Cardiology Board Review Jennifer Carlquist PA-C, CAQ ER Medicine - - PowerPoint PPT Presentation

Cardiology Board Review

Jennifer Carlquist PA-C, CAQ ER Medicine

Disclosure

I have a relationship with CME4Life, LLC, and sell DVDs of my lectures with their company.

Objectives

Common arrhythmias and their treatment Demystifying Bundle Branch and AV Blocks Coronary Artery Disease: Identify patients at risk for CAD, prevention and treatment  Heart Failure: Identify, manage and prevent it

Four parts

• f the heart

Arrhythmias

Things that go bump in the night

Normal conduction

Getting to the root of the cause

SVT AFIB/Flutter WPW Sick sinus VT PVC’s

Palpitations tree

Sinus Tachycardia

Rate: >100 – 160 BPM Regularity: Regular P wave: Present, PR interval constant

__________________ and ________________ can cause sinus tachycardia.

Does he need to go to the ER?

Sinus Pause/Arrest

Rate: Varies Regularity: Irregular, but PR intervals are the same P wave: Present intermittently Sick sinus syndrome:

• Digitalis, CA ++ blockers, Antiarrhythmic drugs, CAD,

collagen vascular diseases and or mets

• Reversible? Pacer?

Atrial Fibrillation

Rate: Variable, ventricular response can be fast or slow. Atrial rate is usually over 350 BPM. Regularity: Irregularly irregular P wave: None; chaotic atrial activity

Patients lose their ___________ in atrial fibrillation.

Atrial Fibrillation Causes

Things we can fix

• Thyrotoxicosis
• High blood pressure
• Heart disease (Valvular)
• High cholesterol

Things the patient can fix

• Obesity
• Smoking
• Caffeine
• Alcohol abuse
• Sleep apnea

Complications

?

Stroke CHF

Assessing stroke risk

 If elevated risk, need to choose: Xarelto, Apixiban, Pradaxa, ASA  Warfarin

Rate vs Rhythm Assess/address stroke risk CHADS Score Ablation/Cardiovert

AC choices

 Warfarin: needs frequent monitoring  Pradaxa (Direct thrombin inhibitors) – non valvular $8-12 day  No monitoring  No reversal

Defining AF

 Paroxysmal: Atrial fibrillation that lasts from a few seconds to days, then stops on its own  Persistent: Does not stop by itself but will stop if cardioverted  Permanent (long standing persistent) AFIB begets AFIB wont retain sinus  Normal LA with structurally normal hearts are better candidates

Atrial Flutter

Rate: Atrial: 250–350 BPM, Vent: 125–175 BPM Regularity: Regular P wave: Saw toothed, “F waves”

The mechanism behind atrial flutter is generally reentrant in nature.

Atrial Flutter Causes

 PE  ETOH  Ischemic heart disease  Hypoxia  Digitalis toxicity  Mitral or tricuspid valve disease  AMI

What is the rhythm?

SVT

These patients will most likely have a ___________ blood pressure.

PSVT

 Etiology

 Rapid atrial depolarization overrides the SA node  Stress, pathway, caffeine, drugs

 Clinical Significance

 Decrease in cardiac output = angina, hypotension, or CHF

 Clinical Features

 Regular, Rapid, No discernable P wave HR – 160-220

 Drugs  Pathway

Ectopy

The Troublemaker

What causes ectopic beats?

Lots of angry cells…  Atrial  Ventricular  Come in patterns

This ectopy pattern is called ______________ .

ECTOPY

Where’s the PAC?

Junctional Premature Contraction (JPC)

 A junctional premature contraction (JPC) is a beat that originates prematurely in the AV node.  It can occur sporadically or in a grouped pattern.  If PR interval is present, it does NOT represent atrial stimulation of the ventricles.

PVC

What is this called?

Just how mad are you??

