Download Cardiology Board Review

Cardiology Board Review
Jennifer Carlquist PA-C, CAQ ER Medicine
 Common arrhythmias and their treatment
 Demystifying Bundle Branch and AV Blocks
Objectives
 Coronary Artery Disease: Identify patients at
risk for CAD, prevention and treatment
 Heart Failure: Identify, manage and prevent it
Arrhythmias
Things that go bump in the night
Normal
conduction
Sinus
Tachycardia
Rate: >100 – 160 BPM
Regularity: Regular
P wave: Present, PR interval constant
__________________ and ________________ can cause sinus tachycardia.
Rate: Varies
Regularity: Irregular, but PR intervals are the same
P wave: Present intermittently
Sinus
Pause/Arrest
Sick sinus syndrome:
- Digitalis, CA ++ blockers, Antiarrhythmic drugs, CAD,
collagen vascular diseases and or mets
- Reversible? Pacer?
Palpitations
tree
Getting to the
root of the
cause
AFIB/Flutter
SVT WPW
PVC’s
Sick sinus VT
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.
Things we can fix
Atrial
Fibrillation
Causes
•Thyrotoxicosis
•Hyperlipidemia
•High blood pressure
•Heart disease
(Valvular)
Things the pt can fix
•Obesity
•Smoking
•Caffeine
•Alcohol abuse
•Sleep apnea
Complications
Stroke
CHF
Rate vs Rhythm
Assess/address
stroke risk
CHADS Score
Ablation/Cardiovert
 If elevated risk, need to choose: Xarelto, Apixiban, Pradaxa, ASA
 Warfarin
Assessing
stroke risk
 Warfarin: needs frequent monitoring
 Pradaxa/Xarelto (Direct thrombin inhibitors) – non
valvular $8-12 day
AC choices
 No monitoring
 No reversal
 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
Defining
AF
 Permanent (long standing persistent) AFIB
begets AFIB wont retain sinus
 Normal LA with structurally normal hearts are
better candidates
Afib with RVR
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.
 PE
 ETOH
 Ischemic heart disease
Atrial Flutter
Causes
 Hypoxia
 Digitalis toxicity
 Mitral or tricuspid valve disease
 AMI
SVT
These patients will most likely have a ___________ blood pressure.
 Etiology
 Rapid atrial depolarization overrides the SA node
 Stress, pathway, caffeine, drugs
 Clinical Significance
PSVT
 Decrease in cardiac output = angina, hypotension, or
CHF
 Clinical Features
 Regular, Rapid, No discernable P wave HR – 160-220
 Drugs
 Pathway
SVT
Ectopy
The Troublemaker
Lots of angry cells…
What causes
ectopic beats?
 Atrial
 Ventricular
 Come in patterns
This ectopy pattern is called ______________ .
ECTOPY
Where’s the
PAC?
 A junctional premature contraction (JPC) is a beat that originates
prematurely in the AV node.
 It can occur sporadically or in a grouped pattern.
Junctional
Premature
Contraction
(JPC)
 If PR interval is present, it does NOT represent atrial stimulation of
the ventricles.
PVC
 Bigeminy - every other beat
 Trigeminy - every third beat
Just how mad
are you??
 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
 You are driving into the EKG.
 You need to turn.
 You signal. Right or left.
Bundle Branch
BLOCKS
 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
LAFB is NOT
benign
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
Sinus
tachycardia
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?
 First degree AV block is a constant and
prolonged PR interval
1st Degree AV
Block
 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
Regularity: Regularly irregular
P wave: Present
PR interval: Variable
QRS width: Normal
Dropped beats: Yes, patterned
Long, Longer, Longest, DROP! Rinse and repeat. - Wenchebach
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
SecondDegree 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
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
Third-Degree
Heart Block
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
Dead? Defib
VT
Alive?
Synch
Adenosine
Stable?
SVT
Unstable?
Synch
 Rate: Generally 100 to 220 bpm
 Width of QRS>0.12 sec
Ventricular
Tachycardia
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
.
Rate: 200–250 BPM
Torsade de
Pointes
Regularity: Irregular
P wave: None
P:QRS ratio: None
PR interval: None
QRS width: Variable
Grouping: Variable sinusoidal pattern
Dropped beats: None
Prolonged __________________ can cause torsades.
 Changing polarity of the QRS complex from
positive to negative and back to positive again
Torsades De
Pointes
 Its still VTACH – why do I need to identify it
further?
Treatment is different!
Torsades
Magnesium sulfate
 Felt unwell “like the water ran out of me”
 Under stress
 HX: HTN, psyche, chronic neck pain
 Drank alcohol and did cocaine
Case
Called
911…
 “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
EMS says…
 Then goes into torsades….
Is shocked at 200 j once, brief CPR
Post shock
in ER
K was 2.7
Qt prolonging meds
Did cocaine
What were her
risks?
