Cardiology
Ischemic Heart Disease
Coronary artery disease (CAD) is the most common cause of death, by far, and kills
10 times more women than breast cancer.
Risk factors are useful for 2 things:
1.
2.
Help answer diagnostic questions in equivocal cases
Modifying them can lower mortality
For family history to be significant as a risk factor, the family member must be
young (female relatives < 65, male relatives < 55).
Emotional stress is not a clear risk factor. It is not possible to measure precisely.
Risk factors include the following:
• Diabetes mellitus
• Hypertension
• Tobacco use
• Hyperlipidemia
• Peripheral arterial disease
• Obesity
• Inactivity
• Family history
Coronary artery disease (CAD) presents with chest pain that does not change with
body position of respiration. CAD is not associated with chest wall tenderness. The
single worst or most dangerous factor for CAD is diabetes. When any one of the
following 3 features is present, the patient does not have CAD.
Pleuritic Pain (changes
with respiration)
Pulmonary embolism
Pneumonia
Pleuritis
Pericarditis
Pneumothorax
Positional Pain
(changes with bodily
position)
Pericarditis
Tenderness (pain on
palpation)
Costochondritis
The most common cause of chest pain that is not cardiac in etiology is a
gastrointestinal (acid reflux) problem.
1.
2.
3.
A patient comes to the emergency department with chest pain. The pain
also occurs in the epigastric area and is associated with a sore throat, a
bad metallic taste in the mouth, and a cough. What do you recommend?
An alcoholic patient comes to the emergency department with chest
pain. There is nausea and vomiting and epigastric tenderness. What do
you recommend?
A patient comes to the emergency department with chest pain. There is
right-upper quadrant tenderness and mild fever. What do you
recommend?
Answers:
1. Give a proton pump inhibitor.
2. Check amylase and lipase levels.
3. Order an abdominal sonogram for gallstones.
Beside chest pain, other clues to ischemic disease as the cause of chest pain
are as follows:
•
•
•
•
•
Dull pain
Lasts 15–30 minutes
Occurs on exertion
Substernal location
Radiates to the jaw or left arm
Physical Findings
There is nothing unique or pathognomonic about the physical findings of ischemic
heart disease. Physical findings such as tenderness only tell you the patient does
not have ischemic disease. There is no buzzword for physical examination of CAD
that indicates, “Aha! This is coronary disease.”
Piece of Physical Exam
Cardiovascular (CV)
Chest
General exam
Extremities
Basic Science Correlate
Findings That Could Be Abnormal
S3 gallop: Dilated left ventricle
S4 gallop: Left ventricular hypertrophy
Jugulovenous distention
Holosystolic murmur of mitral
regurgitation
Rales suggestive of congestive heart
failure
Distressed patient, short of breath,
clutching chest
Edema
The mechanism of an S3 gallop is rapid ventricular filling during diastole. As
soon as the mitral valve opens, blood rushes into the ventricle, causing a splash
sound transmitted as an S3.
S4 gallop is the sound of atrial systole into a stiff or noncompliant left ventricle. It
is heard just before S1 and occurs with any type of left Ventricular hypertrophy.
S4 is the bang of atrial systole.
Holosystolic Murmur: Mitral Regurgitation
Diagnostic Testing
An EKG is always the best initial diagnostic test for ischemic-type pain. If the case
present to you is very clearly a case of ischemic pain and the examiners ask you
to choose between an EKG and aspirin, nitrates, oxygen, and morphine, then
choose treatment first.
ST Elevation
ST Depression
T Wave Inversion
The wrong “best initial tests” of steps are troponin, CK-MB, stress testing,
echocardiogram, or angiography. These tests do not eliminate the need to give
aspirin first.
CCS Tip: When the question requests what the most accurate test is, answer CKMB or troponin.
CK-MB and troponin levels both rise at 3–6 hours after the start of chest pain.
They have nearly the same specificity. The main difference between CK-MB and
troponin is that CK-MB only stays elevated 1–2 days while troponin lasts elevated
for 1–2 weeks. Therefore, CK-MB testing is the best test to detect a reinfarction a
few days after the initial infarction.
CCS Tip: Always the wrong answer: LDH level or LDH isoenzymes.
Basic Science Correlate
Troponin C: Birds to calcium to activate actin:myosin interaction
Troponin T: Binds to tropomyosin
Troponin l: Blocks or inhibits actin:myosin interaction
Myoglobin elevates as early as 1–4 hours after the start of chest pain. Myoglobin
is the answer to the question “Which of the following will rise first?” when the
choices are all cardiac enzymes.
Stress testing is the answer when the case is not acute and the initial EKG and/or
enzyme tests do not establish the diagnosis.
Answer: Stress test when the case is equivocal or uncertain for the presence of
CAD. Do not do an angiography unless the stress test is abnormal. Exercise
tolerance, or “stress,” testing detects coronary artery disease when the heart rate
is raised and ST segment depression is detected. This case is asking you to know
that a stress test is a way of increasing the sensitivity of detection of CAD
beyond an EKG and enzymes.
When do I answer dipyridamole or
When do I answer exercise thallium
adenosine thallium stress test or
testing or stress echocardiography?
dobutamine echo?
Patients who cannot exercise to a
EKG is unreadable for ischemia:
target heart rate of > 85% of maximum:
• Left bundle branch block
• COPD
• Digoxin use
• Amputation
• Pacemaker in place
• Deconditioning
• Left ventricular hypertrophy
• Weakness/previous stroke
• Any baseline abnormality of the ST
• Lower-extremity ulcer
segment of the EKG
• Dementia
• Obesity
Sestamibi nuclear stress testing is used in obese patients and those with large
breasts because of the greater ability of this radioisotope to tissue.
Answer: Angiography is the next diagnostic test to evaluate an abnormal stress
test that shows “reversible” ischemia. Reversible ischemia is the most dangerous
thing that a stress test can show. If the stress test shows “fixed" defects—that is, a
defect unchanged between exercise and rest—this is a scar from a previous
infarction. Fixed defects do not need angiography. Coronary bypass is the answer
only if the angiogram has already been done. Echocardiography is the best initial
test to evaluate valve function or ventricular wall fiction. Nuclear ventriculogram
is the most accurate method to evaluate ejection fraction.
Basic Science Correlate
Mechanism of Thallium
Nuclear isotopes are picked up by the Na/K ATPase of normal myocardium. If
cardiac tissue is alive and perfused, it will pick up the nuclear isotope. To the
myocardium, thallium looks like potassium.
Decreased uptake = Damage
Answer: The CK-MB level should return to normal 2–3 days after a myocardial
infarction. If a reinfarction has occurred, the level will go back up again 5 days
later, while the troponin level will still be up from the original infarction. Troponin
can be elevated for 2 weeks after an infarction. Angiography can detect
obstructive, stenotic lesions but cannot detect myocardial necrosis. Stress testing
should never be performed if the patient is having current chest pain; chest pain is
a reason to stop a stress test. Echo will show decreased wall movement, but this
could have been present from the previous cardiac injury.
Acute Coronary Syndrome (ACS)
The definition of acute coronary syndrome (ACS) is as follows:
•
•
•
•
•
Causes acute chest pain
Can be with exercise or at rest
Can have ST segment elevation, depression, or even a normal EKG
Not based on enzyme levels, angiography, or stress test results
Based on a history of chest pain with features suggestive of ischemic
disease
Treatment
Aspirin
The best initial therapy for all cases of ACS is aspirin. Aspirin can be administrated
orally or chewed and absorbed under the tongue. It has an instant effect on
inhibiting platelets. Aspirin alone reduces mortality by 25 percent for acute
myocardial infarction and by 50 percent for “unstable angina,” which may become
a non-ST segment elevation myocardial infarction (NSTEMI). Nitrates and
morphine should also be administered in acute coronary syndromes, but they do
not lower mortality. Oxygen has no benefit if the patient is not hypoxic.
Clopidogrel or ticagrelor is added to aspirin for all patients with acute myocardial
infarction. Prasugrel is given only when angioplasty is done.
Prasugrel, clopidogrel, or ticagrelor is added to everyone getting angioplasty and
a stent. These meds inhibit ADP activation of platelets.
Basic Science Correlate
Mechanism of P2Y₁₂ Antagonists: Clopidogrel, Prasugrel, Ticagrelor
These agents block aggregation of platelets to each other by inhibiting ADPinduced activation of the P2Y₁₂ receptor. Clopidogrel and prasugrel are in the
thienopyridine class.
Thrombolytics and Primary Angioplasty
Thrombolytics and primary angioplasty both lower mortality in ST segment
elevation myocardial infarction (STEMI) and are dependent on time; in other
words, their benefit markedly diminishes with time.
Prasugrel added only for angioplasty.
Primary angioplasty means angioplasty during an acute episode of the chest
pain, and infarction is the single best evidence for mortality benefit with
angioplasty. Angioplasty is one type of “percutaneous coronary intervention” (PCI).
PCI must be preformed within 90 minutes of arrival at the emergency department
for a STEMI. Angioplasty has not been shown to decrease mortality in stable
angina more than medical therapy (aspirin, beta blockers, and statins) alone.
If PCI cannot be performed within 90 minutes of arrival in the emergency
department, the patient should receive thrombolytics. The question will clearly
state that “the patient is at a small rural hospital” or “the nearest catheterization
facility is over an hour away.” The question must be clear on this point.
