chapter 4e internal medicine

8/2/2019 Chapter 4e Internal Medicine

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4.5 Internal Medicine

Sushama Rich, MD

Cardiovascular System

Approach to the Cardiac Patient

Most common presenting symptoms:

Chest Pain

Chest pain of cardiac origin is commonly these types:

Pericardial

Anginal

Myocardial infarction

Aortic dissection

Pericardial pain

Sharp pain that radiates to the trapezius and is aggravated by breathing. Relieved by leaning forward and

remaining still.

Causes Pericarditis

Diagnosis

On auscultation shows pericardial friction rub

ECG shows ST segment elevation

Anginal pain

Substernal chest pain that is squeezing in nature radiates to the jaw, left arm, or left shoulder.

It is aggravated or brought on by exercise.

Relieved by rest or nitroglycerin

Chest pain usually never lasts more than 20 minutes

Diagnosis

Usually clinical ECG shows ST segment changes

Myocardial Infarction

Same as anginal pain

Duration usually greater than 20 minutes

Not relieved by rest

Diagnosis

ECG: ST segment changes

Blood tests show CPK-MB, Troponin

Aortic dissection

Sudden onset, tearing type of pain that radiates to the back mid scapular

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Cardiac Dyspnea

Cardiac dyspnea is labored breathing that is caused by edema in the bronchial walls and stiffening of the lungs

due to alveolar edema.

Dyspnea is due to a reduction in cardiac output

Dyspnea is aggravated by exercise and relieved sometimes by rest

Causes of cardiac dyspnea

Congestive heart failure

Coronary artery disease

Types of cardiac dyspnea

Orthopnea: dyspnea that occurs in the recumbent position due to increased paroxysmal nocturnal dyspnea

Paroxysmal nocturnal dyspnea: dyspnea that wakes a patient up in the middle of the night

Palpitations

Palpitations are the perception of ones own heart beat. Most common cardiac cause is arrhythmias.

Diagnostic and cardiovascular procedures

Chest X-ray

Shows

Heart size

Heart shape

Great vessels

Electrocardiogram

Can diagnose old or current heart attacks

Disturbances of heart rhythm

Detects thickening of the wall

Holter Monitoring

Uses a portable recording device worn by the patient under the clothing for 24 hours. This procedure is used for:

Documents arrhythmias

Classifies arrhythmias Diagnoses silent ischemia

Assess results of antiarrhythmic drugs

Exercise Stress Test

Used to:

Diagnose CAD

Evaluate known CAD

Contra-indications

A M.I.-within the last 48 hours

Severe aortic stenosis


Echocardiography

Echocardiography reveals the anatomy of the heart. This technique is use for:

Valvular disease

Congenital heart disease

Function of the heart muscle

Flow of blood- this can be seen by color Doppler (blue and red)

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Coronary Angiography

Coronary angiography is the best test for CAD

Vessels as small as 1mm can be visualized

Any occlusion of the artery is seen as narrowing, beading or occlusion of the vessel

Myocardial perfusion

Myocardial perfusion imaging uses radioactive thallium. Indications

Initial evaluation of patients

Prognosis after an acute M.I.

To detect extent of scarring after an acute M.I.

MUGA Scan Equilibrium Radionuclide Angiography

After receiving a small injection of a radioisotope, the patient lies on a table and multiple images are recorded

by scintillation camera.

Uses

Evaluates cardiac function

Measures ejection fraction

Show the contraction of different regions of the heart

Coronary Artery Diseases

Two types of coronary artery disease:

Atherosclerotic coronary artery disease (ASCAD)

Non atherosclerotocic coronary artery disease (NASCAD)

Atherosclerotic Coronary Artery Disease (ASCAD)

Definition

The basic lesion is atherosclerosis of the coronary arteries. The pathological hallmark of this disease is athero-

sclerotic plaque. Plaque is made up of hypertrophied intimal smooth muscle cells, lipids, and a fibrous cap.

Risk factors for the development of ASCAD

Increases with age

Gender: more common in men

Serum cholesterol: high levels of LDL. This is the single most important risk factor, low levels of HDL

Smoking

Hypertension

Diabetes mellitus

Family history

Oral contraceptives

Pathogenesis of ASCAD

As the typical plaque develops, it begins to occlude the coronary arteries; this leads to a reduction of blood flow

to the myocardium. In order for ischemic symptoms to develop at least 70% of the coronary artery has to be occlud-

ed by the plaque. A variety of factors influence the clinical course of CAD, like the length of the lesion, vasomotor

tone, rupture of the plaque, erosion of the plaque and ultimately thrombus formation.



