Clinical med 1 ( EXAM 2) ( Traumatic-infectious & inflammatory heart conditions)

pericardial effusion

is excess fluid between the heart and the sac surrounding the heart, known as the pericardium. Most are not harmful, but they sometimes can make the heart work poorly

Definition Pericardial Effusion

•Effusion present when accumulated fluid within pericardial sac exceeds small amount that is normally present

•Acute or chronic

•Hemodynamically stable - unstable

Epidemiology Pericardial Effusion

•Small effusions are often asymptomatic

•Found in 3% of subjects in autopsy studies

•Observed in all age groups

•Mean occurrence 30-49yo

•Mortality/morbidity dependent on etiology/comorbid conditions

•M = F

Etiology Pericardial Effusion

•Can occur as a component of almost any pericardial disorder

•Acute pericarditis

•Autoimmune disease/Neoplastic disease

•Postmyocardial infarction or cardiac surgery

•Sharp or blunt chest trauma

•Drugs (procainamide, hydralazine, isoniazid)

•Acute pericarditis : Viral

•Enteroviruses: coxsackie, enterovirus and echoviruses

Clinical history-hemodynamically stable Pericardial Effusion

•Will have no symptoms specific to effusion

•May have symptoms of underlying cause

Clinical history-hemodynamically unstable Pericardial Effusion ( 1.This is when pericardial effusion is progressing to cardiac tamponade)

•Fatigue

•Dyspnea

•Elevated jugular venous pressure

•Edema

•Chest pain, pressure, discomfort

Improved by sitting up/leaning forward

Intensified by lying supine

Physical examPericardial Effusion

•Pulsus paradoxus

Decrease in systolic blood pressure of more than 10mm Hg with inspiration

•Friction rub left lower sternal border

•Tachycardia/Tachypnea

Muffled heart tones

•Ewart sign

Dullness to percussion beneath angle of left scapula

•Extremities

Weak peripheral pulses

Edema

Cyanosis

1.Decrease in systolic blood pressure of more than 10mm Hg with inspiration, signaling falling cardiac output during inspiration

2.Ewart's sign - Dullness to percussion beneath angle of left scapula from compression of left lung by fluid

Physical exampulsus paradoxus - Pericardial Effusion

•Place a blood pressure cuff on patient's arm

•Very slowly deflate cuff while listening for Korotkoff sounds

•Note pressure you first hear sounds during expiration

•Repeat process and record pressure where sounds are heard during inspiration

•Difference between the two numbers is pulsus paradoxus

Differential diagnosis Pericardial Effusion

•Acute Pericarditis

•Cardiac Tamponade

•Dilated Cardiomyopathy

•Acute MI

•Pulmonary Embolism

WorkupPericardial Effusion : Imaging

•Echocardiogram (initial test of choice)

•PA and lat CXR

•CT chest

•MRI chest

Workup Pericardial Effusion

•CBC w/ diff

•CMP

•Cardiac Biomarkers + EKG

•Pericardial effusion >>>> diagnostic purposes

•Fluid analysis

How's it diagnosed? Pericardial Effusion

•Confirming presence of a pericardial effusion

•Assessing any hemodynamic impact

•Establish cause if possible

Echocardiography*

•Imaging modality of choice for diagnosis*

CXR Pericardial Effusion

•Findings are variable, depending on etiology and size of effusion

•*Not specific and or diagnostic

•< 250 mL may not result in significant findings

•Larger effusions present with an enlarged cardiac silhouette/clear lung fields

*Water bottle-shaped heart

EKG Pericardial Effusion

•Early pericardial effusion

•ECG typically displays diffuse ST elevation*

EKG Pericardial Effusion Triad

•Low QRS voltage

•Tachycardia

•Electrical alternans

Clinical managementPericardial Effusion

Consultations

•Cardiologist/Cardiothoracic surgery

Medical care

•Focused to determine etiology

•Treatment of underlying disease(s)

Clinical interventionpericardiocentesis - Pericardial Effusion

Pericardial fluid drainage : •Indications for urgent drainage depend on level of hemodynamic compromise