Thrombolytics are indicated when the patient has chest pain for < 12 hours and
has ST segment elevation in 2 or more leads. A new left bundle branch block
(LBBB) is also an indication for thrombolytic therapy. Thrombolytics should be
given within 30 minutes of a patients arrival in the emergency department with
pain.
Basic Science Correlate
Mechanism of Thrombolytics
Thrombolytics activate plasminogen into plasmin. Plasmin chops up fresh or newly
formed fibrin strands into D-dimers. This is why all clots elevate levels of D-dimers.
After several hours, the fibrin clot has been stabilized (made more permanent) by
factor XIII. Plasmin will not cleave fibrin once stabilized by tar XIII.
Beta Blockers, ACE Inhibitors, and Angiotensin Receptor
Blockers
Beta blockers lower mortality, but the timing of their administration is not critical.
Beta blockers, such as metoprolol, should be given, but they are not as urgent to
give as aspirin, thrombolytics or primary angioplasty. ACE inhibitors or
angiotensin receptor blockers (ARBs) should be given to all patients with an
acute coronary syndrome, but they only lower mortality if there is left ventricular
dysfunction or systolic dysfunction. Make sure there is a lipid profile and start
the patient on HMIG CoA reductase inhibitors, if indicated (i.e., if LDL is not at
goal).
Basic Science Correlate
Mechanism of Beta Blockers in Myocardial Infarction
The most common cause of death in both CHF and MI is ventricular arrhythmia
brought on by ischemia. Beta blockers are both anti-arrhythmic and anti-ischemic.
Slower heart rate means more time for coronary artery perfusion. Increased left
ventricular filling time increase both stroke volume and cardiac output.
Answer: Angioplasty will lower the risk of mortality most for this patient. If it can
be obtained within 90 minutes, angioplasty is the best therapy. Metoprolol lowers
mortality but is not dependent on how soon you give it, as long as the patient
receives it before going home.
Statins
Statin medications, such as atorvastatin, should be given to all patients with an
acute coronary syndrome, regardless of what the EKG shows or troponin or CKMB levels.
Effects of Therapy Used in Acute Coronary Syndromes
Always Lower Mortality Lower Mortality in
Do Not Lower Mortality
Certain Conditions
• Aspirin
• Thrombolytics
• Primary angioplasty
• Metoprolol
• Statins
• Clopidogrel, prasugrel,
or ticagrelor
•
⁃
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•
⁃
⁃
⁃
•
⁃
⁃
⁃
⁃
⁃
•
⁃
⁃
• ACE inhibitors if
ejection fraction is low
• ARBs if ejection fraction
is low
• Oxygen
• Morphine
• Nitrates
• Calcium channel
blockers
• Lidocaine
• Amiodarone
When is prasugrel, clopidogrel, or ticagrelor the answer?
When a platelet antagonist is to be used for acute chest pain, there is aspirin
allergy, the patient is to undergo angioplasty, or an acute infarction is
occurring. Ticlopidine is associated with neutropenia.
Add one of them to aspirin when there is an acute MI.
When are calcium channel blockers (verapamil, diltiazem) the answer?
The patient has an intolerance to beta blockers, such as severe reactive
airway disease (asthma).
There is cocaine-induced chest pain.
There is coronary vasospasm/Prinzmetal's angina.
When is a pacemaker the answer for acute MI?
Third-degree AV block
Mobitz Il, second-degree AV block
Bifascicular block
New left bundle branch block
Symptomatic bradycardia
When is a lidocaine or amiodarone the answer for acute MI?
Only when there is ventricular tachycardia or ventricular fibrillation.
Do not give antiarrhythmic medications to prevent ventricular arrhythmias.
Clopidogrel, or ticagrelor is used when:
• There is aspirin allergy.
• The patient undergoes angioplasty and stenting.
• There is acute MI.
Prasugrel has greater efficacy than clopidogrel but causes more bleeding.
Prasugrel increases bleeding in:
• Age > 75
• Weight < 60 kg
Complications of Myocardial Infarction (MI)
All the complications of myocardial infarction result in hypotension.
Diagnosis
Diagnostic Test
Treatment
Cardiogenic shock
Valve Rupture
Septal rupture
Echo, Swan-Ganz (right
heart) catheter
Echo
Myocardial wall rupture
Echo, right heart catheter
showing a step up in
saturation from the right
atrium to right ventricle
Echo
Sinus bradycardia
EKG
Third-degree (complete)
heart block
Right ventricular
infarction
EKG, canon “a” waves
EKG showing right
ventricular leads
ACEI, urgent
revascularization
ACEI, nitroprusside, intraaortic balloon pump as a
bride to surgery
ACEI, nitroprusside, and
urgent surgery
Pericardiocentesis,
urgent cardiac repair
Atropine, followed by
pacemaker if there are
still symptoms
Atropine and a
pacemaker even if
symptoms
resolve
Fluid loading
Basic Science Correlate
Mechanism of Septal Rupture Systolic Murmur
Left ventricular pressure is greater than till right ventricular pressure. This causes
left-to-right shunt of oxygenated blood. Oxygen saturation in the right ventricle is
markedly increased compared with the right atrium.
Post-MI Discharge Instructions
All patients post-MI should go home on aspirin, clopidogrel (or prasugrel), a beta
blocker, a statin, and an ACE inhibitor.
Answer: Some waiting is necessary to have sex after an infarction. Sex minimally
increases the risk of infarction. The duration and the intensity of exertion are
sufficient to provoke ischemia in some cases.
Non-ST Segment Elevation Myocardial Infarction
The predominant differences in the management of non-ST segment elevation MI
(NSTEMI) are as follows:
•
•
•
No thrombolytic use.
Heparin is used routinely. Low molecular weight (LMW) heparin is superior
to IV unfractionated heparin.
Glycoprotein IIb/IIIa inhibitors lower mortality, particularly in those under
going angioplasty
The single greatest benefits from GPIIb/IIIa inhibitors with ACS come in
combination with angioplasty and stent placement. Abciximab does not benefit ST
segment elevation MI.
Answer: Heparin is the only one of these choices that has been shown to produce
lower mortality. Thrombolytics do not lower mortality, unless there is ST elevation
or a new LBBB. Positive cardiac enzymes are not an indication for thrombolytics.
Other answers that could be right if they were choices GPIIb/IIIa inhibitors, such
as eptifibatide, tirofiban, or abciximab, or the use of angioplasty/PCI.
Basic Science Correlate
Mechanism of Heparin
Heparin potentiates the effect of antithrombin. Antithrombin actually inhibits almost
every step of the clotting cascade. This is why it does not work with antithrombin
deficiency. Heparin only prevents new clots from forming.
Chronic Angina
Office-based cases of further management will emphasize the same issues
mortality benefit.
Thrombolytics are only used if there is ST segment elevation or a new LBBB within
12 hours of the onset of chest pain.
ARBs are used interchangeably with ACE inhibitors, especially if the patient has
a cough with ACE inhibitors. Both ACE and ARBs cause hyperkalemia.
Treatment
Aspirin and metoprolol are the 2 main routinely indicated medication because of
their benefit on mortality. Nitrates should be used for those with angina pain but
they do not lower mortality.
ACE inhibitors and ARBs should only be used in further management for stable
cases if the question describes any of the following:
•
•
•
Congestive failure
Systolic dysfunction
Low ejection fraction
Coronary angiography is predominately used to determine who is a candidate
for coronary artery bypass grafting (CABG). You do not need to do angiography
to diagnose CAD. Stress test can show “reversible ischemia.” However, you must
do angiography to see who needs CABG.
You do not need to do angiography to initiate the following:
•
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•
•
•
•
Aspirin + metoprolol (mortality benefit)
Nitrates (pain)
ACE/ARB (low ejection fraction)
Clopidogrel, prasugrel, or ticagrelor (acute MI or can not tolerate aspirin)
Statins
If pain persists, add ranolazine or ivabradine
Answer: The main difference between saphenous vein grafts and internal
mammary artery grafts is that vein grafts start to become occluded after 5 years
but internal mammary artery grafts are often patent at 10 years. There is no
difference in the need for medications.
Indications for CABG:
•
•
•
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Three coronary vessels with> 70 percent stenosis
Left main coronary artery stenosis > 50–70 percent
2 vessels in a diabetic
2 or 3 vessels with low ejection fraction
Ranolazine:
• Anti-angina med
• Added if other meds do not control pain
Lipid Management
The single strongest indication for lipid-lowering therapy is for a statin in a patient
with an acute coronary syndrome. The goal of therapy in those with CAD is an
LDL < 70. You will answer “statin therapy” for any case of CAD or an equivalent
with an LDL > 100. Anyone with an acute coronary syndrome needs to be on a
statin. The entire concept of “goal directed” therapy to a specific LDL is not clear
at this time.
If a question requests for the LDL goal in a patient with CAD and diabetes, the
answer is LDL goal at least < 70.
There are also other risk factors to consider. If the 10-year risk of CAD is > 7.5%,
your answer is a statin.