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Clinical Features of ASCAD

The most common feature of ischemia to the myocardium is angina pectoris

Ischemia could proceed without any symptoms to an M.I.

Ischemia may cause sudden death

Angina could present in three forms.

Stable angina Chest pain or pressure produced by exertion

Radiates to the jaw or arm

Brought on by exercise

Relieved by rest

Associated with exertional dyspnea

Does not last more than 20 minutes

If pain lasts more than 20-30 minutes and is not relieved by nitro, suspect M.I.

Unstable angina

Chest pain same as above

It is progressive in nature: The episodes are more frequent and last longer but never more than 20 minutes

It is of increasing severity, duration, or frequency Printzmetals angina

The hallmark of this disease is S-T segment elevation on ECG

S-T segment elevation indicates transmural infarction of the myocardium

It is classically caused by coronary vasospasm that occurs near an atherosclerotic plaque

It more commonly affects women; it occurs more often at night, not associated with exertion

There is no increase serum markers for an M.I.

Diagnosis of Angina

Clinical symptoms are key

Resting ECG: is usually normal between episodes

Sometimes one may see new horizontal or down sloping S-T segment

New T wave inversion

S-T segment elevations indicates variant angina

Exercise stress test: The appearance of horizontal or down sloping of S-T segment depression of more than 1

mm indicates ischemia

Exercise stress test associated with thallium stress test is much more valuable

Coronary angiography is done for confirming a suspicion, diagnosis, risk stratification, assessment of CABG

or angioplasty

Treatment of Angina

Nitrates

B-adrenergic blockers: limit myocardial oxygen demand

Calcium antagonists: prevent coronary spasm, hence ideal for variant angina

PCTA: percutaneous transluminal angioplasty

Rotational atherectomy

Coronary artery bypass surgery: indicated for multi-vessel disease

Beta blockers should not be used in variant angina because blockade of the alpha receptors cause alpha

receptor mediated vasoconstriction



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Myocardial infarction

Occurs when there is 100% occlusion of the coronary artery.

Pathogenesis

Acute M.I is almost always associated with a thrombus superimposed upon a significant plaque

It takes at least 20 minutes of ischemia to cause an irreversible injury

Most often occurs in the morning when there is decreased adrenergic activity Myocardial necrosis begins in the sub-endocardium and spreads to the epicardium

Most common artery to be blocked is the left anterior descending

Table 1. Classification of Myocardial Infarction

Characteristic Q-Wave MI Non-Q Wave MI

Prevalence 47% 53%

Complete coronary obstruction 80-90% 15-25%

Elevated ST-T segment 80% 25%

Depressed ST-T segment 20% 75%

Postinfarction angina 15-25% 30-40%

Early reinfarction 5-8% 15-25%Infarct size Moderate to large Usually small

Acute complications Common Uncommon

Therapy

Thrombolysis Indicated Not indicated

Beta Blockers Indicated Not indicated

Clinical Features

Chest pain for more than 30 minutes

Associated symptoms: dyspnea, diaphoresis, nausea, vomiting, palpitations, and light-headedness.

Symptoms simulate: GI-upset

Physical Exam Signs of ischemia: S4, new MR murmur

Signs of heart failure: increased JVP, crackles in lung fields, S3

Diagnostic Studies

ECG: diagnostic in 85% of cases

ST segment elevation, Q waves, T wave inversion

Serum markers: CPK MB is increased within six to ten hours post MI, troponin I increases within 6-10 hours

post MI, LDH1 increases within 48-72 hours

Echocardiogram: New wall motion abnormality

Treatment

Treatment of pain: Nitroglycerine, morphine sulfate

Thrombolysis

Indications for thrombolytic therapy are the following:

Chest pain

ECG: ST segment elevation

Less than 12 hours from onset

No contra indication



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Absolute contra-indications for thrombolytic therapy:

Active internal bleeding

Suspected aortic dissection

Recent head trauma

Blood pressure greater than 200/120

Pregnancy

CVA

Trauma or surgery within two weeks

Relative contra-indications:

Active peptic ulcer disease

Known bleeding diathesis

Menstruation

Prolonged CPR

Drugs used for thrombolytic therapy:

Alteplase (TPA): Fifteen mg IV-bolus, .75 mg per kilogram over 30 minutes, 5 mg per kilogram over 60

minutes

Streptokinase (SK): 1.5 Mu IV over 30-60 minutes

Reteplase (RPA): 10 u IV repeat in 30 minutes

Drugs used for arrhythmias

Prophylactic Lidocaine

Procainamide for acute recalcitrant arrhythmias

Treatment of conduction disturbances

Atropine

Treatment of heart failure

Diuretics for mild congestive heart failure

Digitaliscontroversial

Treatment of mitral regurgitation and acute ventricular septal defect

Arteriolar vasodilator therapy Intra-aortic balloon pumping

Adjunct therapy

Beta-blockers reduce early mortality by reducing ventricular arrhythmias

ACE inhibitors reduce the extent of remodeling and incidents of late mortality

Anti-coagulants: heparin

Aspirin

Diltiazem: for non Q wave infarcts

Angioplasty



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Complications of MI

Ventricular arrhythmias

Acute conduction abnormalities

Ventricular aneurysm

Pump failure

Mitral regurgitation Ventricular septal defect

Cardiac rupture

Left ventricular aneurysm

Dresslers syndrome occurs in 2-10 weeks post MI. Presents as fever, malaise, pericarditis and pleuritis

Pericarditis

Prognosis

Depends on the number of vessels affected. Extent of left ventricular damage

Non-atherosclerotic Coronary Artery Disease

Causes Coronary embolism occurs in infective endocarditis, atrial fibrillation

Collagen vascular disease affects medium-sized arteries. Ex: SLE RA, Wegeners granulomatosis

Radiation therapy

Cardiac transplantation

Heart Failure

Heart failure is the inability of the heart to pump blood to meet the oxygen requirement of the body tissues.

Heart failure is a syndrome of many diseases that interfere with cardiac function. There are two types of heart fail-

ure, low output and high output. Low-output failure occurs due to reduction in the cardiac output. High-output

failure occurs due to an increase in cardiac output.

Etiology Ischemic heart disease

Hypertensive heart disease

Cardiomyopathies

Valvular heart disease

Pericardial disease

High output failure: AI, MR, VSD, AV fistulas, severe anemia, sepsis, thyrotoxicosis, beri beri

Pathophysiology

Systolic dysfunction: Could be of two types, decrease in contractility or increased after load

Decreased contractility occurs due to MI valvular heart disease, hypertension, cardiomyopathies

Increased after load occurs due to hypertension, aortic stenosis or dilated cardiomyopathy and valvular

regurgitation Diastolic dysfunction: Hypertrophic cardiomyopathy may occur in hypertension and amyloidosis

Descriptive Terminology

High-output failure occurs due to increased cardiac output. Example, chronic severe anemia causes volume

overload

Left-sided failure occurs when the left ventricle is failing. Example, MI

Right-sided failure: Most common cause is left ventricular failure. It may also occur due to COPDs in which

case it is called corpulmonale



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Clinical Features

Dyspnea

Orthopnea that leads to nocturnal cough

Paroxysmal nocturnal dyspnea

Nocturia

Edema

Anorexia

Right upper quadrant pain

Fatigue

Physical Signs

Acute heart failure

Hypo or hypertension, tachycardia, diaphoresis, cyanosis, cold and pale extremities

Left-sided failure

Pulmonary rales, cardiac murmurs, tachypnea

Right-sided failure

Increased JVP, pleural effusions, congestive hepatomegaly, ascites, jaundice, peripheral edema

Diagnosis

Chest X-ray shows pulmonary edema, bilateral pleural effusions

Echocardiogram: Decreased ejection fraction and increased chamber size indicate systolic dysfunction, hyper-

trophy and or abnormal inflow across the mitral valve indicates diastolic dysfunction

