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Chung from AMCA

Cardiology Notes

Yuan Chung February 12th, 2017

1. ECG Review. I would encourage you to go on

library/basics/ for an overview of ECG basics. Another book which I would
recommend is called ECG Made Ridiculous Simple. We will attempt a quick review
of basic ECG Principles on Saturday, February 18 th, 2017. On the exam, you should
be able to recognize basic ECG abnormalities. Anything below mark RED means
that you should be able to recommend the ECG patterns.

2. Arrhythmias. Arrhythmias are essentially abnormal rhythms. They are

characterized as either bradyarrhythmias or tachyarrhythmias. Bradyarrhythmias
are abnormal rhythms which have a ventricular rate of <60bpm (beat per minute).
Tachyarrhythmias are abnormal rhythms which have ventricular rate of >100bpm.
The differentials of bradyarrhythmia, first of all, include the following: sinus
bradycardia, first degree AV block, second degree block (Mobitz Type 1 and Mobitz
Type 2), and third degree AV block. Lets now look at each one of these in the
context of relevance to the MCCEE/QE Exam.

2.1 Bradyarrhythmias.

Sinus Bradycardia. This can result from a normal response to cardiovascular

conditioning. However, considerations should also be given from medications
(particularly beta blockers as well as calcium channel blockers). Generall, patients
are asymptomatic. The treatment is mostly conservative but atropine may be
considered in certain cases.

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.

Tachyarrhythmias, first of all, are characterized into supraventricular

tachyarrhythmias and ventricular tachyarrhythmias. Supraventricular
tachyarrhythmias are also known as narrow complete tachyarrhythmias.
Ventricular tachyarrhythmias, on the other hand, are wide complex. The term
narrow and wide refers to the length of the QRS interval. QRS interval>120ms
is considered wide. QRS interval <120 is considered short. Lets now take a look at
important differentials here.

2.2.1 Supraventricular Tachyarrhythmias

Sinus tachycardia. As you can imagine, sinus tachycardia can be a normal

physiologic response to sympathetic output (fear). However, we must also consider
the possibility of endocrinologic causes (hyperthyroidism, Pheochromocytoma,
among others), hypovolemia, infections and/or PE. Patient may or may not
demonstrate cardiac symptoms including shortness of breath and palpitations. It Is
important hear to treat the underlying cause.

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.

Multifocal atrial tachycardia



Paroxysmal Atrial Tachycardia

2.2.2 Ventricular Tachycardia

VT (Management per ACLS Protocol. We will discuss this in Emergency Medicine)

VF (Management per ACLS Protocol. We will discuss this in Emergency Medicine).

Torsades de pointes (Association with long QT Syndrome. Long QT can be a result

of hypokalemia, alcoholism, congential long QT, and/or medications such as
antidepressants and antipsychotics).

3. Congestive Heart Failure

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.

Now, lets start our discussion by focusing on HFrEF

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.

Cardiomyopathy refers to the disorders of the heart myocytes (heart muscles). We

can group cardiomyopathies into the following three categories: restrictive,
hypertrophic, and dilated cardiomyopathies. While isolated right-sided
cardiomyopathies exist (called ARVS, or arrhythmogenic right ventricular
cardiomyopathy, or ARVC), most cardiomyopathy, regardless of type, is primarily a
left sided heart issue prior to spreading to the right side.

4.1 Dilated Cardiomyopathy

Dilated cardiomyopathy is the most common cardiomyopathy which results in left

ventricular dilatation and reduced ejection fraction, causing left sided reduced
ejection fraction heart failure. Many causes exists and include alcohol, myocarditis,
postpartum status infections (HIV noted), and doxorubicin (a chemotherapy
medication). The most common result, as you may remember from section 3.1, is
reduced ejection fraction heart failure with onset of left sided symptoms or right
sided symptoms alongside left sided symptoms. Diagnosis is the same with the
workup for 3.1. However, echocardiography is considered for evaluation of
dynamic heart function. Treatment is based on section 3.1 with an additional focus
on addressing the underlying etiologies (such as HIV).

4.2 Restrictive Cardiomyopathy

Restrictive Cardiomyopathy leads to a stiffer ventricle with impaired diastolic

filling while ejection fraction is maintained. It is, as mentioned before, an important
cause of HFpEF. It is most frequently caused by infiltrative diseases (sarcoid,
amyloid, and hemochromatosis) or scarring. Echocardiography again is key for

4.3 Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy is a result of hypertrophy of the myocytes with

resulting impaired filling defects, resulting in diastolic heart failure. An important
one to remember is HOCM (or Hypertrophic Obstructive Cardiomyopathy). A key
finding is a systolic ejection murmur which increases with decreased preload (such
as valsava or standing).