Hx of previous long qt….
Female
 “I think I need something stronger for pain…”
 I didn’t take my blood pressure medication as it
was too expensive…
At clinic visit
 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,
Rispiridal
Clinic EKG
Routine EKG in
2012
Coronary Artery Disease
Atherosclerosis, Angina, Unstable Angina, NSTEMI, STEMI
The menu
MI vs. NSTEMI vs.Unstable angina vs
Angina
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
 Variant Angina (Prinzmetal’s or atypical),
Not all chest
pain is CAD
caused by arterial spasm most often occurs at
rest
No fixed occlusion
CAD
Pathophysiology
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
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
 3 high risk patients: Diabetics, females and
elderly
 20 % with proven mi have only upper abd pain
 40% pain radiates to right side
Atypical
Presentations
Common
 Character: 1/3 pressure, but others sharp stab
aching or indigestion
only 1/3 with exertion
JAMA. 2005 Nov 23;294(20):2623-9
You can’t find it if you don’t look for it.
High index of suspicion
 Nausea, vomiting, diaphoresis
 Fatigue
 (Levine’s) sign, dyspnea
CAD
Signs &
Symptoms
 Unstable angina vs stable
 Gut instinct
 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)
Physical EXAM
 PAD
 Denial
“I feel like I am going to die.”
 Early morning hours common (circadian BP surge)
 Similar to CAD - longer duration and more severe
 More N&V, diaphoresis, anxiety or weakness
Worrisome
 Usually > 30 minutes
 If lasts > 15 minutes despite 2 nitroglycerin SL
 separated by 5 minutes, suspect MI
 15% of MIs are painless
 May present as sudden onset SOB due to CHF
 Previous EKG!! One EKG begets another
 ~50% of people normal
EKG
 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
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
Wellens
 A Can’t Miss EKG Finding
 42 y/o male presented with intermittent chest
pain.
Case
 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.”
What
happened?
5 vessel bypass.
EF of 40%.
AVR
 Elevation of more than 1mm in aVR in the
setting of Acute Coronary syndrome is
associated with left main disease
Ominous
finding!
 Not a STEMI, but should be treated like one
 PCI
 Associated with an increase in mortality
 TST
 2 mm depression of ST segment lasting greater
than 0.08 seconds (ST flat or downsloping)
Stress
TESTING
 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
of AMI
Labs
Troponin:
 Rises in 3-5 hours/peaks in 12 hours
 Closest to ideal
“MONA”
Morphine
O2
Nitrates
ASA
Why guess when you could know?
 Cardiac catheterization (Angiogram)
 Invasive
Gold Standard
 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
Treatment
Nitrates
BB
Ca channel blocker
Diuretics
Statin
ACEI
 Beta Blockers (Toprol XL, Coreg)
 ACEI particularly with E.F. <40%
 If DES, then Plavix plus ASA for one year
Special
Populations
 Cardiac rehab
MI
Complications
Dressler's syndrome (Pericarditis)
CHF
Arrhythmia
Left ventricular Aneurysm
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.
 DOE, PND, orthopnea, rales
 Weight loss/gain, poor appetite
 S3, MR murmur, displaced PMI, ↑ HR
EXAM
 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?
Pressure =
BiPap
L=Lasix
M=Morphine
N=Nitrates
O=Oxygen…
P = Pressure
 Patients with LVEF 40% or less with symptoms
or prior symptoms, unless contraindicated, to
reduce morbidity and mortality
ACEI
 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
If: Fluid retention
 Loops preferred, but thiazides can be considered for patients with
hypertension and mild fluid retention.
Diuretics
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 betablocker 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
Things we can fix
 Anemia
 Arrhythmia
 Lifestyle, diet
 HTN
 Infection
 Thyroid disease
 CHF: TREATMENT
 Less fluid in
 More fluid out = Loop diuretics
Treatment
 Low salt (2 g max/d)
 ACEI
 Cardiac Rehabilitation
 Patient education
Cardiomyopathies
Dilated 95%
(floppy)
Hypertrophic
4% (bulky)
Restrictive 1%
(squished)
Dilated:
Floppy
Heart
 Males
 Idiopathic 30%
 Drugs
(Cocaine/Adriamycin)
 Thyroid (hypo or hyper)
 Peripartum
 Infection
Mechanism=Bad
Muscle Function
 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
Restrictive
Cardiomyopathy
Least common cause of cardiomyopathy
About 70% of people die within 5 years
after symptoms begin
 Symptomatic treatment usually not helpful
Treatment
 Hemachromatosis, the exception
HOCM
 Syncope
Something is
in the way.
 Chest pain
 DOE
MR
 Dyspnea at rest
 Palpitations
S4
S3
HOCM Clues
 DOE in a young patient
 Athlete syncopal during exercise
 Palpitations, orthopnea
ECG Findings
Which would you
rather have as your
“wine glass”?
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