Chapter 1 Cardiology

7/26/2019 Chapter 1 Cardiology

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Andrew Reid PA-C

Physician Assistant

Boards

PANCE/PANREREVIEW

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TABLE OF CONTENTS

INTRODUCTION .................................................................................... 1

CHAPTER 1: CARDIOLOGY ................................................................. 2

-REVIEW QUESTIONS ................................................................................................. 34

-REVIEW ANSWERS .................................................................................................... 37

-QUICK FACTS/ASSOCIATIONS ................................................................................. 43

CHAPTER 2: PULMONOLOGY ............................................................. 46


-REVIEW ANSWERS .................................................................................................... 74


CHAPTER 3: MUSKULOSKELETAL/RHEUMATOLOGY .................... 81


-REVIEW ANSWERS .................................................................................................... 124


CHAPTER 4: GASTROENTEROLOGY ................................................. 135

-REVIEW QUESTIONS .................................................................................................. 166-REVIEW ANSWERS .................................................................................................... 169


CHAPTER 5: REPRODUCTION ............................................................. 176

-REVIEW QUESTIONS .................................................................................................. 210

-REVIEW ANSWERS ..................................................................................................... 213


CHAPTER 6: GENITOURINARY ............................................................ 220


-REVIEW ANSWERS ..................................................................................................... 255


CHAPTER 7: EENT ................................................................................ 262


-REVIEW ANSWERS .................................................................................................... 295


CHAPTER 8: ENDOCRINOLOGY .......................................................... 301


-REVIEW ANSWERS ..................................................................................................... 322

-QUICK FACTS/ASSOCIATIONS .................................................................................. 327

CHAPTER 9: NEUROLOGY ................................................................... 329-REVIEW QUESTIONS .................................................................................................. 350

-REVIEW ANSWERS ..................................................................................................... 353

-QUICK FACTS/ASSOCIATIONS .................................................................................. 358

CHAPTER 10: HEMATOLOGY .............................................................. 360


-REVIEW ANSWERS ..................................................................................................... 381



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CHAPTER 11: PSYCHIATRY ................................................................. 387


-REVIEW ANSWERS ..................................................................................................... 405


CHAPTER 12: DERMATOLOGY ............................................................ 409

-REVIEW QUESTIONS ................................................................................................... 434

-REVIEW ANSWERS ...................................................................................................... 436

-QUICK FACTS/ASSOCIATIONS ................................................................................... 440

CHAPTER 13: INFECTIOUS DISEASE .................................................. 442

-REVIEW QUESTIONS ................................................................................................... 463

-REVIEW ANSWERS ...................................................................................................... 466

-QUICK FACTS/ASSOCIATIONS ................................................................................... 477

TABLE OF CONTENTS


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Medicine can be overwhelming, but its not complicated. What makes it sochallenging is the amount of information you are expected to retain. So, what doyou need to know and what can you ignore?

This book will give you a straight forward way to learn the many disease processesout there. I didnt write a lot of bullet points with a lot of random facts. Instead, Iwrote down what is done first, and what will be done next. The boards want tomake sure that you know the order in which to do things, even though everythingis usually done simultaneously in clinical practice.

This book contains everything you need to know to pass your boards. The firstsection of each chapter is filled with all the diseases required by the NCCPAblueprint. The second section is a set of review questions that goes over the entirechapter. The third section is a set of tables that detail important facts andassociations. This third section is a nice way to rapidly review everything the nightor morning before an exam.

Purchasing this book is much more than just a book purchase. You will also have

access to me should any questions arise. If there are ever any questions orclarification that is needed, please dont hesitate to email me:

[email protected]

I am here to make this process as painless as possible. I am here to help you. Itook a great deal of time to put this together, and I know it will help.

Study hard. Visualize your self passing. Go in with confidence.

Before you know it, you will be out in clinical practice helping others. Alwaysbelieve in your abilities, and remember:

Every artist was first an amateur - Ralph Waldo Emerson

PhysicianAssistantBoards.com Andrew Reid PA-C

INTRODUCTION


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Cardiology

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Congestive Heart Failure (CHF)

Introduction

Heart failure is a pump problem. There may be a problem with filling (diastolic dysfunc-

tion) or a problem with pumping (systolic dysfunction). The net result is a decrease in per-fusion to tissues, resulting in under-oxygenation.

Diastolic dysfunction: Decreased filling due to poor relaxation of the ventricle. Because

the problem here is filling, and not pumping blood out, the ejection fraction will remain

normal.

Systolic dysfunction: Decreased ejection fraction usually less than 50%. This percentage

correlates to the amount of blood that leaves the left ventricle (50% of the blood is

pumped out of the ventricle).

The most common etiology is coronary artery disease.

Signs and Symptoms

The most common presenting symptoms of heart failure are fatigue and shortness of

breath. This is largely a clinical diagnosis based on a good history and physical exam.Other key features that lead you to the diagnosis are: orthopnea (SOB upon lying), paroxys

mal nocturnal dyspnea (sudden feeling of su#ocation mid sleep prompting the patient to

get out of bed), pedal edema, jugular venous dystension, and an S3 gallop.

Diagnostic Testing

The first and most useful test that should be performed is an echocardiogram. An ECG

should be done to screen for arrhythmias and to look for Q waves (old in-farct). ECG

might also show signs of ischemia and/or left ventricular hypertrophy. Stress testing is

used to asses exercise tolerance and risk stratification. Chest X-ray is used in the

evaluation of dyspnea (not to diagnose CHF).

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Treatment

ACE/ARBs and beta blockers are your main drugs in terms of lowering mortality.

Specific beta blockers you should know are carvedilol, bisoprolol, and metoprolol

succinate- these have the most proven benefit in reducing mortality. Small caveat:

never give beta blockers during an acute exacerbation.

Diuretics are given to reduce symptoms: fluid overload. Digoxin is also used for symptom

control such as SOB. Digoxin decreases the time spent hospitalized, but does not reduce

mortality in patients. Spironolactone or eplerenone (less endocrine side e#ects than spiro-

nolactone) are only beneficial to those who are classified as having class 3 or class 4 CHF.

Be careful with the use of calcium channel blockers, as they may increase mortality in CHF

patients.

For those patients who continue to be symptomatic, the addition of nitrates andhydralazine has proven benefit (more so with African Americans).An ICD (implantable car-

diac defibrillator) is used when the ejection fraction is below 35%, those with sutained VT,

and/or those with unexplained syncope to prevent a fatal arrhythmia.

Caveat:An ICD should only be used if the patient is expected to survive for at least one

year. If everything up to this point has failed, the final option includes transplantation.

ACUTE EXACERBATION

An ECG is done to look for arrhythmias and myocardial infarction. What about BNP?

Well, this is used as an attempt to distinguish between CHF exacerbation and COPD exac-

erbation as the cause of dyspnea. This is a sensitive, but nonspecific test. Meaning, a

normal BNP will exclude CHF, but an elevated BNP can be caused by a variety of

reasons.A severely elevated BNP (>400) increases the likelihood of CHF exacerbation;


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Oxygen

Position (head up)/positive pressure

CARDIOMYOPATHY

Introduction

This is a disease of the heart muscle associated with cardiac dysfunction. The strict defini-

tion requires that no etiology is found (but most will usually have a genetic component).