Pulmonary artery catheterization: Increased PCWP, decreased CO and increased SVR indicates low-output

failure

Classification

Class 1: Symptomatic only with greater than ordinary activity

Class 2: Symptomatic with ordinary activity

Class 3: Symptomatic with minimal activity Class 4: Symptomatic at rest

Treatment

Diet: reduction in sodium

Diuretics: Loop or thiazide diuretics

ACE inhibitors

Digoxin

Beta-blockers

Spironolactone

Anti-coagulants

Cardiomyopathies

Cardiomyopathies is myocardial dysfunction that is not due to ischemic valvular hypertensive or congenital

heart disease. Types of cardiomyopathy:

Dilated cardiomyopathy

Restrictive cardiomyopathy

Hypertrophic cardiomyopathy



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Dilated cardiomyopathy: Occurs due to ventricular dilation with decrease in contractile function of the left,

right or both ventricles in the absence of pressure overload, volume overload or CAD. It almost always results in

congestive heart failure.

Etiologies

Ischemia

Valvular disease: Chronic AI or MR, hypertension

Toxic: most common cause is alcohol induced

Drug therapy: Example, Doxirubicin therapy

Infectious: Example, viral HIV

Idiopathic

Endocrine disorders: Example, thyrotoxicosis, hypothyroidism, acromegaly

Metabolic disorders: Example, hypophosphotemia, hypocalcemia, thyamine deficiency

Hemoglobinopathies: Example, sickle cell anemia, thalassemia

Collagen vascular disease: Example, SLE, and scleroderma

Clinical Features

Include both left and right-sided heart failure Chest pain

Physical Signs

Signs of left-sided heart failure

Diagnosis

History

Stress test

Cardiac catheterization

Lab studies

Echocardiography is the most important test that reveals dilated, poorly contracting left and right ventricles

Treatment

Standard heart failure therapy

Immuno suppressants

Cardiac transplantation

Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy is a disorder in which there is hypertrophied septum, mitral valve prolapse, and

left ventricular outflow obstruction.

Etiology

Inherited autosomal dominant Some sporadic cases are known to occur

Specific abnormalities of cardiac myosin occurs



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Pathophysiology

Hypertrophied septum encroaches upon the left ventricular outflow

Obstruction of the anterior leaflet of the mitral valve

Systolic anterior motion of the anterior leaflet of the mitral valve

Which then leads to papillary muscle displacement

Diastolic dysfunction, the left ventricle is so stiff that it does not fill properly during diastole Decreased coronary perfusion occurs

Leads to syncope

Clinical Features

Dyspnea

Angina

Syncope

Arrhythmias

Palpitations


Physical Examination

Murmur: mid- to late-holosystolic murmur

The murmur is reduced in intensity with the valsalva murmur, and increased in intensity from squatting

Carotid upstroke has a spike and a dome character to it

Diagnosis

ECG; left ventricular hypertrophy

CXR; cardiomegaly

Echocardiogram is the gold standard for diagnosis: shows septal hypertrophy, mitral regurgitation, outflow

tract obstruction

Treatment

Medical Therapy

Beta blockers

Calcium channel blockers

Digitalis: only in the end stage of the disease

Surgical treatment

Myomectomy; surgical reduction of the septum

Mitral valve replacement

Pacemaker implantation

Restrictive Cardiomyopathy

Definition: Impaired ventricular filling due to decreased compliance caused by increased stiffness of the wall

Etiology

Infiltrative diseases; examples are amyloidosis, hemochromatosis, carcinoid syndrome, sarcoidosis, idiopathic

eosinophilia

Metastatic diseases

Radiation therapy

Idiopathic

Scleroderma



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Pathology

Increased diastolic stiffness

Systolic function is usually normal in the early stages

Left ventricular pressure is above normal

Systolic function is compromised in the late stages

Decreased ventricular cavity size Decreased cardiac output

Clinical Features

Right-sided failure is greater than left-sided failure

Peripheral edema

Dyspnea

Refractory to treatment with diuretics

Thromboembolic events

Physical Examination

Increased JVP

Cardiac S3 and S4 Congestive hepatomegaly

Ascites

Jaundice

Peripheral Edema

Diagnostic Studies

Chest X-ray shows normal chamber size, enlarged atria, pulmonary congestion

ECG

Echo shows symmetrical wall thickening, increased diastolic end pressure, decreased atrial filling