Risk factors in lipid management:
•
•
Tobacco use (cigarette smoking)
High blood pressure (≥ 140/90 mm Hg or on blood pressure medication)
•
•
•
Low HDL cholesterol (< 40)
Family history of early coronary heart disease (female relatives < 65, male
relatives < 55)
Age (males ≥ 45, females ≥ 55)
Answer: The statins have a greater effect on lower mortality compared with the
other medicines. Recent guidelines will be further clarified over time. Give statins if
the 10-year risk is > 7.5%.
Coronary artery disease equivalents:
•
•
•
•
Diabetes mellitus
Peripheral artery disease
Aortic disease
Carotid disease
Answer: The goal of LDL can be < 70 for patients at the very highest risk of
infarction. This includes those with acute coronary syndromes or the combination
of coronary disease and a very severe risk factor, such as diabetes.
The most common adverse effect of statin medications is liver toxicity. As many
as 1 percent of patients will stop a statin because of its effect on raising
transaminases. Liver function tests should be routinely checked. Rhabdomyolysis
is not the most common adverse effect. There is no routine indication to check
CPK levels.
PCSK9 Inhibitors
Evolocumab and alirocumab inhibit proprotein convertase subtilisin kexin type 9
(PCSK9). PCSK9 blocks the clearance of LDL by the liver from the blood, PCSK9
inhibitors can bring down enormously elevated levels of LDL in familial
hypercholesterolemia. They massively increase hepatic clearance of LDL but they
do not lower mortality. PCSK9 inhibitors are injectable medications. They are the
answer when the question says a statin is used at the maximum dose and the LDL
is not controlled in severe hyperlipidemia.
Summary of Lipid Management
Overall, the standards for the management of hyperlipidemia are in a state of
change. The clear answers are:
•
•
•
•
•
•
Statins are by far superior to any other drug.
Every patient with coronary disease and stroke should be on a statin.
Most patients with diabetes should be on a statin.
If the question says “> 10% ten-year risk,” then answer “a statin.” It is likely
the answer with > 7.5% as well.
Goal-directed therapy to a particular LDL is not clear.
PCSK9 inhibitors bring the LDL down but the mortality benefit is not clear.
Sex and the Heart
Answer: Anxiety is the most common cause of erectile dysfunction postinfarction.
Although beta blockers may be the most common medication associated with
erectile dysfunction, anxiety is still a more common cause of erectile dysfunction
than beta blockers.
Answer: Nitrates are contraindicated when medications such a sildenafil are to be
used. When used at the same time, they can cause a dangerous level of
hypotension.
Congestive Heart Failure (CHF)
The mechanism that matters for congestive failure has to do with the difference in
treatment between systolic dysfunction with a low ejection fraction and
diastolic dysfunction and a normal ejection fraction. There is no clear way to
distinguish systolic from diastolic dysfunction from symptoms alone. Clues in the
history are hypertension, valvular heart disease, and myocardial infarction.
CHF present with shortness of breath, particularly on exertion, in person with any
of the following:
•
•
•
•
•
•
•
•
Edema
Rales on lung examination
Ascites
Jugular venous distention
S3 gallop
Orthopnea
Paroxysmal nocturnal dyspnea
Fatigue
S3: Splash
S4: Bang
Basic Science Correlate
Mechanism of Rales
Increased hydrostatic pressure develops in the pulmonary capillaries from left heart
pressure overload. This causes transudation of liquid into the alveoli. During
inhalation, the alveoli open with a “popping” sound referred to as rales
Pulmonary Edema
Answer: Oxygen, furosemide, nitrates, and morphine are the mainstay of therapy
for acute pulmonary edema. Although they are not associated with a concrete
mortality benefit, they are the standard of care for pulmonary edema, which is the
worst manifestation of CHF. Removing volume from the vascular system and,
therefore, the lungs is more important than any form of diagnostic testing.
Pulmonary edema is a clinical diagnosis. Shortness of breath, rales, S3, and
orthopnea are more important in establishing the diagnosis than any single test.
CCS Tip: On CCS, move the clock forward no more than 15–30 minutes at a time
for acutely unstable ICU or emergency department patients.
Basic Science Correlate
Mechanism of Carvedilol
Carvedilol is an antagonist of both beta-1 and beta-2 receptors as well as alpha-1
receptors. This makes it anti-arrhythmic, anti-ischemic, and antihypertensive.
Diagnostic Testing
All of the following should be ordered on the first screen on the CCS portion of the
exam. They should be ordered with the initial therapy (i.e., with the oxygen,
furosemide, nitrates, and morphine).
Initial Tests to Be Ordered
Chest x-ray
EKG
Oximeter (consider ordering arterial
blood gases [ABG])
Echocardiogram
Basic Science Correlate
What the Tests Show
• Pulmonary vascular congestion
• Cephalization of flow
• Effusion
• Cardiomegaly
• Sinus tachycardia
• Atrial and ventricular arrhythmia
• Hypoxia
• Respiratory alkalosis
• Distinguishes systolic from diastolic
dysfunction
Mechanism of "Cephalization" of Flow
The bases or bottom of the lungs are generally more “full” of blood because of
gravity. As fluid builds up in the lungs, it fills the vessels from the bottom to the top,
like a cup filling with water. This moves the fluid towards the head, a process called
“cephalization.”
Mechanisms of Dobutamine, Inamrinone, and Milrinone
Inamrinone and milrinone are phosphodiesterase inhibitors. They increase
contractility and decrease afterload as vasodilators, yielding much the same effect
as dobutamine. Dopamine increases contractility, but dopamine's alpha-1 agonist
activity causes vasoconstriction. This increases afterload.
Mechanism of Respiratory Alkalosis in CHF
Fluid overload causes hypoxia. Hypoxia causes hyperventilation. Hyperventilation
decreases pCO₂. Decreased pCO₂ causes alkalosis. Hence, hypoxia causes
respiratory alkalosis.
Cases of pulmonary edema and myocardial infarction should be placed in the
intensive care unit.
CCS Tip: Pulmonary edema is the perfect example of a CCS in which all the tests
should be ordered at the same time as the treatment.
Further Management
The vast majority of patients with pulmonary edema will respond to preload
reduction alone to control the acute symptoms.
In a small number of patients, acute management with a positive inotrope will
be necessary. There is no evidence that any positive inotrope or contractility
inducing agent will lower mortality. They are also the answer on a CCS case of
pulmonary edema when furosemide, oxygen, nitrates, and morphine are given and
the patient is still short of breath after the clock is moved forward.
Digoxin is never the right answer as an acute treatment for pulmonary edema.
Digoxin can be used to slow the rate of atrial fibrillation.
Positive Inotropic Agents Used Intravenously in the Intensive Care Unit
Dobutamine (drug of choice)
These are used as further management
Inamrinone
of acute pulmonary edema cases after
the clock is moved forward 30–60
Milrinone
minutes and there is no response to
preload reduction.
Answer: Synchronized cardioversion is used when ventricular tachycardia is
associated with acute pulmonary edema. The same answer would have been
used if the acute pulmonary edema was associated with the onset of atrial
fibrillation, flutter, or supraventricular tachycardia. Unsynchronized cardioversion is
used for ventricular fibrillation or ventricular tachycardia without a pulse. Medical
therapy, such as lidocaine, amiodarone, or procainamide, can be used for
sustained ventricular tachycardia that is hemodynamically stable.
“Synchronized” = Timing with cardia cycle
Answer: Nesiritide is a synthetic version of atrial natriuretic peptide that is
used for acute pulmonary edema as a part of preload reduction. It decreases
symptoms of shortness of breath and is not clearly associated with a reduction in
mortality. There is no clear indication that the answer is nesiritide.
Answer: BNP or brain natriuretic peptide level is a blood test that can be used to
establish a diagnosis of CHF in a patient who is short of breath. If the
presentation is not clear, a BNP level can be used to help distinguish between
pulmonary embolus, pneumonia, asthma, and CHF. BNP level goes up in CHF but
is rather nonspecific normal BNP level excludes CHF.
Answer:
Cardiac
Output
a.
Decreased
Systemic
Vascular
Resistance
Increased
Wedge
Pressure
Right Atrial
Pressure
Increased
Increased
b.
Decreased
Increased
Decreased
Decreased
c.
Increased
Decreased
Decreased
Decreased
d.
Decreased
Increased
Decreased
Increased
Pulmonary edema is associated with a decrease in cardiac output due to pump
failure, which results in the backup of blood into the left atrium and an
increased wedge pressure. There is also an increase in right atrial pressure,
which is the same as saying jugular venous distention. Increases in sympathetic
outflow will increase systemic vascular resistance in an attempt to maintain
intravascular filling pressure. Choice B represents hypovolemic shock, such as
dehydration. Choice C representations septic shock, which is driven by massive
systemic vasodilation, such as from gram-negative sepsis. Choice D represents
pulmonary hypertension.
Basic Science Correlate
Mechanism of Increased Wedge Pressure in CHF
Wedge pressure = Left atrial (LA) pressure
The inflated balloon blocks pressure from behind catheter, making the catheter tip
pick up flow from “in front,” or downstream. “Downstream" for the pulmonary
capillaries means the left atrium.