Because there usually is no etiology, cardiomyopathies can be present during any decade

of life, including childhood. There are three main types: Dilated cardiomyopathy, hypertro-

phic cardiomyopathy, and restrictive cardiomyopathy.All of these can lead to heart

failure.

Signs and Symptoms

Symptoms will usually be identical to thosediscussed incongestive heart failure.

Diagnostic Testing

The echocardiogram is the test of choice to distinguish between the three.



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Specifics

Distinguish hypertrophic cardiomyopathy from hypertrophic obstructivecardiomyopathy.In HOCM, the septum will cause an obstruction to normal blood flow out of the aorta.

Classically, HOCM is the diagnosis when a young healthy athlete dies suddenly. However,

the most common symptom is shortness of breath, not death. This is also treated with

beta blockers; but do not use diuretics, as they are contraindicated in HOCM.

ATRIAL SEPTAL DEFECT

This is a direct connection between both atria through a defect in the septum. These chil-

dren are usually asymptomatic, but over time can lead to heart failure or recurrent

respira-tory infections. You will hear a systolic ejection murmur withafixed wide splitting

of S2.


Cardiomyopathy Introduction Dysfunction Treatment

Dilated

Ventricle is dilated,

leading to decreasedcontraction of the

ventricle

Systolic Same as CHF

Hypertrophic

Normal or impaired

ventricular filling with

ventricular hypertrophy

and preserved systolic

function.

Diastolic

Beta Blockers, followed

by Calcium Channel

Blockers.

Restrictive

Impaired ventricular

filling without

hypertrophy of the

ventricle.

Also has

impaired contractility.

This is the least

common cause of

cardiomyopathy in the

states.

Diastolic dysfunction,

which can lead to

systolic dysfunction

No specific Treatment

available


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The best test for diagnosis is an echocardiogram. The ASD will usually close spontane-

ously, but surgery may be performed at age 4 or in those who are severely symptomatic.

COARCTATION OF THE AORTA

Narrowing of the aorta at the ductus arteriosus. May present with hypertension or

respira-tory distress. There will be a reduced blood pressure and a reduced pulse in the

lower extremities. Diagnosed by echocardiogram. Chest x-ray will show rib notching or a3 sign at the site of coarctation. These are surgically corrected.

PATENT DUCTUS ARTERIOSIS

The ductus arteriosis is a connection between the main pulmonary artery andtheaorta. It

usually closes the first two days of life. The ductus arteriosisis kept open by a low

oxygen environment and prostaglandins. Failure to close is termed PDA. You will hear a

machine like continuous murmur. Diagnosis is made with echocardiogram. Premature

infants are treated with indomethacin.All othersare treated with percutaneous catheter

closure or surgical ligation.



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TETRALOGY OF FALLOT

Cyanotic heart disorder that is characterized by:

$Right ventricular hypertrophy

$VSD

$Overriding aorta

$Right ventricular outflow obstruction

Harsh systolic ejection murmur heard best at the left sternal border.

Tet spells: hyper cyanotic episodes that develop during crying or feeding. Bringing the

childs knees to the chest will decrease venous returnand increase vascular resistance,

which will in turn make the child more comfortable.

Diagnosed with echocardiogram. Treated by surgical repair.

VSD

A direct connection between both ventricles through a defect in the septum.

Eisenmenger syndrome: First, there will be a left to right shunting of blood, which will

eventually lead to pulmonary hypertension.As the pressures increase in the pulmonary

vasculature,more so than the right ventricle, a shunt reversal occurs. This means that

deoxygenated blood will be shunted from the right ventricle to the left and out into the

systemic circulation.

A holosytolic murmur is heard that does not increase with respiration. Diagnosed with

echocardiogram. This will usually close without treatment, but surgical repair is done for

symptomatic children.



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HYPERTENSION

Introduction

The definition is a systolic pressure over 140 or a diastolic over 90. Diabetes and CKD are

treated to the same value. Patients >60 years of age are treated when the systolic pres-

sure is over 150 or the diastolic is over 90 (unless they have diabetes or CKD - they are

then treated when pressures rise >140/90). Hypertension also requires that it be elevated

on at least two separate occassions. There are two stages of hypertension:

Stage 1

Systolic: 140-159

Diastolic: 90-100

Stage 2

Systolic: over 160

Diastolic: over 100

Etiology

Over 95% of hypertension is termed essential (meaning idiopathic or no one really knows

why). The other 5% are from secondary causes. The most common secondary cause is

from renal disease. If a person states they regularly have a normal BP at home, but ele-

vated in the o%ce, they might su#er from white coat hypertension. The numbers at home

are valid.

Signs and Symptoms

Patient are usually asymptomatic at the time of diagnosis. Hypertension does not

cause headache!



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Diagnostic Testing

After diagnosis, it is important to look for end organ damage. Routine labs that are or-

dered include: urine analysis, urine micro albumin, EKG, CBC, BMP, and lipid panel. The

physical should focus on: fundoscopy (hemorrhage or papilledema), thyroid assessment,

carotid bruit, size and rhythm of heart, crackles in lungs, renal bruit, pedal edema, confu-

sion or weakness.

Treatment

First, initiate lifestyle recommendations such as weight loss, DASH diet,smoking

cessation, moderate alcohol use, decrease sodium consumption, and exercise. If these

do not work, a young healthy adult should be treated with a diuretic (hydrochlorothiazide

or chlorthalidone), ACE/ARB, or a long acting dihydropyridine (amlodopine). Those in

stage two should be treated with 2 medications (usually one will include a diuretic). If a

person has co-morbid conditions, then the first line therapy is dictated by that condition:

Diabetes: ACE/ARB

CHF/Ischemia/CAD: Beta blocker or ACE/ARB

Angina: Beta blocker or calcium channel blocker

BPH: Alpha blockerHyperthyroid: Beta blocker

CKD: ACE/ARB

Reynauds: Calcium channel blocker

Migraine: Beta blocker or calcium channel blocker

Resistant hypertension is hypertension that is not responsive to at least three medications,

one of which must include a diuretic.

Secondary hypertension

So, who should undergo evaluation for secondary hypertension?



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& $Severe or resistant hypertension

& $Age less than 30 who are otherwise healthy

& $Malignant or very rapidly occurring hypertension

Renovascular hypertension is the most common cause of secondary hypertension.

Clues to diagnosis:

Renal artery stenosis: abdominal bruit

Hyperaldosteronism: hypokalemia and hypernatremia

Primary kidney disease: elevated creatinine

Pheocromocytoma: acute episodes of elevated BP with headache, palpitations, and

sweat-ing

Cushings: moon face, central obesity, bu#alo hump, proximal muscle weakness

Sleep apnea: Obese men who snore

Coarctation of aorta: hypertension in a child. Hypertension of upper extremeties,

diminished femoral pulses, and decreased blood pressure in the lower extremeties.