5. Acute Coronary Syndrome

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.

5.1 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

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

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)


STEMI refers to ST elevation myocardial infarction. Typically presentation, as you all

known, is acute onset substernal chest pain with radiation to the jaw/left arm. It
should be noted that sweating (diaphoresis) is the most specific finding of STEMI.
Physical examination, again, should focus on cardiovascular, respiratory, and
peripheral arterial changes as a result of the STEMI. ECG frequently shows ST-
segment elevation in vascular territories alongside peaked T waves. Normalization
of ST segment and T waves are often observed later. Pathologic Q waves and poor
R wave progressions are often evidence of residual (past) infarcts. Laboratory
studies, therefore, focus on ECGs and cardiac enzymes. The management is
described as below.

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.

Complications from a STEMI to remember would be the following. Heart failure

(within hours, preserved or reduced ejection fractuion), pericarditis and arrhythmia
(days), left ventricular wall rupture (1 week) with onset of mitral regurgitation, and
Dressler syndrome (post MI autoimmune pericarditis, months following).

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.

There are essentially two causes of hypertension, primary or secondary. Primary

implies that the hypertension has no known etiology at present. Risk factors (as we
can all imagine) would involve family history, dyslipidemia, past MI/strokes,
smoking, obesity, high fat/sodium diet, and age. Secondary hypertensions refer to
causes which have a confirmed etiologies. The ones you should remember for the
QE/EE would be renal artery stenosis, OCP use, Conns Syndrome, Primary
Aldosteronism, Hyperthyroidism, Coarctation, and Pheochromocytoma.

Now, in any patient with hypertension (primary or secondary), it is important on

history and physical to focus on ruling out secondary causes and to examine for
evidence of END-ORGAN injury. We have discussed relevant history and physicals of
most if not all of the secondary causes in prior topics. Lets instead focus on
understanding the evidence of END-ORGAN injury. Clinically, I usually remember
them by going head to down.
Neurologically, we worry about hypertensive encephalopathy and/or SAH. Ischemic
changes is also possible. As such, a general neurological history and physical is
warranted. I also do a fundoscopy looking for evidence of hypertensive changes,
particularly hemorrhages and exudates.

Cardiovascular, HTN, as we have mentioned before, is a key cause of congestive

heart failure. It can also result in MIs as well as aortic dissection. We discussed the
symptoms and physical examinations of CHF prior. We also discussed MIs prior.
Aortic dissection generally presents with excruciating tearing back pain.

Nephrology, HTN results in hypertensive nephropathy with possible metabolic

disturbances. I, therefore, focus my history and physical on screening the
downstream sequelae of these electrolytes changes (will be discussed in
nephrology) as well as the history and physical of hypertensive induced nephrotic
syndrome (will be discussed in nephrology).

Appropriate investigations, as you can imagine, would focus on evaluation for

secondary causes as well as examination for end organ injury. What does that
entail? Renal artery stenosis (abdominal ultrasound), OCP (dont have a test for it),
Conn Syndrome/Aldosteronism (Aldosterone to Renin Ratio, Sodium, and
Potassium), Cushing Syndrome (24 Hour Cortisol, Dexamethasone Suppression
Test), Pheochromocytoma (Urine catecholamines). End organ evaluations focus on
CT (Non contrast head, if necessary in presence of neurologic symptoms), and
nephrology workup (will be discussed in nephrology). Please, do not order them all.
If you dont have a suspicion for pheochromocytoma, for example, dont order an
urine catecholamine.

If the patient is deemed to have primary hypertension, it is important than to

initiate treatment. Treatment should start with lifestyle modifications alongside
blood pressure medications. The choice of medications vary depending on
underlying comorbidity. A safe choice, for all intent and purposes, would be ACE
inhibitors except in pregnancy where it is contraindicated (we use hydraline or
labetalol, as Dr. Nik likely discussed in ObGyn).

Now, if the patient is in a hypertensive crisis (urgency or emergency), the

management is a bit different. Hypertensive urgency refers to presentation of
symptoms (primarily headaches and chest pain) without end organ damage.
Hypertensive emergency refers to presentation of symptoms with end organ
damage. Hypertensive urgency is treated with oral antihypertensives with the goal
of gradually lowering the BP in 1-2 days. Hypertensive emergency is treated witH IV
labetalol or nitroprusside with the goal of lowering mean arterial pressure by no
more than 25% within the first two hours.

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.

