CARDIOLOGY STEP 3 REVIEWBy James K. Rustad, M.D.

Copyright © 2009 All Rights Reserved.

Outline

Arrythmias and Chest Pain Pericarditis Endocarditis Rheumatic Fever Hypertension Valvular Heart Disease Congential Heart Diseases

Arrhythmias

Wolf Parkinson White Syndrome Accessory

pathway between atria and ventricle

Short PR interval (no AV nodal delay) and delta wave at onset of wide slurred QRS complex

WPW (continued)

If symptomatic – best initial therapy Procainamide (for VT or SVT from WPW)

Long term treatment: Radiofrequency ablation

Avoid digitalis, beta blocker and calcium channel blocker (may precipate arrhythmia)

Atrial fibrillation

Irregularly irregular heart beat

EKG – no P wave, irregular RR interval

Rule out Thyrotoxicosis Often patient has

history of HTN, ischemia, or cardiomyopathy.

If patient is unstable > Synchronized Cardioversion

Rate control and anticoagulation Rate control medications including beta

blockers (metoprolol, esmolol), calcium channel blockers (diltiazem), or digoxin.

Once rate is controlled, anticoagulation with warfarin for INR 2-3 for all patients with atrial arrhythmia lasting beyond 48 hours.

Clinical Scenario

23 year old woman comes for evaluation of “rapid heart beat.” Pulse is 130 but otherwise VSS. EKG shows Paroxysmal Supraventricular Tachycardia. The next most appropriate step in management is:

A) IV heparin B) Load digoxin C) Carotid Massage D) Immediate Cardioversion

Management of SVT

1) Valsalva 2) Carotid massage 3) Adenosine (if 6 mg ineffective give 6

mg more) 4) Verapamil, Diltiazem 5) If hemodynamically unstable:

Synchronized Cardioversion

Clinical Case: Syncope

62 yo woman comes to clinic complaining of fainting spells. Investigation with Holter Monitor shows two episodes of arrhythmia, one of sinus brady 40/min and one SVT with 200/min.

The most appropriate step in management is: A) Start atenolol B) Start verapamil C) Echocardiogram D) Recommend Dual chamber pacemaker E) Refer for cardiac catheterization

Tachy-Brady Syndrome (Sick Sinus)

Treatment: Dual Chamber Pacemaker

Initially try to D/C digitalis, calcium channel blocker, beta blocker –

If still symptomatic - PACEMAKER

Chest Pain

Risk factors for CAD

Men >45, Women >55

Male gender Diabetes, HTN,

Lipid abnormality (increased LDL)

Smoking Physical inactivity Increased

Homocysteine

Differential Diagnosis Nonpleuritic CP

Cardiac: MI/infarction, myocarditis Esophageal: spasm, esophagitis,

ulceration, neoplasm, achalasia, diverticula, foreign body

Referred pain from subdiaphragmatic GI structures

Gallbladder and biliary: cholecystitis, cholelithiasis, impacted stone, neoplasm

Gastric and duodenal: hiatal hernia, neoplasm, PUD

Differential (continued)

Chest pain associated with MVP Pulmonary: neoplasm, pneumonia,

PE/infarction Mediastinal tumors: lymphoma,

thymoma Pain originating from skin, breasts and

musculoskeletal structures: herpes zoster, mastitis, cervical spondylosis

Dissecting aortic aneurysm Pancreatic: pancreatitis, neoplasm

Angina

Exertional chest pain relieved by rest.

Tightness, squeezing, pressure like.

Short duration 3-20 minutes.

EKG during chest pain: T wave inversion and ST depression.

Stable angina: Aspirin and Metoprolol have benefit on mortality; nitrates helpful for pain.

Unstable angina

1. History of chronic angina but recent increase in frequency, intensity.

2. New onset (less than 2 months) severe and 3 or more episodes a day.

Angina at rest.

Unstable Angina Management S/L NTG for chest pain (IV next option),

Aspirin, Bed Rest, O2 Clopidrogrel, Heparin for 48 hours,

platelet glycoprotein IIb/IIIa receptor antagonist

Beta Blocker (or Ca channel blocker) Enzymes X 3 and admit to CCU

Clinical Scenario

55 year old man with diabetes comes to clinic for follow-up after ED visit for L sided chest pressure 2 weeks lasting 10-20 min in duration with no radiation. Escalation of symptoms 2 days prior to ED visit, SOB on exertion, and diaphoresis on onset of pressure.