HYPERTENSIVE URGENCY

Introduction

Severely elevated hypertension is considered to occur when the systolic is over 180

and/orwhen the diastolic is over 120.

Signs and Symptoms

By definition, the patient is asymptomatic and cannot have end organ damage.

Treatment

Do not bring down blood pressure rapidly, and do not use sublingual nifedipine (this is con-



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traindicated)! When a patients body is used to having elevated pressures, and then sud-

denly those pressures drop, there wont be enough pressure to circulate oxygen to the

brain and heart. This decrease in oxygenation can lead to MI or CVA, and has been most

described with sublingual nifedipine.A gradual reduction over 1-2 days is the preferred

approach. The general consensus is to initiate control with two BP medications and followup in 2 days as an outpatient. There isnt an agreement for the ideal first line medication.

HYPERTENSIVE EMERGENCY

Introduction

Severely elevated hypertensionusually over 180/120.

Signs and Symptoms

A hypertensive emergency must include end organ damage. Two subcategories under the

hypertensive emergency include: malignant hypertension and hypertensive encephalopa-

thy.

Malignant hypertension will present with papiledema, exudates, retinal hemorrhage, acute

kidney injury (hematuria or proteinuria), and/or focal neurological findings. Encepalopathy

will present with cerebral edema: Headache, N/V, confusion, seizure, coma.

Diagnostic Testing

When there are focal neurological findings, an MRI should be done to rule out stroke.

Treatment

The goal is to decreasethediastolic pressure to 100 in 6 hours.After the blood

pressure has been controlled, begin oral therapy to bring the diastolic


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CARDIOGENIC SHOCK

Introduction

Shock is a state characterized by decreased perfusion and decreased oxygenation of

tissues. This will cause disruption at the cellular level. If caught early, all of the damage

will be reversible, but over time, will lead to cell death, organ failure, and eventually

death.

Cardiogenic shock stems from the heart not being able to pump normally.

Etiology

The etiology will be anything that causes the heart to stop pumping e%ciently, but will usu-

ally occur from an MI.

Signs and Symptoms

Classically, they will behypotensive, altered,and havecool clammy skin. Ultimately meta-

bolic acidosis develops. Systemic vascular resistance and heart rate will be increased.

Look for chest pain and dyspnea in someone with a history of cardiac disease. There will

also be pulmonary congestion and elevated cardiac enzymes.

Treatment

Always stabilize the patient before trying to attempt to find an etiology. This means aggres

sive fluid resuscitation, followed by pressors (norepinephrine or dopamine) if needed.



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ORTHOSTATIC HYPOTENSION

Introduction

This usually occurs because of autonomic dysfunction and is an inadequate physiological

response to postural changes. This will usuall occur in patients over the age of 65.

Etiology

Medications, hypovolemia, anemia, heart disease, diabetes, and or Parkinsons disease.

Signs and Symptoms

When the patient suddenly stands, they will feel dizzy, have palpitations, and become syn-

copal.

Diagnostic Testing

Take the blood pressure lying down, then have the patient stand for a couple minutes,

and then repeat the blood pressure. The diagnosis is made if the systolic blood pressure

falls 20mmHg or if the diastolic falls 10mmHg or more. Order tilt table testing if suspicion

is high, but orthostatic vital signs are normal.

Treatment

Treat the underlying etiology. If noneisfound, attempt to increase fluid and sodium

intake. If no response, give fludrocortisone(mineralcorticoid) as first line medical therapy.

ATRIAL FIBRILLATION/FLUTTER

Introduction

Atrial fibrillation is the most common cardiac arrhythmia. Fibrillation can be thought of as



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a worsening of flutter. These patients are at increased risk for stroke due to the potential

for thrombus formation. This is because of the constant quivering from the atria. The

blood will become stagnant and a clot will form. It takes a couple of days after atrial fibril-

lation starts, for a thrombus to form.

Signs and Symptoms

Both types may present with palpitations, shortness of breath, and/or chest pain.

Diagnostic Testing

Diagnosed on ECG. Fibrillation will have an irregularly irregular rhythm without any Pwaves.Atrial flutter will present as a regular rhythm with a saw tooth pattern. Flutter will

usually have an atrial rate of 300 and a ventricular rate of 150.

Treatment

Unstable patientsare treated the same:

Cardioversion

If this is the first episode, order an echocardiogramto evaluate for thrombus formation.

Trans esophageal echo is more sensitive than trans thoracic. If the patient has been

symptomatic for less than two days, you may rate control or cardiovert (may be safely

done because it is too soon for a thrombus to form). If symptoms have been present for

more than 2 days, then the possibility of thrombus exists, and ideally you want to rate

control (beta blockers or calcium channel blockers) as the first line option. If a calcium

channel blocker is used, use the non dihyropyridines (verapamil or diltiazem).

If the patient requests cardioversion and symptoms have been present over 2 days, order

an echo to rule out a thrombus. If no thrombus exists, give heparin and cardiovert. If the

echo shows a thrombus, you must anticoagulate with warfarin for four weeks before car-

dioverting.



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Finally, make sure you provide long term anticoagulation with either aspirin or warfarin.

So, when do we use warfarin and when do we use aspirin? CHADS2 score:

C-CHF (1point)

H-Hypertension (1point)A-Age of 75 (1point)

D-Diabetes (1point)

S-Stroke or TIA in past (2 points given here)

Score:

0: Aspirin

1: Aspirin or warfarin

2: warfarin

HEART BLOCK

First Degree Long PR Interval (>.20) No Treatment

Mobitz 1/Wenckebach

PR progressively lengthens,

until it fails to produce a p wave

and QRS complex.

No treatment if patient is asymptomatic.

Pacemaker if symptomatic (signs of

hypo perfusion)

Mobitz 2

Patient will have a continuously

dropped QRS complex just like

Mobitz 1, however, no

lengthening of the PR is noted.

May present with syncope

Treat everyone with a pacemaker to

prevent progression to complete block.

Third Degree

Signal from the atria does not

reach the ventricle. Therefore,

you will have P waves that are

independent from the QRS

complex

Treat with a pacemaker. May be fatal.



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BUNDLE BRANCH BLOCK

Right bundle branch: electrical activity in the his-purkinje fibers are slowed. The right

bundle receives most of the blood supply from LAD. Wide QRS (over .12), RSR pattern

in leads V1 or V2, S wave wider than R wave in V5 and V6. There may also be altered ST

segments and T waves.Asymptomatic patientsdo not need treatment. Those who

develop symptoms due to other electrical conductions should be placed on a

pacemaker.

Left bundle branch: Same pathophysiology as the right bundle branch, however, the left is

instead a#ected. Wide QRS (over .12), notched R wave in V5 and V6. ST and T waves dis

placement are opposite to the direction of the QRS complex. Remember, a new LBBB

must be treated as an MI when infarction is being considered. Treatment is the same as a

right bundle branch block.

