-

Cardiology with Dr. Conrad Fischer, MD

Chest Pain
* 47yo woman comes to your office complaining of substernal chest pain. The
pain has been going on for months. It is intermittent and exertional, sometimes
when she goes up two flights of stairs, sometimes at rest, sometimes she goes
up three flights of stairs and nothing happens. She also has nausea and
vomiting. She has not past medical history. What is the most likely diagnosis?
Answer is gastroesophageal reflux disease.

* What is the most common cause of non-cardiac chest pain? Gastrointestinal

problems like gastritis, esophagitis,duodenitis, peptic ulcer disease, reflux
disease, etc.

* What is the best initial diagnostic test for her? Answer is ECG. Why not pH
monitor or upper endoscopy? To rule out the most dangerous thing first.

* Which of the following is the most accurate test for her? Well then it might be
pH monitor or upper endoscopy.

* 47yo woman now suddenly remember she has had diabetes since she was a
child and has been taking insulin for 30 years. She also remembers hypertension
and hyperlipidemia with low HDL. She forgot to mention she smoked three packs
of cigarettes a day. Oh yea also most of her family members had heart attacks in
the 40s and she is a high-stress type A person. Now, what is the most likely
diagnosis in this patient? Answer is ischemic heart disease.

* Correcting which of the risk factors will improve her long term survival? Answer
is correcting all of them. Correcting which of the results in the most immediate
improvement in outcome? Tobacco smoking. But what kind of question is that,
its not like a managed care plan would only allow for you to correct a single
problem so you would need to choose the best one to correct. In real life you try
to fix all of the risk factors.

* What is the most common risk factor for coronary disease and myocardial
infarction? Hypertension. What is the most common cause of hemoptysis?
Bronchitis. Not TB, mitral stenosis, cancer, Wegener, Goodpasture, etc. What is
the most common cause of atrial fibrillation in the United States? Hypertension.

* Smoking related deaths are about 2/3 COPD and 1/3 lung cancer.

* In real life, you can have an MI with no chest pain and with a normal ECG. But
for a board exam, if they want you
to know an answer they have to tell you something. Otherwise no one can know
the answer. 4% of the time
myocardial infarction pain is pleuritic. For boards, that is too small a chance so if
a patient has pleuritic pain on a
board exam question it is not an MI.
* Pleuritic chest pain (worse with respiration) causes include viral pleurisy (i.e.
pleurodynia, Devils grip, Bornholm
disease), pneumothorax, pneumonia, pericarditis, pulmonary embolism. They all
start with Ps.
* Pneumothorax and pulmonary embolism are different from the other pleuritic
chest pain in that they are associated
predominantly with shortness of breath. Patient complains of not being able to
breath, with a little chest pain.
Myocardial infarction patient complains of crushing chest pain, with a little
shortness of breath.
* Myocardial infarction chest pain changes with position 4% of the time. Most of
the time, it is not positional.
Pericarditis chest pain is positional, better when leaning forward or worse with
leaning back.
* Chest wall is non-tender in myocardial infarction. Chest wall is tender in
costochondritis (Tietze syndrome).
* Anything that can give pleuritic pain can simulate shortness of breath. The
patient is splitting and does not want to
take a deep inspiration.
* Fever is not specific enough to differentiate between causes of chest pain.
Fever seen in infections and
inflammation like pneumonia and pleuritis as well as others like MI, PE,
pneumothorax (any form of atelectasis).
* Any clot or collection of blood can give fever; like DVT clot, MI clot,
hemarthrosis in the knee, subdural
hemorrhage, subarachnoid hemorrhage, ruptured ectopic pregnancy.

- 92 -

* Sympathetic outflow (diaphoresis, pain, tachycardia, pale, cold and clammy

extremities) does not help you specify
between causes of chest pain.
* Sense of impending doom and Levine sign also do not help you determine the
cause of chest pain.
* Most common cause of death in the United States is myocardial infarction. For
every 100 people who go to the
hospital with chest pain, 50 have a non-cardiac problem, 10 have unstable
angina, < 10% have an MI.
* Therefore, you must have the ability to distinguish between the causes of chest
pain. They are largely based on
positional changes, pleuritic pain, tenderness on chest wall. Positional, Pleuritic,
Tender.
* How is it that an attending can know about a list of patients while you can only
remember information about 2-3
as a new student? It is because they are not listening to most of what you say.
They are not smarter than you, they
just know what is important to listen to. The attending knows the important
symptoms that distinguish between
diseases and also knows the most appropriate management.
* In terms of determining the diagnosis, which is the most important: risk factors
or individual presentation? Answer
is individual presentation. Even with a history that includes every risk factors, it
is not as important as presentation
of positional, pleuritic, and tender. Profiling is less accurate.
Stress Testing & Coronary Artery Disease Management
* 47yo lady with intermittent chest pain, what is the best initial diagnostic test?
Answer is ECG. No matter what
happens, you want to rule out the most dangerous thing first.
* Say the ECG is normal. Now what will you do for her? Answer is cardiac stress
test.
* Reasons to stop a stress test include chest pain, hypotension, shortness of
breath, lightheadedness.
* Major measure of sufficient exercise (test adequacy) is heart rate. Patient must
be able to exercise, doctor must be
able to read ECG: look for ST segment depression (ischemia, not infarction).
* What if patient has baseline ST segment changes, like hypertension (left
ventricular hypertrophy) or drugs (patient