Transient 1.5 mm ST elevation anterior leads, no Q waves, and negative enzymes. BP 150/80.

Total cholesterol of 290 with HDL 33 and LDL 222 Most appropriate next step in management?

Unstable Angina

A) Continue Aspirin 325 mg daily and close follow up

B) Stop Aspirin and start Clopidrogrel C) Schedule him for coronary

angiography D) Start therapy with Lovastatin E) Initiate therapy with Nifedipine

Unstable angina (continued) The answer is D: Long term goals include

LDL <100. patient should be managed conservatively by managing risk factors optimally.

Coronary angiography is accepted for those who continue to report symptoms despite aggressive management, escalation of symptoms/severity, or hemodynamic instability.

Stress test Poor Prognosis ST depression

over 2 mm at < 6 min on BRUCE protocol

ST dep. persists > 5 min post exercise

ST elevation Hypotension HR < 70%

predicted max

Indications of CABG

Left main disease Triple vessel

disease with low EF

Diabetes with 2 or more vessels involved

MI

Chest pain greater than 30 min. Diaphoresis, SOB, weakness, pain.

Cardiac Enzymes: CK-MB, Troponin I, Troponin T

ST elevation MI

Q wave, transmural

ST elevation greater or = to 1 mm in two consecutive leads.

O2, S/L NTG, Morphine, Aspirin or Clopidrogrel, B-blocker, IV heparin.

PTCA OR Thrombolytic (less than 12 hours post MI, ST elevation, New LBBB)

Non ST elevation MI

Sub-endocardial, ST depression or T-wave inversion

No Q wave but cardiac enzymes up

Manage similar to unstable angina.

With continued Chest Pain – Cardiac Cath

Clinical Scenario

61 year old male with CAD and history of 2 MI’s comes to ER because of chest pain and SOB.

EKG shows sinus rhythm with ST-segment elevation in leads II, III and aVF

Next appropriate diagnostic step to order?

A) cardiac stress test B) chest X-ray C) EKG with R-sided

leads D) green dye cardiac

output measurement E) Ventilation-

perfusion scan

Right Ventricular Infarct

Check Right sided lead V4 for ST elevation!

Hypotension but elevated JVD (increased right atrial pressure)

Positive Kussmaul’s, clear lung field

Treat with IV fluids and manage like MI

Knowledge test

A 58 year old man comes to the office several days after going to the ER with an episode of chest pain. He had a normal EKG and normal CK-MB and was discharged. What is most appropriate for further management?

Stress testing

When the case is not acute and initial EKG/enzymes do not establish diagnosis: the stress test is a way of increasing the sensitivity of detection of CAD.

What if the stress test is abnormal?

If the stress test shows an area of “reversible ischemia,” angiography is the next diagnostic test.

“Fixed defects” – unchanged between exercise and rest – is a scar from a previous infarction.

Clinical Scenario

52 year old man comes to ED unresponsive with no pulse. After assessing ABC’s, the next appropriate step is which of the following?

Amiodarone load, defibrillate, intubate, push adenosine or push epinephrine?

ACLS Protocol

CPR until defibrillator ready.

3 shocks: 200, 300 then 360 J then intubation.

1 mg of epinephrine Shock again w/ 360 J If no stable rhythm:

Amiodarone loading

Aortic Dissection

Type A: intimal tear at ascending aorta just distal to aortic valve. Look for new aortic regurgitation murmur. SURGICAL EMERGENCY!!!!

Type B: just distal to L subclavian artery. Mostly managed medically but still call SURGERY!

Symptom: sudden onset of chest pain radiates to back.

Signs: Widening of mediastinum in CXR

Asymmetrical pulse, BP (R 180/100 and L 130/70)

Aortic dissection investigation and treatment

Stable vitals: CT chest with contrast

Vitals unstable: TEE Keep pulse around 60+,

decrease reflex tachy and tear propagation with IV Propranolol or Labetalol

Keep systolic BP around 100 with IV Nitroprusside or Verapamil

Aortic dissection

Actor John Ritter (1948-2003)

Special topic: Diastolic Dysfunction

Diastolic dysfunction refers to an abnormality in the heart's (LV) filling during diastole (phase of the cardiac cycle when the heart (ventricle) is not contracting but is actually relaxed and filling with blood that is being returned to it, either from the body (into RV) or from the lungs (into LV).

DD

Ventricle = balloon made thick rubber. Fills with high pressure, volume can’t expand.