•Choice of pericardiocentesis/open drainage based on local preference and experience

Prognosis Pericardial Effusion

HIV/AIDS, cancer or otherwise immunocompromised ® high mortality rates

Complications

•Ventricular rupture

•Dysrhythmias

•Pneumothorax

•Myocardial injury

•Infection

Recurrence may be 90% in cancer patients

May progress to cardiac tamponade

Cardiac tamponade

compression of the heart by an accumulation of fluid in the pericardial sac

clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise.

medical emergency, the complications of which include pulmonary edema, shock, and death

Definition Cardiac Tamponade

•Pericardial effusion that causes accumulation of enough fluid to compress the heart enough to cause cardiac function impairment

•Results in a stiffening of the pericardium if not corrected

•Classification

Acute

Subacute

Epidemiology Cardiac Tamponade

•Approximately 2 cases/10,000 in US

•2% of penetrating trauma cases have cardiac tamponade

•M > F [1.5 : 1]

•Traumatic and infectious sources more common in younger people

•Uremic and Neoplastic more common in older populations

Etiology Cardiac Tamponade

•Rate of fluid accumulation is very important

•Rapid

•Slow

Risk factors Cardiac Tamponade

•Pericarditis of any etiology

•Active Cancer

•Penetrating Trauma

•Acute Renal Failure/Uremia

•Tuberculosis infection

•Systemic Autoimmune Disease

•History of HIV/IV drug abuse

•H/O chest radiation

•Recent pacemaker/AICD implantation or other recent cardiac surgery

•Recent MI

Clinical history Cardiac Tamponade

•Chest Pain

•Dyspnea/tachypnea

•Cough

•Pulsus paradoxus

Physical examCardiac Tamponade

Beck's Triad

•Hypotension

•Jugular Venous Distention (JVD)

•Muffled Heart Tones

•Decreased urine output (UOP)

•Confusion

•Tachycardia

•Pulsus Paradoxus

•More than 10mmHg drop in systolic BP with inspiration

•Skin/Extremities

•Pale/mottled skin

•Cool extremities

•Peripheral edema

Differential diagnosisCardiac Tamponade

•Pericarditis/Myocarditis

•Acute Coronary Syndrome (ACS)

•Pneumothorax

•Pulmonary Embolism

•Pleural Effusion

•Thoracic Aortic Dissection

•Hemopericardium

WorkupCardiac Tamponade LABS

•CBC wiTh differential

•CMP

•Cardiac Biomarkers + EKG

•

WorkupCardiac Tamponade Imaging

•CXR

•Cardiomegaly → effusion > 250mL

•Ultrasound (diagnostic test of choice for imaging)*

•FAST Exam

•Focused Assessment with Sonography for Trauma

EKG of cardiac tamponade

1.Low voltage and PR segment depression are ECG signs that are suggestive, but not diagnostic, of pericardial effusion and cardiac tamponade.

2.Because these ECG findings cannot reliably identify these conditions, we conclude that 12-lead ECG is poorly diagnostic of pericardial effusion and cardiac tamponade.

How's it diagnosed? Cardiac Tamponade (Echo)

•An echo-free space posterior and anterior to the left ventricle and behind the left atrium

•Early diastolic collapse of the right ventricular free wall

•Late diastolic compression/collapse of the right atrium

•Swinging of the heart in the pericardial sac

•Left ventricular pseudohypertrophy

•Inferior vena cava plethora with minimal or no collapse with inspiration

•A greater than 40% relative inspiratory augmentation of blood flow across the tricuspid valve

•A greater than 25% relative decrease in inspiratory flow across the mitral valve

ECHO cardiac tamponade

1.An important sign of tamponade seen in 2D echocardiography is dilatation of the IVC (>20 mm in an adult size heart) and hepatic veins

2.This is known as IVC plethora, and, although not very specific, it is a very sensitive sign of cardiac tamponade (92%)

Clinical intervention Cardiac Tamponade

•Mechanical drainage/removal of fluid

•ER treatment

•Pericardiocentesis 1st line

•Open drainage

•Pericardial window (recurrent)