Treatment

Treat underlying disease

Symptomatic therapy with diuretics

Valvular Disease

Aortic Stenosis

Etiology

Congenital (e.g. bicuspid valve): In young and middle-aged adults, bicuspid aortic valve with progressive

scarring and calcification is the most common cause

Rheumatic Disease Degeneration and calcification of a tricuspid valve

Aortic stenosis is more common in men

Disease Process

The outflow obstruction leads to left ventricular hypertrophy

Symptoms

Symptoms are not usually present until the obstruction is advanced



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Cardiac symptoms

Angina Pectoris

Syncope

Dyspnea

Physical Findings

Ejection murmur is typically harsh and is often loud. The duration of the murmur is proportional to the

severity of the obstruction

The carotid pulse is characteristically reduced in amplitude and prolonged in duration

Diagnosis

Echocardiography and the Doppler confirms the diagnosis

The Doppler flow velocity can determine the severity

Treatment

Surgery for patients with cardiac symptoms and severe aortic stenosis

Avoid vigorous activities

Cardiac catheterization for patients with severe aortic stenosis

Chronic Aortic Regurgitation

Etiology

Bicuspid Aortic valve

Aortic root dilatation

Endocarditis

Associated with some connective tissue disorders. (e.g. Marfans Syndrome)

Disease Process

Aortic regurgitation results in a volume overload of the LV with ventricular dilatation. The stroke volume is

increased as the LV ejects both the forward output and the blood that regurgitated into the ventricle duringdiastole

Symptoms

Palpitations/pounding in the chest or head

Dyspnea due to elevated pulmonary venous pressure

Angina pectoris due to decreased diastolic coronary perfusion

Physical Findings

Wide pulse pressure

Systolic ejection murmur

Third heart sound

Diagnosis

Endocardiography can determine the cause of aortic regurgitation in many patients



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Treatment

Surgery for patients with LV systolic dysfunction and onset of symptoms

Oral vasodilator therapy for asymptomatic patients with significant aortic regurgitation and normal systolic

function. By decreasing systemic resistance regugitant volume is reduced

Acute Aortic RegurgitationEtiology

Infective endocarditis

Prosthetic aortic valve dysfunction

Proximal dissection of the aorta

Disease Process

Severe acute condition places a volume overload on a left ventricle that has not had the time to dilate in a

compensatory manner. The increased ventricular diastolic pressure leads to left atrial pressure and pul-

monary congestion

Physical Findings

Sinus tachycardia is often present

Diastolic murmur may be less prominent and shorter in duration

Third heart sound gallop can be heard

Diagnosis

Endocardiography and Doppler assess the status of Aortic regurgitation, its cause, and the underlying ven-

tricular function

Treatment

Vasodilator therapy

IV nitroprusside for severe heart failure

Surgical therapy is the definitive treatment

Mitral Stenosis

Etiology

Rheumatic Fever

Occurs twice as frequently in female patients as male

Disease Process

Progressive thickening of the valve leaflets and fusion of the commisures. Calcification contributes to the

valve immobility and stenosis

The chora tendinae also may thicken and fuse

The valve scarring progresses slowly before symptoms arise. Elevated left atrial pressure leads to pulmonaryartery hypertension that can provoke RV failure and functional tricuspid regurgitation

Symptoms

Exertional dyspnea, orthopnea and paroxysmal nocturnal dyspnea due to pulmonary venous congestion

Fatigue and weakness when the cardiac output decreases

Symptom onset is most common in the third or the fourth decade of life

These patients, who may get atrial fibrillation, a common complication, may not tolerate increased heart rate

Embolism from enlarged left atrium can cause stroke, especially when atrial fibrillation is present



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Physical Findings

Left atrium is enlarged because mitral stenosis increases the left atrial pressure

Loud first heart sound

As the severity of mitral stenosis increases, the interval between the 2nd heart sound and opening snap

decreases

Diagnosis Echocardiography can detect mitral valve thickening, provide information about valve mobility and the

degree of calcification.