LV failure = Increased LA pressure = Increased wedge pressure
Chronic Management of CHF
All patients, having been stabilized from acute pulmonary edema, should have an
echocardiogram to establish whether there is systolic dysfunction with a low
ejection fraction or diastolic dysfunction with a normal ejection fraction. Long-term
management of dilated cardiomyopathy or systolic dysfunction is based on the
use of ACE inhibitors, beta blockers, and spironolactone. Diuretics are also
used but have not been proven to lower mortality. Digoxin is used to decrease
symptoms and decrease the frequency of hospitalization but has not been shown
to decrease mortality in congestive failure. ARBs can be used interchangeably with
ACE inhibitors. The beta blockers with evidence for lower mortality in CHF are
metoprolol, carvedilol, and bisoprolol. ACE inhibitors and beta blockers are
indicated for CHF patients with systolic dysfunction at any stage of disease.
Hydralazine combined with nitrates is used if ACE inhibitors and ARBs cannot be
used; hydralazine acts to reduce afterload. Spironolactone lowers mortality but
has only been proved to do so for more advanced, symptomatic disease; any
patient originally presenting with pulmonary edema should get spironolactone.
Spironolactone is anti-androgenic. Spironolactone causes gynecomastia and
erectile dysfunction in men; switch to eplerenone. Eplerenone is a
mineralocorticoid antagonist. Eplerenone lowers mortality in CHF without the antiandrogenic side effects of spironolactone.
The patient is still dyspneic after wine ACE Inhibitors, beta blockers,
diuretics, digoxin, and mineralocorticoid inhibitors.
Answer:
•
Ivabradine: SA nodal inhibitor of “funny channels” that slows the heart rate.
Add it to systolic dysfunction if the pulse is > 70/minute or beta blockers
can't be used. There is mortality benefit with ivabradine.
•
Sacubitril/valsartan: This combination is used instead of an ACE inhibitor.
Sacubitril is added only to an ARB; this neprilysin inhibitor has a mortality
benefit for systolic dysfunction.
Diastolic dysfunction is treated with beta blockers and diuretics. However, you
have to be careful not to overuse diuretics. The benefit of ACE inhibitors for
diastolic dysfunction is not clear. Digoxin and spironolactone definitely do not help
diastolic dysfunction.
Further management of CHF calls for the following treatments:
Systolic Dysfunction (Low Ejection
Fraction)
• ACEI or ARB
• Metoprolol, carvedilol, or bisoprolol
• Spironolactone or eplerenone
• Diuretics
• Digoxin
• Hydralazine/nitrates
Diastolic Dysfunction (Normal
Ejection Fraction)
• Metoprolol, carvedilol, or bisoprolol
• Diuretic
The single most important fact about the “further management” of CHF is that
mortality is decreed by ACE/ARB, beta blockers, and spironolactone. Digoxin
decreases symptoms but does not lower mortality.
Answer: Implantable cardioverter/defibrillators are indicated in dilated
cardiomyopathy. The most common cause of death in CHF is sudden death froIn
arrhythmia. Those with an ejection fraction below 35 percent that persists are
candidates for implantable defibrillator placement.
Answer: Biventricular pacemaker is associated with a decrease in mortality in
those with severe congestive failure with an election fraction < 35 percent and
a QRS duration > 120 msec. This is also referred to as "cardiac resynchronization
therapy.”
If the patient is still short of breath and QRS is wide (> 120), then resynchronize
with a biventricular pacer.
Basic Science Correlate
Mechanism of Biventricular Pacemaker
Wide QRS means ventricles not beating together. Ventricles not beating together
means inefficient forward flow, like trying to hop on one leg. Biventricular pacemaker
means both ventricles go back to beating at same time. Effect instant.
Answer: There is no place for routine anticoagulation with warfarin, no matter how
low the ejection fraction may be in CHF in the absence of a clot of chronic atrial
fibrillation. Warfarin is a wrong answer for CHF.
Answer: Symptomatic bradycardia is an absolute contraindication for the use of
beta blockers. The overwhelming majority of patients with peripheral artery disease
can still use beta blockers. In a patient with a myocardial infarction, the mortality
benefit of metoprolol far exceeds the risk of its use when asthma, emphysema, or
peripheral artery disease is present. Two thirds of asthma patients can tolerate
beta blockers.
Valvular Heart Disease
All valvular heart disease presents with shortness of breath as the chief
complaint. Look for the phrase “worse with exertion or exercise.” Hypertension,
myocardial infarction, ischemia, increasing age, and rheumatic fever will be in the
history but, with the exception of rheumatic heart disease, are probably too
nonspecific to give you the diagnosis. Young patients with valvular heart disease
will have mitral valve prolapse, hypertrophic obstructive cardiomyopathy, mitral
stenosis, or bicuspid aortic valves.
Following are clues to the diagnosis:
Clue to Diagnosis
Young female, general population
Likely Diagnosis
Mitral valve prolapse
Healthy young athlete
Hypertrophic obstructive
cardiomyopathy (HOCM)
Mitral stenosis
Immigrant, pregnant
Turner’s syndrome, coarctation of aorta Bicuspid aortic valve
Palpitations, atypical chest pain not
with exertion
Mitral valve prolapse
Physical Findings
All valvular heart disease can be expected to have murmurs and rales on lung
exam. Possible findings on exam are as follows:
•
•
•
Peripheral edema
Carotid pulse finds
Gallops
Therefore, when you suspect valvular disease, select the cardiovascular, chest,
and extremities portion of the physical exam.
Murmurs
The most difficult important aspect for the exam is the part of the valvular heart
disease section that concerns understanding auscultation, particularly the effects
of various maneuvers on these murmurs. Systolic murmurs are most commonly
aortic stenosis, mitral regurgitation, mitral valve prolapse, and hypertrophic
obstructive cardiomyopathy (HOCM). Diastolic murmurs are most commonly
aortic regurgitation and mitral stenosis. All right-sided murmurs increase in
intensity with inhalation. All left-sided murmurs increase with exhalation.
Murmur intensity
increases with…
Side of murmur
Exhalation
Inhalation
Left
Right
Associated disease
Mitral and aortic valve
lesions
Both stenosis and
regurgitation of tricuspid
valves
Effects of Valsalva, Standing, Squatting, and Leg Raise
Maneuvers predominately affect the volume of blood entering the heart. Squatting
and lifting the legs in the air increase venous return to the heart. Valsalva
maneuver and standing up suddenly decrease venous return to the heart.
Valsalva maneuver is exhaling against a closed glottis, like bearing down a bowel
movement or blowing against a thumb stuck in the mouth. This increases
intrathoracic pressure, which decreased blood return to the heart.
When suddenly squat, you are squeezing the veins of the legs, which are rather
large. This essentially squeeze blood up into the heart like squeezing on a tube
of toothpaste. For those too weak to squat suddenly, the physician can lift up the
legs. This has the same effect as squatting, which is to drain blood into the chest
from the lower extremities.
The majority of murmurs increase in intensity with squatting and leg raise. Aortic
stenosis (AS), aortic regurgitation (AR), mitral stenosis (MS), mitral regurgitation
(MR), and all right-sided heart lesions will become louder with squatting and leg
raising. The only two murmurs that become softer with these maneuvers are mitral
valve prolapse (MVP) and hypertrophic obstructive cardiomyopathy (HOCM).
The following table shows the effect of venous return on murmurs.
Aortic stenosis (AS)
Effects of Change in
Venous Return
Increase (squat, leg
raise)
Increased murmur
Effects of Change in
Venous Return
Decrease (stand,
Valsalva)
Decreased murmur
Aortic regurgitation (AR)
Increased murmur
Decreased murmur
Mitral stenosis (MS)
Increased murmur
Decreased murmur
Mitral regurgitation (MR)
Increased murmur
Decreased murmur
Ventricular septal detect
(VSD)
Hypertrophic obstructive
cardiomyopathy (HOCM)
Mitral valve prolapse
(MVP)
Increased murmur
Decreased murmur
Decreased murmur
Increased murmur
Decreased murmur
Increased murmur
Valvular lesion
Effects of Handgrip and Amyl Nitrate
Handgrip is a maneuver that increases afterload by compressing the arteries of
the arm by contracting the muscles of the arm. Handgrip does not significantly
increase venous return to the heart: the veins of the arms are not as large as those
of the legs, so compressing them does not make much difference in venous return
to the heart. Handgrip, because it increase afterload, essentially functions as the
opposite of an ACE inhibitor, worsening the murmurs of conditions that would
get better with an ACE inhibitor. For instance, AR and MR are treated with ACE
inhibitors, because afterload reduction increases the forward flow of blood into the
aorta. Handgrip will, therefore, worsen AR and MR murmurs by pushing blood
back into the heart. Handgrip will make the murmurs of AR and MR louder and
more intense. The same is true for VSD. Handgrip worsens the murmur of VSD,
because more blood now goes from the left ventricle into the right ventricle.
Amyl nitrate is a vasodilator that decreases afterload by dilating peripheral
arteries. Amyl nitrate has the opposite effect of handgrip. Giving amyl nitrate is
like giving an ACE inhibitor or ARB. If handgrip worsens AR and MR, then amyl
nitrate improves AR and MR.
Handgrip improvements or lessens the murmurs of MVP and HOCM. The
murmurs of MVP and HOCM lessen when the left ventricular chamber is larger or
more full. What happens to the size of the left ventricular (LV) chamber if there is
increased afterload? The LV chamber will not empty and, therefore, the LV will be
larger. A larger LV chamber relieves or lessens the obstruction in HOCM.