•Need for Intubation

•Ventilatory support

•IV Fluid (IVF) bolus 500-1000mL

•Be aware of adverse effects to include pulmonary edema/↓ cardiac output

Clinical managementCardiac Tamponade

•IV Fluid (IVF)

•Bolus 500-1000mL

•Vasopressors

•If needed

•Not contraindicated

Prognosis Cardiac Tamponade

•Outcome associated with etiology of cardiac tamponade and pre-existing comorbidities

•Mortality

•1-year mortality rate 77% for malignant effusion

•13% mortality rate for non-malignant effusion

medical complication of IVC filters

.cardiac tamponade, or a buildup of fluid around the heart.

Explanation : IVC filters fracture and migrate, they can reach the heart and compromise the pericardium, letting blood into the space between the pericardium and the heart.

Pharmacotherapeutics (Cholestyramine)Pregnancy and Lactation

•Pregnancy category: C

•

•Lactation: Drug does not enter breast milk; use with caution because of potential vitamin loss in mother

•

Clinical pharmacotherapeuticsBile Acid Sequestrants (Muddy Points)

•Bile Acid Sequestrants are used to treat hyperlipidemia (HLD) in pregnancy (true)

•Q1 - patients who have osteopenia or high risk of developing osteoporosis should be treated with bile acid sequestrants (false)

•Bile acid sequestrants increase the risk of developing osteoporosis so they should not be used to treat HLD in patients who are already at risk or who have osteopenia/osteoporosis

•Q2 - using a combination of ezetimibe and a statin in pregnancy or patient with osteopenia/osteoporosis (or at high risk of developing)

•Statins are C/I in pregnancy and ezetimibe is pregnancy category C (should not be used)

•There is no C/I for use of ezetimibe + statin in patients with osteopenia or osteoporosis

•There does not seem to be a "protective" feature to prevent or reduce risk of developing osteopenia/osteoporosis

Pregnancy Categories

•A: Generally acceptable. Controlled studies in pregnant women show no evidence of fetal risk.

•

•B: May be acceptable. Either animal studies show no risk but human studies not available or animal studies showed minor risks and human studies done and showed no risk.

•C: Use with caution if benefits outweigh risks. Animal studies show risk and human studies not available or neither animal nor human studies done.

•D: Use in LIFE-THREATENING emergencies when no safer drug available. Positive evidence of human fetal risk.

•X: Do not use in pregnancy. Risks involved outweigh potential benefits. Safer alternatives exist.

NA: Information not available

DefinitionInfective Endocarditis

•Infection in the heart valves or endocardium

1.is a bacterial or fungal infection of the valvular and/or endocardial surface of the heart

2.May include one or more heart valves, the mural endocardium, or a septal defect

3.The endocardium is the lining of the interior surfaces of the chambers of the heart.

4.This condition is usually caused by bacteria entering the bloodstream and infecting the heart.

5.Bacteria may originate in the: mouth.

Distinction between acute subacute bacterial endocarditis

Acute :

1- Heart may be normal

2- Organism: S.Arues ;pneumococcus;s.pyogenes,Emteroccoucs

3-Prompt,vigorus and initiated on emprical ground

Subacute :

1- RHD,CHD

2-Organism : Viridians ,streptococci,enterococcus

3- Therapy : Can often be delayed until culture report and susceptibilities available

EpidemiologyInfective Endocarditis

•M > F

•No racial predilection

•Prevalence > 60 yo

Dx at younger age often related to IV drug abuse (IVDA

EtiologyInfective Endocarditis

Rheumatic valve disease

•Mitral MC

•Tricuspid Valve MC in IVDA

•Aortic

Congenital heart disease

•PDA

•VSD

•Tetralogy of fallot

MVP

•S. viridans MC pathogen of subacute bacterial endocarditis - dental procedures and upper respiratory infections

Part of oral flora

Infection of abnormal heart valves

Infects damaged valves

Pathogens Infective Endocarditis

Native valve endocarditis

•S. aureus and streptococcal species account for majority of cases

•Fungi account for a small percentage (MC IVDA)

