Introduction Largest Section of

PANCE/RE 16% of Test 48 Questions There are not any heart

sounds!!

Review: Hypotension Hypertension Cardiomyopathy Heart Failure CAD

Congenital Disorders Valvular Disease Conduction Disorders Vascular Disease Infectious Disease

Hypotension Causes in adequate oxygen to body tissue Types of Shock

Hypovolemic- hemorrhage, loss of plasma, third spacing, anything to decrease volume

Cardiogenic Shock-MI, arrhythmias, heart failure, valve defects, HTN, myocarditis, cardiac contusion

Obstructive Shock-Tension pneumo, pericardial tamponade, PE

Poor blood flow Regulation- Sepsis, anaphylaxis, neurogenic shock

Sepsis is most common 40-80%!

Hypotension Presentation-

Abnormal Vital Signs Hypotension, tachycardia, AMS, metabolic acidosis,

orthostatic changes Treatment

Life Support Trendelenburg position O2, Fluids Monitor urine output (0.5mL/kg/hr) Continuous cardiac monitoring Pressors to increase GFR, help with HR and cardiac

contractions

Orthostatic or Postural Hypotension Causes:

Reduced Cardiac Output, arrhythmias, volume loss, medications, metabolic disorders

Consider this with syncope work up Presentation:

Greater than 20 mmHg drop in systolic blood pressure between supine and sitting or standing

With rise in pulse by >15 bpm

Hypertension Primary (Essential)

95% of patients Causes: Genetics, Increased salt intake, Obesity, ETOH,

Tobacco, Lack of exercise Definition: BP > 140/90 on three occasions Most common symptom: vague, non specific HA

Secondary (5%) Causes: Sleep Apnea, estrogen use, pheochromocytoma,

RAS, Cushing’s, thyroid disease, etc

Hypertension Hypertensive Urgency- BP that must be reduced

within an hour, are they symptomatic? BP > 220/125 HTN Emergency- must be reduced with 1 hour to

prevent End Organ Damage or death Diastolic >130 Presentation: encephalopathy, nephropathy,

intracranial hemorrhage, aortic dissection, preeclampsia/eclampsia, unstable angina, MI

Hypertension Hypertensive Urgency

BP that must be reduced within an hour Are they symptomatic? BP > 220/125

HTN Emergency Must be reduced with 1 hour to prevent End Organ

Damage or death Diastolic >130 Presentation: encephalopathy, nephropathy, intracranial

hemorrhage, aortic dissection, preeclampsia/eclampsia, unstable angina, MI

Hypertension Work up:

Labs: Check for end organ damage (CBC, CMP, Cardiac Enzymes, UA, Lipid Profile)

EKG-LVH? Treatment:

DASH! Deitary Approach to Stop HTN:

low fat, low sodium, low cholesterol, increase fruits/veggies, weight loss…..HEALTHY LIFESTYLE!

Initial Medications ACE inhibitors, Diuretics,

Beta-Blockers

HTN Emergency Treatment Preferred is sodium nitroprusside

NTG if MI Aortic Dissection- nitroprusside and labetalol Other IV Meds: nicardipine, enalpril, hydralazine,

lasix PO Meds: Clonidine, captopril, nifedipine

Heart Failure CHF- dyspnea, water and sodium retention Adversely affects cardiac output and left atrial pressure Left Sided Failure

Excertional dyspnea, cough, fatigue, orthopnea, rales, gallops

Right sided Failure Distended neck veins, hepatomegaly, pitting edema,

(often caused by left sided HF) Hallmark of CHF is nocturnal paroxysmal dyspnea

Heart Failure Testing:

Check for: anemia, renal insufficiency, hyperkalemia, hyponatremia, elevated LFTs, elevated BNP

CXR- cardiomegaly, edema, effusion EKG- Low voltage Treatment:

Correct any reversible causes Low sodium diet, exercise Diuretics to reduce volume-thiazide or loop with ACE Calcium Channel Blockers (amlodipine) if angina is present

Defibrillators are becoming more common

Heart Failure Low Voltage EKG CXR- cardiomegaly ,

edema, effusion

Coronary Artery Disease Decreased oxygen to cardiac muscle Most common cause atherosclerotic narrowing Risk Factors-

male, age, low estrogen state, smoking, family history, obesity, inactivity, cocaine use

Metabolic Syndrome- abdominal obesity, triglycerides >150, HDL <40 men, <50 women, glucose >110, and HTN