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA

These are supraventricular tachycardias that are intermittent and occur abruptly. Patients

will present with abrupt onset of palpitations and the EKG will show a narrow complex

tachycardia. The first step is to assess hemodynamic instability (hypotension, SOB,

chest pain, and altered mental status). If hemodynamic instability exists, then cardiovert.

If stable, the patient may be given vagal maneuvers to slowdownthe rate (valsalva or

carotid massage). This will allow you to see the P waves, as they are usually

superimposed into the QRS complex. If this does not work, adenosine may be given, and

will be diagnostic and therapeutic.

Note: If the diagnosis is thought to be WPW, the addition of adenosine will worsen the ar-

rhythmia and may lead to ventricular tachycardia and ventricular fibrillation.



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PREMATURE BEATS

PVC

Ectopic beats originating in ventricular foci. Patientsare usually asymptomatic, but if

symptoms occur, they will present with palpitations. The EKG will show a wide complex

QRS without P waves. Following the wide complex QRS, there will usually be a

compensatory pause (the AV node will be blocked for a short periodnotallowingthe sig-

nal from the SA node to reach the ventricle). The AV node then clears, and a normal p

wave and QRS complex are seen.Asymptomatic patientsdo not require treatment.

Those who are symptomatic may be given a beta blocker.

PACEctopic beatsoriginating from the atria outside the SA node. Patientsare usually

asymptomatic, but if symptoms occur, theywill present with palpitations. The EKG will

show a P wave before expected and will havea di#erent morphology from the previous P

waves. The closer the ectopic foci is to the SA node, the more similar the P wave will

appear.Asymptomatic patients do not require therapy. If symptoms occur, treat with a

beta blocker.

SICK SINUS SYNDROME

This is SA node dysfunction, usually from fibrous tissue covering the SA node. EKG will

show: alternating bradycardia and tachycardia, sinus arrest without an appropriateescape rhythm, andaninappropriate response to stress. Symptoms are very

inconsistent, and not helpful in the diagnosis. Treatment is with a pacemaker.



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VENTRICULAR TACHYCARDIA

WIDE COMPLEX TACHYCARDIA (requires at least 3 consecutive wide complexes). Do not

try and di#erentiate between SVT or aberrant conduction.Always treat a wide complex

tachycardia as ventricular tachycardia. If unstable, cadiovert. If stable treat with ami-

dorone or procainamide. If medication does not convert to sinus rhythm, then cardiovert.

Torsades de pointes:

This is a polymorphic ventricular tachycardia that arises from a prolonged QT interval. In

the technical sense, if the baseline QT interval was normal, it is simply referred to as poly-

morphic ventricular tachycardia.

Treatment: withdraw the o#ending drugs, correct electrolyte abnormalities, and cardiac

pacing. Magnesium sulfate may be o#ered in the acute setting for drug induced torsades.

VENTRICULAR FIBRILLATION

No organized electrical activity.

Cardioversion immediately -> cpr->shock->epinephrine->shock->amiodarone



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STABLE ANGINA AND PRINZMETAL ANGINA

Introduction

Stable angina is myocardial ischemia secondary to exertion (increased oxygen demand).

A variant, known as prinzmetal angina, is ischemia secondary to coronary artery spasm.RISK FACTORS: hypertension, smoking, hyperlipidemia, diabetes, and obesity.

Signs and Symptoms

Stable angina presents as chest discomfort with exertionand is relieved by rest or

nitroglycerin. The discomfort is predictable in nature, and never occurs at rest. The

physical exam will usually be normal. This is a diagnosis based on the patients history

and risk factors for coronary artery disease. Prinzmetal angina typically occurs at rest.

Diagnostic Testing

The ECG will be normal in stable angina. The ECG in prinzmetal angina will show ST

segment elevations that will return to baseline immediately after the episode (usually 5-15

min). Neither will have elevated cardiac enzymes (STEMI will have elevated enzymes,

and will not have the ST segment return to baseline so quickly).

If the diagnosis is unclear, refer the patient for stress testing. Stress testing (either with

medication or treadmill) will increase oxygen demand, and will demonstrate ischemia

on ECG.

Treatment

Treat with lifestyle modifications (same as those in the hypertension section).Also, make

sure to control hypertension, diabetes, and hyperlipidemia.All patients are treated with an

aspirin and beta blocker. The beta blocker will be used to slow the heart, allow increasedventricular filling, and reduce oxygen demand. The patient will also be given nitroglycerin

(decreases pre load) to be used on an as needed basis for chest pain. Those who cannot

be controlled with medication should be referred for angiography and revascularization.

Only use calcium channel blockers when beta blockers are contraindicated, or as an ad-

junct to beta blockers.



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Prinzmetal angina will be treated with calcium channel blockers as the pathophysiology

is spasm of the smooth muscle. Do not use beta blockers in prinzmetalanginaas this

can predispose the patient to a worsening in spasm from unopposed alpha receptors.

ACUTE CORONARY SYNDROME

Introduction

This encompasses UNSTABLE ANGINA, NSTEMI, and STEMI.All will present identical

and testing is necessary to arrive at thediagnosis. Remember, time is muscle, so the

faster you treat, the better the outcome. Women and diabetics can present atypically

without chest pain.

Diagnostic Testing

ECG: Unstable angina and NSTEMI will have signs of ischemia (ST depression or T wave

inversion). STEMI will have ST elevation of 1mmor morein at least two contiguous leads

Remember to repeat the EKG every 10 minutes if ACS is suspected,as the initial EKG

may be normal. The first EKG abnormality usually seen with infarction will be hyperacute

T waves. Remember, that a new left bundle branch block should be treated as an

infarction.

Cardiac enzymes:

CK-MB will rise after 4 hours, and will stay elevated for a couple days.

Troponins (Preferred cardiac marker and troponin-I is most specific) rises after 4 hours

but will stay elevated for up to two weeks. Most patients with negative enzymes can be

excluded by 6 hours, but for those high risk patients, you should continue serial labs for

12 hours. Reinfarction is diagnosed if troponin increases over 20%. CK-MB can also be



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used to evaluate reinfarction, as the numbers should return to baseline after a couple

days. CK-MB is now second line to diagnose reinfarction.

Unstable angina will NOT have an elevation in cardiac enzymes.

NSTEMI and STEMI WILL have an elevation in cardiac enzymes.Initially, unstable angina and NSTEMI will present identical, as it takes time for cardiac en-

zymes to rise.

Treatment

All patients presenting with ACS should immediately be given morphine, oxygen, nitrates

(avoid if the patient is on phosphodiesterase-5 inhibitors as this will cause hypotension),

and aspirin (chewed). Caveat: If patient has inferior MI, and suspected involvement ofthe

right ventricle, avoid nitrates as this can cause a severe drop in blood pressure.All

patients should also receive a beta blocker (metoprolol or atenolol) and a statin

(atorvastatin) immediately if no contraindication exists.