S. aureus most common cause among injection drug users

•Prosthetic valve endocarditis

•Early disease MC caused by S. epidermis

Enterococci

•Recent GU or GI infection

Etiology with ivda Infective Endocarditis

•2/3 of patients have no prior hx of heart disease or murmur

•Murmur may be absent with tricuspid valve involvement

•MC pathogen is MRSA

•Present with pleuritic chest pain

Risk factorsInfective Endocarditis

•IV drug use/abuse (IVDA)

•Poor dentition or dental infection

•Structural (valvular) heart disease

•History of infective endocarditis

•Hemodialysis

•HIV infection

Endocarditis : Bacterial source

Intravascular catheter >>>>> Bacteria in bloodstream

Endocarditis : Abnormal substrate

Prothetics valve

Native valve damage

>>>>>> Thrombi

Endocarditis treatment

Emproc treatement : Vancomycin

Clinical historyInfective Endocarditis

•MC sx is persistent fever

•Pleuritic chest pain

•Malaise/fatigue

•Anorexia

•Chills/sweats

•Cough

•Headache

•Myalgia/arthralgia

•Confusion

•Clues suggesting bacteremia

•IV catheters

•Orthopedic hardware

•IVDA= intravenous drug abuse

•Recent bacterial infection

•Pre-existing cardiac lesion

•Valvular heart disease

Fever is usually low grade

Physical exam Infective Endocarditis

New onset or worsening murmur

•mitral valve > aortic valve > tricuspid valve > pulmonic valve

IVDA - Tricuspid valve

Derm

•Painful or tender raised violaceous nodules on the pads of the digits and palms

•Painless erythematous macules on the palms and soles

•Linear reddish-brown lines under the nail bed (splinter hemorrhages)

•Petechiae (skin or mucous membranes)

EENT

•Roth spots

Abd exam

•Splenomegaly

Neuro exam to establish baseline

Physical exam Infective Endocarditis others aspects

1.Murmur - IVDA - systolic murmur LLSB ® tricuspid regurg; otherwise - mitral valve regurg best heard at heart apex with radiation to the left axilla

2.Derm exam - note size, shape, type and location of lesions

3.EENT - get visual acuity, fundoscopic exam

4.Osler Nodes - Painful or tender raised violaceous nodules on the pads of the digits and palms

5.Janeway Lesions - Painless erythematous macules on the palms and soles

6.Roth spots - retinal hemorrhages with central clearing

Physical exam - petechiae Infective Endocarditis

•Most common skin manifestation

•Petechiae & splinter hemorrhages

•Nonspecific for endocarditis

Physical exam "Splinter hemorrhages" Infective Endocarditis

Linear reddish-brown lesions in nail bed

More Specific Findings than Splinter Hemorrhages

•Janeway lesions

•Osler's nodes

•Roth spots

Physical exam-"Janeway lesions" Infective Endocarditis

•Macular, painless, erythematous lesions on palms and soles

Physical exam - Osler nodes Infective Endocarditis

•Painful, violaceous papulopustules located on fingers, toes, feet

Physical Exam - Roth spotsInfective Endocarditis

Exudative, edematous hemorrhagic lesions of retina

Bacterial endocarditis mnemonics

FROM JANE

Fever

Roths spots

Osler

Murmur

Janeway lesions

Anemia

Nail bed hemorrhage

Emboli

Differential diagnosis Infective Endocarditis

•Pulmonary embolism

•Deep Vein Thrombosis

•Lyme Disease

•Lymphoma

•Vasculitis

•Polymyalgia rheumatic

•Reactive arthritis

•Myocarditis

WorkupInfective Endocarditis labs

•CBC w/ diff

•CMP

•Cardiac biomarkers + EKG + BNP

•UA (Å protein & hematuria)

•RF/ESR/CRP ()

•Blood cultures x 3 (1 hour apart)

•S. aureus

•Strep viridans and bovis

•Enterococci

WorkupInfective Endocarditis Imaging

•CXR

•Transesophageal Echocardiogram (TEE more sensitive than TTE)