Presentation: Squeezing or pressure sensation Stable occurs with excretion and relieved by rest, unstable occurs at rest Prinzmetal’s-vasospasm at rest, usually early morning, will have

normal cath Levine’s Sign- clenched fist held over chest with clenched teeth when

describing pain

Coronary Artery Disease Testing:

ST segment elevation or down sloping (25% of EKG will be normal during attack)

ST segment depression during stress test

Consider Stress images: Nuclear Stress test, Echo, Cardiac CT/MRI

Cath- can diagnosis and treat at same time

Coronary Artery Disease Treatment:

Lifestyle changes Underlying conditions: HTN, DM, cholesterol NTG to help with Pain Beta Blockers- first line of therapy Calcium Channel Blockers- reduce cardiac muscle

demand

Coronary Artery Disease http://www.cdc.gov/heartdisease/coronary_ad.htm

Acute Coronary Syndrome EKG- ST elevation, Q waves Elevated Cardiac Enzymes: Troponin, CPK-MB 20% die from VF before reaching hospital 1/3 of acute MI’s have silent pain or minor pain, think of

atypical presentation (women, age, DM) Presentation:

CP, usually lasting >30 minutes Diaphoresis, weakness, syncope, cough, dyspnea, orthopnea,

n/v Dressler’s Syndrome- (Post MI) pericarditis, fever,

leukocytosis, pericardial or pleural effusion, occurs 1-2 weeks after MI

ACS EKG Findings ST elevations (or

depressions), T wave inversion, NEW LBBB?

Inferior-Leads II, III, aVF

Posterior- Leads V1, V2

ACS EKG Findings Anteroseptal- Leads V1, V2 Anterior- Leads V1, V2, V3 Anterolateral- Leads V4, V5, V6

ACS Treatment IV fluids, O2, ASA, NTG, morphine, Serial

Enzymes/EKG, consider anticoagulation and Beta Blockers

If ST elevation is present- need to have intervention within 3 hours of onset of pain….SEND TO CATH LAB!!

Non Stemi- Use TIMI score or risk stratification

TIMI Score

Congenital Disorders Either Cyanotic or Noncyanotic Cyanotic-Right to left shunt Tetralogy of Fallot-

1) Subaortic septal defect 2) Right Ventricular outflow Obstruction 3) Overriding Aorta 4) RVH

Crescendo-decrescendo holosystolic murmur, cyanosis Pulmonary Atresia

Closed pulmonary valve Atrial septal opening and patent ductus arteriosus Tricuspid regurg sudden onset of severe cyanosis

Tetralogy of Fallot

1) Subaortic septal defect

2) Right Ventricular outflow Obstruction Pulm Stenosis

3) Overriding Aorta 4) RVH

Noncyanotic Disorders Atrial Septal Defect

Opening between right and left atria, most common

Systolic ejection murmur, early to mid systolic rumble

Ventricular Septal Defect most common of all congenital

cardiac abnormalities Systolic murmur at LLSB

Patent Ductus Arteriosus Continuous (Machinery) murmur

Coarctation of Aorta narrowing of proximal thoracic

aorta Systolic LUSB murmur, may be

continuous

Figure 3 sign on CXR prestenotic dilatation of the aortic

arch and left subclavian artery

Valvular Disorders Most common presentation is fatigue, exercise intolerance EKG is not useful, consider CXR and Echo Aortic and Mitral Valves

Aortic Stenosis- Location 2nd RICS, will radiate to neck and LSB, loud with thrill

Aortic Regurgitation- Location 2-4th LICS, radiates to apex, high pitch blowing

Mitral Stenosis- Location Apex, no radiation, Low Pitch at midsystolic

Mitral Regurgitation- Location Apex, radiates to axilla, soft to loud occurring pansystolic

Valvular Disorders Tricuspid and Pulmonic Valves

Right sided pressure overload causes right sided cardiomegaly and right sided failure

Patients have exercise intolerance, easily fatigue JVD, hepatomegaly, peripheral edema

Tricuspid Regurg- Location LLSB, holosystolic, radiates to rt sternum, JVD

Pulmonic Stenosis- Location 2-3 LICS, midstolic crescendo – decrescendo, possible thrill, occurs systolic

Supraventricular Arrhythmias Sinus Bradycardia <60 Sinus Tachycardia >100 Atrial Fibrillation is most

common chronic arrhythmia

Presentation: Palpitations, angina,

fatigue, weakness, asymptomatic

Atrial Fibrillation Irregular Rate and Rhythm Loss of P waves Rate Controlled <100, uncontrolled >100

Treatments Paroxysmal Supraventricular Tachycardia (PSVT)

