigan pulse
Optimum auscultation: diaphragm, pt leaning forward, breath held in expiration
Austin Flint: Aortic Regurg may be associated with low pitched mid-diastolic murmur
at apex
Recommended drugs
Diuretic BB ACE-
I
ARB CCB Aldosterone
antagonist
Heart
Failure
X X X X X
Post-MI X X X
High CAD X X X X
DM X X X X X
Chronic
kidney dz
X X
Recurrent
stroke
prevent
X X
Mitral Stenosis Opening snap following A2
Low pitched diastolic rumble heard best at apex, Lt Lat position, using bell
Left sided after expiration
Mitral Regurgitation Holosystolic murmur heard best at left sternal border and radiates to axilla
Loudest over PMI
Begins with S1 and ends at or after A2
Mitral Valve Prolapse Mid systolic click with late systolic murmur
Ausculatory findings accentuated in the standing position or valsalva
Pulmonic Insufficiency diastolic decrescendo murmur
Pulmonary Stenosis systolic murmur with S2 split
Tricuspid Regurgitation pansystolic murmur, right heart failure
Best heard at third to fifth ICS along left sternal border
Can be hard to hear, blowing, coarse or musical
Begins with S1 and fills systole
Louder during inspiration
Tricuspid Stenosis Rumble often follows audible opening snap
Heard at third to fifth ICS along lefts sternal border out to apex.
Murmur increases with inspiration
Murmurs in Stable Angina Occasionally a gallop rhythm and apical systolic murmur due to transient mitral
regurg from papillary muscle dysfunction
**Here is a youtube video with a mnemonic to remember the diastolic vs systolic murmurs **
http://www.youtube.com/watch?v=sL0vHiXLZ-4

INTERNAL MED EOR EXAM STUDY GUIDE: VALVULAR HEART DISEASE

Definitions
Stenosis- abnormal narrowing
Regurgitation- backward flowing of blood
Aortic Stenosis (AS)
Congenital: Unicuspid or bicuspid valves, younger population
Rheumatic
Untreated Strep pharyngitis- usually between 5-15y
Fusion of the leaflets, also effects mitral valve
Degenerative calcific (most cases > 70y)
Lipid accumulation, inflammation and calcification
AS pathophysiology
Bulky calcification > obstruction of the outflow tract leads to hypertrophy of the left ventricle > eventually leads to less
compliance > diastolic dysfunction (elevated LVEDP)
AS symptoms
3 cardinal symptoms: Angina, Syncope, Dyspnea
AS treatment
Surgical aortic valve replacement (gold standard)
Mechanical vs bioprosthetic
Transcatheter aortic valve replacement (TAVR)
Palliative percutaneous aortic balloon valvuloplasty
Medical therapy
Aortic Insufficiency
Regurgitation of aortic valve into left ventricle
Multiple etiologies- endocarditis, iatrogenic, bicuspid vs acute in setting of aortic dissection
Prognosis determined by symptoms and LV size/function
AI clinical manifestations
Diagnosed with auscultation/echocardiogram
AI treatment options
Medical therapy to help slow progression of symptoms
ACEi, Diuretics
Surgical valve replacement if evidence of LV systolic dysfunction with or without symptoms
Mitral Stenosis
Thickening and immobility of mitral valve leaflets (fusion or shortening of chordae tendonae)> increased pressure in
left atrium > increased pressure in pulmonary vasculature > elevated pressures in right heart
Etiology: Rheumatic fever (majority), Congenital
MS clinical manifestations
Dyspnea
Pulmonary hypertension- can progress to right heart failure
Hemoptysis
Embolic events (mostly with Afib)
Atrial fibrillation
PE: Evidence of right heart failure- JVD, lower extremity edema, hepatomegaly
MS management
Medical management: Diuretics, Beta blockers, +/- Anticoagulants (if Afib), Statins
Mitral balloon valvuloplasty (PMBV)
Surgical valve replacement
Mitral Regurgitation (MR)
Etiologies: Mitral valve prolapse, Rheumatic , Flail leaflet, Endocarditis
MR manifestations
Exercise intolerance, Dyspnea on exertion, Easy fatigability
MR treatment
Medical therapy- ACEi/ARB, beta blockers, diuretics
SURGERY if severe MR with LV impairment and/or pulmonary hypertension or new onset atrial fibrillation (with or
without symptoms)
Mitral Valve Repair (ring annuloplasty) may be superior to replacement
Mitral Valve Prolapse
female predominance
Causes: myxomatous degenerative changes, connective tissue disorders, ruptured chord or papillary muscles, enlarged
annulus or trauma
Non-specific symptoms- chest pain, dizziness, dyspnea, lightheadedness, exercise intolerance, anxiety disorders
Pulmonic Insufficiency
Causes: Dilation of pulmonic ring, Abnormality of leaflets, Congenital
Pulmonary stenosis
Congenital is MC
Tricuspid Regurgitation
Causes: Abnormality of valve leaflets , Endocarditis, Dilation of right
ventricle
Treatment: diuretics, surgery