•Valve vegetation

•Abscesses

•New valve insufficiency

HACEK organims for Endocarditis

Haemophilus Parainfluemzae

Actinobacillus Actim=nomycetemcomitans

Cardiobacterium hominis

Eikenella corrodens

Kingellla Kingae

Endocarditis diagnostic

Diagnosis requires 2 major OR 1 major + 3 minor OR 5 minor

Clinical interventionInfective Endocarditis

Indications for surgical (operative) intervention ® valve replacement

•Refractory CHF

•Persistent infection

•Invasive infection

•Previous prosthetic valve

•Recurrent systemic emboli

•Fungal infections

Clinical pharmacotherapeutics empiric therapy - Infective Endocarditis

Non-Operative Management

•Native valve endocarditis (NVE) ® 4-6 weeks

•Ceftriaxone OR Gentamicin

•MRSA or PCN allergy ® vancomycin

Prosthetic valve endocarditis (PVE) ® 4-6 weeks

•Vancomycin + Gentamicin + Rifampin

Critically ill/unstable

•Vancomycin + cefepime + piperacillin-tazobactam

•Suspect pseudomonas a

Fungal endocarditis

•Amphotericin B (6-8 weeks)

•Surgical intervention often needed with fungal pathogens

Prognosis Infective Endocarditis

•Largely dependent on whether or not complications resulted from the infection

•Best cure rates by organism

•Strep viridans and strep bovis ® 98%

•Enteroccoci and s. aureus (IVDA) 90%

•Non-IVDA community acquired S. aureus 60-70%

•Aerobic gram-negative organisms 40-60%

•Fungal organisms < 50%

•Complications include HF, new valve disease, conduction abnormalities, cerebral embolism, renal embolism and/or infarct

•Untreated almost always fatal

Infective Endocarditis ACUTE

Toxic presentation

Progressive valve destruction and metatstic infection developing in days to weeks

most commonly caused by S.Aureus

Acute malaise

shaking chills

leukocytosis

normal gamma globulins

Rheumatoid factor +

Infective Endocarditis Subacute

Mild toxicity

Presentation over weeks to months

Rarely leads over weeks to months

Rarely leads to metattastic infection

Most commonly S.Viridians

Weight loss

fatigue

night sweats

low or no fever

normal white cell counts or leukopenia

elevated gamma globulins

Rheumatoid factor +

Duke criteria for endocarditis?

2 major // 1 major or 3 minor // 5 minor

Major Duke Criteria

Two positve blood cultures

positive echo

new regurgitant murmur

Duke minor criteria

Predispostion condition

fever

Immunologic signs

One positive blood culture

Positive echo not meeting major criteria

Infection endocarditis seens on a patient

Roth spots of retina

splinter hemoorahges

Janey lesions

Oslers nodes

Function of the pericardium : Mechanical function

•Limiting acute dilation

•Maintaining ventricular compliance

•Distributing hydrostatic forces

Function of the pericardium : Membranous function

•Reduces external friction

•Barrier against infection and malignancy

•Ligamentous function

•Anatomically fixes heart

Definition Acute Pericarditis

Inflammation of pericardium characterized by :

•Chest pain

•Pericardial friction rub

•Serial electrocardiographic changes

Epidemiology Acute Pericarditis

•Uremic etiology common in patients with advanced renal disease (before dialysis)

•Malignant disease is the most common cause of pericardial effusion with tamponade in developed countries

•M > F

•More common in men under age 50

•More common in adults than children

Etiology Acute Pericarditis

•MC cause in immunocompetent patients ® post-viral infection or idiopathic (80%)

•Uremic pericarditis is a common complication associated with chronic renal failure

•Inflammatory disorders

RA, SLE, Rheumatic fever

•Cardiovascular

AMI

Dressler syndrome = post MI + fever + pleural effusion

Aortic dissection

•Metabolic disorders

•Neoplasms, drugs, trauma

MC viruses are coxsackie virus and echovirus

Clinical history Acute Pericarditis

•Presentation depends on underlying etiology

•Major clinical manifestations

•Acute onset chest pain

Substernal and may radiate to neck/shoulders

Typically pleuritic

Improved by sitting up and leaning forward

Physical Exam Acute Pericarditis

Pericardial friction rub

•Superficial scratchy/squeaking sound

•Best heard with diaphragm over left sternal border

EKG changes

•New widespread ST elevation or PR depression

•Serial exams may be necessary for detection

•Transient and present in 50% of cases

What are the 5 P's of pericarditis seeing on physical exam ?

