INTERNAL MED EOR EXAM STUDY GUIDE: CHFScientific 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 acutelyo 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 blockersCHF History and Physical

Sympso Dyspnea (at rest and exertional)o Orthopneao Paroxysmal Nocturnal Dyspnea (PND)o Chronic cough (non-productive) –vascular congestiono Nocturiao Fatigueo With RV Failure: RUQ Pain, Nausea, Loss of appetite, Peripheral edema, Ascites

PEo Vitals: can be normal, may have Tachycardia, Hypotension , Decreased pulse pressure,

Diaphoresis, Cool extremitieso WEIGHT! Follow very closelyo JVD

o Thyromegalyo Carotid pulse- Aortic Stenosis (AS)o Lungs: Crackles, Wheezes, Rhonchi, Pleural effusionso LV lift or sustained pulsationo Diminished first sound: annulus around the valves change, not getting closing snapo S3 gallopo Murmurso 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 ventricleso 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 Underlyingo Valvular diseaseo MI : Stent, Angioplasty, CABGo HTNo Arrhythmiaso Alcoholo Drugs: CA++ channel blockerso Pericardial disease

Diureticso Most effective for symptomso Careful for excessive useo 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, titrateo Bumetinide (Bumex) 0.5-2 mg Dailyo Torsemideo BID preferredo Watch electrolytes

K+ sparing drugs (aldosterone antagonists)o Spironolactone (Aldactone) 25-50 mg Dailyo Triamterene, Amiloride, Eplerenone (Inspra)o Along with ACE and diuretics, reduction in mortality and improve symps

ACEIo Prevents hospitalizationso Increased exercise toleranceo Decreases symptomso 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

ARB’so Not to be used with ACEIo Chronic Failure: Candesartan or valsartan can benefit as alone or in addition to diuretico 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/Digitaliso Only oral positive inotropeo Used in conjunction with patients with atrial fibrillationo Enhances sympathetic tone which delays AV conductiono Can be given with other medso Amiodarone (CORDARONE)o Quinidineo Propafenone (RYTHMOL)o Verapamil

Vasodilators/Nitrateso Reduction of AV afterloado Need an agent or a combination of agents to improve both factorso NTG, Sodium Nitroprusside, Isosorbide 20-80 mg TID, NTG pasteo 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: CCB’s 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 deathNon-Pharm Tx Diet, exercise management

o Reduction in weight, sodium intakeo 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: HYPERTENSIONJNC7 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 HTN3. 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, NSAID’s, Low potassium intake

History and Physical Symptomso Asymptomatic : “Silent killer”o Nonspecific: HA, Blurred vision, Dizziness, Facial flushingo Severe Symps: N/V, Irregular HR, Tinnitus, Dyspnea

PEo BMIo Verify contralat armo Funduscopic examo Palpate peripheral pulseso Bruits (carotid, renal, femoral)o Thyroid gland enlargement or masseso Cardiac (LVH)o Kidney enlargemento Abdominal masses and AAA pulsationo BLE edema and pulseso 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 betterComplications 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 providedo 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 treatmento 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 Effectso Increase K, uric acid; elevated BUN/Cro 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 ACEIso Prevention of stroke,o Possibly diminish progression of Alzheimer’s

ADE’s similar to ACEICalcium 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 Cardioprotectiveo Useful in patients with angina, prior MI, stable CHFo Treatment for migraines and anxiety

Adverse reactionso Worsen chronic lung disorderso Possibly worsen heart failure and peripheral vascular diseaseo Abrupt withdrawal may trigger angina or MI in patients with heart diseaseo Dizziness, fatigue, insomnia, depression, erectile dysfunction, Raynaud’s, increase TG

Treatment: Compelling Indications

INTERNAL MED EOR EXAM STUDY GUIDE: HEART MURMURSAortic Stenosis Harsh systolic ejection murmur heard best at right upper sternal border (RUSB)

o Mid to late peako Reduced intensity of second heart soundo Radiates to carotidso Pulses-parvus et tardus (slow and late)o Narrow pulse pressureo Begins after S1, ends before A2