INTERNAL MED EOR EXAM STUDY GUIDE: CAD/MI/ACS
Acute Coronary
Syndrome
The spectrum of disease and clinical presentations resulting from myocardial ischemia and/or
necrosis
ACS = UA + NSTEMI + STEMI
Angina CP brought on by exertion/emotion, may radiate to neck, arm or jaw. Relieved with rest or
NTG, may be associated with nausea, sweating, or SOB, usually short lives (3mins)
EKG often normal, but in an active episode: ST depression, T wave inversion/flattening
Angina Equivalent: SOB, DOE, Diaphoresis in the absence of CP, Prevalent in elderly
Evaluation: Exercise treadmill test, Nuclear stress, Echo, MR/CT, angiography
Exercise treadmill: confirms presence of angina, positive test is 1 mm horizontal or downsloping
ST-T wave beyond baseline
Chronic Stable Angina Tx Prevent further attacks
Long acting nitrates: Isosorbide
Beta blockers: Prolongs life CAD pts with chronic angina
Ranolazine
Antiplatelets: ASA, Clopidogrel
Revascularization: PCI, Stent, CABG
Unstable Angina Angina that is new onset, occurs at rest, or is increasing in frequency, severity, or duration
Rest angina: anginal pain that persists for 20 minutes despite cessation of activity
New onset angina: symptoms that began within 2 months of presentation
Coronary Vasospasm NOT caused by thromboembolic state
Two examples: Cocaine and Prinzmental Angina
Prinzmental Angina Variant angina due to coronary artery vasospasm +/- fixed lesion
MC in women <50 y/o
Usually occurs early morning, a/w arrhythmias
2/3 of victims have underlying CAD
Acute MI NSTEMI + STEMI = AMI
Up to 90% of STEMI occurs from a thrombus that is occluding a coronary artery (plaques
thicken rupture thrombus)
Typical Rise and Fall of either Troponin or CPK-MB associated with ONE of these
o Ischemic Symptoms
o Diagnostic ECG Changes
o Pathologic Q Waves
o PCI data confirming CAD
3 primary tools for risk stratification: H&P, Initial EKG, I-Stat Troponin
EKG Most AMI pts present with non-diagnostic EKG changes
Diagnostic findings: Pathologic Q waves, S-T segment deviation, T-wave inversion, New onset
LBBB
Low risk: Normal EKG, Non-specific ST-T wave changes, Unchanged from prior
High risk: any dx findings, LVH with strain, LBBB, Paced rhythm
TIMI Risk Stratification Estimates mortality for patients with unstable angina and NSTEMI
AMERICA
Age 65+, Markers, EKG, Risk (>= 3 risk factors), Ischemia (2 or more angina episodes in 24 hrs),
CAD (Stenosis >50%), ASA within 1 week
Physical Exam S3,S4, or new murmur, Rales, Pitting edema, Arrhythmia, diaphoresis
PE may be normal
DO NOT try to rely on reproducible CP
Bio-Markers CPK MB: Historical gold standard, detectable at 4-6 hrs peaks 12-24 hrs
Troponin T & I: Detectable 3 hrs, may remain 14 days. highly specific cardiac muscle, more sens
and specific than CPK-MB, Troponin I preferred
Acute Inferior MI Typical ST Elevation in II, III, and AVF
Often have reciprocal changes in the anterolateral leads (V2-V6)
RCA lesions - serves both the RV and SA node
Infamous for brady-dysrhythmias and pump dysfunction
Acute Anterior MI Typically caused by occlusion of the LAD
Termed the widow-maker
Changes typically seen in V1 through V4
Acute Lateral MI Typically associated with larger inferior (inferolateral) or anterior (anterolateral) infarctions that
involve the Left Circumflex
Reciprocal Depression often seen in II and AVF
High Lateral Infarction has ST-Elevation isolated to leads I, AVL,V5, and V6
Acute Posterior MI Posterior MI can occur alone, but most commonly occur in the setting of a large Inferior MI
Culprit lesion can be either RCA or Left Circumflex
V1 - prominent R wave, with flat ST-depression
V2 - prominent R wave with upright T-wave
AMI Treatment Door to Drug time of 60 minutes
Door to Balloon time of 90 minutes
MONA-B
o Morphine: Theoretically reduces pain and anxiety and therefore decreases myocardial
workload and oxygen demand. May cause anaphylaxis and hypotn.
o O2: Good face value, but no proven benefit in either morbidity or mortality
o Ntg: Reduces BOTH preload and afterload as well as myocardial oxygen demand.
o ASA: Thromboxane A2 inhibitor - inhibits platelet aggregation, 325 mg , Reduces M&M
by 25% to 50% !!
o Beta blockers (Metoprolol, Esmolol): B-Blockers decrease contractility and myocardial
oxygen demand. Significant mortality reduction
Antiplatelet Therapy ASA, Clopidogrel, Prasugrel, Ticagrelor
Patients with definite UA/NSTEMI at medium or high
risk and in whom an initial invasive strategy is selected should receive dual antiplatelet therapy
on presentation
ASA: 325 on presentation but 81 mg thereafter
Other treatments Heparin, effects intrinsic pathway (IX, X, XI, XII), measure PTT
o Should be administered at known onset of ACS
o Does not dissolve clot, prevents further development
LMWH (Enoxaparin): easy admin, no need to monitor coag levels
Factor Xa Inhibitors: Rivaroxaban, Apixaban
Glycoprotein IIb/IIIA inhibitors (Eptifibatide, Tirofiban, Abciximab): useful in those undergoing
PCI, used in STEMI or AMI. Avoid if no ST elevation
Reperfusion: Fibrinolytics , PCI
o PCI superior, but if prolonged transport or delay consider early fibrinolysis
Fibrinolytics T-PA or R-PA
Indications: 1 mm STE in 2 contiguous leads, or new LBBB, in a story that fits
Contraindications: Persistent HTN 200/120, STEMI only!!
Health Maintenance Begin statins post tx
Lifestyle!