on digoxin) or pacemaker spike or LBBB? Then do a stress echo or stress thallium

test, both have similar
indications. Thallium is injected or an echocardiogram done right after walking
on treadmill.
* Stress echo should look for dysmotility or hypokinesis (decreased wall motion);
the ischemic portion does not
move well during ischemia. If infracted, you see akinesis (no wall motion).
* Thallium looks like potassium to the cardiac myocyte. If you are a myocyte in
the heart, you will pick up
potassium because of the sodium-potassium ATPase. If there is poor perfusion,
the capillary cannot delivery the
thallium. An ischemic or infracted area will have decreased thallium uptake. How
do you tell the ischemia from the
infarct if they both have decreased thallium uptake? You re-scan 4 hours later.
The scan will be the same 4 hours
later if there is infarct. If there is ischemia, the area will reperfuse showing
thallium uptake.
* 47yo lady is morbidly obese, has claudication with peripheral vascular disease,
diabetic foot ulcers, dyspnea at rest
due to COPD, and one leg. Can she do an exercise stress test? Nope. No need to
memorize the list, just think of
things that make it so you cannot exercise. You could memorize digoxin, LHV,
pacemaker for abnormal baseline
ECG, but what if your test has procainamide (causes ST down scooping)? Or
some other drug/condition that was not
in a list to memorize? Understand the basic question, is there a baseline
abnormality to the ECG such that I would
need to order an echo or thallium stress test?
* Dipyridamole (Persantine) thallium stress test used when patient cannot
exercise. Also called a chemical stress
test. Or, dobutamine echo stress test can be used when patient cannot exercise.
Both have similar indications.
* Maximum heart rate = 200 - age.
* Sub-maximal stress test should reach 85% of maximum heart rate: 85% of (220
- age)
* Exercise tolerance decreases as you get older, just as indicated in the equation.
* Dipyridamole thallium stress test abnormalities found by looking for decreased
thallium uptake. Dipyridamole

dilates coronary arteries, so more thallium should be picked up normally.

* Dobutamine echo stress test abnormalities found by looking for decreased wall
motion. Dobutamine increases
contractility and can provoke ischemia, so increased wall motion normally.
* Real exercise is always better than simulated exercise.
* Bicycle ergometry (hand bicycle) is not enough exercise to get the heart rate
up. There is much more muscle in the
thighs than arms in nearly all the population.
* 47yo lady gets an exercise stress test and it is positive. What is the next best
step? As a side note, what does this
question mean? Youre being asked what is the next step in management, so
diagnosis or treatment. If you were
asked next step in diagnosis then pick angiogram, or best diagnostic test then
pick angiogram.
* Best next step in management for patient with chest pain and ischemic heart
disease seen on stress test is
medication. Give aspirin (lowers mortality), nitrates (no change in mortality),
beta blockers, ACE-I (if left
ventricular dysmotility, congestive failure), calcium channel blockers (only if
patient cannot tolerate beta blockers as
beta blockers can decrease mortality and calcium channel blockers do not).

- 93 * What is the most accurate test for any disease? Autopsy.

* How to you differentiate Prinzmetal angina (from unstable angina)?
Angiography, not history, not ECG.
Angiography shows clean coronary arteries for Prinzmetal angina.
* 47yo woman with positive stress test and aspirin allergy. What do you give?
Clopidogrel or ticlopidine.
* Nitrates and digoxin do not lower mortality.
Hyperlipidemia
* When determining if a patient should get anti-lipid medications, do you look at
LDL, HDL, total cholesterol,
triglycerides, VLDL, or waist circumference? Answer is LDL. We do not know if
triglycerides are associated with
disease as well as we know that LDL are related to disease.

* 47yo woman with chest pain being treated and LDL is 191. What do you do
next? Answer is statins, not
cholestyramine, niacin, or fibric acid derivatives. Statins are first. All of those
drugs lower total cholesterol and all
raise HDL. All lower triglycerides as well. Statins are first because they lower
mortality.
* Which raises HDL the most? Niacin. Which lowers triglycerides the most? Fibric
acids like gemfibrozil.
* 47yo woman with positive stress test but no risk factors and LDL is 171?
Answer is statins. 141? Statins. What is
most important, risk factors or individual presentation? Again, individual
presentation. She has disease. Once you
have disease, it does not matter how many risk factors you have.
* Diet and exercise only prevent the disease. So when disease is present, diet
and exercise is not primary treatment.
* Risk factors <=1, start diet at 160 LDL and drugs at 190 LDL.
* Risk factors >=2, start diet at 130 LDL and drugs at 160 LDL.
* Disease, start diet at 100 LDL and drugs at 130, get LDL < 100.
* Patient with coronary artery disease (or MI, angina, unstable angina) who has
LDL > 130, start statin.
CABG & PCI
* 47yo woman with positive stress test, why do angiography? To determine if she
needs a coronary artery bypass
graft (CABG) or percutaneous coronary intervention (PCI) with medications.
* For every 100 people who undergo CABG, 1 person dies; Surgical mortality is
1%, which seems small when it is
someone elses mortality. Its better to be alive with chest pain.
* Bypass if severe disease, meaning 3 vessel disease or left main affected.
* PCI (angioplasty, stenting) if 1 or 2 vessel disease.
* This is why you hear he had triple bypass or she had quadruple bypass or
David Letterman had quintuple
bypass. You do not hear yea, he had single bypass.
* CABG is not done for single or double vessel disease because there is no
benefit in mortality. Let the mortality
difference drive you.
Unstable Angina & Myocardial Infarction Management

* 64yo man with a history of hypertension and hyperlipidemia comes to the ED

with chest pain. The pain goes to his
neck and arm, lasting for the past hour. He is diaphoretic, short of breath, S4
gallop, Levine sign, sense of
impending doom. You wont be asked diagnosis (unstable angina) or what test to
order (ECG). ECG shows ST
segment depression in V2-V4. What is the next step in management? Give
aspirin and beta blockers.
* What if the patient is allergic to aspirin? Give clopidogrel or ticlopidine.
* Would giving oxygen help? Not really, it does not remove the thrombus from
the heart and has not been shown to
significantly improve mortality. The patient is not hypoxic in the sense of low
arterial PO2.
* Thrombolytics do not lower mortality either.
* What else should the man having a possible MI get? Nitrates, although they do
not lower mortality they help
relieve chest pain. Aspirin and beta blockers reduce mortality. Oxygen also given
as well as morphine (analgesic)
but they are not the most important part. Mnemonic is MONA for morphine,
oxygen, nitroglycerine, aspirin. Only
aspirin matters there. Better mnemonic is MONAB for morphine, oxygen, nitrates,
aspirin, beta blockers.
* This is unstable angina because the patient has ST depression. ST elevation is
the best you can do to tell if there is
a myocardial infarction now.
* ACE-I only helpful if CHF or decreased left ventricular function.
* Calcium channel blockers helpful when you cannot use beta blockers or patient
has Prinzmetal angina.
* What other medication lowers mortality in addition to the beta blockers and
aspirin? Answer is heparin.
* In a myocardial infarction, a clot has formed and completely occluded the
artery.
* In unstable angina, a clot is forming and has not occluded the artery, although
it is working on occluding.
* Heparin prevents clots from forming. Thrombolytics do not prevent clots from
forming, they lyse clots.
* Heparin is useful for unstable angina. Thrombolytics is useful for myocardial
infarction.