STEMI: Everyone gets heparin. PCI is the preferred to thrombolytics. PCI must be done

within 90 minutes of arrival. If PCI is unavailable, or if unable to get to a center in 90

minutes, give thrombolytics. Thrombolytics are only indicated if chest painhas been

presentunder 12 hours and lacks contraindications (coagulation disorder, severehypertension, internal bleeding, or history of hemorrhagic stroke).

NSTEMI and unstable angina are managed identical to STEMI with the following excep-

tions:

NO thrombolyticsare given.Give either ticagrelor or GP IIb/IIIa inhibitor instead.

Post STEMI/NSTEMI: all patients should be continued on aspirin, beta blocker (metoprolol

or atenolol), ACE, and statin. Clopidogrel is used for those with aspirin allergy.

Cocaine associated MI should be treated the same as those with other forms of ACS with

the following modifications: Avoid beta blockers and give benzodiazepines.



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AORTIC ANEURYSM/DISSECTION

Introduction

Abdominal aortic aneurysm is a dilation of the aorta, usually below the renal artery. One

time screening with ultrasound should be o#ered to men over 65 who have a history ofsmoking. Dissection is a tear in the aortic wall and is associated with Marfan syndrome

and Ehlers-Danlos syndrome.

Signs and Symptoms

The majority of patients with AAA are asymptomatic. When patients have symptoms, they

might present with abdominal or back pain. The exam will show a pulsatile abdominal

mass.

Dissection will present in an older man with sudden severe tearing chest pain or in-

terscapular back pain.

Diagnostic Testing

AAA is diagnosed on ultrasound. Dissection may have a blood pressure di#erential be-

tween both arms. Widened mediastinum will be present on chest Xray. CT, MRI, and TEE

are more specific than CXR.

Treatment

AAA:

Under 3 cm: No further workup

3cm-3.9cm require repeat ultrasound in 2-3 years

4cm-5.4cm require repeat ultrasound in 6 months

Over 5.5 cm should be surgically repaired.

Dissection:

Type A = Ascending aorta=surgery

Type B = Descending aorta= beta blocker. Surgery is indicated if complete rupture or end

organ damage.



27/48

Imaging should then be done every 6 months to yearly to look for degeneration.

ARTERIAL EMBOLISM/THROMBOSIS

The majority will originate in the heart secondary to MI or AFIB, and will travel to the lower

extremities. These emboli will lodge in areas of excess plaque formation or where there

are bifurcations; the femoral artery being the most prevalent.Acute ischemia may cause

pain, weakness, or numbness; however, the majority are from chronic plaque formation, al-lowing enough collateral circulation, to render the patient asymptomatic. Treatment for an

acute embolism includes anticoagulant therapy.

Giant Cell Arteritis

This is a vasculitis of the extracranial branches of the carotid artery. The patient will pre-

sent with headache, jaw claudication, and visual disturbances. Exam will show scalp

tenderness. The majority will be women over 50 and have an elevated ESR.A normal

ESR virtually excludesthedisease. Diagnosis is made with temporal artery biopsy.

Treated withprednisone to avoid blindness from optic nerve ischemia. Do not wait on

biopsy resultsto starttheprednisone if GCA is suspected.



28/48

25

SYSTOLIC MURMURS

Aortic Stenosis

Usually seen in the

elderly due to

calcification of the

aorta. The other

two etiologies

include congenitalbicuspid/unicuspid

valve and

rheumatic disease

The most common

symptoms include

dyspnea, angina,

dizziness. Patients

may also present

with syncope.

Systolic

crescendo-

decrescendo

murmur. Heard

best at the second

right intercostal

space radiating to

the neck.

Patients who

present with any

symptoms need

surgical correction

immediately due tothe high risk of

sudden death.

Pulmonic Stenosisdyspnea, fatigue,

and syncope.

Heard best at the

left upper sternal

border and may

have ejection click.

Treatment is with

balloon valvotomy.

If severe, then

surgery is

indicated.

Mitral Regurgitation

The main etiology

is mitral valve

prolapse and

coronary disease.

Patients are usually

asymptomatic, but

may have dyspnea

and fatigue.

Murmur:

holosystolic

murmur. Heard

best over apex and

radiates to axilla.

Asymptomatic

patients are not

treated. Those with

symptoms are

given vasodilators.

If severe,

worsening, or no

improvement in

symptoms with

medications, thenext step Is

surgery.

Mitral Valve

Prolapse

This is usually

asymptomatic, but

may cause chest

pain, palpitations,

and anxiety.

Usually present in

women

Murmur: Has a

mid-systolic click,

with a possible late

systolic murmur

depending on the

severity of

regurgitationpresent.

Beta Blockers

Tricuspid

Regurgitation

Most commonly

from dilation of

right atrium and

ventricle

Symptoms are non-

specific, might be

those of right sided

heart failure if

present.

Murmur:

holosystolic

murmur. Heard

best left mid sternal

border. When

regurgitation is

severe, the murmur

will fade.

Diuretics are used

for symptoms.

For

those with heart

failure, therapy

should be aimed at

that.

For severe

disease, surgery is

performed.


29/48

PERIPHERAL ARTERIAL DISEASE

Peripheral arterial disease is synonymous to coronary artery disease. The presentation is

that of angina in the legs (leg pain with exertion and relieved with rest). This can be diag-

nosed with the ankle-brachial index. This is the ratio of the blood pressure in the ankles

to the arm. This is a positive test when the ratio is under .9 (normally the blood pressures

should be equal).All patients receive aspirin. Blood pressure, lipids, and glucose should

be normalized, similar to those with CAD. The first step in treatment is a supervised 12

week exercise regimen. Cilostazol is the only medication that has any proven medical

benefit for the treatment of PAD.

26

DIASTOLIC MURMURS

AorticRegurgitation

Dilation of aortic

root or congenital

bicuspid valve.

Outside the US the

most common

cause is rheumatic

disease

Asymptomatic.

Will present with

wide pulse

pressure (water

hammer pulse).

Blowing quality.

Will become

holosystolic as the

regurgitation

worsens. Heard

best at the left

sternal border.

Treatment is with

surgery for those

who are

symptomatic, orthose with

progressive

enlargement if

asymptomatic.

Pulmonic

Regurgitation

Pulmonic

hypertension

Decrescendo

murmur. Identical

to aortic

regurgitation.

Mitral Stenosis Rheumatic disease

Shortness of

breath. Pregnancy

will exacerbate

symptoms, or

cause initial

symptoms in those

who were

asymptomatic

Low pitch rumble.

Best heard at the

apex.

Treatment is with

balloon valvotomy

or surgery.

Diuretics and beta

blockers may be

used for symptom

control only.

Tricuspid Stenosis

Rheumatic

disease. Will

occur with other

valve abnormality

Symptoms are

similar to other

valvular disorders.

Heard best at 4th

intercostal space

at the lower left

sternal border.

Ace inhibitors and

diuretics may be

used for symptom

control. If no

improvement

balloon valvotomy

or surgery is done.

