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Cardiology Notes
2.1 Bradyarrhythmias.
First degree AV block. First degree AV block can occur in physiologically normal
individuals. Similar to sinus bradycardia, however, beta blockers and calcium
channel blockers are also possible etiologies to note. Particularly, these patients
are generally asymptomatic with no treatment required.
Second degree AV block (Mobitz Type 1 and Type 2). Mobitz Type 1 block
characteristically happen as a result of beta blockers and/or calcium channel
blockers. Right sided ischemia should be considered as well. Patients are generally
asymptomatic. The treatment generally involve stopping the medications and/or
atropine as clinically indicated. Mobitz Type 2 block results from acute/subacute MI
and or fibrotic diseases of the conduction system. Frequent syncope can be noted.
Progression to third-degree AV block can also be observed as well. Pacemaker
placement is warranted.
Third Degree Block. Here there is no communication between the atria and the
ventricles. As such, patients are generally symptomatic as a result of disjoint heart
function. Pacemaker placement is warranted. (Screen for cardiovascular symptoms
such as chest pain, (pre)syncope, edema, hypotension, among others).
2.2 Tachyarrhythmias.
Atrial Fibrillation. You should have a good differential for atrial fibrillation. A way to
remember it is PIRATES (Pulmonary Diseases, Ischemia, Rheumatic Diseases,
Anemia, Thyroidtoxicosis, Ethanol, and Sepsis). Patient are often asymptomatic.
However, presentation with cardiac symptoms and a irregularly irregular pulse is
possible. You should also have a good approach to management of atrial
fibrillation. Essentially, consider, first, the hemodynamic stability of the patient.
If the patient is not stable, cardioversion is warranted. If the patient is stable, start
the patient on rate control agent, particularly beta blockers and CCBs. These
stable patients, however, should also be considered for possible cardioversion as
well. If the atrial fibrillation happens outside of a 48 hour window (or if the time
period of onset is unknown), a TEE is warranted to rule out thrombus. If thrombus is
present, patients should be anticoagulated for 3 weeks prior to cardioversion. If no
thrombus is present, immediate cardioversion is warranted. Finally, if the atrial
fibrillation happens within a 48 hour window, immediate cardioversion is warranted.
Particularly important also is the decision to start on long term anticoagulation
(warfarin) following atrial fibrillation. For this, we use the CHA 2DS2-VASc score (CHF,
HTN, Age>75 (2 points), Diabetes, Strokes/TIA History (2 points), Vascular Disease,
Age 65-74, Sex Category (Female)). A CHAD2DS2-VASc score of greater than 2
warrants warfarin anticoagulation regimen.
Atrial Flutter.
AVNRT
Congestive Heart Failure is an often tested topic on the QE/EE. You should be
comfortable with the management and pathologic principles of congestive heart
failure. Essentially, we can separate congestive heart failures in systolic or
diastolic heart failure. Systolic Heart Failure is also known as reduced ejection
fraction heart failure with an ejection fraction of <50%. It is labelled as HFrEF.
Diastolic heart failure, on the other hand, is known as preserved ejection fraction
(>50%) heart failure. It is labelled as HFpEF.
It is important also to know that both HFrEF and HFpEF can be either left sided or
right sided. Since most right sided heart failures we will encounter result from left
sided heart failures. We can essentially group it in the following way. HFrEF (1. Left
sided; 2. Right sided from left sided failure). HFpEF (1. Left sided; 2. Right sided
from left sided failure).
Now, what are the symptoms of a left sided only heart failure and what are the
symptoms of the right sided from left sided failure, irrespective of whether the
ejection fraction is reduced or not? Well, we can remember the symptoms by
nothing that left sided failure tends to result in pulmonary congestion and right
sided failure (which, again, tend to result from left sided failure and will therefore
have left sided symptoms also) tends to have peripheral congestion. Pulmonary
congestions imply basilar crackles, pleural effusions, shortness of breath, pulmonary
edema, PND, orthopnea. Peripheral congestions imply elevated JVPs, peripheral
edemas, ascites, sacral edema, among others.