 Bigeminy - every other beat  Trigeminy - every third beat  Quadrigeminy - every fourth beat  Couplets - two in a row  Triplets - three in a row  V-Tach - 5 or more PVC’s  Multifocal – More than one focus

PVC Couplet

Multifocal

Bigeminy

Trigeminy

Quadrageminy

BBB Hemiblock

Bundle Branch BLOCKS

 You are driving into the EKG.  You need to turn.  You signal. Right or left.  J point: the junction between the end of the QRS segment and the beginning of the ST segment

Turn signal theory

• Courtesy of Mike Taigman

“Drive your car”

LBBB Causes Aortic stenosis Dilated cardiomyopathy AMI/Extensive CAD Primary disease of the cardiac electrical conduction system Long standing hypertension leading to aortic root dilatation = aortic regurgitation

RBBB Causes

• RVH / Cor pulmonale
• PE
• Ischemic heart disease
• Rheumatic heart disease
• Myocarditis or cardiomyopathy
• Degeneration of conduction

system

“Drive your car”

Sinus Tachycardia Causes

Fever Pain Hypovolemia Drugs

Supraventricular Tachycardia

Criteria Rate: 140 - 220 bpm Rhythm: Regular QRS: Normal or prolonged (>.12 sec) Usually starts and stops suddenly

AV Blocks

What is actually blocked? A vessel? Is something really “blocked?”

Heart Blocks Defined by PR Interval

First-Degree Heart Block

Regularity: Regular P wave: Normal PR interval: Prolonged >0.20 sec QRS width: Normal

Does this rhythm normally cause symptoms?

1st Degree AV Block

 First degree AV block is a constant and prolonged PR interval  Insult to AV node, hypoxemia, Inferior MI, dig toxicity, ischemia of the conduction system and increased vagal tone  Criteria Rhythm: Regular PRI: > .20

2nd Degree

AV Block - Type I

Long, Longer, Longest, DROP! Rinse and repeat. - Wenchebach

Regularity: Regularly irregular P wave: Present PR interval: Variable QRS width: Normal Dropped beats: Yes, patterned

2nd Degree AV Block, Type I Wenkebach

 Wenkebach: Long, longer, longest….drop.  Same causes as 1st degree AV block  Criteria Rhythm: Irregular PRI: Progressive lengthening of PRI until dropped beat  QRS's appear to occur in groups.

Mobitz II Second- Degree Heart Block

Regularity: Regularly irregular P wave: Normal PR interval: Normal QRS width: Normal Dropped beats: Yes

2nd Degree AV Block Type II Mobitz

 Can lead to third degree AV block  AV conduction normal…then drop.  Criteria PRI: Constant on conducted complexes until a sudden block of AV conduction

Third-Degree Heart Block

Rate: Separate rates for underlying (sinus) rhythm and escape rhythm Regularity: Regular, but P rate and QRS rates are different P wave: Present P-QRS ratio: Variable PR interval: Variable, no pattern QRS width: Normal or wide Grouping/dropped beats: None

3rd Degree AVB Complete

 Caused by:

 Acute MI  Dig Toxicity  Conduction System Disease

Something wicked this way comes

Ventricular Tachycardia (VTach)

Rate: 100–200 BPM Regularity: Regular PR interval: None QRS width: Wide, bizarre

VT

Dead?

Defib Alive?

Synch

SVT

Stable?

Adenosine

Unstable?

Synch

Ventricular Tachycardia

 Rate: Generally 100 to 220 bpm  Width of QRS>0.12 sec Rhythm: Regular  Stable = treated with lidocaine or Amiodarone  Hemodynamically unstable VT (with a pulse) is cardioverted  VT without a pulse is defibrillated  Three or more beats of ventricular origin (PVCs) in succession at a rate greater than 100 beats per minute .

Torsade de Pointes

Rate: 200–250 BPM Regularity: Irregular P wave: None QRS: Changing polarity Grouping: Variable sinusoidal pattern

Prolonged __________________ can cause torsades.

Torsades

How do we treat this?

Case

 Felt unwell “like the water ran out of me”  Under stress  HX: HTN, psyche, chronic neck pain  Drank alcohol, etoh, did cocaine

Called 911…

EMS says…

 “Had an episode of urinary incontinence, pt felt weak”  Dizzy, dyspnea, chest discomfort  Field EKG: Sinus tachycardia with borderline st elevation in V1, V2 with one PVC  Then goes into torsades…. Is shocked at 200 j once, brief CPR

Post shock in ER

What were her risks?

