Inflammatory + valvular heart disease

IE, Pericarditis

IE Cause

Blood flow turbulence within heart allows causative organisms to infect previously damaged valves and other endothelial surfaces

What is IE (infective endocarditis)

• infection of heart valves and endothelial surfaces

4 categories of IE

1. L sided native IE

2. L prosthetic valve IE

3. R IE (IV drug)

4. intracardiac, intravascular devices (pace maker, defibrillator)

What is the most common organism from IV drug use

staph Aureus

What organisms cause IE

staph aureus

oral streptococcus

enterococci

GRAM +’ve bacteria

Risk factors of IE

• prior IE

• prosthetic valves

• acquired valvular disease

• cogenital heart defects

• cardiac lesions

Etiology + patho

Vegetations → primary lesions of IE consists → fibrin, leukocytes, platelet, microbes

vegetation leads to emboli → portion of vegetation falls off into circulation → emboli arise from left

left → brain , systemic circulation, kidney, spleen

right → lungs

•Risk is greatest first few days after antimicrobials are started.

L and Right differential causes

Left: Underlying heart disease, bacterial infections

Right: illicit drug use

IE clinical manifestation

Non-specific symptoms

• chills, weakness, malaise, fatigue, anorexia

low grade fever

• absent in older adults or autoimmune 90%

• janeway

• oslers

• splinter hemorrhage

• petechiae

onset murmur

aorta and mitral

embolizations

spleen

kidney

peripheral BV

brain

lung → PE → R sided endocarditis

Diagnosis for IE

• past and present medical Hx

• lab → blood cultures

• echo → surgery candidate, active infections

• ECG → AV block

• CXR → in enlarged heart

• cardiac catheterization → surgery candidate, coronary artery patency, valvular fx

Prophylatic Tx

Abx for specific cardiac conditions prior to dental and surgery procedure

• 4-6 weeks

long term treatment

Key to successful treatment → accurate identification of bacteria

hospitalize with Abx

blood culture → effectiveness of Abx

collab + nursing (goals)

1) achieve / reachieve normal cardiac fx

2) physical activity ADLs without fatigue

3) prevent recurrent of IE

Health promotions IE

• ambulatory + care home

• abx 4-6 weeks

• adequate physical + mental rest at home

• repeat blood culture → assess effectiveness of Abx

Rheumatic Fever

• inflammation of connective tissues ( brain, joint, heart, skin)

• may also impact all layers of the heart

Rheumatic heart disease

result of rheumatic fever → characterized by scarring and deformity of heart valves

ARF ( acute rheumatic fever) what is it from

complication of delayed treatment of Group A streptoccocal Pharyngitis

Rheumatic endocarditis

•Rheumatic endocarditis→ swelling & erosion of valve leaflets, on which vegetations form (deposits of fibrin & blood)→ thickening of valves and fusion of commissures and chordae tendineae →valves becomes thickened and calcified →stenosis

• reduction of mobility with failure of valves → regurgitation

Rheumatic fever clinical clinical manifestations

•Chest pain

•Excessive fatigue

•Heart palpitations

•Dyspnea

•Swollen ankles, wrists, or stomach

Best treatment of Rheumatic fever

THE BEST TREATMENT IS EARLY DETECTION AND TX OF GpA STREP PHARYNGITIS (aka “Strep throat”)

Acute pericarditis

inflammation of pericardium

Etiology of Pericarditis

Non-infective: Acute MI, radiation, neoplasm

infective: viral, bacterial, fungal

hypersensitivity: Drug reaction or autoimmune

Pericarditis after MI ( two distinct syndromes)

Acute Pericarditis: within 48-72 hours

Dresslers syndrome: 4-6 weeks ( late)

Inflammatory response (of acute pericarditis)

influx of of neutrophils → characteristic of acute pericarditis

Clinical manifestation of Pericarditis

• progressive, worsening pain → sharp, pleuritic in nature

• worsens with deep inspiration → leads to dyspnea

• worsens with supine position → relief upon sitting upright

• hallmark: pericardial friction rub, change in ECG

• ECG - ST wide spread elevation and PR depression, depolarozation

Complications of Pericarditis

• cardiac tamponade

• Pleural effusion

cardiac tamponade

Develops as fluid accumulates in the pericardial sac

(pericardial effusion), causing an increase in intrapericardial

pressure and producing compression of the heart.

sx:  confused, anxious, and restless.

The patient will develop tachypnea, tachy-

cardia, and a decreased cardiac output (CO). The neck veins are

usually markedly distended because of increased jugular venous

pressure, and a significant pulsus paradoxus is present. Pulsus

paradoxus is a decrease in systolic BP with inspiration that is

exaggerated in cardiac tamponade

pleural effusion

accumulation of excess fluid in the pericardium.

It can occur rapidly (e.g., chest trauma) or slowly (e.g., tuber-

culous pericarditis). Large effusions may compress adjoining

structures. Pulmonary tissue compression can cause cough,

dyspnea, and tachypnea. Phrenic nerve compression can induce

hiccups, and compression of the recurrent laryngeal nerve may

result in hoarseness. Heart sounds are generally distant and

muffled, although blood pressure (BP) is usually maintained by

compensatory mechanisms.

Pericarditis DX

ECG, CXR, labs ( leukocytosis, elevated CPR, ESR, trops) ECHO

Pericarditis Treatment

ID and treat underlying problem

abx for acute pericarditis

corticosteroids for patients with pericarditis to autoimmune conditions or no NSAIDs

CP and inflammation → NSAIDs or high dose ASA and colchicine

pericardiocentesis - if drainage necessary

bedrest and pain relief