•Pleuritic

•Postural

•Persistent chest pain

•Pericardial friction rub

1.Pericardial friction rub (Pathognomonic) and is best heard at the end of expiration while pt is sitting upright and leaning forward

2.Pleuritic pain that is sharp and worse with inspiration

3.Pain is worse lying supine and improves with leaning forward

Diagnostic criteriaAcute Pericarditis

•Two of the following four criteria:

•1. Non-ischemic chest pain

•2. ECG evidence of PR depression or ST segment deviation

•3. Detection of a pericardial rub on auscultation

•4. Pericardial effusion on 2-D echocardiography (best INITIAL test)

•BEST TEST - T2 Weighted Cardiac MRI (does NOT require contrast)

•Make the "best test" better by using gadolinium contrast

Workup stage 1 ekg Acute Pericarditis

•Diffuse ST elevation at onset of acute pain: Hallmark of acute pericarditis

subsequent ekg changes •Stage 2

•ST segment returns to baseline in a few days

subsequent ekg changes •Stage 3

•T waves become inverted

subsequent ekg changes •Stage 4

•Returns to baseline in weeks to months

EKG showing diffuse ST segment elevations seen

leads II, aVF, V2 to V6

Imaging Acute Pericarditis

Echocardiogram

•Often normal

•Essential for evaluation of pericardial effusion

CT scan

•Provides details of entire pericardium

•Normal thickness by CT is < 2 mm

•Thickening suggestive of acute pericarditis

MRI

•Provides details without contrast or radiation

Clinical intervention Acute Pericarditis

Cardiology consultation

Surgical intervention

•Pericardiectomy (best for constrictive pericarditis)

•Pericardiocentesis (effusions > 250mL)

•Pericardial window placement

•Pericardiotomy (refractory cases)

Clinical pharmacotherapeutics Acute Pericarditis

Aspirin and NSAIDS 1st line

•For all patients without a contraindication

•Duration based upon persistence of symptoms

•Tx usually < 2 weeks

Colchicine is 2nd line

•Used as an adjunct to NSAID therapy

•Reduces symptoms and rate of recurrences

•Use in all refractory/recurrent cases

•Continued for 3 months

Refractory to NSAIDS/Colchicine

•Glucocorticoids (not for initial tx)

Prognosis Acute Pericarditis

•Depends on etiology

•Idiopathic and viral etiologies usually have a self-limited course

•Most post-MI cases have a benign course

•With 1st occurrence co-existing pleural effusion is common

Acute pericaditis = Inflammation of the pericadium

when the pain is going down or up ?

Sitting = pain down

supine = pain up

EKG triad of Pericarditis

PR elevation in aVR

PR depression

Diffuse Concave ST elevation

Etiology of Acute periodontitis : causative agents

Viral

Neoplastic

Uremic

Connective tissue disorder

Basic line TX

NSAIDS/Aspirin

Colchicine

Steroid

Definition Constrictive Pericarditis

•Long term/chronic inflammation of the pericardium

Thickening and scarring

•Restriction of ventricular diastolic filling

Epidemiology Constrictive Pericarditis

•Effects those with conditions related to the Etiology

Etiology Constrictive Pericarditis

Occurs due to things that cause inflammation to develop around the heart

•Heart Surgery

•Radiation therapy to the chest

•Tuberculosis

•Any cause of acute pericarditis can cause constrictive pericarditis

Clinical history Constrictive Pericarditis

•Dyspnea that develops slowly and gets worse (MC sx)

•Fatigue

•Orthopnea

•Chronic edema of the legs and ankles

•Ascites

•General weakness

Physical exam Constrictive Pericarditis

•Fever

•Tachycardia

•Palpitations

•Paroxysmal nocturnal dyspnea

•Diaphoresis

•Heart tones

•"Pericardial knock"