Amyl nitrate will do the opposite. It increases ventricular emptying and, therefore,
decrees the size of the LV. Amyl nitrate worsens the murmurs of MVP and
HOCM by increasing the obstruction and the degree of prolapse of the valves in
MVP.
The effect of handgrip and amyl nitrate on aortic stenosis can be hard to
understand. Handgrip softens the murmur of aortic stenosis. This happens by
preventing blood from leaving the ventricle; you can't have a murmur if blood is not
moving. If afterload goes up, blood can't eject from the LV, and the AS murmur will
soften. Another way of saying it is that the murmur of AS is based on the gradient
between the LV and the aorta. If the LV pressure is greater than the aorta pressure,
then the gradient or difference is high. The higher the gradient, the louder the
murmur and the more sever the AS is considered. Handgrip increases pressure in
the aorta; therefore, the gradient or difference between the LV and aorta
decreases. Handgrip is like covering up a trombone or trumpet. You can't produce
music if you put a hand over the front of a wind instrument.
Amyl nitrate has exactly the opposite effect on AS compared to handgrip. Amyl
nitrate decreases afterload and decreases the pressure in the aorta, thus
increasing the gradient between LV and aorta and worsening (making louder)
the murmur of AS.
Mitral stenosis (MS) is little affected by either handgrip or amyl nitrate. These
generally do not affect ventricular filling, which is the major component of MS. ACE
inhibitors, likewise, have very little effect on MS.
Aortic stenosis (AS)
Effect on Murmur
Volume
Handgrip (Increased
Afterload)
Decrease
Effect on Murmur
Volume
Amyl Nitrate
(Decreased Afterload)
Increase
Aortic regurgitation (AR)
Increase
Decrease
Mitral stenosis (MS)
Negligible effect
Negligible effect
Mitral regurgitation (MR)
Increase
Decrease
Ventricular septal detect
(VSD)
Hypertrophic obstructive
cardiomyopathy (HOCM)
Mitral valve prolapse
(MVP)
Increase
Decrease
Decrease
Increase
Decrease
Increase
Valvular Lesion
Location and Radiation of Murmurs
One of the main clues to the identity of a murmur is the location at which the
murmur is heard.
•
•
•
•
Aortic stenosis is heard best at the second right intercostal space and
radiates to the carotid arteries. It is classically described as a crescendo
decrescendo murmur.
Pulmonic valve murmurs are heard at the second left intercostal space.
Aortic regurgitation and tricuspid murmurs, as well as VSD murmurs,
are heard at the lower left sternal border.
Mitral regurgitation (MR) is heard at the apex and radiates into the axilla.
The apex is at the level of the 5th intercostal space, below the left nipple.
Intensity of Murmurs
•
•
•
•
•
I/VI: Only heard with special maneuvers (e.g., Valsalva, handgrip)
II/VI and III/VI: Majority of murmurs; no objective difference between them
IV/VI: Thrill present (a thrill is a palpable vibration you can feel from severe
valve lesion)
V/VI: Can be heard with stethoscope partly of the chest
VI/VI: Stethoscope not needed to hear it
Diagnostic Testing
The best initial diagnostic test for valve lesions on single best answer questions is
an echocardiogram. The most accurate test is a left heart catheterization. This
can also measure pressure gradients, such as in aortic stenosis, most accurately.
On CCS cases, you should also add an EKG and chest x-ray for valvular lesion
assessment.
Treatment
Regurgitant lesions are best treated with vasodilator therapy, such as ACE
Inhibitors, ARBs, or nifedipine. Afterload reduction will slow the profession of
regurgitant lesions. If handgrip makes it worse, then ACE inhibitors are the “most
effective medical therapy.” If the patient still progresses despite medical therapy,
then surgical replacement of the valve should be preformed. Valve replacement
with a catheter can be done in some patients.
Order transthoracic echocardiography (TTE) first on CCS. Then order a
transesophageal echocardiogram (TEE) if the TTE is not fully diagnostic.
Stenotic lesions are best treated with anatomic repair. Mitral stenosis should
undergo balloon valvuloplasty, even if the patient is pregnant. Aortic stenosis that
is severe must be surgically replaced. Aortic valve replacement is well tolerated
even in the very old. Diuretics can decrease pulmonary vascular congestion with
stenotic lesions, but they are not as effective or important as anatomical repair.
•
•
Valsalva improvements murmur = Diuretics indicated
Amyl nitrate improvements murmur = ACE inhibitor indicated
Valvular Lesion
Aortic stenosis (AS)
Standing/Valsalva
Decrease
Diuretics Indicated
Yes (replace best)
Aortic regurgitation (AR)
Decrease
Yes
Mitral stenosis (MS)
Decrease
Yes (balloon best)
Mitral regurgitation (MR)
Decrease
Yes
Ventricular septal detect
(VSD)
Hypertrophic obstructive
cardiomyopathy (HOCM)
Mitral valve prolapse
(MVP)
Decrease
Yes
Increase
No
Increase
No
Valvular Lesion
Aortic stenosis (AS)
Amyl Nitrate
Increase
ACE Inhibitor Indicated
No
Aortic regurgitation (AR)
Decrease
Yes
Mitral stenosis (MS)
Negligible effect
No
Mitral regurgitation (MR)
Decrease
Yes
Ventricular septal detect
(VSD)
Decrease
Yes
Hypertrophic obstructive
cardiomyopathy (HOCM)
Mitral valve prolapse
(MVP)
Increase
No
Increase
No
Aortic Stenosis (AS)
Aortic stenosis most commonly present with chest pain. Syncope and CHF are
less common presentations. The patient will be older and often has a history of
hypertension. Coronary artery disease will be present in as many as 50 percent of
patients.
Prognosis is as follows:
•
•
•
Coronary disease: 3- to 5- year average survival
Syncope: 2- to 3- year average survival
CHF: 1.5- to 2- year average survival
Basic Science Correlate
Mechanism of Syncope/Angina in AS
In AS, a stiff valve just proximal to the entry point of coronaries blocks blood flow
into the vertebral and basilar arteries and carotids. No flow to brain = Passing out.
Thus, AS causes LV hypertrophy. LV hypertrophy = Increased demand.
AS = Blocked flow with increased demand = Chest pain
Physical Exam
Choose the cardiovascular (CV) exam, chest, and extremities.
AS gives a crescendo-decrescendo systolic murmur. The murmur will be heard
best at the second right intercostal space and radiate to the carotid arteries. The
murmur will increase in intensity with leg raising, squatting, and amyl nitrate. The
murmur will decrease with Valsalva, standing, and handgrip. The case may
describe delayed carotid upstroke as well.
Normal aortic valve gradient is zero.
Basic Science Correlate
Mechanism of Crescendo/Decrescendo Murmur of AS
The first part of the Cardiac cycle is isovolumetric contraction. With isovolumetric
contraction, no blood moves. No blood moving = No murmur. Peak flow occurs in
mid-systole. Peak flow = Peak noise. Here, AS yields a diamond-shaped crescendodecrescendo murmur.
Diagnostic Testing
The transthoracic echocardiogram (TTE) is the best initial diagnostic test. A
transesophageal echocardiogram (TEE) is more accurate. Left heart
catheterization is the most accurate diagnostic test and allows the most accurate
method of assessing the pressure gradient across the valve. Mild disease is a
gradient < 30 mm Hg. Moderate disease is indicated by 30–70 mm Hg, and severe
disease is indicated by a gradient > 70 mm Hg. For CCS cases, also choose an
EKG and a chest x-ray, which will show left ventricular hypertrophy.
Treatment
Diuretics are the best initial therapy but will not alter long-term prognosis. Further,
overdiuresis is dangerous, and use of diuretics needs to be very judicious.
The treatment of choice is valve replacement. Bioprosthetic valves (porcine,
bovine) will last 10 years on average, but do not require anticoagulation with
warfarin. Mechanical valves do not have to be replaced as often, but must also be
treated with warfarin to an INR of 2—3. Valve replacement is well tolerated, even in
the elderly. Valve replacement by catheter is done when a patient can’t tolerate
surgery.
Balloon dilate AS only if the patient is to sick to go surgery.
Mechanical values can wear out after 15-20 years.
Aortic Regurgitation (AR)
Hypertension, rheumatic heart disease, endocarditis, and cystic medial
necrosis cause AR. Rarer causes are Marfan’s syndrome, ankylosing spondylitis,
syphilis, and reactive arthritis. Reactive arthritis is an inflammatory arthritis tis of
large joints, inflammation of the eyes (conjunctivitis and uveitis), and urethritis,
previously commonly referred to as Reiter's syndrome. Shortness of breath and
fatigue are the most common presentation.
Physical Exam
Choose the cardiovascular (CV) exam, chest, and extremities.
The murmur of AR is a diastolic decrescendo murmur heard best at the left
stern border. There are several unique physical findings that are rarely seen with
AR. The murmur will increase in intensity with leg raising, squatting, and handgrip.
•
•
•
Quincke pulse: Arterial or capillary pulsations in the fingernails
Corrigan's pulse: High bounding pulses (also known as a “water-hammer
pulse”)
Musset's sign: Head bobbing up and down with each pulse
•
•
Duroziez's sign: Murmur heard over the femoral artery
Hill sign: Blood pressure gradient much higher in the lower extremities
Diagnostic Testing
TTE is the best initial diagnostic test. TEE is more accurate. Left heart
catheterization is the most accurate test. For CCS cases, also choose an EKG
and a chest x-ray, which will show left ventricular hypertrophy.