* How can you tell now to give heparin or thrombolytics? Answer is ST elevation
or not.
* If ST segment elevation present, give thrombolytics. If no ST segment
elevation, give heparin.

- 94 * Beside thrombolytics or heparin, the management is the same for unstable

angina and MI.
* For MI, thrombolytics dissolves the clot then give heparin afterwards to keep it
open.
* 64yo man with a history of hypertension and hyperlipidemia comes to the ED
with chest pain. The pain goes to his
neck and arm, lasting for the past hour. ECG shows ST segment depression in V2V4. He has melena, a subdural
hematoma, epidural hematoma, subarachnoid hemorrhage, petechiae, heavy
periods. Now what do you do?
* What do you do different when you have a major contraindication to
thrombolytics and heparin? Answer to open
the vessel is do angioplasty.
* Glycoprotein IIb/IIIa inhibitors are abciximab, eptifibatide, and tirofiban. These
are antiplatelet drugs and can
make you bleed, thus you would not give these in an acutely bleeding patient.
* Most common cause of death immediately post-MI is arrhythmias. Prophylactic
lidocaine suppresses those
arrhythmias, so why not use lidocaine? Because it does not change the mortality.
Lidocaine also causes arrhythmias.
* All patients who get angioplasty also get a stent to keep the vessel open.
Atheromatous plaque gets covered by a
little later of endothelium. During times of exertion, the plaque ruptures which
causes a sudden clot to occlude the
artery. Angioplasty is when a catheter is placed through the partially occluded
artery then a balloon is expanded to
open the vessel. The problem is when you remove the catheter the plaque can
bulge back out. Thus you leave a
meshwork stent scaffolding to keep it expanded.
* CK-MB and troponins do not begin to arise for 4 hours. If they do not change
management, why order them? If

the CK-MB is up with ST segment elevation, you will still give aspirin, beta
blockers, thrombolytics. If CK-MB not
up, maybe it is just not up yet since they begin to rise at 4-6 hours and take 1224 hours to reach peak.
* Also, thrombolytics can be given up to 12 hours from the onset of chest pain (3
hours for stroke).
* CK-MB last 1-2 days, troponins last 1-2 weeks. CK-MB (97-99%) is specific, but
troponins are even more specific
(99.9%). Troponin I is the most sensitive and specific. Uterus can still make a
little CK-MB but no troponins.
* LDH is no longer used in the diagnosis of myocardial infarction. LDH is not
abnormal from 12-24 hours.
* When a patient comes in with chest pain and ECG abnormalities, do not wait
around for enzyme changes. The
mortality benefit with thrombolytics is enormous in the first 1-2 hours, up to a
50% reduction in mortality within the
first hour. Overall reduction in mortality with thrombolytics is 25%.
* Efficacy is the same with tPA (tissue plasminogen activator) and streptokinase.
Use tPA if patient previously got
streptokinase, because streptokinase can produce antibodies resulting in
anaphylaxis.
Post Myocardial Infarction Management
* 65yo man in the coronary care unit (CCU) after having an inferior wall
myocardial infarction last night. He
received all the appropriate therapy. You are called by the nurse because he is
confused. Patients blood pressure
is 70/40, pulse is 40, has cannon a waves, a chest that is clear to auscultation.
Heart exam reveals 3/6 murmur.
Which of the following is the most likely diagnosis?
* Right coronary artery feeds the right ventricle, AV node, and inferior wall. 40%
of inferior wall MIs also have RV
infarcts. This is not the right answer though.
* Myocardial wall rupture with cardiac tamponade would lead to hypotension and
confusion. But no.
* Think about what it could be. We could go to sermons all day long to become
saints, but it doesnt work that way.
* Valve rupture with chordae tendineae rupture (after a week) could cause a
murmur and hypotension. Nope.

* What about extension of the MI with cardiogenic shock? Not that either.
* Cardiogenic shock would give rales. Valve rupture would regurgitate into the
lungs, causing rales. This patient has
a clear lung auscultation exam. RV infarct and cardiac tamponade could give
clear lungs, but the heart would beat
faster to compensate (here the patient has bradycardia).
* Complications of an MI can all cause hypotension and hypotension can cause
confusion.
* Answer is third degree complete AV heart block, described first in 1826 by
Stokes and in 1846 by Adams near the
University of Dublin. Wait, they didnt have ECG back then. Stethoscope invented
shortly before by Laennec in
France (1816). They saw lightheadedness, syncope, cannon a waves,
bradycardia. No hypotension because the blood
pressure cuff did not exist then.
* What is the best initial diagnostic test? ECG, showing complete heart block.
* What is the best initial management? Atropine. This blocks the
parasympathetic, allowing the sympathetics to
work without inhibition and thus speeds up the impulses through the AV node. It
is like a car that has an accelerator
(sympathetics) and brakes (parasympathetics). Atropine cuts the brake lines for
a while.
* Transcutaneous pacer makes the heart beat with capture, but it also makes all
the chest muscles contract.
* Transvenous pacing cannot be setup fast enough and requires an invasive
procedure.
* If cardiac tamponade, do a pericardiocentesis or a cardiac window then repair
the hole.
* If valve rupture, may need to go in and emergently replace the valve.
* If cardiogenic shock and extension of the MI, may need emergency bypass
surgery.