PhysicianAssistantBoards.com Andrew Reid PA-C


30/48

PHLEBITIS/THROMBOPHLEBITIS

This is a thrombus in a superficial vein, most commonly the saphenous vein, causing in-

flammation of the surrounding tissue. This usually developsin those with varicose veins.

The patient will present with pain, tenderness, and erythema.A palpable cord

(thrombus) will be felt. This is a clinical diagnosis, but a duplex ultrasound is done to rule

out DVT. Treat with elevation, warm compress, compression stockings, and NSAIDs.

Those with concomitant DVT or at high risk for DVT, should be treated with anticoagulation

(low molecular weight heparin or warfarin) for four weeks instead of supportive therapy.

DeepVein Thrombosis

IntroductionClot formation arising from Virchows triad: hypercoagulability, stasis, and endothelial

injury. Virchows triad risk factors include OCP use, pregnancy, cancer, recent hospitaliza-

tion, and/or immobilization.A small percent will not have risk factors and are termed un-

provoked DVT.

Signs and Symptoms

The patient will present with unilateral lower extremity pain, erythema, and swelling. Ho-man sign will be positive on exam: calf pain with dorsiflexion of the ankle. In reality, this

test lacks sensitivity and specificity and should never be used (but for exams this points to

DVT).



31/48

Diagnostic Testing

Begin with wells criteria; if the patient has a score under 2 (meaning low probability) order

a D-DIMER.A normal D-dimer virtually excludes all DVTs.An elevated D-dimer or a well

score over 2 requires duplex ultrasound.

Treatment

Heparin and warfarin are started together. You must overlap the two medications for 5

days, as it takes a few days for warfarin to take e#ect.Also, warfarin inhibits protein C

and S initially, and therefore might increase risk for clot formation the first few days.

Continue warfarin for 3-6 months (INR should be 2-3). Those who have unprovoked DVT

should be kept on warfarin indefinitely as long as there arent any contraindications.

VARICOSE VEINS

Defined as veins that become dilated over3mm. Faulty valves causing blood to pool is

the most common cause leading to dilation of the vein. Patients will often feel leg pain

and swelling. Duplex ultrasound is done to evaluate reflux. Compression hose stockings

and leg elevation are first line treatment followed by sclerotherapy.

VALVULAR DISEASE

The boards want you to know the murmur associated with these valvular disorders.A

defi-nite diagnosis for all is reached with echocardiogram. Most symptoms are similar tothat of CHF: shortness of breath and chest discomfort. Certain maneuvers will a#ect mur-

mur intensity-know them:

Inspiration increases right ventricular filling, but decreases left ventricular filling.

Right sided murmurs Increase with Inspiration.

Left sided murmurs increase with expiration.



32/48

Squatting/leg raise/handgrip increases vascular resistance (afterload) and increases

ven-tricular filling (preload). Increasing preload and afterload increases the sound of all

mur-murs, except that of mitral valve prolapse (this will decreases).

Standing and valsalva decrease venous return (preload). Decrease in preload decreases

the sound of all murmurs, except that of mitral valve prolapse (this will increase).

29

Systolic Murmur

Aortic Stenosis

Usually seen in the

elderly due to

calcification of the

aorta. The other two

etiologies include

congenital biscupid/unicuspid valve and

rheumatic disease

The most common

symptoms include

dyspnea, angina,

dizziness. Patients

may also presentwith syncope.

Systolic crescendo-

decrescendo

murmur. Heard best

at the second right

intercostal spaceradiating to the neck.

Patients who pres

with any sympto

need surgical

correction

immediately due

the risk of sudde

death.

Pulmonic StenosisDyspnea, fatigue,

and syncope

Heard best at the left

upper sternal border

and may have

ejection click

Treatment is wit

balloon valvotomy

severe, surgery

indicated.

Mitral Regurgitation

The main etiology is

mitral valve prolapse

and coronary

disease

Asymptomatic. May

have dyspnea and

fatigue

Holosystolic murmur

heard best over apex

and radiates to axilla

Asymptomatic

patients arent

treated. Those w

symptoms are giv

vasodilators. I

severe, worsenin

or no improveme

with meds, the n

step is surgery

Mitral Valve Prolapse

Asymptomatic. But,

may cause

palpitations, chest

pain, and anxiety.

Usually present in

women.

Mid systolic click

with possible latesystolic murmur

depending on the

severity

Treat with beta

blockers

Tricuspid

Regurgitation

Most commonly from

dilation of right

atrium and ventricle

Symptoms are non

specific. Symptoms

can be the same as

right sided heart

failure

Holosystolic murmur

heard best left mid

sternal border.

When regurgitation

is sever, murmur will

fade.

Diuretics for

symptoms. Thos

with heart failur

treat accordingl

Surgery in seve

disease.


33/48


Diastolic Murmurs

Aortic Regurgitation

Dilation of aortic

root or congenital

bicuspid valve.Outside the US the

most common

cause is rheumatic

disease

Asymptomatic. Will

present with wide

pulse pressure

(water hammer

pulse).

Blowing quality. Will

become

holosystolic as the

regurgitation

worsens. Heard

best at the left

sternal border.

Treatment is with

surgery for those

who are

symptomatic, orthose with

progressive

enlargement if

asymptomatic.

Pulmonic

Regurgiation

Pulmonic

hypertension

Decrescendo

murmur. Identical to

aortic regurgitation.

Mitral StenosisRheumatic disease

Shortness of

breath. Pregnancy

will exacerbate

symptoms, or

cause initial

symptoms in those

who were

asymptomatic

Low pitch rumble.

Best heard at the

apex.

Treatment is with

balloon valvotomy

or surgery.

Diuretics and beta

blockers may be

used for symptom

control only.

Tricuspid Stenosis

Rheumatic disease.

Will occur with

other valve

abnormality

Symptoms are

similar to other

valvular disorders

Heard best at 4th

intercostal space at

the lower left

sternal border

Ace inhibitors and

diuretics may be

used for symptom

control. If no

improvement

balloon valvotomy

or surgery is done


34/48

ENDOCARDITIS

Introduction

Infection of the endocardial surface oftheheart, which extends to the heart valves.

Risk factors include prosthetic heart valves and injection drug users.

Etiology

Streptococci viridans is the most common bacteria in prosthetic and native valves.

Staphylococcus aureus is the most common bacteria in those who are injection drug us-

ers (vegetation will appear on the right).

Sign and Symptoms

The patient will present with a new or change in murmur plusfever. Look for Jane way

lesions (painless plaques on palms and soles), Osler nodes (painful nodes on fingers and

toes), and/orRoth spots (pale retinal lesions surrounded by hemorrhage).

Diagnostic Testing

The first thing to do istoobtain blood cultures (three separated by one hour). Make sure

to obtain the blood culturesbefore antibiotics are given. Next, order an echocardiogram.

DUKE CRITERIA:

Two major, or one major and three minor, or 5 minor:

Major: Positive blood culture, vegetations on echocardiogram, new regurgitant murmur

Minor: Fever, vascular phenomenom (emboli to organs), immunologic phenomenon (roth,

osler,jane), or positive culturesof uncommon pathogen.