K was 2.7 Qt prolonging meds Did cocaine Hx of previous long qt…. Female

At clinic visit

 “I think I need something stronger for pain…”  I didn’t take my blood pressure medication as it was too expensive…  I did take my nieces medication, it starts with an “L”  I did take two methadone that day for pain…  Meds: Prozac, Methadone, Trazadone, Pepcid, Risperdal

Clinic EKG

Coronary Artery Disease

Atherosclerosis, Angina, Unstable Angina, NSTEMI, STEMI

How many people die

1,500,000 M.I.s in the US annually Acute mortality ~ 30% 5-10% of survivors die in the first year

CAD Etiology

 Coronary artery atherosclerosis  Coronary artery spasm (Prinzmetals, drug use)  Congenital abnormalities (less than 1% of population)  Clot

Not all chest pain is CAD

 Variant Angina (Prinzmetal’s or atypical), caused by arterial spasm most often occurs at rest No fixed occlusion

CAD Risk factors

 High plasma LDL ( > 100 )  Low plasma HDL ( < 40 )  DM  Hypertension, Smoker, couch potato  Family hx of heart disease <age 55; female <65

BEWARE OF Vasculopaths

THE BIG ONE

 Provoking: Emotion or exertion  Quality: Heaviness, squeezing, pressure, smothering, crushing  Radiation: L arm, R arm, jaw, neck, back  Relieved: By rest  Severity: Quiet patient with a 10/10 pain  Time: Variable

Atypical Presentations Common

 3 high risk patients: Diabetics, females and elderly  20 % with proven mi have only upper abd pain  40% pain radiates to right side  Character: 1/3 pressure, but others sharp stab aching or indigestion

• nly 1/3 with exertion
• JAMA. 2005 Nov 23;294(20):2623-9

CAD Signs & Symptoms

 Nausea, vomiting, diaphoresis  Fatigue  (Levine’s) sign, dyspnea  Unstable angina vs stable  Gut instinct

Worrisome

 Usually > 30 minutes  If lasts > 15 minutes despite 2 nitroglycerin SL  separated by 5 minutes, suspect MI  May present as sudden onset SOB due to CHF

Physical EXAM

 Quiet, still, diaphoretic patients

 ¼ of patients with anterior M.I. have ↑HR and/or HTN

 S4, S3, signs of CHF  New murmur (Mitral regurgitation – in systole)  PAD  Denial

“I feel like I am going to die.”

Obvious MI

EKG

 Previous EKG!! One EKG begets another  ~50% of people normal  repolarization abnormalities  T wave or ST segment changes (depressed,  elevated, flipped) NSSTW  New BBB

ST segment elevation WITH reciprocal ST segment depression

OR new LBBB

Stages of MI

 First: T wave flips in early ischemia.  Then: ST elevation either  flat or tombstoning  Finally: We see Q waves.

Where is the MI

The EKG is a snapshot.

63 y/o male : Chest pain – EMS responds…

“ My pain is getting worse…”

“I really don’t feel so well…”

50 y/o male with “indigestion”

T wave inversion can be seen as the sole ECG change in 10% of AMI.

58 y/o female with chest pain

Deep anterior T waves are consistent with LAD (left anterior descending) disease and represent a high-risk group

Her cath report

Lesion on mid LAD 99% stenosis

Post hospital clinic visit

The Cardiology “Happy Meal”

 BB  ACEI  Statin  ASA/Antiplatelet  “I feel dizzy now”  “I don’t want to be on all these medications”  Phase II Cardiac Rehab

Case

 42 y/o male presented with intermittent chest pain.  HX: HTN, smoking, hyperlipidemia severe, possible ehlers danlos. High stress lifestyle. Worked as a mechanic. Thin framed.

42 year old male C/P clinic EKG

PMD note “Has chest tightness after dinner, worse laying down, sometimes when

• sitting. Connection to activity, but not

consistently so. Eases with doing less. No lightheadedness, dizziness, sweats.”

Wellens

 A Can’t Miss EKG Finding

What happened?

5 vessel bypass. EF of 40%.

AVR

Ominous finding!

 Elevation of more than 1mm in aVR in the setting of Acute Coronary syndrome is associated with left main disease  Not a stemi, but should be treated like one  PCI  Associated with an increase in mortality

Stress TESTING

 TST  2 mm depression of ST segment lasting greater than 0.08 seconds (ST flat or downsloping)  15% false positives, 15% false negatives  Stress echo  Radionuclide (Lexiscan scanning) How do you choose which test to order?