- 95 Congestive Heart Failure (CHF)

* 67yo woman with a history of MI, valve disease, hypertension, adriamycin use,
radiation to her heart and chest,
Chagas disease, beri beri, and alcoholic cardiomyopathy. She comes in while
chowing down on an entire pizza.

Presentation is dyspnea with rales to apices, JVD to ears, S3 gallop, edema to

waist, enlarged liver, enlarged spleen,
ascites, and hemorrhoids. She says she has shortness of breath while laying flat
but feels better when she goes to the
window and puts her head outside (what makes her feel better in reality is just
getting up). You will not be asked the
diagnosis here, which is CHF in its worst form called pulmonary edema.
* What is the most common cause of developing congestive heart failure in the
United States? Post-MI. Myocardial
infarction killed off part of the heart, so you have a weak leaky heart.
* There are many causes of CHF and the initial diagnostic tests and management
are all the same.
* There needs to be an event causing (acute) pulmonary edema in a patient with
underlying CHF. Common causes
are stopping medications, increased salt load, myocardial infarction (more
ischemia), arrhythmia. Wall motion gets
worse when your heart becomes ischemic, worsening the congestive failure.
* How much cardiac output is based on atrial contribution? Answer is 10-20% in
normal person. So you can live
without the atrial kick. But that is because your heart is not weak
(cardiomyopathy), dead (post-MI), leaky (valve
regurgitation). These patients need atrial contribution.
* If you have congestive failure and you develop atrial fibrillation, now you may
have lost 40-50% of your cardiac
output because you need the atrium to push blood forward.
* Valvular rupture occurring a week after an MI would cause regurgitation leading
to acute pulmonary edema.
* For this 67yo patient, what is the next best step in management? Answer is
oxygen then loop diuretics.
* Patient will not die from lower extremity edema or organomegaly. They die from
pulmonary edema. This patient
has lungs filled with fluid and thus is not oxygenating. The fastest was to get
fluid out of your body is diuretics.
* ACE-I will decrease mortality in the long-term, but they will not help acutely.
Getting fluid out of the lungs now
will help reduce preload. Preload reduction will save this patients life, give loop
diuretics.

* Many years ago before IV furosemide was around physicians did phlebotomy
and rotating tourniquets.
* Loop diuretics are used because they are intravenous and work fast on the
ascending loop of Henle. Loop diuretics
are furosemide, bumetanide, ethacrynic acid, torasemide.
* Nitrates also work at pre-load reduction because they dilate both arteries and
veins, but dilate veins more.
* Morphine can reduce pre-load as well.
* 67yo woman with CHF and now acute pulmonary edema. Give her medication
for her shortness of breath and to
reduce preload: oxygen, loop diuretics, nitrates, morphine. 80-90% of patients
will get better with this therapy.
* CXR would show enlarged heart with congestion, pulmonary vascular
redistribution, effusions, Kerley B lines, but
we know all this. A CXR does not change our management in this patient. Patient
comes in short of breath saying
they feel like they are filled up with fluid. You do a CXR and tell her that her lungs
are filled with fluid. Thats great
doc, but she already knew that and she doesnt care. What are you going to do
to help her is the question.
* ABG would show hypoxia and low CO2 (hyperventilating). But you know this, it
does not change management.
* Say you give this patient oxygen and preload reduction but she is still short of
breath. This is dilated
cardiomyopathy, also known as systolic dysfunction. The goal now is to decrease
afterload.
* Why not use digoxin now since it is a positive inotrope? It takes time, weeks to
fully take effect.
* Dopamine and dobutamine are both positive inotropes. Which do you give for
this patient though? Dobutamine.
They will both increase contractility (positive inotropes) and myocardial oxygen
consumption.
* Dopamine increases the afterload. Dobutamine decreases the afterload, and
thus does not change blood pressure.
* Dopamine is only used if you need to raise the blood pressure. It is only used as
a pressor here.
* Afterload reduction is best achieved with ACE-I (-pril drugs). Most common
adverse reaction to ACE-I is cough

and hyperkalemia. If you have an intractable dry cough, give an ARB (-sartan
drugs, like losartan or valsartan).
* ARB drugs are angiotensin II receptor blockers.
* Most accurate way to measure ejection fraction is MUGA scan.
* Catheterization and angiogram is less accurate, but more accurate than an
echocardiogram.
* The least accurate method to assess ejection fraction is an echocardiogram.
Echo is the best initial method of
measuring ejection fracture. They are cheap, clean, easy, but not the most
accurate test.
* MUGA scan is a nuclear ventriculogram (radionuclide ventriculography).
Nuclear isotope is injected into the body
and the scan measures the amount of nuclear energy emitted from the heart in
diastole and systole. The difference in
this measurement corresponds to the ejection fraction, stroke volume to be
precise. Since it is nuclear energy, it is
not based on a cross sectional diameter like an echo or catheterization. You could
look at a soda bottle and take a
cross sectional diameter to get an estimate of the amount of soda inside. But the
better way is to pour fluid into the
bottle and measure how much actually comes out, and that is what a MUGA scan
is about.

- 96 * 67yo lady with pulmonary edema and CHF was treated with oxygen,
furosemide, nitrates, morphine. She feels all
better the next day, what is the most important medication to discharge her on?
Answer is ACE-I, diuretics, and beta
blockers. Sometimes you may need digoxin.
* ACE-I can raise potassium and help offset diuretics. You give potassium if the
patient is only on diuretics and
digoxin, as the diuretic would make you hypokalemic and the digoxin would then
become toxic.
* Diuretics and digoxin have not been show to lower mortality. ACE-I has been
shown to improve mortality.
* Aspirin has been shown to decrease mortality in coronary disease but not
congestive failure.