Cardiac tamponade is an extreme version of pericarditis with excessive fluids in the

pericardiac space. This typically results from trauma, particularly trauma directly to
the medial side of the left nipple. Physical examination, as we will review in
emergency medicine, is extremely telling, with the presentation of Beck Triad
(Hypotension, Muffled Heart Sounds, and JVP elevation). ECG often shows evidence
of electrical alternans. Treatment involves aggressive resuscitations alongside
pericardiocentesis. We will review ABCDEs of emergency medicine during our
emergency medicine class.

8. Vascular Surgery

8.1 Peripheral Arterial Diseases.

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.

8.2 Aortic Aneurysm.

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.

8.3 Aortic Dissection.

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.

9. Basic Anatomy Review.

Anatomy of vessels following the ascending aorta.

Anatomy of cardiac heart vessels (coronary vessels)

Neurology Concise (Headaches and Peripheral Neuropathy)

1. Headaches

It is essentially important here to differential migraine, tension, and cluster

headaches from each other with, in addition, an understanding of associated
secondary headache causes.

1.1Migraine Headaches: Migraines are characteristically headaches which last for 1-

2 days described as unilateral, pulsating, and severe with exacerbation by light,
sound, or physical activity. Associated phonophobia or photophobias are often
observed. It frequently affects young females with OCPs and menstral periods,
and stresses being notable triggers. Migraine can be with or without aura. A
classical migraine with aura which presents with reversible neurologic deficit,
particularly scotomas or visual cuts prior to the migraine itself. Treatment
generally involves avoidance of triggers. Abortive therapy (during aura) with
triptans should be considered. Prophylaxis can be considered for severe cases
with TCs or Beta Blockers.
1.2Cluster Headaches: Cluster headaches are excruciating but brief unilateral
orbital headaches that last for a few hours. They, interesting tend to occur in
clusters. That is, they tend to occur at the same time of the day, same side of
the head, same seasons as well. First episode presentations, given its unilateral
nature as well as associated neurologic changes (particularly Horners) often
requires working with CT head. Repeated attacks however do not require
further workup. Cluster headaches primarily affect men more than women.
Treatment is general triptans for abortion as well as prophylactic CCB

1.3Tension Headaches: Tension headaches typically present with a bandlike pain

triggered by stress. This tends to be mild/moderate in quality. Avoidance of
exacerbating factor is a focus. NSAID/acetaminophen should be considered for
management of pain.

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.

2. Peripheral Neuropathy (Harrisons Chapter 53 and 54).

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.

Mononeuropathy Multiplex refers to simultaneous involvement of noncontiguous

nerve trunks. Pattern, therefore, is generally asymmetric. However, disease
progression makes it difficult clinically to truly differentiate it from polyneuropathy.
Multiple causes are noted. Diabetes, infectious etiologies (Lymes, Hepatitis B/C,
HIV, CMV), and infiltrative diseases should be considered (amyloidosis, sarcoidosis).
Cryoglobulinemia in context of gamma globulinopathy of unknown significance
should also be considered. Diagnostically difficult.

Polyneuropathies: Polyneuropathies refer to diseases to the peripheral nerves in

roughly the same areas on both sides of the body. Based on electrophysiologic
recordings, we can separate polyneuropathies into distal axonopathies and
myelinopathies. Distal axonopathies are frequently a recent of toxins, drugs, or
chemotherapy. Diabetes, alcohol use, and renal failures should be considered.
Myelinopathies refers to the loss of the myelin and/or loss of the peripheral
Schwann cells. The most common cause is Guillain Barre Syndrome as well as
CIDP, OR Chronic Inflaammatory Demyelinating Polyradiculopathy.

Guillain Barre Syndrome is a rapidly progressing autoimmune disorder of the

peripheral nerves associated with recent viral infections, C. jejuni infections. It
classically presents with ascending paralysis and areflexia in a symmetric manner
over days. Autonomic dysregulation can also be observed. This is known as the
AIDP (acute inflammatory demyelinating polyneuropathy) subtype Three other
subtypes (AMAN, AMSAN, as well as Miller Fisher Syndrome) are known. CSF
finding is particularly distincting, with elevated CSF protein with no pleocytosis, a
phenomenon known as albuminocytologic dissociation. If there is evidence of
pleocytosis (white blood cell on CSF, alternative diagnosis, particularly viral myelitis
or a HIV neuropathy) should be considered. Treatment is focused on
plasmapheresis as well as IVIG. Combination treatment has not been shown to be
clinically significant. Specific choice depends on subtype. Particularly, AMAN and
Millar Fisher may respond better to IVIG better than plasma exchange. It is
expected that 85% of patients with GBS would achieve a full functional recovery.

A noted differential of Guillain Bareer Syndrom is CIDP, or chronic inflammatory

demyelinating polyneuropathy. In short, this is GBS with a much longer and chronic
course. Details beyond the scope of QE/EE.