Cardiac Enzymes

Myoglobin: Sensitive/not specific

 Rises in 2-3 hours/peaks in 3-6 hours  Doubling over 90 minutes highly predicative

• f AMI

Troponin:

 Rises in 3-5 hours/peaks in 12 hours  Closest to ideal

Labs

“MONA”

Morphine O2 Nitrates ASA

Gold Standard

Why guess when you could know?  Cardiac catheterization (Angiogram)  Invasive  Risks: Infection, hematoma, death

Indications for CABG

 CABG is the preferred treatment for: 1. Left main coronary artery 2. Disease of all three coronary vessels LAD,LCX and RCA 3. Diffuse disease not amenable to treatment with a PCI. The 2005 ACC/AHA guidelines: Also high-risk patients: severe ventricular dysfunction (i.e. low ejection fraction), or diabetes mellitus

Special Populations

 Beta Blockers (Toprol XL, Coreg)  ACEI particularly with E.F. <40%  If DES, then Plavix (or novel) plus ASA for one year  Cardiac rehab

MI Complications

Dressler's syndrome (Pericarditis) CHF Arrhythmia Left ventricular Aneurysm LV Thrombus

Prevention

Diet, exercise for lipid lowering Stop smoking Treat HTN, DM Reduce inflammation Reduce stress

Heart Failure

Growing problem

 one million Americans are admitted for heart failure per year...and up to 20% are readmitted within 30 days.

EXAM

 DOE, PND, orthopnea, rales  Weight loss/gain, poor appetite  S3, MR murmur, displaced PMI, ↑ HR  JVD, HJR, pedal edema, ascites  CXR (pulmonary edema)  Decreased mentation  Oliguria

Causes

MI Valve disease Anemia Thyroid Toxins

NYHA HF Classification

Can have both

How do we acutely treat CHF?

L=Lasix M=Morphine N=Nitrates O=Oxygen… P = Pressure

Pressure = BiPap

ACEI

 Patients with LVEF 40% or less with symptoms

• r prior symptoms, unless contraindicated, to

reduce morbidity and mortality  Asymptomatic patients with LVEF 35% or less  Common ACEI: Lisinopril, Ramipril, Enalapril  Check potassium, serum creatinine, and blood pressure within one week of initiation or dosage increase in the elderly, and within one to two weeks of initiation or dose

Diuretics

If: Fluid retention  Loops preferred, but thiazides can be considered for patients with hypertension and mild fluid retention. Furosemide: initial 20 to 40 mg once or twice daily, max total daily dose 600 mg  Bumetanide: initial 0.5 to 1 mg once or twice daily, max total daily dose 10 mg  Torsemide: initial 10 to 20 mg once daily, max total daily dose 200 mg

Beta blockers

Stable patients with LVEF 40% or less with sx If hypotension occurs, separate beta- blocker from other hypotensive agents (e.g., ACEI), or decrease diuretic dose Don’t stop abruptly Use Metoprolol Succinate (Toprol XL, Coreg)

Special Populations

 Use an aldosterone antagonist for patients with class II to IV heart failure...if CrCl is > 30 mL/min and potassium is < 5 mEq/L.  Consider adding hydralazine plus isosorbide dinitrate in African Americans with class III or IV symptomatic heart failure.

Don’t make it worse

NSAIDS Glitazones Diltiazem Verapamil Procardia Sotolol Dronaderone

Fight or flight

 Rubber band theory  Heart fails = stress = catecholamine release  RAAS activates  Retain sodium, heart rate goes up  Increased sodium = increased fluids = more failure

Things the patient can fix  Lifestyle, diet Things we can fix  Anemia  Arrhythmia  HTN  Infection  Thyroid disease

Treatment

 CHF: TREATMENT  Less fluid in  More fluid out = Loop diuretics  Low salt (2 g max/d)  ACEI  Cardiac Rehabilitation  Patient education

Cardiomyopathies

Dilated 95% (floppy) Hypertrophic 4% (bulky) Restrictive 1% (squished)

Dilated: Floppy Heart

Mechanism=Bad Muscle Function

 Males  Idiopathic 30%  Drugs (Cocaine/Adriamycin)  Thyroid (hypo or hyper)  Peripartum  Infection  CHF = SOB/Rales and JVD/S3

Restrictive Cardiomyopathy

“I have CHF symptoms, with a normal size heart.”

Heart is normal size, but is too stiff to relax Least common cause of cardiomyopathy About 70% of people die within 5 years after symptoms begin Restrictive Cardiomyopathy

 Symptomatic treatment usually not helpful  Hemachromatosis, the exception

Treatment

When is it usually diagnosed? HOCM

HOCM

Something is in the way.

 Syncope  Chest pain  DOE  Dyspnea at rest  Palpitations

S3 S4 MR

HOCM Clues

 DOE in a young patient  Athlete syncopal during exercise  Palpitations, orthopnea

ECG Findings

Which would you rather have as your “wine glass”?

Jennifercarlquist@yahoo.com