INTERNAL MED EOR EXAM STUDY GUIDE: ARRHYTHMIAS AND CONDUCTION DISORDERS
Sinus Tach > 100 bpm
Usually physiologic: Pain, fever, anemia, anxiety
Treat underlying
Sinus Brady < 50 bpm
Normal (training) high vagal tones
Vagal (N/V/ABD pain)
Beta Blockers
Wandering Atrial Pacemaker P waves vary in at least three ways

Junctional Rhythm Not P waves, too close to QRS
Usually due to high vagal tone=usually asymptomatic, no treatment
May require pacing
Can happen with elevated junctional rate =DIG toxicity
Ventricles and atria are stimulated at the same time

SVT Poor nomenclature it includes all of these things:
Sinus tac, A- fib, Atrial flutter, Multifocal atrial tachycardia, AV nodal reentrant
tachycardia- goes in a loop. Usually what is meant with SVT
AV nodal Reentrant Tachycardia
(AVNRT)
Narrow QRS (supraventricular)
Paroxysmal in onset, Sudden in termination
Cause: Dual AV nodal pathways
Impact: Sudden onset/variable duration/palpitations to syncope
Treatment
o Acute: Vagal (ie Valsalva, carotid sinus massage), Medical: Adenosine
o Chronic: Medical (AV nodal blockers)/Ablation
Atrial Flutter

Atrial rate of 300, Reentry rhythm
May require carotid massage to slow rate and see flutter waves
Cause
o Usually pathologic due to atrial pathology; scar/dilation/ischemia
o Hyperthyroidism
o Acute illness (CVA/pneumonia/sepsis)
Impact
o Symps dependent on ventricular rate
o Risk of cardioembolism like atrial fib
Mgmt
o Confirm Dx with vagal and medication
o Slow rate: slow AV node conduction. Betas or CCB
Cardioversion: Electrical or Medical
A-Fib