Aortic Insufficiency (aka regurgitation)

High pitched diastolic decrescendo murmuro 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 apexMitral Stenosis Opening snap following A2

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

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/ACSAcute Coronary Syndrome

The spectrum of disease and clinical presentations resulting from myocardial ischemia and/or necrosis

ACS = UA + NSTEMI + STEMIAngina 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 baselineChronic 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 Symptomso Diagnostic ECG Changeso Pathologic Q Waveso PCI data confirming CAD

3 primary tools for risk stratification: H&P, Initial EKG, I-Stat TroponinEKG 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 weekPhysical 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 preferredAcute 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 mortalityo 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 reductionAntiplatelet Therapy ASA, Clopidogrel, Prasugrel, Ticagrelor

Patients with definite UA/NSTEMI at medium or highrisk and in whom an initial invasive strategy is selected should receive dual antiplatelet therapy on presentation

ASA: 325 on presentation but 81 mg thereafterOther treatments Heparin, effects intrinsic pathway (IX, X, XI, XII), measure PTT

o Should be administered at known onset of ACSo 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 fibrinolysisFibrinolytics 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 DISORDERSSinus 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 SVTAV 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: Adenosineo 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/ischemiao Hyperthyroidismo Acute illness (CVA/pneumonia/sepsis)

Impacto Symps dependent on ventricular rateo Risk of cardioembolism like atrial fib

Mgmto Confirm Dx with vagal and medicationo Slow rate: slow AV node conduction. Betas or CCB

Cardioversion: Electrical or MedicalA-Fib

Focal Firing or multiple wavelets Choatic, rapid atrial rate at 400-600 bpm Irregularly irregular

o Supraventricularo May be rapid, or narrow in absence of bundle branch

Impact of A-fib/fluttero Common post CABG, etiology similar to fluttero Also common in acute illness, infection, stress, hyperthyroid, Acute ETOH

poisoningo CVA, Peripheral embolization

Sympso 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 therapyo Ibutelide for acute cardioversiono DC cardioversiono Pace termination for a flutter

Ablation therapyo A flutter ablation, highly successful

o A fib ablation, complex, but highly successfulMgmt fib/Flutter (prevent embolism)

Anticoagulationo Pre and post cardioversiono Short term risk increases if duration >48 hourso 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 CCB’s 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 toneo AV nodal blocking agentso high vagal tone associated with ischemiao 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, CCB’s, Betas Avoid AV blocking agents MAY on occasion benefit from pacing

Second Degree AV block Type II Almost always due to organic dz, Usually due to block within His bundle system

(Mobitz II) 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 Causeso CAD, HTN, Aortic valve disease, Cardiomyopathyo Prognosis is determined by the severity of the organic heart disease

presento No specific therapy is required for this conduction abnormality by itself

Ventricular Arrhythmias PVC’s, 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

PVC’s Usually benign and insignificant, like PACs Occasionally a harbinger of underlying structural heart disease Mgmt

o Asymp = reassuranceo Symp = reassurance, pharm- betas and CCB’s DON’T work!!, ablation. Even

in pt with severe CAD no evidence of benefit from treating asymp PVC’s, 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 DOPAMINEo LEVOPHEDo 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 (ICD’s)

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 millisecondso Aborted cardiac arresto Torsades de pointes or complex ventricular arrhythmiao More than two episodes of syncope in the past two yearso 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, TCA’s, 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, CCB’s or beta’s, Procainamide, Amiodarone Wide complex: Procainamide Amiodarone, AVOID AV-nodal blocking agents

(adenosine, dig). Cardioversion for extreme tachydysrhythmias >250 bpmBrugada 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, Beta’s CONTRAINDICATED (exacerbates symps), teach family

and friends CPR, NO sports

INTERNAL MED EOR EXAM STUDY GUIDE: CARDIOMYOPATHYCardiomyopathy (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 DzEjection 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, dysrhythmiasHCMO Tx Beta’s, CCB’s, Myomectomy, ETOH septal ablation

AICDRestrictive 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, CCB’s, 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 2nd line