* But wont beta blockers worsen ejection fraction? Actually, they increase
ejection fraction and cardiac output.
Basic sciences in medical school will tell you over and over that beta blockers are
negative inotropes that worsen
ejection fraction and worsen cardiac output. That was because beta blockers had
not been studied in congestive
failure because everyone thought it would make things worse.
* There is an interesting thing that happens to patients with congestive failure
who are on beta blockers and they like
it quite a bit. That thing is that they do not die.
* Beta blockers lower mortality more than ACE-I in congestive failure.
* What is the bigger problem in cardiac failure with systolic dysfunction, the
weak heart or the ischemia? Ischemia,
and that is why beta blockers are good as they lower heart rate and cardiac
contractility, because they are antiischemic.
Going back to stress testing, what is the major determinant of exercise? Heart
rate. When you lower the
heart rate you reduce ischemia and the patient is less likely to die.
Valvular Heart Disease
* Valvular disease is organized into stenosis and regurgitation, more than by
valve location.
* Fundamental symptom of all valve disease is CHF (rales, S3 gallop, edema).
* The ease of availability and use of the echocardiogram has led to a decline in
our ability to auscultate murmurs.
The echo has greater sensitivity and specificity than the stethoscope.
* What is the most common cause of mitral stenosis? Rheumatic fever, but it can
cause any valvular disease.
* What else causes mitral stenosis? Congenital, but it can cause any valvular
disease.
* Calcification can cause mitral stenosis and aortic stenosis, but not a regurgitant
loose/floppy lesion.
* Infections (e.g. endocarditis) can cause regurgitant lesions from vegetations,
but not stenotic lesions.
* When your heart dilates, the valve leaflets do not change in size. Anything that
dilates the heart has to cause
regurgitation because the leaflets separate. Infarction can cause regurgitant
lesions through this mechanism.

* Rare aortic regurgitation causes include ankylosing spondylitis, reactive

arthritis, syphilis, Marfan syndrome,
Ehlers-Danlos, HLA-B27 stuff. These all added together and multiplied by 10 are
still not even close to causes of
aortic regurgitation compared with myocardial infarction and dilation of the
heart.
* Mitral stenosis is the most likely valvular disease to have hemoptysis, atrial
fibrillation (with emboli to brain), and
dysphagia. Dysphagia because the enlarged left atrium (most posterior heart
structure) presses on the esophagus.
There can also be hoarseness as the atrium presses against the recurrently
laryngeal nerve.
* Aortic stenosis is associated with syncope, CHF, and angina. Mnemonic: SAD for
syncope, angina, dyspnea
(CHF). Most common symptom of aortic stenosis is angina, because the ostia
(entry points) for the coronary arteries
are distal to the aortic valve. The stenotic aortic valve blocks blood flow into the
coronary arteries. Also, coronary
artery disease is common in patients with aortic stenosis (older men), thus
another cause of angina. Worse prognosis
is with CHF, 1-2 years average until death. Syncope prognosis is 3 years, angina
prognosis is 5 years.
* What can be done to restore a heart to normal shape and size once it dilates?
Nothing, heart transplant needed.
Cardiomyoplasty, slicing a piece of the dilated heart out, does not work (e.g.
Batista partial ventriculectomy). The
actin and myosin filaments have become separated and cannot contract well.
When your butt gets really big and
your underwear stretches, do you cut out a piece of underwear to fix the size?
No, you need an underwear transplant.
* ACE-I may stop the dilation problem from getting worse, but they do not alter
anatomical heart size.
* Since nothing can be done after the heart dilates, if you plan to replace the
valve you should not wait for the heart
to dilate up in size. If you wait, it will be too late.
* Exotic findings for aortic regurgitation are largely archaic, like Watson water
hammer pulse, Corrigan pulse (rapid
upstroke and collapse of the carotid artery pulse), de Musset sign (head nodding
in time with the heart beat),

Quincke sign (pulsation of the capillary bed in the nail), Traube sign (a double
sound heard over the femoral artery
when it is compressed distally), Duroziez sign (systolic and diastolic murmurs
described as 'pistol shots' heard over
the femoral artery when it is gradually compressed). Dont forget the even less
common Lighthouse sign, Landolfi
sign, Becker sign, Mller sign, Mayen sign, Rosenbach sign, Gerhardt sign, Hill
sign, Lincoln sign, Sherman sign,
and Ashrafian sign. None of these have utility in making a diagnosis. Hearing a
diastolic murmur is more reliable.
* These exotic findings are usually only seen in longstanding non-treated
disease. We replace the valve before these
patients join the American Iatrogenic Association.

- 97 * Initial test of choice for any valvular disease is echocardiogram.

* Cardiac catheterization is the only way to get direct pressure readings for any
valvular disease.
* Transthoracic echo (TTE) or transesophageal echo (TEE) first? Answer is TTE
first. Which is best? TEE.
* Mitral stenosis treatment includes preload reduction (diuretics, salt restriction).
* 27yo pregnant woman with much worse symptoms from her mitral stenosis.
Why? Plasma volume goes up but the
size of the mitral valve does not. She delivers here baby but still has bad
shortness of breath despite diuretics and
salt restriction. What is the next best step in the management of this patient?
Balloon valvotomy.
* ACE-I help get blood out of the ventricle, and we do not have a problem with
that in mitral stenosis. Digoxin will
not help because it helps blood squeeze out of the ventricle. Digoxin would help
with atrial fibrillation because it
helps decrease the heart rate and ventricle fills during diastole.
* Commissurotomy would help increase the size of the stenotic hole. But this is
very invasive.
* The ultimate step in management for all valvular heart disease is replacement
of the valve. But what can you do in
the meantime before replacing the valve, that is the question. How do you get
the valve into the heart? Open heart