Focal Firing or multiple wavelets
Choatic, rapid atrial rate at 400-600 bpm
Irregularly irregular
o Supraventricular
o May be rapid, or narrow in absence of bundle branch
Impact of A-fib/flutter
o Common post CABG, etiology similar to flutter
o Also common in acute illness, infection, stress, hyperthyroid, Acute ETOH
poisoning
o CVA, Peripheral embolization
Symps
o Palpitations, Lightheadedness/syncope, Angina, SOB
Rate Mgmt Fib/Flutter Rate slowing agents: Increase vagal tone, DIGOXIN
Decrease sympathetic tone: Beta blockers
AV nodal blocking agents: Calcium channel blockers
AV node ablation/permanent pacing for uncontrollable rates
Rhythm Mgmt Fib/Flutter Antiarrhythmic therapy
o Ibutelide for acute cardioversion
o DC cardioversion
o Pace termination for a flutter
Ablation therapy
o A flutter ablation, highly successful
o A fib ablation, complex, but highly successful
Mgmt fib/Flutter (prevent
embolism)
Anticoagulation
o Pre and post cardioversion
o Short term risk increases if duration >48 hours
o Long term risk depends on CHADS2 score (2 is high risk and need
anticoagulation)
CHF = 1
HTN = 1
Age > 75 = 1
DM = 1
Stroke or TIA = 2
Multifocal Atrial Tachycardia Associated with respiratory failure
Poorly responsive to usual Afib therapy
Treat the underlying non cardiac problem
Rate > 100 bpm
> 3 P wave morphologies
Beta blockers and CCBs do not work.
Severe COPD, Bronchodilators increasing sympathetic tone treat underlying
condition

First Degree AV block Prolonged AV delay, PR interval > .21 seconds with all atrial impulses conducted
Etiology
o normal vagal tone
o AV nodal blocking agents
o high vagal tone associated with ischemia
o Especially inferior MI
Mgmt: Avoid exacerbating agents

Second Degree AV block Type 1
(Mobitz Type 1, Wenkebach)
PROGRESSIVE AV delay with the PR interval lengthening and RR interval shortening
before the dropped beat.
2:1, 3:2, 4:3, etc
Elevated vagal tone, frequently asymptomatic
May be from drugs: Digoxin, CCBs, Betas
Avoid AV blocking agents
MAY on occasion benefit from pacing

Second Degree AV block Type II
(Mobitz II)
Almost always due to organic dz, Usually due to block within His bundle system
Intermittently non-conducted atrial beats not preceded by lengthening AV
conduction
Occasional P waves conducted

Third Degree Heart Block (complete
heart block)
no relationship b/w atrial and Ventricular rate
P waves walk through the QRS
Transmission of atrial impulses through AV node completely blocked, ventricular
pacemaker maintains slow, regular ventricular rate, usually less than 45 bpm.
Syncope common, weakness, dyspnea.
Tx: pacing

RBBB Delayed or blocked conduction through the right bundle
Potential causes
o Organic Heart Disease, CAD *MC, Myocarditis, Degenerative conduction
system disease, Congenital Heart Disease

LBBB Potential Causes
o CAD, HTN, Aortic valve disease, Cardiomyopathy
o Prognosis is determined by the severity of the organic heart disease present
o No specific therapy is required for this conduction abnormality by itself

Ventricular Arrhythmias PVCs, Non-sustained VT, VT, VF
Etio
o Structural heart disease, ischemic and non ischemic CMO, CAD, Primary
electrical abnormalities, Long QT syndrome, Brugada syndrome, Severe
metabolic disorders
Mgmt: Underlying, antiarrhythmics, device therapy, ablation, transplant
PVCs Usually benign and insignificant, like PACs
Occasionally a harbinger of underlying structural heart disease
Mgmt
o Asymp = reassurance
o Symp = reassurance, pharm- betas and CCBs DONT work!!, ablation. Even
in pt with severe CAD no evidence of benefit from treating asymp PVCs, tx
can cause harm!!!
Idioventricular Rhythm something lower than the SA Node is running the show
Sinus arrest
Much depends on the clinical state
Usually short lived
Tx: Beta agonists
o DOPAMINE
o LEVOPHED
o ISOPROTERENOL
Manage the underlying issue (hypoxia/metabolic disturbance)
If persistent permanent pacing


Ventricular Pacing Ventricular paced beats are ALWAYS wide
Looks like LBBB and has pacer spikes


VT Does NOT respond to vagal maneuvers or AV nodal blocking agents
Frequently complication of Acute MI, CMO, CAD, mitral valve prolapse, or
myocarditis.
Torsade de Pointes: occurs in Prolonged QT, hypokalemia, hypomagnesemia
Non-sustained VT: 3 or more consec beats lasting <30 secs and terminating
spontaneously.
Treatment
o Acute: Pulseless (ACLS) Shock, CPR, Epi or Vasopressin, Amiodarone. Pulse
Unstable = cardioversion, stable = Amiodarone, Lidocaine, or
Procainamide.
o Chronic recurrent sustained VT: In pts with LV dysfunction, implantable
cardioverter defibrillators (ICDs)

Torsades, Tx is IV Mag
VF Pulseless!! ACLS
Shock, CPR, Epi or Vasopressin, Amiodarone