Treatment
ACE inhibitors, ARBs, and nifedipine are the best initial therapy. For CCS
cases, you should add a loop diuretic, such as furosemide. Surgery is the answer
when the ejection fraction drops below 55 percent or the left ventricular end
systolic diameter goes above 55 mm; surgery should be done in patients with
these criteria even if they are asymptomatic.
Basic Science Correlate
Why Does High Pressure Dilate the Aortic Valve?
The law of LaPlace says: The wall tension, or force dilating a vessel, is proportionate
to the radius of the vessel times the pressure on the inside.
Tension = Radius x Pressure
The wider a vessel is, the faster it will get dropped apart. Here, the more the aortic
ring of aorta is dilated, the faster it will get folded apart. Likewise, the higher the
interior pressure, the faster the interior will be pulled apart. This force of being
“pulled apart,” or dilation, is called “wall tension” in the law of LaPlace.
ACE and ARB drugs vasodilate peripheral arterioles. Lower pressure = Lower wall
tension.
Mitral Stenosis (MS)
Rheumatic fever is the most common cause of MS. Look for an immigrant
patient because of the low rates of rheumatic fever in the United States. Also look
for a pregnant patient because of the large increase in plasma volume with
pregnancy. Special features of MS are as follows:
•
•
•
Dysphagia: Large left atrium pressing on the esophagus
Hoarseness: Pressure on recurrent laryngeal nerve
Atrial fibrillation leading to stroke
Basic Science Correlate
Mechanism of Increased MS Symptoms in Pregnant Women
Pregnant women have a 50 percent increase in plasma volume. More volume with
the same valve diameter Tears more pressure, backflow, and symptoms. Pregnancy
also changes the hypothalamic osmolar receptors. ADH levels stay higher in
pregnancy, so the collecting duct absorbs more free water.
Physical Exam
Choose the cardiovascular (CV) exam, chest, and extremities.
The murmur of MS is a diastolic rumble after an opening snap, which can be
described as an “extra sound” in diastole. The S1 is louder. As the mitral stenosis
worsens, the opening snap moves closer to S2. The murmur will increase in
intensity with leg raising, squatting, and expiration.
Basic Science Correlate
Mechanism of Opening Snap Earlier in Worsening MS
The mitral valve opens when LA pressure > LV pressure. Worse MS = Higher LA
pressure. Higher LA pressure pushes the mitral valve open earlier.
Diagnostic Testing
TTE is the best initial diagnostic test. TEE is more accurate. Left heart
catheterization is the most accurate test. For CCS cases, also choose an EKG
and a chest x-ray, which will show left atrial hypertrophy. On chest x-ray, there is
straightening of the left heart border and elevation of the left mainstem
bronchus. There may also be a description of a double density in the cardiac
silhouette (from left atrial enlargement).
Treatment
Diuretics are the best initial therapy. They do not alter progression. Balloon
valvuloplasty is the most effective therapy. Pregnant women can and should be
readily treated with balloon valvuloplasty. Pregnancy is not a contraindication to
valvuloplasty.
Basic Science Correlate
Balloon valvuloplasty works in MS because the stenosis results from excess fibrosis
of the valve. Rheumatic fever causes cardiac endomyocardial and valvular fibrosis.
Fibrosis can be stretched by the balloon. By contrast, aortic stenosis is calcified,
and calcification does not stretch or rip easily with a balloon.
MS = Balloon fibrosis
AS = Remove/replace calcification
Mitral Regurgitation (MR)
MR is caused by hypertension, ischemic heart disease, and any other
condition that leads to the dilation of the heart. You cannot have dilation of the
heart without the mitral valve leaflets separating. Dyspnea on exertion is the most
common symptom.
Physical Exam
Choose the cardiovascular (CV) exam, chest, and extremities.
S3 gallop is associated with fluid overload states, such as congestive heart failure
or mitral regurgitation. An S3 can be normal in patients under the age of 30.
The murmur of MR holosystolic and obscures both S1 and S2. MR is heard
best at the apex and radiates to the axilla. The murmur increases in intensity
with leg raising, squatting, and handgrip. Standing, Valsalva, and amyl nitrate
decrease the intensity S3 gallop is often present.
Diagnostic Testing
TTE is the best initial diagnostic test for MR. TEE is more accurate.
Treatment
ACE inhibitors, ARBs, and nifedipine are the best initial therapy and the
medications most likely to decrease the rate of progress of the disease. For CCS
cases, you should add a loop diuretic, such as furosemide. Surgery is the answer
when the left ventricular ejection fraction drops below 60 percent or the left
ventricular end systolic diameter goes above 40 mm. Surgery should be done in
patients with these criteria even if they are asymptomatic. Surgery can be valve
repair or replacement. Repair means placing clips or sutures on the valve to tighten
it up.
The operative criteria for regurgitant lesions in asymptomatic patients are as
follows (repair is preferred to replacement):
Ejection fraction
Left ventricular end
systolic diameter
Aortic Regurgitation
< 55%
Mitral Regurgitation
< 60%
> 55 mm
> 40 mm
Ventricular Septal Defect (VSD)
Asymptomatic patients may present with only a holosystolic murmur at the
lower left sternal border. Larger defects leads to shortness of breath. The
murmur worsens with exhalation, squatting, and leg raise.
Diagnostic Testing
Echocardiography is the diagnostic test to use first, but catheterization is used
to determine the degree of left-to-right shunting most precisely.
Treatment
Mild defects can be left without mechanical closure.
Atrial Septal Defect (ASD)
Small ASDs are asymptomatic. Larger ones may lead to shortness of breath or
signs of right ventricular failure, such as shortness of breath and a parasternal
heave. The most frequently tested knowledge is that ASD is associated with
fixed splitting of S2.
Basic Science Correlate
Mechanism of Fixed Splitting of S2 in ASD
S2 splitting is caused by different pressures on different sides of heart. Same
pressure on both sides means no splitting.
LA/RA pressure no change in respiration = No change in splitting
Diagnostic Testing
Diagnose with an echocardiogram.
Treatment
Percutaneous or catheter devices are the best therapy. Repair is most often
indicated when the shunt ratio exceeds 1.5 to 1.
Splitting of S2
Wide, P2 Delayed
• Right bundle branch
block
• Pulmonic stenosis
• Right ventricular
hypertrophy
• Pulmonary hypertension
Paradoxical, A2
Delayed
• Left bundle branch
block
• Aortic stenosis
• Left ventricular
hypertrophy
• Hypertension
Cardiomyopathy
Dilated Cardiomyopathy
Fixed
ASD
Dilated cardiomyopathy presents and is managed in the same way as the case
of CHF described above.
Diagnostic Testing
Echocardiography is the best initial test to determine the ejection fraction and
look for wall motion activity. MUGA or nuclear ventriculography is the most
accurate method of determining ejection fraction.
Treatment
Besides ischemia, the most common causes of dilated cardiomyopathy are
alcohol, adriamycin, radiation, and Chagas’ disease. The treatment for all forms
of dilated cardiomyopathy, no matter their cause, is with ACE inhibitors, ARBs,
beta blockers, and spironolactone. Spironolactone and eplerenone are
mineralocorticoid or aldosterone antagonists. They are used to decrease the work
of the heart; they are not given for their diuretic effect. Spironolactone is antiandrogenic and inhibits testosterone. Eplerenone does not inhibit androgens.
Digoxin decreases symptoms but does not prolong survival. Ivabradine is a
sodium funny channel blocking the SA node. Add ivabradine if the heart rate is >
70 after the use of beta blockers.
Hypertrophic Cardiomyopathy
This condition presents with shortness of breath on exertion and an S4 gallon
on examination.
S4 gallop is a sign of left ventricular hypertrophy and decreased compliance or
stiffness of the ventricle. S4 gallop does not automatically indicate the need for
additional therapy.
Diagnostic Testing
Echocardiography shows a normal ejection fraction.
Treatment
The mainstay of therapy is with beta blockers and diuretics. ACE inhibitors can
be used, but their benefit is not as clear. Digoxin and spironolactone do not benefit
hypertrophic cardiomyopathy.
Restrictive Cardiomyopathy
Restrictive cardiomyopathy presents with a history of sarcoidosis, amyloidosis,
hemochromatosis, cancer, myocardial fibrosis, or glycogen storage diseases.
Shortness of breath is the main presenting complaint in all forms of
cardiomyopathy. Kussmaul's sign is present: this is an increase in jugular venous
pressure on inhalation.
Diagnostic Testing
Cardiac catheterization shows rapid x and y descent. The EKG shows low
voltage. Echocardiography is the mainstay of diagnosis Endomyocardial biopsy
is the single most accurate diagnostic test of the etiology.
Amyloid:
• Low-voltage EKG
• Speckled pattern on echo
Treatment
Diuretics and correcting the underlying cause are the best treatments.
Takotsubo Cardiomyopathy
This is a rare, sudden systolic dysfunction brought on by extreme emotions. Look
for a vignette involving a postmenopausal woman with sudden psychological
stress. Takotsubo cardiomyopathy presents like acute myocardial infarction with
ventricular dysfunction. Coronary arteries are normal.