HTN = LV muscle hypertrophies to deal with the high pressure, and LV becomes stiff

Aortic Stenosis =ventricular muscle has hypertrophied and becomes stiff, due to the increased pressure load placed on it by the stenosis.

Special topic: Jugular Venous Pressure

A: Atrial contraction

C: Closure of Tricuspid

X: Atrial RelaXation

V: Venous filling Y: opening of

Tricuspid

JVP is Right Atrial Pressure

Large right sided “a” wave is Tricuspid stenosis

Large left sided “a” wave is Mitral Stensosis

Rapid x and y descent is Constrictive Pericarditis (rapid x only = cardiac tamponade)

Canon “a” wave = complete heart block (atria and ventricle have own rhythm, no coordination)

Pericarditis

Acute Pericarditis

Mid sternal chest pain, non radiating.

Relieved by sitting up and leaning forward.

Worst with supine and inspiration.

Associated hx: viral fever, breast cancer, s/p radiation therapy, renal failure, MI

EKG: Diffuse ST elevation and PR depression.

Confirm with Echo Treatment:

Aspirin, NSAIDS.

Clinical scenario

58 year old woman with metastatic lung cancer and HTN admitted for CP, SOB.

s/p radiation Transthoracic echo

shows constrictive pericarditis, but no pericardial effusion present.

On physical, what would you expect?

A) increase in JVP with inspiration.

B) inspiratory stridor C) jugular venous

flattening D) muffled cardiac

sounds E) tracheal deviation

to right

Kussmaul’s sign

Increase in jugular pressure with inspiration.

Increased R-sided pressure exerted by noncompliant pericardium as heart moved inferiorly by descending diaphragm during inspiration.

Endocarditis

Endocarditis

Most present with a fever for a few days.

Other possible s/sx: splinter hemorrhage of finger nail (sub-ungal hemorrhage), palate/conjunctival petechia

Osler Node (painful,violaceous raised lesions of fingers/toes/feet)

Roth’s spot: exudative lesions in the retina

Fever + New or Changed murmur Blood cultures

first! If positive, do an

ECHO to look for vegetations.

Common organisms/treatment Common: Strep

viridens Virulent: Staph

aureus S/P cardiac

surgery: Staph epidermis (for this or prosthetic valve give vanco + rifampin + genta)

Strep: Penicillin with Gentamicin or Ceftriaxone

Staph: Nafcillin + Genta

Best empiric therapy (or for MRSA or Penicillin allergy): Vanco + Gent

Give Ceftriaxone if c/s shows: Haemophilus Actinobacillus Cardiobacterium Eikenella Kingella

IV Drug Abuse

Endocarditis typically involves R side of heart (injecting in veins) – usually staph aureus, MRSA

Fever, pleuritic chest pain, cough, hemoptysis

CXR: nodular density in both lung fields, cavitary lesion

Endocarditis Prophylaxis

Previous endocarditis. Prosthetic cardiac

valve. Congenital Cyanotic

cardiac disease. First 6 mos after repair with prosthetic material (or with residual effects after repair).

Cardiac Valvulopathy in transplanted heart.

Procedures which need prophylaxis:

Dental procedures that cause bleeding (amoxicillin - or clindamycin if patient allergic to penicillin)

Respiratory tract surgery or surgery of infected skin.

Valve replacement surgery Anatomic defects –

difficult to correct with only ABX!

Valve rupture/prosthetic valve

Abscess Fungal endocarditis Embolic events

after starting ABX.

Rheumatic Fever

Acute RF usually develops after 2-4 weeks of pharyngeal infection with Group A streptococcus.

Can erysipelas lead to rheumatic fever?

No --- skin goes to kidneys only. Throat goes to kidneys and heart.

Earliest Symptomatic manifestation

Arthritis --- migratory and involves large joints mainly lower extremity. Subjective pain greater than objective inflammation.

Erythema marginatum

Non-pruritic Erythematous

lesion with pale center, mostly on trunk, rounded margin.

Early manifestation

Evanescent (appear, disappear)

Syndenham chorea

Commonly on one side and ceases during sleep.

Abrupt, purposeless, non rhythmic involuntary movement.

Rheumatic Fever (continued)

Early: Mitral Regurgitation

Late: Mitral stenosis, secondary to scarring and calcification of damaged valve.

Nodule: mostly over bony surface.

Firm, painless, usually disappears within a month.