surgery in general with median sternotomy. If the porcine valve needs to be

replaced every 10 years and we have a
27yo pregnant female here, is valve replacement at the top of your list for
management? Lets hope not.
* With balloon valvotomy a vascular catheter is threaded across the valve and a
balloon dilates, opening the valve.
* With aortic stenosis, balloon valvotomy does not work well. Valve replacement
with vessel bypass is the therapy.
* Aortic stenosis calcifications are from calcium, thus balloons do not work as
well.
* Mitral regurgitation and aortic regurgitation are managed with the same
medications used for CHF. Treatment is
preload reduction, positive inotrope, and afterload reduction. ACE-I and
vasodilators are the most important. This
makes it easier for blood to get out of the heart. Treatment is valve replacement
if symptoms persist.
Cardiac Auscultation
* Auscultation locations are APTM (all physicians take money), aortic at upper
right sternal border, pulmonic at
upper left sternal border, tricuspid at lower left sternal border, mitral at lower left
midclavicular area.
* Valsalva maneuver decreases preload. Exhalation against closed glottis, which
increases intrathoracic pressure and
decreases venous return to the heart. Have patient bear down like they are
having a bowel movement is another way.
* Squatting maneuver increases preload. Leg veins are compressed pushing
blood up into the heart.
* Standing suddenly decreases preload, blood pools in the legs so less blood in
the heart.
* Leg raising increases preload. Blood is brought away from the legs and into the
heart.
* Right atrial pressure when sitting is zero, when standing it could be almost subatmospheric, 5mmHg laying flat.
There is no pressure pushing blood back into the heart, blood basically just falls
into the right atrium. If you increase
the intrathoracic space pressure (valsalva) it pushes blood out of the thorax.
* Mitral stenosis (MS): opening snap moving closer to S2 as stenosis worsens
because left atrial pressure increases

so it pushes the valve open earlier. Murmur will increase with more blood in heart
(leg raise, squatting). Decreases
with preload reduction (standing, Valsalva).
* Aortic stenosis (AS): crescendo-decrescendo murmur, upper right sternal
border. Murmur will increase with more
blood in heart (leg raise, squatting). Decreases with preload reduction (standing,
Valsalva).
* Mitral regurgitation (MR): S1 and S2 are obscured by constant murmur,
pansystolic or holosystolic murmur.
Decreases with preload reduction (standing, Valsalva).
* Aortic regurgitation (AR): decrescendo murmur because blood gets shot up out
of the aortic valve and you do not
hear anything, then you hear the blood crashing down on the ventricle.
Decreases with preload reduction (standing,
Valsalva).
* Do not give beta blockers to AS, MS, AR, MR because it would make the
murmur/problem worse.
* Hypertrophic obstructive cardiomyopathy (HOCM): crescendo-decrescendo
murmur, lower left heart apex. Most
common presentation is dyspnea. It is the most common cause of sudden death
in healthy young athletes. Unlike the
other murmurs of the left heart, there is more murmur with less blood and less
murmur with more blood.
Asymmetric septal hypertrophy is in the way, so anything that makes the heart
larger (more blood) pushes away the
obstruction and decreases the murmur. When a patient exercises, the heart
contracts more completely causing more
obstruction. When dehydrates, the heart empties more fully causing more
obstruction. Digoxin, diuretics, and ACE-I
would thus cause more obstruction. Do not give HOCM or MVP patients diuretics.
Best initial therapy for HOCM is
beta blockers because it decrease the heart rate thus more filling and thus less
obstruction.
* Occasionally a myomectomy is needed for HOCM to remove the obstruction.
* Mitral valve prolapse (MVP): mid-systolic click due to leaflets stopping short.
Most common cause is congenital.
Presentation is most commonly pain (atypical chest pain), palpitations, panic
attacks. Mnemonic: Prolapse, Pain,

Palpitations, Panic attacks. Initial therapy is beta blockers.

* Note treatment and maneuvers are the opposite in HOCM and MVP compared
with AS, MS, AR, and MR.

- 98 * If a diuretic is used to treat a murmur (preload reduction), then a Valsalva will

make the murmur less intense by
the same concept of preload reduction. Thus all left sided murmurs get more
intense with more blood (leg raise,
squatting) and less intense with less blood (Valsalva, standing). Exceptions are
HOCM and MVP.
Restrictive Cardiomyopathy, Pericarditis, & Pericardial Tamponade
* Beta blockers are not used in restrictive cardiomyopathy because it is not
hypertrophic. ACE-I and diuretics are
not used because it is not dilated.
* Causes of restrictive cardiomyopathy include amyloidosis (protein accumulation
from inflammatory disease),
sarcoidosis, hemochromatosis, cancer, and fibrosis.
* Causes of pericarditis include tuberculosis, viral (e.g. coxsackie), strep, staph,
klebsiella, pseudomonas, rickettsia,
cytomegalovirus, toxoplasmosis, anaerobes, Gram negatives, syphilis, yep
anything. Viral is the most common.
* Inflammatory causes include SLE, scleroderma, rheumatic fever, rheumatoid
arthritis, Sjgren syndrome, Dressler
syndrome, uremia, mixed connective tissue disorder, yep any connective tissue
disorder or inflammatory disorder.
* Trauma causes include open heart pericardiotomy trauma, chest wall trauma,
yep stop cause its any trauma.
* Say youre in a lecture and someone is listing all the causes of pericarditis. By
the 20th item on the list the
audience will look like the old Maxell tape ads with the guy in front of the speaker
being blown back. What are you
going to learn from this? Pretty much nothing. All the attendings and residents
who know the lists will love the ever
so complete lecture, while the medical students will look at each other and say
Uhh, wanna go get a beer?
* There are over 50 separate causes of pericarditis. Any major textbook will list
these items in completeness, but you

can bundle any one of the causes into these main topics. Try to do this for any
disease with a long list.
* Cancer causes include...yea no point, its any cancer near the heart. Lungs,
breast, esophagus, mediastinal lymph
nodes are all near the heart.
* Symptom of pericarditis is pain that is positional and pleuritic.
* ECG shows ST elevations everywhere. Pathognomonic ECG finding is PR
segment depression.
* Treatment of pericarditis is to correct the underlying etiology. If no etiology
(mainly viral), NSAIDs. If NSAIDs
do not work, then use prednisone.
* Causes of pericardial tamponade are pneumonia, pleuritis, pleural effusion.
* What are the causes of pneumonia? Anything, pneumococcus most often.
* Which connective tissue disorders have pulmonary involvement? Any
connective tissue disorder.
* What cancer can affect the lung? The ones that are anatomically near the lung.
* Can trauma cause a pleural effusion? Yep. And pulmonary contusion with
atelectasis leading to pneumonia.
* Causes of pericardial tamponade are the same as pericarditis. Infections,
inflammatory, trauma, cancer.
* What about peritonitis? Yep, same causes there too.
* Chronic pericardial tamponade becomes constrictive pericarditis from fibrosis.
* Presentation is jugular venous distension (JVD), tachycardia, and hypotension.
But that could be pulmonary
edema, so how do you distinguish? Answer is pulsus paradoxus and clear lungs.
* First test of choice is echocardiogram.
* Treatment of choice is needle pericardiocentesis.
* The problem with the pericardiocentesis is that the fluid can keep reaccumulating. So what do you do to treat a
chronic pericardial effusion? Pericardial window, a hole in the pericardium and
fluid drips into pleural space.
* Constrictive pericarditis symptoms are JVD, ascites, enlarged liver.
* What occurs in constrictive pericarditis that does not occur in CHF. Pericardial
knock.
* CXR or CT for diagnosis.
* Treatment is to remove the pericardium.