Initial: Valsalva maneuver, coughing, unilateral carotid massage

Synchronized cardio version DO Not Cardiovert if you suspect Digitalis Toxicity IV Adenosine can terminate rhythm Prevention: Beta Blocker, digoxin and/or verapamil

A-Fib Rate Control Cardio version Amiodarone for chronic a-flutter Ablation can terminate pathway Consider anticoagulants, increased risk for thrombus

Antiarrhythmic Drugs 1a Sodium Channel Blockers

Slows conduction and prolongs repolarization phase (Guanidine, procainamide, disopyramide, moricizine) SVT, VT, V Fib

1b Shorten Repolarization (Lidocaine, phenytoin) V tach, V Fib

1c Depress phase 0 repolarization Slows conduction (Flecainide) Life threatening V tach, SVT

II Beta Blockers, Slow AV conduction Supraventricular tachycardia

Antiarrhythmic Drugs III Prolong Action Potential

(Amiodarone) IV Slow calcium channel blockers

(Verapamil, diltiazem) Supraventricular tachycardia

V slows conduction time through AV node Interrupts reentry pathways Adenosine or Digoxin, SVT

EKGs V Fib

No measurable rate, but tachycardia No P waves No QRS complex

EKGs Sinus Tachycardia

>100 P waves Regular Rhythm

Ventricular Arrhythmias V Tach

3 or more consecutive ventricular premature beats

Frequent complication of MI Torsades de points

V tach with QRS complex twisting around baseline

French Term “twisting of points”

V Fib No effective pumping,

without immediate treatment death

Torsades De Pointes V tach with QRS complex twisting around baseline French Term “twisting of points”

Ventricular Arrhythmias Presentation:

Asymptomatic, syncope, dizziness, palpations Treatment:

Ventricular premature beats use Beta Blockers if symptomatic

V tach cardioversion Meds: lidocaine, procainamide, amiodarone,

magnesium may help Consider implantable defibrillators

Sick Sinus Syndrome Sinus node dysfunctions Mostly in infants and elderly Most patients are asymptomatic Can have syncope, dizziness, confusion, heart

failure, palpitations, angina

Sick Sinus Syndrome Causes:

Meds: (digitalis, calcium channel blockers, antiarrhythmic)

Other: metastatic disease, surgical injury, rare but CAD can cause

Reversible if caused by digitalis, quinidine, Beta Blockers, aerosols

Treatment: If symptomatic usually require pacing

AV Block Presentation:

Weakness, fatigue, light-headed, syncope Treatment: only effective long term treatment is cardiac pacing Types: First Degree

Prolonged PR Interval Second Degree

Mobitz type I (Wenckebach) PR interval gets longer then a dropped QRS complex

Mobitz type II PR interval is the same but will then have dropped QRS

Third Degree (complete heart block More P waves than QRS and no relationship between them

AV Block Which One?

AV Block Which One?

AV Block Which One?

AV Block Which One?

Cardiomyopathies 3 types

Dilated Hypertrophic Restrictive

Dilated Cardiomyopathy Most Common (95%) Reduced strength of ventricular contraction Results in Dilated Left Ventricle Presentation is similar to patient in heart failure Causes:

Genetics (around 25%) Idiopathic ETOH abuse Postpartum Chemotherapy, MUGA Endocrinopathies Myocarditis

Dilated Cardiomyopathy Testing:

ECG- maybe nonspecific CXR-cardiomegaly and

pulmonary congestion Echo is great test, also

nuclear stress, cath- will show left ventricular dilation and dysfunction with poor cardiac output

Treatment: Avoid ETOH Supportive treatment of

CHF

Hypertrophic Obstructive Cardiomyopathy Accounts for about 4% of cardiomyopathies Symptoms:

Dyspnea, angina, syncope, asymptomatic PE:

May have a sustained PMI Loud S4 gallop Systolic murmur Bisferiens carotid pulse

Hypertrophy of myocardium, mostly in septum Will have small LV, diastolic dysfunction Almost exclusively Genetic

Hypertrophic Obstructive Cardiomyopathy Presentation:

Think: Young athlete with syncope Sudden Cardiac Death in patients <30

Testing: CXR- usually unremarkable EKG- nonspecific ST changes, septal Q waves, LVH Imaging (Echo, nuclear stress test, MRI, Cath) – LVH, asymmetric

septal hypertrophy, small LV, diastolic dysfunction Treatment:

Intial start on Beta Blocker or calcium channel blockers Ablation of hypertrophic septum may be required **Dual Chamber Pacing, Defibrillator** May require mitral valve replacement

Restrictive Cardiomyopathy Around 1% of cardiomyopathies Fibrosis of ventricular wall Presentation:

Decreased exercise tolerance Right-sided congestive failure Pulmonary HTN is also common

Causes: collagen-defect Most common cause is Amyloidosis, Radiation, diabetes,

Restrictive Cardiomyopathy LV is usually small and firm with reduced function Testing:

CXR- may show mild to moderate enlarge cardiac silhouette

EKG-may show low voltage Echo is the Key to diagnosis Can consider biopsy to

r/o pericarditis

Treatment: Steroids and diuretics

Pericarditis Usually result of infection Can be autoimmune, neoplasm, radiation, chemo toxicity TB is major cause outside of US Presentation:

Pleuritic pain, relieved sitting upright and leaning forward Can have a friction rub

Testing: CBC CXR, Echo to show extent of effucion EKG- Electrical Alternans, may show low voltage Consider PE?

Pericarditis MI? ST segment will be regional, in Percarditis it is global

Pericarditis Treament:

Pericardiocentesis If only inflammatory- steroids and NSAIDS Infectious- ABX Constrictive requires diuresis

Pericardial Effusion Causes:

Pericarditis, uremia, cardiac trauma Pressure on the heart

Presentation: Cough, dyspnea, can have pain or be painfree

Cardiac Tamponade occurs when fluid reduces ability to fill and thus reduces output

Presentation: Tachycardia, tachypnea, narrow pulse pressure, pulsus

paradoxus

Pericardial Effusion

Endocarditis Most common

pathogens: Strep viridans, Staph aureus,and enterococci IV drug users- Staph

aureus, usually involves tricuspid valve

Prosthetic values-Staph, gram negative, or fungus

Usually occurs in first 2 months of surgery

Endocarditis Presentation:

Fever, nonspecific complaints,

90% have a stable murmur Subungal petechiae Splinter Hemorrhages Olser Nodes- painful

rasied lesions on fingers, toes, feet

Janeway Lesions-painless red lesions on palms and soles

Roth Spots- exudative lesions on retina

Endocarditis Testing:

3 sets of blood cultures taken 1 hour apart

Echo is great to identify the valves

Duke Criteria: Must have 2 major, One major and one minor, or Three minor

Major: 2 positive blood cultures Evidence on echo Development of new murmur

Minor: Predisposing Factors Fever >100. Vascular Phenomena (Olser

nodes, Roth Spots, glomerulonephritis)

Positive blood culture not meeting major critera

Treatment: Consider ABX before dental

work Valve replacement may be

needed Anticoagulation if valve

replacement is done IV ABX

Peripheral Arterial Disease Type 1- limited to aorta, common iliac artery Type 2- aorta, common iliac and external iliac Type 3-multilevel extends to femoral, popliteal, tibial

arteries Presentation:

Lower leg pain with exercise Doppler study is helpful Ankle Brachial Index – less than 0.8 significant disease

Peripheral Arterial Disease Treatment:

Reduce risk factors Stop smoking Lipids Clopidogrel, Warfarin Lower extremity revascularization

Deep Vein Thrombosis Virchow’s Triad

Vascular injury Hypercoagulability Venous stasis

Presentation: Single LE swelling, pain,

erythema, Positive Homan’s Sign Doppler study confirms

Treament: Lovenox, Coumadin,

Xeralto Education for PE

Giant Cell Arteritis Systemic inflammatory condition of medium and large vessels >50 More common in patients with polymyalgia rheumatica Involves temporal artery Can cause blindness if not treated Presentation:

Scalp tenderness, HA, visual changes Temporal Artery can be tender or normal

Testing: Elevated Sed Rate and CRP Temporal Biopsy

Treatment: High Dose Prednisone for 1-2 months followed by Taper

Aortic Aneurysms Weakness in vessel that causes dilation Causes:

Atherosclerosis is most common causes Also: congenital, syphilis, giant cell arteritis, vasculitis,

trauma 90% are abdominal Dissection leads to death in 90% of patients Presentation:

Usually asymptomatic Pulsating abd mass

Aortic Aneurysms Dissecting:

Tearing pain that radiates into back Hypotension Tachycardia Unequal pulses Pain out of proportion

Testing: CT or MRI are better than US

Treatment: Surgical Repair 5 year survival rate after repair is 60%

Summary Huge % of Test Need to devote a lot of time on Cardiology Review Know MI EKG locations EKG/CXR will help confirm your answer, not make it

for you Worst Case Scenario’s

ACS, AAA

learnekgs.com frca.co.uk education.science-thi.org med.umich.edu http://www.cdc.gov/heartdisease/coronary_ad.htm