Carditis Subcutaneous Nodule

Diagnosis: Jones Criteria

Carditis Polyarthritis Chorea Subcutaneous

Nodule Erythema

Marginatum

Fever Arthralgia Previous RF or

Rheumatic Heart disease

Major Minor

Rheumatic Fever treatment

Aspirin Oral Penicillin V for

10 days or Benzathine Penicillin G IM X 1 dose

Penicillin allergic: Erythromycin X 10 days

Oral Penicillin V or oral sulfadiazine daily or Pen. G IM q4 weeks

Until patient is approx. 20 years old (approx. 10 years from attack)

Acute Treatment Prophylaxis

Hypertension

Management of Blood PressureBlood Pressure

Systolic Diastolic Management

Recheck

Stage I 140-159 90-99 Thiazide unless other indication

Within 2 months

Stage II Greater than or equal to 160

> Or = to 100

2 Drug Combo

If greater than 180/110 treat right away, otherwise recheck within one month

Thiazide diuretics

They work by inhibiting reabsorption of Na+ and Cl− ions from the distal convoluted tubules by blocking the thiazide-sensitive Na+-Cl− symporter. Thiazides also cause loss of potassium and an increase in serum uric acid.

Hypokalemia, Hyponatremia and Hyperuricemia

Recommended starting dose: Hydrochlorothiazide 25 mg once daily

K+ sparing diuretics (think SAT) Spironolactone inhibits

the effect of aldosterone by competing for intracellular Ald. receptor in the distal tubule cells (it actually works on Ald. receptors in the collecting duct). This increases the secretion of water and sodium, while decreasing the excretion of potassium.

Amiloride works by directly blocking the epithelial sodium channel (ENaC) thereby inhibiting sodium reabsorption in the distal convoluted tubules and collecting ducts in the kidneys.

Triamterene with similar Mechanism to Amiloride.

Loop Diuretics

Loop diuretics act on the Na+- K+ - 2Cl- cotransporter in the thick ascending limb of the loop of Henle - inhibit sodium and chloride reabsorption.

Loop (of Henle) diuretics

Loop diuretics prevent the urine from becoming concentrated and disrupt generation of hypertonic renal medulla. Water has less of an osmotic driving force to leave the collecting duct system, ultimately resulting in increased urine production.

Furosemide, Bumetanide, Ethacrynic acid, Torsemide

Beta Blockers

Cardioselective (Beta 1)

Atenolol 50-100 mg/day

Metoprolol 25-100 mg/day

Non-selective: Propranolol 40-80 mg PO BID

Alpha and Beta blocker: Labetolol (The recommended initial dosage is 100 mg twice daily - usual maintenance dosage of labetalol HCl is between 200 and 400 mg twice daily).

ACE inhibitors

Lisinopril: recommended initial dose is 10 mg qdaily. Usual dosage range is 20 to 40 mg per day administered in a single daily dose.

Side effects: Dry cough, hyperkalemia, angioedema.

ACE inhibitors (continued)

Angiotensin II receptor blockers Losartan Irbesartan Valsartan Candesartan

Calcium Channel Blockers Non-

Dihydropyridine (bradycardia)

Diltiazem Verapamil

(constipation)

Dihydropyridine (cause Tachycardia)

Amlodipine 5-10 mg/day

Felodipine Nifedipine 30-60

mg/day

Calcium channel blockers: Ankle Edema

Valvular Heart Disease

Presents with Shortness of breath ---“worse with exertion or exercise.”

Physical findings: Murmur, Rales on lung exam. Possibly peripheral edema, carotid pulse findings, gallops.

Heart Sounds

S1: Closing of the mitral valve. S2: Aortic valve closes first, followed by

pulmonic. Right sided murmurs increase on

inspiration because the lung expands and intrathoracic pressure goes down > blood to the heart increases.

Wide splitting of S2

Aortic valve closes earlier Pulmonic valve closes later MR, VSD, Pulmonary Stenosis, Pulmonary

Artery Hypertension, RBBB

Mitral Regurgitation

MR

Holosystolic murmur best heard at apex radiates to the axilla.

Blood travels from Left Ventricle to Left atrium.

There is less blood for LV to pump out and the Aortic Valve closes earlier.

MR

Test of choice: Transthoracic Echocardiogram

Acute MR caused by rupture of chordae tendinae during MI or Endocarditis. Tx: Emergency Surgery.

Chronic MR should be referred for surgery when symptomatic or asymptomatic with EF < 55% or LV end systolic dimension greater than 45 mm.

Ventricular Septal Defect

Holosystolic murmur, Lower left sternal border

Most common acyanotic congenital cardiac anomaly.