Treatment

-blockers

Control atrial fibrillation

Anticoagulants to decrease the risk of thromboembolism

Percutaneous mitral valve balloon valvuloplasty

Valve replacement

Mitral Regurgitation

Etiology

Mitral valve prolapse

Ischemic heart disease can cause papillary muscle ischemia

Left ventricular (LV) dilation

Mitral Annulus calcification

Rheumatic heart disease

Acute mitral regurgitation can result from the rupture of chorda tendinae or papillary muscle

Disease Process

Chronic mitral regurgitation produces a volume overload

Left atrium is moderately enlarged and there is elevation of left atrial pressure, which can lead to pulmonary

congestion and dyspnea

Physical Findings

Holocystic murmur is characteristic, which begins immediately after a soft 1st heart sound. It is high-pitched

Diagnosis

Echocardiography can assess mitral valve structure, cardiac chamber size, and left ventricle function

Doppler assesses the severity of the mitral regurgitation

Treatment

Vasodilater therapy to decrease the afterload (e.g. ACE inhibitors)

Valve replacement

Mitral Valve Prolapse (MVP)Etiology

MVP is common and can cause mitral regurgitation ranging from trivial to severe

Can be isolated, or associated with connective tissue diseases (e.g. Marfans)

More common in women

MVP can be inherited (autosomal dominant)

MVP is benign in most patients



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Disease Process

Mitral valve in these patients is usually large, floppy, and redundant with elongated chorda tendinae

Middle-aged or older men may be more likely to develop severe regurgitation or complications

Complications

Ineffective endocarditis

Cardiac arrhythmia

Thromboembolism

Symptoms

Most MVP patients are asymptomatic, but the following symptoms can be present:

Atypical chest pain

Palpitations

Fatigue

Anxiety

Postural phenomena

Neuropsychiatric symptoms

Diagnosis

Echocardiography is used to confirm the diagnosis

Treatment

Antibiotic endocarditis prophylaxis in all MVP patients with structural valve changes and/or murmur of

regurgitation

-blockers

Pericardial Diseases

Pericarditis and pericardial effusion

Pericardial tamponade Constrictive pericarditis

Pericarditis is an inflammation of the pericardium. Pericardial effusion is an accumulation of fluid within the

pericardial cavity.

Etiologies

Infectious

Viral: Coxsackie B virus, echovirus, adenovirus, EBV, VZV, HIV

Bacterial: (From endocarditis, pneumonia or cardiac surgery), S. Pneumoniae, S. Aureus, and TB

Non-infectious

Idiopathic

Uremia Acute MI

Post MI: Dresslers syndrome

Post pericardiotomy

Neoplastic: Lung, breast, renal cell

Trauma: Chest trauma

Pericardial effusion without pericarditis, CHF, cirrhosis



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Clinical Features

Chest pain: Burning, stabbing increased by breathing, reduced by leaning forward, radiates to the trapezius

Fever

Physical Exam

Pericardial friction rub is the gold standard for clinical diagnosis

Pericardial effusion will cause distant heart sounds, dullness over the left posterior lung field (Ewarts sign due

to compressive atelectasis)

Diagnostic Studies

ST segment elevation throughout the ECG, depression of the PR segment is diagnostic and unique to peri-

carditis

Echocardiography will show pericardial effusion. Echo-free space between the two layers of the pericardium

Chest X-ray: Water bottle appearance of the heart

Treatment

NSAIDS

Steroids for refractory idiopathic disease Treat underlying cause

Cardiac Tamponade

Cardiac tamponade is a life-threatening condition due to a rapid development of pericardial effusion that is

compressing the heart.

Pathophysiology

The heart cannot fill adequately

Increased intra-pericardial pressure

Diastolic pressure is elevated

Pulsus paradoxus: Inspiration causes a decrease in intra-pericardial and right atrial pressures which leads toan increase in venous return, which leads to increased RV size which leads to septal shift to the left which

leads to decrease in left ventricular stroke volume and output

Clinical Features

Dyspnea on exertion

Fatigue

Orthopnea

Physical Exam

Pulsus paradoxus: When the systolic blood pressure falls more than 10 mm of mercury during inspiration.

This implies that stroke volume is falling during inspiration due to compression

Neck vein distension

Diagnosis

Echocardiogram shows effusion

Treatment

Emergency pericardiocentesis



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Constrictive Pericarditis

Constrictive pericarditis is caused by diffuse thickening of the pericardium due to inflammatory process

Etiology

Post viral

Radiation

Uremia

TB

Idiopathic

Post surgical

Clinical Features

Dyspnea

Orthopnea

Ascites

Edema

Jaundice

Typical symptoms are right-sided heart failure

Diagnosis

ECG shows atrial arrhythmias

Echocardiography is not as valuable

MRI is capable of measuring pericardial thickness

Treatment

Surgical removal of the pericardium

Aortic Diseases

Aneurysms of the aorta Aortic dissection

Aneurysms of the Aorta

An aneurysm of the aorta is permanent dilation of an artery due to weakness of the wall.