Prolonged QT The following factors indicate that a patient is at high risk for LQTS:
o A QTc of greater than 500 milliseconds
o Aborted cardiac arrest
o Torsades de pointes or complex ventricular arrhythmia
o More than two episodes of syncope in the past two years
o Males 10 to 12 years old
QTc should never exceed 0.42 in young adults (0.44 in children)
QTc > 0.55 = very high risk for sudden death
Drug Causes: Procainamide, Erythromycin, TCAs, Phenothiazine, Quinidine,
Organophosphates
Metabolic Causes: Hypokalemia, Hypomag, Hypocalcemia, Myocarditis
Tx: Betas to suppress arrhythmias, AICD placement. If progress to Torsades, IV
Magnesium

WPW Wolff-Parkinson-White syndrome, MC pre-excitation
Paroxysmal tachycardia at a rate of 150-300 BPM resulting from loss of conduction
through the AV node
MC seen in children and young adults
May be asymp, may present as SVT or V-Fib (sudden cardiac death)
Short PR interval (<0.12/120 ms)
QRS > 0.12/120 ms with slurred onset of QRS waveform (Delta wave)!!!


Mgmt: Stable or unstable, wide or narrow, regular or irregular
Unstable: cardioversion 100J
Narrow complex: Vagal, adenosine, CCBs or betas, Procainamide, Amiodarone
Wide complex: Procainamide Amiodarone, AVOID AV-nodal blocking agents
(adenosine, dig). Cardioversion for extreme tachydysrhythmias >250 bpm
Brugada Syndrome syndrome of recurrent ventricular dysrhythmias with saddle or cove shaped ST
elevation in V1 to V3
One of MC causes non-ischemic cardiac death worldwide, can lead to VT/VF
Presentation: syncope, cardiac arrest, nightmares, thrashing in bed
Tx: AICD placement, Betas CONTRAINDICATED (exacerbates symps), teach family
and friends CPR, NO sports



INTERNAL MED EOR EXAM STUDY GUIDE: CARDIOMYOPATHY
Cardiomyopathy (CMO) Scientific
Concepts
Alteration myocardial function, usually leads to decreased CO and symps CHF
Reduced Spare Capacity: Heart works harder to meet basic metabolic demands
= decreased cardiac reserve
Risk factors: Ischemic heart dz (MC), tobacco, HTN, obesity, DM, Valvular heart
Dz
Ejection Fraction (EF) EDV ESV/EDV
o Normal : 55 65%
o EF <40% in systolic CHF
CMO Workup EKG, Echo, CXR, BNP, BMP, CBC, Stress test, Viability study, Coronary
Angiography, Holter
Hypertrophic CMO Small or NML cavities, marked hypertrophy, normal systolic function, abnormal
diastolic function
Leading cause of sudden cardiac death in athletes
Screen 1st degree relatives
Avoid competitive athletics, dehydration
Obstructive vs Non-obstructive
o Dynamic outflow tract obstruction
o Septum bulges into LVOT (left ventricular outflow tract)
o Idiopathic hypertrophic subaortic stenosis (IHSS)
Hypertrophic CMO H&P Symps: SOB, Exercise intol, angina, syncope
PE
o S3 in children, S4 secondary to contraction against a noncompliant left
ventricle
o Systolic ejection murmur
Increased intensity of murmur
Decrease in preload, decrease in afterload
Valsalva
rising from a squatting position
Decreased Intensity of murmur: Increase in preload
(squatting)
EKG: LVH with ST-T wave changes, dysrhythmias
HCMO Tx Betas, CCBs, Myomectomy, ETOH septal ablation
AICD
Restrictive CMO Normal wall thickness, dilated atria, normal systolic function, abnormal
diastolic function
NO respiratory variation of valvular inflow
Causes: Fibrosis, Amyloid, Sarcoid, Radiation
Symps: Fatigue, SOB, Edema, Ascites
Tx: Underlying, betas, CCBs, Diuretics, transplant
Constrictive Respiratory variation of mitral and tricuspid inflow by echo
Ischemic CMO Dx: Nuc stress test, catheterization , Both tests to see extent coronary dz
Tx: Revascularization, ASA, betas, ACEI/ARB, statin, diuretic, aldactone, isordil
Dilated CMO Enlarged cavities, normal wall thickness, decreased systolic function, abnormal
diastolic function
Causes: Idiopathic, ischemia, infectious, rheum, meds, peripartum, stress
(takotsubo)
Dx: Echo, nuc stress for underlying coronary dz, MUGA
Symps: DOE, impaired exercise capacity, Orthopnea, PND, peripheral edema
Tx: ACEI, Betas, diuretics, aldosterone antag, Digoxin 2
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