TreatmentTreat empirically with [ceftriaxone or vancomycin] AND gentamicin until cultures return.

Then, treat according to the culture.

Prophylaxis against endocarditis is done with amoxicillin and is indicated for those with



35/48

$History of endocarditis

$Prosthetic valves

$Unrepaired cyanotic congenital heart disease.

$Cardiac transplant patients

AND are undergoing:

$Dental procedures that a#ect gingival tissue

$Invasive respiratory procedures

$Invasive treatment of skin infections

PERICARDITIS

Introduction

Inflammation of the pericardium (two layers that cover the heart). The most common

etiologiesareidiopathic and viral.

Sign and Symptoms

The patient will present with pleuritic chest pain (worsened with inhalation) and positional

chest pain (worse supine and improved with sitting).A friction rub is a very specific

physical exam finding (grating sound heard with the bell of the stethoscope).

Diagnostic TestingThe EKG will show di#use ST elevations with PR depressions. The chest xray will showan

enlarged cardiac silhouette. Troponins will be elevated, but do not signify infarction. An

echocardiogram can distinguish between an MI and pericarditis. Pericarditis will have

pericardial e#usion and will not have wall motion abnormalities.



36/48

Treatment

Treatment is with NSAIDs.

CARDIAC TAMPONADE

Introduction

This is a result of excess pericardial fluid, which exerts pressure onto the heart, leading tofilling and hemodynamic compromise.

Sign and Symptoms

Patient will present with Becks Triad: hypotension, mu'ed heart sounds, and distended

neck veins. Pulses paradoxus may also be present. This occurs when there is a drop in

blood pressure of at least 10mmHg with inhalation.

Diagnostic Testing

The EKG will show electrical alternans (QRS complexes alternate in amplitude). The

chest Xray will show an enlarged cardiac silhouette and clear lung fields. The

echocardiogram will show pericardial e#usion and chamber collapse. Definitive

diagnosis and treatment is done withpericardiocentesis.



37/48

REVIEW QUESTIONS

1. How will the ejection fraction di#er in diastolic and systolic heart failure?

2. What is the most common etiology in CHF?

3. What is the first test that should be ordered in the evaluation of CHF?

4. Which drugs lower mortality in heart failure?

5. Which beta blockers lower mortality?

6. What is the medication of choice for hypertrophic cardiomyopathy?

7. What sound will you hear in a patient with an ASD?

8. What classic x-ray finding will you see in coarctation of the aorta?

9. What classic murmur will be heard in patients with PDA?

10.What are TET spells?

11.What is Eisenmenger syndrome?

12.What is the most common cause of secondary hypertension?

13.What are the first line medications for hypertension in patients who are otherwise

healthy?

14.What is the di#erence between hypertension urgency and emergency?

15.What is the classic clinical presentation for a patient in cardiogenic shock?

16.How will atrial flutter and atrial fibrillation present on EKG?



38/48

17.What will happen if a patient who presents with WPW is accidentally given adeno-

sine?

18.What is the classic presentation for a patient presenting with angina?

19.What arethe medicationsof choice for patients with stable angina?

20.What is the treatment of choice for prinzemtal angina?

21.What will di#erentiate unstable angina from NSTEMI?

22.Why should you proceed with caution in administering nitrates in patients withan

inferior MI?

23.What medications should be given to all patients post MI?

24.What do the guidelines say about screening for AAA?

25.Why should steroids be given to a patient with suspected GCA before doing a bi-

opsy?

26.What is the only medication with proven benefit in peripheral artery disease?

27.What is the most common vein a#ected in patients with superficial thrombophlebi-

tis?

28.What are risk factors for DVT?

29.When should a D-Dimer be ordered for DVT?

30.How does respiration a#ect murmurs?

31.What are the most common symptoms in a patient with aortic stenosis?

32.Which valvular abnormality will present with a water hammer pulse?



39/48

33.What arethe most common etiologiesinendocarditis?

34.How will patients with endocarditis present?

35.What is the first test to order in patients with suspected endocarditis?

36.What is the classic EKG finding present in patients with pericarditis?

37.What is Becks triad and when will it be found?



40/48

Review Answers

1.How will the ejection fraction di#er in diastolic and systolic heart failure?

Diastolic dysfunction will have a normal ejection fraction. The problem here is poor

relaxation leading to impaired filling. Systolic dysfunction will have a decreased ejec-

tion fraction. The problem here is poor contraction.

2. What is the most common etiology in CHF?

Coronary artery disease. ALL patients get aspirin, beta blockers, and a statin.

3. What is the first test that should be ordered in the evaluation of CHF?

Echocardiogram. Remember, this is a clinical diagnosis, butthe echocardiogramis used to give added information, such as:estimatatingventricular size and

ejectionfraction. It is NOT used to diagnose CHF.

4. Which drugs lower mortality in heart failure?

ACE/ARBs and beta blockers lower mortality in all patients with CHF. Spiranolac-

tone and eplerenone lower mortality in those who have class 3 or class 4 disease.

Diuretics and digoxin reduce symptoms only - they do not reduce mortality!

5. Which beta blockers lower mortality?

The only beta blockers that have proven benefit in CHF are carvedilol, bisoprolol,

and metoprolol succinate (think succinate like survival - both start with s).

6. What is the medication of choice for hypertrophic cardiomyopathy?

Beta blockers. Do not confuse this with HOCM (also treated with beta blockers).

Hypertrophic cardiomyopathy is a type of diastolic dysfunction. Diuretics are CON

TRAINDICATED in HOCM, but not hypertrophic cardiomyopathy.

7. What sound will you hear in a patient with an ASD?

Systolic ejection murmur with wide splitting of S2.



41/48

8. What classic x-ray finding will you see in coarctation of the aorta?

You will either see rib notching or a 3 sign.

9. What classic murmur will be heard in patients with PDA?

Machine like continuous murmur.

10.What are TET spells?

These are found in patients with tetralogoy of fallot and are episodes of hyper cya-

nosis. Classically, the child will bend down bringing their knees to their chest.

This will decrease venous return, increase vascular resistance making the child

more comfortable.

11.What is Eisenmenger syndrome?

This is seen in patients with a VSD, meaning a shunt connecting both ventricles.

Normally, the pressure is greatest in the left ventricle, which will push oxygenated

blood to the right ventricle. Over time, this excess blood pushed to the right ventri

cle is too much for the lungs to handle. This will lead to pulmonary congestion.

Eventually, this leads to increased pressure in the pulmonary vasculature,and in

turn to the right ventricle(more so than theleft ventricle). This will lead to a re-versal of blood flow, from the right ventricle to the left. Deoxygenated blood will

then leave the heart into the systemic circulation - this is bad!

12.What is the most common cause of secondary hypertension?

Renovascular disease

13.What are the first line medications for hypertension in patients who are other-

wise healthy?

Diuretics, ACE/ARBs, or Amlodipine (long acting dihydropyridine).

14.What is the di#erence between hypertension urgency and emergency?