Etiology of Aortic Aneurysms

Aneurysms of the ascending aorta is caused by syphilis, Marfans syndrome, and cystic medial necrosis

Aneurysms of the abdominal aorta are caused by atherosclerosis. This type increases with age, smoking, and

hypertension and has increased incidence in men. The most common site is at the bifurcation of the aorta

Aneurysms of the femoral artery occur due to mycotic infections. It most often occurs in IV drug users

Pathophysiology

Atherosclerosis is the hallmark of aneurysms



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Clinical Features

Small aneurysms are asymptomatic. Large aneurysms cause back pain and pulsating sensations

Blue toe syndrome: sudden occurrence of a very painful blue toe most commonly caused by emboli

Aortic aneurysms can rupture causing massive bleeding, syncope, hypotension and diarrhea with Tenessmus

Musculoskeletal pain

Diagnosis

Most of them are found incidentally on physical exam

Ultrasound is the gold standard

CT scan is used to localize ruptures

Aortograms are rarely used

Treatment

Aneurysms less than 4 cm are usually watched

Aneurysms greater than 5 cm or threat of ruptureconsider surgery

Aortic Dissection

Aortic dissection occurs when the tunica intima tears and blood dissects along the media.

Etiology

Aneurysm of the ascending aorta is most commonly caused by hypertensive aneurysm

Dissection of the descending aorta occurs due to rupture of an atherosclerotic plaque

Blunt trauma can cause either an ascending or a descending aneurysm

Clinical Features

Crushing chest pain that radiates to the back and felt between the scapula

Symptoms of aortic insufficiency may occur

Diagnosis

Murmur of aortic insufficiency

Chest X-ray will show widened media stinum

CT scan confirms diagnosis

Treatment

Stabilize hypotension

Lower systolic blood pressuresurgery



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Co

mmonLaboratoryValues

Age

WBCCo

unt

RBCCount

Hemoglobin

Hematocrit

MCH

MCHC

MCV

RDW

(cells/mm

3)

(106/L)

(g/dl)

(%)

(pg)

(g/dl)

(m

3)

[Sl:109/L]

[Sl:1012/L]

[Sl:g/L]

[Sl:pg]

[Sl:g/L]3

[Sl:fL]

Adultmale

4,500-1

1,000

4.73-5.4

9

14.4

0-16.60

42.9-49.1

27-31

33-37

76-100

11.5-14.5

AdultFemale

4,000-1

1,000

4.1-4.87

12.2-14.7

37.9-43.9

27-31

33-37

76-100

11.5-14.5

Age

PlateletCount

Lymphocytes

Neutrophils,

Neutrophils,

Eosin

ophils

Basophils

Monocytes

(103/L)

Total

Band

Segmented

(%W

BC)

(%WBC)

(%

WBC)

(%WBC)

(%

WBC)

(%WBC)

AdultMale

238,000

34%

3.0%

56%

2

.7%

0.5%

4%

AdultFemale

270,000

34%

3.0%

56%

2

.7%

0/5%

4%

Increasedin

Decreasedin

Leukemiasafter

splenectomy,acute

hemorrh

age,

leukemia,

polycyth

emiavera

Anyviral

infection,

AIDS,MMR,

Acuteand

chronic

lymphocytic

leukemias

Severeexercise,

labor,

newborns,

bacterial

infections,

leukemias,non-

infectivetissue

damage

NAACP

Neo

plasms,

allergies,

Add

isons

dise

ase,collagen

vasculardisease,

parasites

Chronic

myeloid

leukemia

Bac

terial

infection,

sub

acute

bac

terial

end

ocarditis

,ch

ronic

infections,

leukemia

Disseminated

intra-vascular

coagulation,

TTP,ITP

,

eclampsiaand

pre-eclampsia

Pancytopenia,

aplastic

anemia,

neutropenia,

severe

infections,

severe

osteomyelitis

Stress,burns,

trauma,

chemotherapy

Steroids,stress,

Cushings

syndrome

Acute

rheumatic

fever,lobar

pneumonia,

steroidtherapy,

stress,

thyrotoxicosis