Arrhythmia Management
* The type of arrhythmia management that you need to know is the first hour of
management, what you would be
expected to managed as a physician intern at a hospital.
* 47yo man comes to the office seeking advice about diarrhea prophylaxis prior
to going to a vacation to Thailand.
You notice that he feels alright but his heart rate of 47. What is the next best
step in management? This patient does
not have symptoms so ECG. If he did have symptoms, give atropine acutely to
increase the heart rate then a
pacemaker later on.
* Side note, pulse rate is not the same as heart rate. Heart rate is seen on ECG,
pulse is palpated.
* Normal heart rate of 60 to 100 is based on thousands of military recruits
between the ages of 18 and 24, two hours
post prandial in the supine position.
* Sinus bradycardia at a rate of 47 in an asymptomatic man, next step is leave
him alone. What if the heart rate was
37 without symptoms and ECG showing sinus bradycardia? Do nothing. It does
not matter how low it gets because
he has no symptoms.

- 99 * First degree AV block without symptoms do nothing. This does not progress to
second degree AV block.
* Mobitz type I AV block (Wenckebach) without symptoms do nothing. This does
not usually progress and is part
of the normal aging of the conduction system.
* Mobitz type II AV block is the dividing line, this can progress to complete block
and ischemia.
* Mobitz type II AV block and type III complete AV block get a pacemaker even
without symptoms. We do not
wait for the patient to have their first syncopal episode while they are driving
down the road.
* 28yo female medical student who has been preparing for an exam and using
the four basic food groups, alcohol,
nicotine, caffeine, chocolate. She comes in complaining of palpitations. ECG
shows supraventricular tachycardia

(SVT) at a rate of 160. What is the first step in management?

* Multifocal atrial tachycardia includes SVT, atrial fibrillation (Afib), atrial flutter
(Aflutter). They are all the same
in their management except adenosine.
* Determine if the patient is unstable. If unstable, do synchronized cardioversion.
What does unstable mean though?
Hemodynamic instability means systolic blood pressure < 90, chest pain,
shortness of breath, or confusion.
* Does that mean a person with a normal systolic blood pressure of 88 gets
shocked in this situation? Yes. We have
to agree on a definition for hemodynamic instability.
* Conduction jelly is used to increase the surface area for the shock and to
decrease the burn because dry skin burns.
* Stable patient atrial arrhythmia (e.g. SVT) first step is vagal maneuvers like
carotid sinus massage, Valsalva
maneuver, mammalian dive reflex (mostly for kids, ice back to face),
circumferential digital rectal examination.
* Eyeball pressure does a good job of slowing the heart rate...and blinding the
patient, so dont do that. Eyeball
massage can cause retinal detachment and it is not needed.
* Stable patient with SVT and vagal maneuvers did not work, then adenosine.
Adenosine only used for SVT.
* If vagal maneuvers and adenosine do not work, then slow the rate. You can
give digoxin, beta blocker, calcium
channel blocker. How do you know which one to use? These all slow the rate but
do not convert the rhythm. The
indications for digoxin, calcium channel blocker, and beta blocker in this scenario
are the same so it does not matter.
* Say patient had a history of asthma? Then do not use beta blockers because it
could cause bronchospasm.
* Mnemonic for SVT meds: ABCD, adenosine, beta blocker, calcium channel
blocker, digoxin.
* 72yo former president of the U.S. is at an important dinner in Japan, gets up to
make a point, leans forward and
vomits all over the Japanese ambassador. He is found to have rapid atrial
fibrillation secondary to Graves disease.
What is the next best step in the management of this patient? If stable, beta
blockers because it will block the effect

of the sympathetic outflow from the hyperthyroidism.

* Rate controlling meds for non-SVT atrial arrhythmias are BCD: beta blocker,
calcium channel blocker, or digoxin.
* Coumadin is used when patient has chronic atrial fibrillation, which means > 48
hours. Because after you have had
Afib for more than two days you are at risk for emboli.
* 57yo man at the opera who gets up, becomes lightheaded and confused. He is
found to have ventricular
tachycardia (Vtach). Blood pressure is 128/88. What is the next best step in the
management of this patient?
* Does he have hemodynamic instability? No, he has lightheadedness and
confusion.
* Vtach that is stable gets lidocaine, unstable gets defibrillation.
* 57yo man at the opera who gets up, falls to the floor and is not moving. What is
the next best step in the
management of this patient? Answer is determine if he is conscious or
unconscious. Determine if the patient is
responsive and not just sleeping.
* Say patient is truly unresponsive to even painful stimuli. What is the next step
in management? Call 911.
American Heart Association has spent a great deal of time working the algorithm
out. Say we skip this step and open
the airway, do a couple of rescue breaths, he has no pulse so we start
compressions. Whats the problem now? Well,
no one is coming to bring a defibrillator or take this man to the hospital.
* Survival without defibrillation declines to zero after ten minutes. After ten
minutes without defibrillation, the
patient has no good chance of survival. There is a 10% decline in mortality per
minute. Thus, you better be sure
about the next step of management. Call for help before moving on to the rest of
the algorithm. Chest compressions
do not restart the heart, they keep you alive while waiting for the important
equipment (defibrillator) to arrive.
* Say the patient is unresponsive and pulseless. What is the differential?
Pulseless ventricular tachycardia,
ventricular fibrillation (Vfib), asystole, pulseless electrical activity (PEA). What is
the only way to distinguish

these? ECG. Thus, you better call for help to get the equipment there so you can
distinguish these.
* After calling for help, then you do ABCs. Open airway, check breathing, give
two breaths if not breathing, check
pulse, start compressions if no pulse.
* Say ECG shows up and patient is in Vfib with no respirations. Now what?
Defibrillation. Not intubation, how long
would it take to intubate in the field? Maybe 3-4 minutes with getting equipment
out, suction, and get the tube in. In
that time, 40% of your patients just died since 10% are lost per minutes.

