Transcript Cardiology Step 3 Review

CARDIOLOGY STEP 3
REVIEW
By James K. Rustad, M.D.
Copyright © 2009 All Rights Reserved.
Outline
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Arrythmias and Chest Pain
Pericarditis
Endocarditis
Rheumatic Fever
Hypertension
Valvular Heart Disease
Congential Heart Diseases
Arrhythmias
Wolf Parkinson White Syndrome
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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)
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If symptomatic – best
initial therapy
Procainamide (for VT
or SVT from WPW)
Long term treatment:
Radiofrequency
ablation
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Avoid digitalis, beta
blocker and calcium
channel blocker (may
precipate arrhythmia)
Atrial fibrillation
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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
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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
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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
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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
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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)
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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
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Men >45, Women
>55
Male gender
Diabetes, HTN, Lipid
abnormality
(increased LDL)
Smoking
Physical inactivity
Increased
Homocysteine
Differential Diagnosis Nonpleuritic
CP
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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)
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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
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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.
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Stable angina: Aspirin
and Metoprolol have
benefit on mortality;
nitrates helpful for
pain.
Unstable angina
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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
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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
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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
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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)
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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
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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
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Left main disease
Triple vessel disease
with low EF
Diabetes with 2 or
more vessels involved
MI
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Chest pain greater
than 30 min.
Diaphoresis, SOB,
weakness, pain.
Cardiac Enzymes: CKMB, Troponin I,
Troponin T
ST elevation MI
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Q wave, transmural
ST elevation greater
or = to 1 mm in two
consecutive leads.
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O2, S/L NTG,
Morphine, Aspirin or
Clopidrogrel, Bblocker, IV heparin.
PTCA OR
Thrombolytic (less than
12 hours post MI, ST
elevation, New LBBB)
Non ST elevation MI
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Sub-endocardial, ST
depression or T-wave
inversion
No Q wave but
cardiac enzymes up
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Manage similar to
unstable angina.
With continued Chest
Pain – Cardiac Cath
Clinical Scenario
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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
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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
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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
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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
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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?
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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
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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
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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
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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!
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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
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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
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Actor John Ritter
(1948-2003)
Special topic: Diastolic Dysfunction
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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
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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
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A: Atrial contraction
C: Closure of Tricuspid
X: Atrial RelaXation
V: Venous filling
Y: opening of Tricuspid
JVP is Right Atrial Pressure
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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)
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Canon “a” wave =
complete heart block
(atria and ventricle have
own rhythm, no
coordination)
Pericarditis
Acute Pericarditis
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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
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EKG: Diffuse ST
elevation and PR
depression.
Confirm with Echo
Treatment: Aspirin,
NSAIDS.
Clinical scenario
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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.
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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
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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
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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)
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Roth’s spot: exudative
lesions in the retina
Fever + New or Changed murmur
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Blood cultures first!
If positive, do an
ECHO to look for
vegetations.
Common organisms/treatment
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Common: Strep
viridens
Virulent: Staph aureus
S/P cardiac surgery:
Staph epidermis (for
this or prosthetic valve