Blood goes from Left Ventricle to Right Ventricle. Less blood in LV available to pump out and aortic valve closes earlier.

Echo for diagnosis, but catheterization can determine degree of L > R shunting most accurately.

Pulmonary Stenosis

Pulmonic valve closes later (Stenotic valves take longer to close).

Pulmonary Hypertension

The pressure is high in the vessel and it is hard to pump blood. The Right Ventricle has to pump blood into pulmonary artery against high pressure. Pulmonary valve closes later.

Right bundle branch block Right ventricle

contracts slowly and pulmonic valve closes later.

Narrow splitting (paradoxical) Aortic valve closes later Pulmonic valve earlier. Sometimes paradoxical splitting where

pulmonic valve closes before aortic valve.

Aortic stenosis, HOCM, LBBB

Aortic Stenosis

Stenotic valves close later.

Midsystolic, upper right sternal border.

Aortic Stenosis

“Crescendo-decrescendo” murmur

Upper right sternal border and radiates to carotids.

Aortic Stenosis

Syncope Angina Dyspnea

Aortic Stenosis

LVH on EKG Treatment of

choice is valve replacement.

Clinical scenario

52 year old woman comes to ED complaining of SOB. History notable for heart murmur and HTN.

Loud ejection murmur at cardiac apex and rales bilaterally in both lung fields. ECG shows LVH.

Most appropriate next diagnostic step? A) cardiac stress test B) Chest CT C) Transesophageal Echocardiogram D) Transthoracic Echocardiogram E) Ventilation-perfusion scan

HOCM

Outflow tract obstruction --- Aortic valve closes later.

Left Bundle Branch Block

Left ventricle closes slowly and Aortic valve closes later.

Blood return

Increases Blood Return (increase venous return to heart).

Decreased Blood Return. All murmurs decrease with standing and valsalva except for…..

Squatting and Leg Raise Standing/Valsalva

HOCM and MVP

Hypertrophic Obstructive Cardiomyopathy

Mitral Valve Prolapse (mid systolic click followed by late systolic murmur)

Hand grip

Increases afterload. Improves or lessens the murmurs of MVP and HOCM as the left ventricular chamber is more full.

Mitral Valve Prolapse

Young thin female with occasional palpitation and mild chest pain.

Treatment: Beta Blocker

Mitral Stenosis

Middiastolic at apex best heard with bell. Diastolic rumble after opening snap.

Rheumatic fever most common cause. Pregnant patient (large increase in plasma volume).

Mitral Stenosis Symptoms Dyspnea (due to

pulmonary edema) Hemoptysis (due to

increased pressure in pulmonary vessels)

Hoarseness due to compression of recurrent laryngeal nerve from enlarged LA – “Ortner’s syndrome”

Treatment of Mitral Stenosis Diuretics are best

initial therapy, but do not alter progression.

MS without MR: Percutaneous Mitral Balloon valvuloplasty.

Aortic regurgitation

Causes: Rheumatic fever, aortic root diseases (Marfan’s, anklosing spondylitis, Reiter’s), congenital bicuspid valve, HTN

Murmur: Diastolic decresendo murmur best heard at L sternal border.

AR: “rapid rise and fall” of pulse Elevated systolic

and low diastolic pressure

Wide arterial pulse pressure

Aortic regurgitation factoids Hill sign: blood

pressure gradient higher in lower extremities.

Corrigan’s pulse: High bounding pulses (“water-hammer”)

Quinke pulse: Arterial or capillary pulsations in fingernails.

Musset’s sign: Head bobbing up and down with each pulse.

Duroziez’s sign: murmur heard over femoral artery

Chronic AR treatment

Medical: reduce afterload with ACE inhibitor, Nifedipine, Hydralazine.

Beta Blocker Surgical indication:

symptoms or LVEF less than 55% or LV end systolic dimension > 50 mm

More Congential Heart Diseases

Patent Ductus Arteriosus

Connects descending aorta and pulmonary artery.

Maternal Rubella infection in early pregnancy.

In premature infant: close with Indomethacin.

More common in girls.

Upper left sternal border continuous machinery murmur.

Tetralogy of Fallot

Most common congential cyanotic cardiac anomaly.

Child while playing may develop SOB, cyanosis.

Coarctation of Aorta

98% occur at origin of left subclavian artery

BP higher in arms than legs

Give PGE1 to maintain patent ductus

Surgical repair after stabilization

Turner’s syndrome

Thank you for your attention!