Treatment
Treat the patient with ACE inhibitors, diuretics, and beta blockers—as in any
other ventricular failure. If there is no acute death, the patient recovers in a few
weeks.
Pericardial Disease
Pericarditis
Chest pain that is pleuritic (changes with respiration) and positional (relieved by
sitting up and leaving forward) is the presentation that is most often given on Step
3. The pain will be described as sharp and brief. Ischemic pain is dull and sore,
like being punched. The vast majority of pericarditis cases are viral. Although any
infectious agent, collagen-vascular disease, or trauma that can be in the history,
remember that Step 3 most often hands you a clear diagnosis and asks what you
want to do about it, such as testing and treatment.
Physical Exam
The only pertinent positive finding is a friction rub, which can have 3 components.
The rub is only present in 30 percent of patients. There is no pulsus paradoxus,
tenderness, edema, or Kussmaul's sign present. Blood pressure is normal, and
there is no jugular venous distention of organomegaly.
Diagnostic Testing
The best initial test is the EKG. ST segment elevation is present everywhere (all
leads). PR segment depression is pathognomonic in lead II, but is not always
present.
Treatment
The best initial therapy is an NSAID, such as indomethacin, naproxen, aspirin or
ibuprofen combined with colchicine. Advance the clock 1–2 days and have the
patient visit the office. If the pain persists, add prednisone orally to the treatment
and advance the clock 1–2 more days. Colchicine adds efficacy to NSAIDs and
prevents recurrent episodes.
Pericardial Tamponade
Tamponade presents with shortness of breath, hypotension, and jugular
venous distention. On CCS, also examine the lungs, because they will be clear.
Following the unique features of tamponade:
•
•
Pulsus paradoxus: This is a reduction of blood pressure > 10 mm Hg on
inhalation.
Electrical alternans: This is alterations of the axis of the QRS complex on
EKG, manifested as the height of the QRS complex.
Basic Science Correlate
Mechanism of Pulsus Paradoxus
Inhalation increases venous return. Increased venous return expands the right
ventricle (RV). Expanded RV compresses the left ventricle (LV). Compressed LV
decreases blood pressure. Tamponade compresses the whole heart.
Inhale = Big RV = Smaller LV = BP drop > 10 mm Hg
Diagnostic Testing
Echocardiography is the most accurate diagnostic test. The earliest finding of
tamponade is diastolic collapse of the right atrium and right ventricle.
Remember that it is normal to have 50 ml or less of pericardial fluid, but there
should be no collapse of the cardiac structures.
EKG will show low voltage and electrical alternans. Electrical alternans is
variation of the height of the QRS complex from the heart moving backward and
forward in the chest.
Right heart catheterization will show “equalization” of all the pressures in the
heart during diastole. The wedge pressure will be the same as the right atrial and
pulmonary artery diastolic pressure.
Treatment
•
•
•
Best initial therapy: Pericardiocentesis
Most effective long-term therapy: Pericardial window placement
Most dangerous therapy: Diuretics
Constrictive Pericarditis
Constrictive pericarditis presents with shortness of breath and the following
signs of chronic right heart failure:
•
•
•
•
Edema
Jugular venous distention
Hepatosplenomegaly
Ascites
Following are the unique features of constrictive pericarditis:
•
•
Kussmaul's sign: Increase in jugular venous pressure on inhalation
Pericardial knock: Extra diastolic sound from the heart hitting a calcified,
thickened pericardium
Diagnostic Testing
•
•
•
Chest x-ray: Showing calcification
EKG: Low voltage
CT and MRI: Showing thickening of the pericardium
Treatment
•
•
Best initial therapy: Diuretic
Most effective therapy: surgical removal of the pericardium (i.e.,
pericardial stripping)
Aortic Disease
Dissection of the Thoracic Aorta
Dissection of the thoracic aorta presents with the following symptoms:
•
•
•
Chest pain radiating to the back between the scapula
Pain that can be described as very severe and “ripping”
Difference in blood pressure between right and left arms
Diagnostic Testing
•
Best initial test: Chest x-ray showing a widened mediastinum
•
Most accurate test: CT angiography
Treatment
When the case describes severe chest pain radiating to the back and
hypertension, order beta blockers with the first screen in addition to an EKG and
chest x-ray. No matter what the EKG shows, move the clock forward and order
either CT angiography, TEE, or magnetic resonance angiography (MRA): all 3
are equally accurate.
•
CT angiography = TEE = Magnetic resonance angiography (MRA)
After starting beta blockers, order nitroprusside to control the blood pressure.
Aortic dissection cases should be placed in the ICU, and a surgical consultation
should be ordered. Survival correction is the most effective therapy.
Abdominal Aortic Aneurysm (AAA)
Screening with an ultrasound should be ordered in 65- to 75- year old men who
are current or former smokers.
Abdominal aortic aneurysm is detected by ultrasound first. AAAs are repaired
when they are > 5 cm. Smaller ones are monitored.
Basic Science Correlate
As an aneurysm enlarges, the rate of expansion increases: Wider aorta = Widens
faster.
This principle is expressed in the law of LaPlace: Wall tension = Radius x
Pressure.
Next step: Lower BP and repair with stent or endovascular procedure when the
aneurysm goes above 5 cm.
Peripheral Arterial Disease (PAD)
PAD presents with claudication (pain in the calves on exertion). The case may also
describe “smooth, shiny skin” with loss of hair and sweat glands, as well as
loss of pulses in the feet.
Spinal stenosis will give pain that is worse with walking downhill and less with
walking uphill or while cycling or sitting. Pulses and skin exam will be normal with
spinal stenosis.
Pain + Pallor + Pulseless = Arterial occlusion
Acute arterial embolus will be very sudden in onset with loss of pulse and cold
extremity. It is also quite painful. AS and atrial fibrillation are often in the history for
arterial embolus.
Diagnostic Testing
•
•
Best initial test: Ankle-brachial index (ABI). (A normal ABI should be ≥ 0.9.)
Blood pressure in the legs should be equal to or greater than the pressure in
the arms. If there is > 10 percent difference, then an obstruction is
present.)
Most accurate test: Angiography
Treatment
•
⁃
⁃
⁃
⁃
⁃
⁃
•
•
Best initial therapy:
Aspirin
Blood pressure control with ACE inhibitors
Exercise as tolerated
Cilostazol
Lipid control with statin a target LDL < 100
Vorapaxar, an antiplatelet drug added to aspirin or clopidogrel
Marginally effective therapy: Pentoxifylline
Ineffective therapy: Calcium channel blocker
Beta blockers are not contraindicated with PAD. If the patient needs them for
ischemic disease, they should be used.
Basic Science Correlate
Mechanism of Calcium Blockers: Why They Don’t Work in PAD
In PAD the atherosclerotic obstruction is on the inside the vessel. Calcium blockers
dilate the muscular layer, which is exterior to the atherosclerosis in the center.
Dilating the outer layer does not expand the inside.
CCS Tip: On CCS, move the clock forward several weeks. PAD is not an
emergency! If initial therapies do not work and the pain progresses, or there are
signs of ischemia such as gangrene or pain at rest, then perform surgical bypass.
Rhythm Disorders
Atrial Fibrillation (A-Fib)
A-fib presents with palpitations and an irregular pulse in a person with a history
of hypertension, ischemia, or cardiomyopathy.
Diagnostic Testing
If the initial EKG does not show the answer, a patient in the hospital should be
placed on telemetry monitoring. Outpatients who are hemodynamically stable
should go under Holter monitoring, which is continuous, ambulatory cardiac
rhythm monitoring for 24 hours or longer.
CCS Tip: For CCS cases, other tests to order once A-fib is found on EKG are the
following:
•
•
•
•
Echocardiography: Looking for clot, valve function, and left atrial size
Thyroid function testing: T4 and TSH levels
Electrolytes: Potassium, magnesium, and calcium levels
Troponin or CK-MB levels: These may be appropriate to test in some
acute-onset cases.
Treatment
Unstable patients should go immediately synchronized electrical cardio
version. Unstable patients should be cardioverted with the first screen, without
waiting for TEE or anticoagulation with heparin or warfarin. Instability is defined as
a systolic blood pressure < 90, congestive failure, confusion related to
hemodynamic instability, or chest pain.
Stable patients should have ventricular heart rate slowed if it is > 100–110 per
minute.
Rate control medications are beta blockers (metoprolol, carvedilol), calcium
channel blockers (diltiazem), or digoxin. In the acute setting, such as the
emergency department, these agents should be given intravenously.
Anticoagulation
Once the rate has been controlled, anticoagulation is the next best step in all
patients with an atrial arrhythmia persisting beyond 2 days. If the question does
not state the duration, you are to treat it as if it were persisting for longer than 2
days.
CHADS
C = CHF
H = Hypertension
A = Age > 75
D = Diabetes
S = Stroke or TIA
CHADS score of 0 – 1 needs aspirin. At 2 or more, use warfarin, dabigatran,
rivaroxaban, apixaban.
Stroke/TIA = 2 points
Dabigatran, rivaroxaban, edoxaban, and apixaban are oral anticoagulants with
similar or better efficiency to warfarin but without the required to monitor the INR.