3.1 HFrEF
Reduced ejection fraction heart failure generally is caused by an MI, HTN, valvular
disorders (aortic stenosis, mitral stenosis, or mitral regurgitation), dilated
cardiomyopathy, and myocarditis. It Is important to remember that it is essentially
a result of inadequant contractility and/or increased in cardiac afterload. The heart,
therefore, compensates by undergoing eccentric hypertrophy. Important tests to
considers would be a CXR (cardiomegaly, Kerly B lines, pulmonary edema, pleural
effusions, vascular redistribution known as cephalization), ECG (consideration for
causes), BNP (Brain natriuretic peptide), and Cr (cardio-renal syndrome. The acute
management of HFrEF is LMNOP (furosemide (Lasix), morphine, mitrates, oxygen,
and upright positioning). ACEI can also be considered. Beta blocker should be
AVOIDED in acute decompensated heart failure. Chronic management consists of
lifestyle modifications alongside pharmacologic therapy (Beta blockers, ACEI/ARBs,
Furosemide, ASA/stain if the underlying cause is MI, spironolactone for class III-IV
heart failure).
3.2 HFpEF. This is not as important for the QE/EE. It is only important to
remember that nonsystolic dysfunction is defined by normal systolic function with
normal or elevated ejection fraction as a result of concentric (rather than eccentric)
hypertrophy. Common causes include HTN, valvular disorders (mitral stenosis,
aortic stenosis, aortic regurgitation), restrictive cardiomyopathy (amyloidosis,
sarcoidosis, and hemachromotosis). We will discuss cardiomyopathy in Section 4.
4. Cardiomyopathy.
Acute Coronary Syndrome is an important focus of the QE/EE. It is, first of all,
important to known that there are three kinds of acute coronary syndrome. They
are unstable angina, NSTEMI, and STEMI. Lets start by talking about unstable
angina and NSTEMI.
Unstable angina and NSTEMI are often discussed together in most internal medicine
textbooks because they are frequently indistinguishable on history. They both
present with new onset chest pain, accelerating frequency of chest pains, or chest
pain which occurs at rest. Physical examination would be focused on a well-
performed cardiovascular, respiratory, and peripheral arterial examinations to rule
out secondary problems (such as a resultant heart failure). The key difference
between the two is in diagnostic tests. ECGs are frequently NOT helpful. NSTEMI,
since it signals impending infarction, results in elevation of cardiac enzymes
whereas unstable anginas do NOT. In terms of treatments, I have summarized it
below.
Unstable angina. Short and long term: (ASA, Clopedigrel (CURE Trial), Beta Blocker,
and Nitrate). Short term only (Heparin based on TIMI Score), and MOAN (Morphine,
Oxygen, ASA, and Nitrogen)). It is not important to know the details of the TIMI
Score.
NSTEMI. Short and long term: (ASA and clopedigrel (30 days for metal stent and 12
months for drug eluting stent), ACEI, Beta blockers, statins, and nitrate). Short term
only (Heparin IV and MOAN)
5.2 STEMI
STEMI. Short and long term: (ASA and clopedigrel (30 days for metal stent and 12
months for drug eluting stent), ACEI, Beta blockers, statins, and nitrate). Short term
only (Heparin IV and MOAN). Intervention with PCI should be considered within 90
minutes. Should PCI not be able to be performed within 90 minutes and there are
no contraindications, thrombolytic therapy should be considered instead.
6. Hypertension
It is important for the QE/EE to have a good working plan for hypertension. First of
all, hypertension definitions vary depending on age and comorbid conditions,
particularly chronic kidney disease and diabetes. It is summarized in the JNC8
Guidelines. The details are not particularly important. For all purposes, remember
that a systolic of more than 140 and a diastolic of more than 90 based on three
measurements separated in time defines hypertension in those <60 years of age.
Anyone with CKD/diabetes is considered hypertensive, regardless of age, with a
systolic pressure of more than 140 or a diastolic of more than 90. Patients more
than 60 years of age are considered hypertensive with systolic pressure of more
than 150 and diastolic of more than 90.
7. Pericardial Diseases.
Pericarditis refers to an inflammation of the pericardial lining of the heart. There are
many causes where this can happen. These include (not too important)
autoimmune causes (SLE, post-MI dressler), uremia, neoplasms, and rheumatic
fevers. The key presentation, as all of you know, is the exacerbation of pleuritic
chest pain on thoracic compression. What does that mean? This means that the
has increased pleuritic pain on lying as well as breathing in, both of which decreases
thoracic volume. Physical examination demonstrates friction rub. Laboratory
investigations should include CXR and ECGs. Echocardiogram can also be
considered if to rule out causes of pericarditis (particularly MI which often result in
wall-motion deficits). ECG, notably, results in diffuse ST-segment elevation and PR
depressions. Treatment is dependent on the underlying etiology. However, it is
generally conservative.