They will both have a blood pressure >180/120. The di#erence is that

hypertension emergency will also have end organ damage.



42/48

15.What is the classic clinical presentation for a patient in cardiogenic shock?

Hypotensive, altered mental status, and cool/clammy skin.

16.How will atrial flutter and atrial fibrillation present on EKG?

Atrial flutter will have a regular rhythm with a saw tooth pattern. Atrial fibrillation

will have an irregularlyirregular rhythm without p waves.

17.What will happen if a patient who presents with WPW is accidentally given

adenosine?

This may place the patient into ventricular tachycardia or fibrillation.

18.What is the classic presentation for a patient presenting with angina?The patient will have chest pain that is relieved with rest or nitroglycerin. The chest

pain is predictable and reproducible. New chest pain or worsening chest pain can

never be classified as stable angina - this is unstable angina.

19.What arethe medicationsof choice for patients with stable angina?

All patients should receive a beta blocker, aspirin, and nitroglycerin. The beta

blocker will increase filling time and decrease oxygen demand. The

nitroglycerin is used on an as needed bases for chest pain relief.

20.What is the treatment of choice for prinzemtal angina?

Give these patients calcium channel blockers. Their pain is due to smooth muscle

spasm. Avoid beta blockers, as this will result in unopposed alpha stimulation and

worsen the their symptoms.

21.What will di#erentiate unstable angina from NSTEMI?

Both will clinically present the same. Both will have similar EKG findings. The only

di#erence will be that NSTEMI will have elevated cardiac enzymes, while unstable

angina will not. Most MIs can reliably be excluded after 6 hours, but if clinical sus-

picion is high, continue to monitor for 12 hours. The most specific cardiac marker



43/48

will be troponin I. Troponin I is also now used to diagnose reinfarction - look for

the trend.

22.Why should you proceed with caution in administering nitrates in patients

withaninferior MI?

If the right ventricle is involved, nitrates will cause a sudden and severe drop

in blood pressure, as this area is preload dependent.

23.What medications should be given to all patients post MI?

Everyone leaves withanaspirin, beta blocker (metoprolol or atenolol), ACE

inhibitor, and a statin. Clopidogrel is given to patients with aspirin allergy.

24.What do the guidelines say about screening for AAA?

Screen males over the age of 65 who have ever smoked. Only a one time screen-

ing with ultrasound is indicated.

25.Why should steroids be given to a patient with suspected GCA before doing a

biopsy?

Optic nerve ischemia can develop leading to blindness. Saving the patients eye

sight is more important then confirming thediagnosis.

26.What is the only medication with proven benefit in peripheral artery disease?

Cilostazol

27.What is the most common vein a#ected in patients with superficial thrombo-

phlebitis?

Saphenous vein

28.What are risk factors for DVT?

Know Virchows triad: hypercoagulability, stasis, and endothelial injury. If risk fac-

tors are not present, this is termed unprovoked DVT.



44/48

29.When should a D-Dimer be ordered for DVT?

D-dimer is only ordered when there is a low clinical suspicion. If DVT is highly sus-

pected, this should never be ordered. DVT has a high sensitivity, but horrible speci

ficity. This means many things can elevate the value, but it is almost always ele-

vated in patients with DVT. Remember, only order iftheclinical suspicion is low.

30.How does respiration a#ect murmurs?

Inspiration will increase right sided murmurs. Expiration will increase left sided mur

murs. Inspiration will increase right ventricular filling, but decrease left ventricular

filling.

31.What are the most common symptoms in a patient with aortic stenosis?

Dyspnea, angina, and dizziness.

32.Which valvular abnormality will present with a water hammer pulse?

Aortic regurgitation

33.What are the most common etiologiesinendocarditis?

Streptococcus viridans and staphylococcus aureus. Staphylococcus aureus is as-sociated with patients who are injection drug users.

34.How will patients with endocarditis present?

They will have a new murmur or a change in murmur with a fever.

35.What is the first test to order in patients with suspected endocarditis?

Blood cultures! The echocardiogram is done after blood cultures have been col-

lected. Antibiotics are given after three blood cultures separated by one hour have

been collected.

36.What is the classic EKG finding present in patients with pericarditis?

Di#use ST elevations with PR depression. An MI will have ST elevations, but they

will not be di#use.



45/48

37.What is Becks triad and when will it be found?

Becks triad is found in patients with cardiac tamponade. The classic triad consists

of hypotension, mu'ed heart sounds, and distended neck veins.



46/48

QUICK FACTS/ASSOCIATIONS

43

CONDITION FACT/ASSOCIATION

CHFOrthopnea, paroxysmal nocturnal dyspnea,

jugular venous distention, S3

HOCM Sudden death in athlete

Atrial Septal

DefectFixed wide splitting of S2

Coarctation of

AortaX-Ray: Rib notching, 3 sign

PDA Machine like murmur

Tetralogy of

FallotCyanosis with crying or feeding

VSD Holosystolic murmur

Cardiogenic

ShockHypotensive, cool, clammy skin

Atrial Fibrillation Irregular irregular rhythm

Atrial Flutter Saw tooth pattern

AV Block Long PR interval

Mobitz 1 Progressivly lengthening PR interval

Mobitz 2 Dropped QRS without lengthening

Third DegreeBlock

Independent P wave and QRS complex

Paroxysmal

Supraventricular

Tachycardia

Narrow complex tachycardia

Stable Angina Chest pain relieved with rest

PhysicianAssistantBoards.comAndrew Reid PA-C


47/48

44

CONDITION FACT/ASSOCIATION

Prinzmetal AnginaDiffuse ST segment elevations, coronary

artery spasm

ACS Morpine, oxygen, nitrates, aspirin

Cocaine Induced

MINO betablockers, give benzodiazepines

Aortic Aneurysm Tobacco

Aortic Dissection

Marfan Syndrome, Ehlers-Danlos

syndrome, tearing chest pain, Wide

mediastinum

GCA Jaw claudicaton, visual disturbance, >50years of age

PAD Leg pain relieved with rest, cilastazol

Superficial

ThrombophlebitisPalpable Cord

DVTVirchows triad, unilateral LE swelling, pain,

and erythema. Homan sign

Murmurs

Right side murmurs increase with

inspiration. Left side murmurs increase withexpiration

Aortic Stenosis

Systolic, second right intercostal space,

radiates to neck

Mitral regurgitation Holosystolic murumur

MVP Women, anxiety, mid-systolic click

Aortic

Regurgitation Wide pulse pressure. Water hammer pulse

Endocarditis

New murmur, fever, injection drug use,

streptococcus viridans , Jane way lesions,

Osler nodes, Roth spots

Pericarditis

Pleuritic chest pain. Worse upon laying,

improves with sitting. ST segment

elevation, PR depression

PhysicianAssistantBoards.comAndrew Reid PA-C


48/48

Condition Facts/Associations

Cardiac Tamponade

Becks triad (hypotension,

muffled heard sounds,

distended neck vein),

pulses paradoxus, electrical

alternans.

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Chapter 1 Cardiology

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