- 100 * If defibrillation did not work, do a cycle of CPR then shock again. Epinephrine
can be given between each cycle as
well. So shock, drug, CPR, shock, drug, CPR, etc. After three cycles with
refractory VT or Vfib, you can give
amiodarone or lidocaine.
* Intracardiac medication has not been show to have greater efficacy so it is not
an answer.
* Thoracotomy with direct cardiac massage is also not an answer, it will not help.
* Magnesium is given for Torsades de Pointes only.
* Precordial thump is like a little defibrillation, 10-20J of energy. The amount of
energy needed for successful
defibrillation is little at the very beginning. Thus, precordial thump used in
witness arrest only with no defibrillator
present. If you have a defibrillator, use that instead.
* What about the dosing of these drugs and shocks? Drug dosing is not asked on
board exams. Exception may be the
advanced cardiac life support (ACLS) drugs here. Epinephrine is 1mg, atropine is
1mg for cardiac arrest and 0.5mg
for bradycardia, lidocaine is 1mg/kg, adenosine is 6mg to start, amiodarone is
300mg.
* Resuscitation of patients beyond 10 minutes only in hypothermia or induced
hypothermia. CO2 production of each
cell and oxygen consumption is directly proportional to body temperature.
* For asystole or PEA, atropine and epinephrine can be given between CPR
cycles.

* Do not shock asystole. It may be important to know the most common wrong
answer in situations like this because
both will be listed on the exam and likely they are the two answer choices you
narrow down to. Defibrillation stops
the heart with the hope that it will reboot normally. Defibrillating asystole will do
nothing because the electrical
system is already stopped; its not like jumper cables for a car, its more like
rebooting an electronic device when it
is not functioning well. Side note: always confirm asystole in a second lead.
* Say youve given epinephrine and atropine through several cycles of CPR and
the patient is still dead. You can
consider a pacemaker. For true asystole, this does nothing. You consider
pacemaker because it could possibly be
very slow bradycardia and you may have missed a beat. Algorithm says consider
because beyond that you are
considering burial or cremation, there is nothing else to do, the patient is dead
anyway.
Electrocardiograms
* There are very few ECGs on USMLE Step 2, maybe two or three.
* Each small box is 40ms. Each large box is 200ms.
* PR interval should be less than 5 small boxes (200ms). QRS should be less than
3 small boxes (120ms).
* Counting rate is done by the 300 method. Count the number of large boxes
between QRS complexes and divide
300 by that number. So if there were 5 large boxes between QRS complexes it
would be 300/5 = 60bpm.
* 300 method points are 300, 150, 100, 75, 60, 50. You can differentiate
tachycardia from bradycardia this way.
* Arrhythmia associated with digoxin toxicity is bigeminy, trigeminy, any
arrhythmia. The most common
arrhythmia seen in digoxin toxicity is SVT with variable block.
* Bigeminy is every other beat being a PVC. Couplets are two PVCs, not
uncommon.
* Supraventricular can be differentiated from ventricular by the width of the QRS
complexes. Wide complexes
always comes from the ventricles. Wide complexes are > 120ms.
Supraventricular impulses follow the normal
conduction pathway through the AV node, which makes them narrow on the QRS.

* Ectopic beats originate from an ectopic focus. One is PVC. Two is couplet. Three
is triplet. Four or more is
ventricular tachycardia.
* ECG showing flat line. Dont think something like the leads came off the
patients chest. This is asystole. There is
some biological variability, so it might not be perfectly flat line. What is the best
next step in management? CPR,
then epi and atropine for a few rounds, then consider a pacemaker, then
consider the patient dead.
* You are at the bedside for a patient with chest pain. They become unconscious
and the ECG shows flat line.
Should you do a precordial thump for the witnessed arrest? No. Precordial thump
is like defibrillation and you do
not defibrillate flat line.
* Consistent wide complexes is ventricular tachycardia. What do you do next if
the patient is conscious and stable?
Give lidocaine.
* What if ECG shows Vtach and patient is unconscious? Defibrillation.
* Know what ventricular fibrillation looks like and do not expect Torsades.
Irregular waves with no consistency
across the rhythm strip. Patient is always pulseless. What do you do? Defibrillate.
* ECG shows Vfib and youve gone through cycles of CPR with defibrillation. Now
you intubated the patient and
give epinephrine during the cycles. How much time do you have to save this
patient? 10 minutes. What medication
can you give for refractory VT or VF? Amiodarone.
* Important Note: There is no minimum and no maximum for running a
resuscitation.
* You get called into a room by a nurse because the monitor shows the patients
rate at 140 per minute. She has the
defibrillator ready and is asking you what to do. You feel a pulse and note that it
is 70 per minute. The patient states

- 101 she missed her dialysis treatment this week. What could it be? Hyperkalemia.
The peaked T-waves are so high that
the monitor is reading them as QRS complexes.

* When talking about peaked T-waves, the size does not matter as much as the
shape. The pointier the worse.
* The most important ECG to know is regular sinus rhythm.
* Keep in mind when you are studying for the exam, if your highest point to
attain is the exam it will feel painful. If
you are conscious of the goodness that comes from the knowledge after that and
what it can do to be of service, then
the exam will feel smaller and your process will be filled with more joy.
------------------------------------------------------------------------------------------------------------------------------------------