8. Vascular Surgery
Peripheral arterial diseases result from chronically atherosclerosis and acutely from
cardiac embolization. Chronically, history and physicals often suggest intermittent
claudication (exercise-induced pain of lower extremities), arterial insufficiencies
(pale/cold extremities), or arterial ulcerations (painful, rapid onset, discret edges
with areas of erythema). Acutely, the symptoms and physical examinations are
often summarized in the 6Ps (Pallor, Pain, Pulse Lacking, Paresthesias,
Poikilothermia (Cold Extremities), and Paralysis). The diagnosis is primarily based
on the ABI, or ankle brachial index, an index of P(systolic of leg)/P(systolic of arm).
ABI is usually around 1.0-1.2 Doppler ultrasounds of extremities can also be
considered. Treatment is based on conservative management with focus on
diet/exercise and control of risk factors (such as diabetes or smoking). The
Fontaine Criteria describes medical and/or surgical management of peripheral
arterial diseases based on extent of occlusion. Detail is not important for QE/EE.
Remember that aortic aneurysms, first of all, can occur anywhere. They are mostly
associated with atherosclerosis. Most are abdominal and infrarenal in origin. People
with aneurysms are generally asymptomatic. However, a pulsatile abdominal mass
or bruits can often be noted on physical examination. Ruptured aneurysms,
however, often present with significant hypotension, tearing abdominal pain with
radiation to the back, as well as shortness of breath. Abdominal ultrasound is
often the first line for screening of aneurysm. In short, aneurysms more than 5cm
warrant surgical repair whereas aneurysms less than 5cm do not. Of course, any
symptomatic aneurysms and/or ruptured aneurysms need urgent vascular surgery
consult following immediate emergency stabilization.
Not as important for the QE/EE. However, it is important to note that they usually
present distal to the left subclavian artery with the most common risk factor being
HYPERTENSION (rather than atherosclerosis with aortic aneurysms). Onset of
sudden ripping pains are often noted in the anterior chest and back. Of note, the
Stanford Classifications describes dissections proximal to the left subclavian. If it is
ascending, it is known as Stanford Class A and requires a URGENT surgical consult.
A descending dissection, however, can be managed with medications, primarily
beta blockages. CT angiography is the standard of imaging. If CT angiography is
not possible (as in context of kidney injury), MR angiography can be considered.
1. Headaches
1.4Secondary Headaches: Secondary headaches are headaches which are likely not
benign in nature. In other words, red flags should be considered. This includes
meningitis (fever, meningeal signs), SAH (thunderclap headaches with
meningeal signs), Giant Cell Arteritis (Jaw Claudications), Increased ICP
secondary to mass effects (Headaches, Nausea/Vomiting, Bradycardia,
Hypotension), and Malignancy (Presence of Constitutional Symptoms).
Treatment and diagnosis would be geared towards management of the individual
associated conditions.
Peripheral nerves are composed of sensory, motor, and autonomic elements. Most
peripheral nerves are mixed. We can subgroup neuropathies into the following
categories: Mononeuropathy (affect one nerve), Mononeuropathy Multiplex (Affect
multiple nerves in distinct areas of the body), and Polyneuropathy (Affect multiple
nerves symmetrically in roughly equal areas of both sides of the body).
Mononeuropathy, first of all, is a type of neuropathy that affects only a single nerve.
Multiple causes are common, including median neuropathy (Carpel Tunnel
Syndrome, with numbness of the median nerve distribution alongside weakness of
wrist flexors and thumb opposition and abduction). It should be remembered that
patient often demonstrates positive Tinels and Phalens sign. Treatment typically
consists of neutral splints with anti-inflammatory medications. Surgical
decompression can also be considered in presence of poor response to medical
treatment. Other mononeuropathy include radial neuropathy, ulnar neuropathy
(Cubital Tunnel Syndrome), Femoral neuropathy, and sciatic neuropathy.