give vanco + rifampin
+ genta)
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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:
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Haemophilus
Actinobacillus
Cardiobacterium
Eikenella
Kingella
IV Drug Abuse
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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
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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:
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Dental procedures that
cause bleeding
(amoxicillin - or
clindamycin if patient
allergic to penicillin)
Respiratory tract
surgery or surgery of
infected skin.
Valve replacement surgery
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Anatomic defects –
difficult to correct with
only ABX!
Valve
rupture/prosthetic
valve
Abscess
Fungal endocarditis
Embolic events after
starting ABX.
Rheumatic Fever
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Acute RF usually
develops after 2-4
weeks of pharyngeal
infection with Group A
streptococcus.
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Can erysipelas lead to
rheumatic fever?
No --- skin goes to
kidneys only. Throat
goes to kidneys and
heart.
Earliest Symptomatic manifestation
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Arthritis --- migratory
and involves large
joints mainly lower
extremity. Subjective
pain greater than
objective inflammation.
Erythema marginatum
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Non-pruritic
Erythematous lesion
with pale center,
mostly on trunk,
rounded margin.
Early manifestation
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Evanescent (appear,
disappear)
Syndenham chorea
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Commonly on one side
and ceases during
sleep.
Abrupt, purposeless,
non rhythmic
involuntary movement.
Rheumatic Fever (continued)
Carditis
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Early: Mitral
Regurgitation
Late: Mitral stenosis,
secondary to scarring
and calcification of
damaged valve.
Subcutaneous Nodule
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Nodule: mostly over
bony surface.
Firm, painless, usually
disappears within a
month.
Diagnosis: Jones Criteria
Major
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Carditis
Polyarthritis
Chorea
Subcutaneous Nodule
Erythema Marginatum
Minor
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Fever
Arthralgia
Previous RF or
Rheumatic Heart
disease
Rheumatic Fever treatment
Acute Treatment
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Aspirin
Oral Penicillin V for 10
days or Benzathine
Penicillin G IM X 1
dose
Penicillin allergic:
Erythromycin X 10
days
Prophylaxis
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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)
Hypertension
Management of Blood Pressure
Blood 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
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They work by inhibiting
reabsorption of Na+ and
Cl− ions from the distal
convoluted tubules by
blocking the thiazidesensitive Na+-Cl−
symporter. Thiazides also
cause loss of potassium
and an increase in serum
uric acid.
Hypokalemia,
Hyponatremia and
Hyperuricemia
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Recommended starting
dose: Hydrochlorothiazide
25 mg once daily
K+ sparing diuretics (think SAT)
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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.
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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
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Loop diuretics act on
the Na+- K+ - 2Clcotransporter in the
thick ascending limb of
the loop of Henle inhibit sodium and
chloride reabsorption.
Loop (of Henle) diuretics
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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
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Cardioselective (Beta 1)
Atenolol 50-100
mg/day
Metoprolol 25-100
mg/day
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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
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Lisinopril:
recommended initial
dose is 10 mg qdaily.
Usual dosage range is
20 to 40 mg per day
administered in a
single daily dose.
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Side effects: Dry
cough, hyperkalemia,
angioedema.
ACE inhibitors (continued)
Angiotensin II receptor blockers
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Losartan
Irbesartan
Valsartan
Candesartan
Calcium Channel Blockers
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Non-Dihydropyridine
(bradycardia)
Diltiazem
Verapamil
(constipation)
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Dihydropyridine (cause
Tachycardia)
Amlodipine 5-10
mg/day
Felodipine
Nifedipine 30-60
mg/day
Calcium channel blockers: Ankle
Edema
Valvular Heart Disease
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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
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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
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Aortic valve closes earlier
Pulmonic valve closes later
MR, VSD, Pulmonary Stenosis, Pulmonary Artery
Hypertension, RBBB
Mitral Regurgitation
MR
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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
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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
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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
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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)
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Aortic valve closes later
Pulmonic valve earlier.
Sometimes paradoxical splitting where pulmonic
valve closes before aortic valve.
Aortic stenosis, HOCM, LBBB
Aortic Stenosis
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
Stenotic valves close
later.
Midsystolic, upper
right sternal border.
Aortic Stenosis


“Crescendodecrescendo” murmur
Upper right sternal
border and radiates
to carotids.
Aortic Stenosis
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Syncope
Angina
Dyspnea
Aortic Stenosis
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LVH on EKG
Treatment of choice is
valve replacement.
Clinical scenario
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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
Squatting and Leg Raise

Increases Blood Return
(increase venous return
to heart).
Standing/Valsalva

Decreased Blood
Return. All murmurs
decrease with standing
and valsalva except
for…..
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!