The long-term use of rate control medications, such as metoprolol, diltiazem or
digoxin, combined with anticoagulation is equal or better than cardioversion with
electricity or medicines.
Routine cardioversion of trial fibrillation is not indicated.
CHADS₂ (CHF, hypertension, age > 75, diabetes, or stroke/TIA) is a screening
system to indicate the need for anticoagulation. A score of 2 or more means
warfarin, apixaban, dabigatran, edoxaban, of rivaroxaban. A score of 0 or 1 means
aspirin.
When CHADS₂ is at 2 or more points, control the rate and anticoagulate. Novel oral
anticoagulants (NOACs) such as rivaroxaban, dabigatran, or apixaban become
therapeutic in a few hours: Unlike warfarin, NOACs do not need several days to
reach the therapeutic levels. Even when warfarin is used for atrial fibrillation, there
is no need to bolus the patient with heparin. Why? Because atrial fibrillation is a
long-term disease that takes months or years to develop a risk of stroke, while fulldose heparin carries a risk of bleeding. Just start the warfarin or NOACs. It is safe.
Heparin treatment bridging to the therapeutic warfarin is a wrong answer.
CHADS-VASc means adding points for Vascular disease such as peripheral artery
disease, Age 65–74, and Sex as in female gender. The same cutoff applies: A
score of 2 or more means use a NOAC.
CHADS-VASc
V = vascular disease
A = age 65—74
S = female sex
A score of 2 or more needs anticoagulation.
Anticoagulation in Atrial Arrhythmias
The novel (or new) oral anticoagulants (NOACs) work either by inhibiting factor Xa
(rivaroxaban, apixaban, edoxaban) or by inhibiting thrombin with dabigatran. If
severe bleeding occurs with warfarin, it is reversible with fresh frozen plasma (FFP).
If bleeding occurs with dabigatran, it is reversible with idarucizumab. If bleeding
occurs with the Xa inhibitors, it is reversible with andexanet. What to know about
NOACs:
•
•
•
•
NOACs prevent more stroke than warfarin.
NOACs cause less intracranial bleeding than warfarin.
NOACs decrease mortality more than warfarin in atrial fibrillation.
NOACs treat DVT and PE.
The main indication for warfarin is a patient with atrial fibrillation who have metallic
heart valves.
Idarucizumab reverses dabigatran.
Atrial Flutter (A-Flutter)
Atrial flutter is administered in the same way as atrial fibrillation. The only
difference is that the rhythm is regular on presentation.
The following table shows how to choose the right rate control medication for a-fib
anal a-flutter.
Beta Blockers
(Metoprolol)
• Ischemic heart disease
• Migraines
• Graves disease
• Pheochromocytoma
Calcium Channel
Blockers (Diltiazem)
• Asthma
• Migraine
Digoxin
• Borderline hypotension
Multifocal Atrial Tachycardia (MAT)
This condition presents like an atrial arrhythmia in association with COPD/
emphysema. EKG will show polymorphic P waves, revealing different atrial foci
for the QRS complexes. As the name implies, patients with MAT have tachycardia
(heart rate > 100). MAT manifests as an irregular chaotic rhythm on EKG. Do not
use beta blockers. Give oxygen first, then diltiazem.
Give oxygen first for MAT.
Supraventricular Tachycardia (SVT)
SVT presents with palpitations and tachycardia and occasionally syncope. It is
not associated with ischemic heart disease. SVT has a regular rhythm with a
ventricular rate of 160–180.
Diagnostic Testing
If the EKG does not show SVT, order Holter monitor or telemetry to increase the
sensitivity of detection.
CCS Tip: On CCS, all cases of dysrhythmia should undergo transthoracic
echocardiography (TTE) after the initial set of orders.
Treatment
•
•
•
•
Best initial management for unstable patients: Synchronized cardioversion
Best initial management for stable patients: Vagal maneuvers (carotid sinus
massage, ice immersion of the face, Valsalva)
Next best step in management if vagal maneuvers do not work:
Intravenous adenosine (Note: This is the most frequently asked SVT
question.)
Best long-term management: Radiofrequency catheter ablation
Wolff-Parkinson-White Syndrome (WPW)
WPW presents as SVT that can alternate with ventricular tachycardia (VT). The
other main due to the diagnosis is worsening of SVT after the use of calcium
blockers or digoxin.
Diagnostic Testing
WPW is diagnosed with finding a delta wave on the EKG. The most accurate test
is electrophysiological studies.
Treatment
Treatment is as follows:
•
•
Best initial therapy if the patient is described as being in SVT or VT from
WPW: Procainamide
Best long-term therapy: Radiofrequency catheter ablation
Basic Science Correlate
Mechanism of WPW
There is an abnormal piece of neutralized cardiac muscle going around the AV node
in WPW. This can result in either atrial or ventricular arrhythmia. The slowest
conduct in the heart is the AV node. Conduction in the aberrant tract is faster; that is
why the PR is short (< 120 mSec) and there is a delta wave on EKG. Calcium
channel blockers and digoxin block conduction more in the normal AV and force the
conduction down the abnormal conduction tract.
Ventricular Tachycardia (VT)
VT can present as palpitation, syncope, chest pain, or sudden death.
Diagnostic Testing
You cannot determine that VT is present without an EKG. If the EKG does not
detect VT, then telemetry monitoring should be ordered. The most accurate
diagnostic test is electrophysiological studies.
Treatment
The table below shows therapy options for persistent VT:
Hemodynamically Stable
• Amiodarone
• Lidocaine
• Procainamide
• Magnesium
Hemodynamically Unstable
• Synchronized cardioversion
Torsade de pointes is ventricular tachycardia with an undulating amplitude.
Magnesium should always be given in addition to medical or electrical therapy.
Ventricular Fibrillation (V-Fib)
V-fb presents as sudden death.
Diagnostic Testing
You cannot tell what caused the loss of pulse without an EKG.
Treatment
Treatment of V-fib is always with unsynchronized cardioversion first. Do not
answer intubation first. Dead people are never breathing. If you shock them back
to life, they are more likely to breathe!
When to deliver
electricity:
Unsynchronized
At any point in cycle
Synchronized
Not during the T-wave
Indications:
V-fib, pulseless VT
Everything except V-fib
and pulseless VT
Basic Science Correlate
Mechanism of Need for Synchronization
The T-wave represents the refractory period. An electrical shock delivered during the
T-wave can set off a worse rhythm—specifically, asystole and ventricular fibrillation
are worse than ventricular tachycardia. Do not deliver a shock during the refractory
period.
Unsynchronized cardioversion (defibrillation) is administrated as follows:
1.
2.
3.
4.
5.
6.
7.
Continue CPR
Reattempt defibrillation
Administer IV epinephrine
Reattempt defibrillation
Administer IV amiodarone or lidocaine
Reattempt defibrillation
Repeat several cycles of CPR between each shock
Syncope Evaluation
The management of syncope is based on 3 criteria:
1.
2.
3.
Was the loss of consciousness sudden or gradual?
Was the regaining of consciousness sudden or gradual?
Is the cardiac exam normal or abnormal?
Diagnostic Testing
On the initial screen, order the following:
•
•
•
•
•
•
Cardiac and neurological examination
EKG
Chemistries (glucose)
Oximeter
CBC
Cardiac enzymes (CK-MB, troponin)
Carotid Dopplers are not useful in syncope. A patient cannot pass out from a
carotid embolus.
CCS Tip: Treat special circumstances as follows:
•
If a murmur is present, order an echocardiogram.
•
•
•
If the neurological exam is focal or there is a history of head trauma due
to syncope, order head CT.
If a headache is described, order head CT.
If a seizure is described or suspected, order head CT and EEG.
Basic Science Correlate
Mechanism of Syncope: Caused by Brainstem Stroke Only
The brainstem control sleep and wake in the brain. Only stroke or TIA of the
posterior circulation can cause syncope. Vertebral/basilar circulation is synonymous
with the posterior or brainstorm circulation. There is no place in the circulation of the
middle cerebral artery that can cause syncope.
CCS Tip: On further management, if the diagnosis is not clear after you move the
clock forward to obtain the results of initial tests, order the following:
•
•
•
•
Holter monitor on outpatients
Telemetry monitoring for inpatients
Repeat check of CK-MB and troponin levels 4 hours later
Urine and blood toxicology screens
CCS Tip: On further management, particularly if the etiology is not clear, order the
following:
•
•
Tilt table testing to diagnose neurocardiogenic (vasovagal) syncope
Electrophysiological testing
Exclude cardiac cases of syncope. More than 80% of mortality from syncope is
from cardiac causes.
The Holter monitor is a 24- to 72-hour continuous ambulatory EKG. This is routine
for most patients with syncope requiring admission.
Treatment
Treatment of syncope is based on the etiology. The majority of cases never get a
specific diagnosis. The most important thing to do in syncope is to exclude a
cardiology etiology, such as an arrhythmia. The majority (> 80 percent) of
mortality from syncope involves a cardiac etiology.
If a ventricular dysrhythmias diagnosed as the etiology of syncope, an
implantable cardioverter/defibrillator is indicated.
CCS Tip: Botton line, order the following for syncope:
•
•
EKG
Enzyme: Troponin/CKMB
•
•
Echocardiogram
Head CT