Week 7: Cardiology Part 3/5: ‘Carditis and Pericardium

Hypertrophic obstructive cardiomyopathy (HOCM) is a genetic primary cardiomyopathy that is the second most common cause of sudden cardiac death in adolescents. It is the leading cause of sudden cardiac death in athletes. It involves asymmetric interventricular septal hypertrophy that causes reduced filling of the left ventricle and diastolic dysfunction. The most frequent initial complaint is dyspnea on exertion, but other symptoms include chest pain, palpitations, and syncope. Syncope usually occurs during or immediately after exercise. Exam findings include an S4 heart sound and a systolic ejection murmur that is intensified with standing up and performing a Valsalva maneuver. Maneuvers that decreased the murmur include hand grip, passive leg raise, and squatting. Diagnosis is ultimately made with echocardiography or cardiac MRI, along with genetic testing. Hospitalization is indicated for patients presenting for syncope who are suspected to have HOCM, as these patients are at significant risk for sudden cardiac death. Beta-blockers are the treatment of choice in patients with HOCM who have chest pain.

The optimal rate for chest compressions is at least 100 compressions/minute. In order to have return of spontaneous circulation (ROSC), patients must have high-quality CPR started early and early defibrillation when indicated. High-quality CPR historically was underappreciated but recent research has brought it to the forefront of care. In addition to an appropriate compression rate of 100 per minute, compression depth of > 5 cm and minimum pauses for CPR must be maintained. Additionally, hyperventilation and resultant hypocarbia is detrimental. A ratio of 30 compressions to 2 ventilations is currently recommended. Compressions should not be held during attempted intubation. Epinephrine should be administered every 3-5 minutes. Rhythm checks should not be performed after shock delivery.

A number of viruses cause myocarditis including adenoviruses, parvovirus 19 and human herpesvirus 6. Cytomegalovirus (CMV) is a common cause in patients with cardiac transplant. Myocarditis occurs via three pathophysiological processes: necrosis from direct invasion of an infectious agent, destruction of myocytes from infiltration of components from the host immune response, and toxic effects of exogenous or endogenous chemicals produced by a pathogen. The pathophysiological process depends on the etiologic agent. In patients with cardiac transplants, CMV and toxoplasmosis gondii are common agents. Patients with myocarditis present with nonspecific symptoms including fever, fatigue, malaise and diarrhea. Dyspnea is the most common presenting complaint in children and is frequently seen in adults as well. Tachycardia out of proportion to temperature elevation should raise concerns for myocarditis. Diagnostically, ECG can have a number of changes including sinus tachycardia, wide QRS complex, prolonged QT interval or ST elevations. Definitive diagnosis is made by endocardial biopsy (MRI is slowly replacing biopsy as the disease can be patchy and biopsy can fail to make the diagnosis).

When fluid accumulates in the pericardial space rapidly (e.g., within minutes), hemodynamic compromise usually occurs. Patients experience hypotension, tachycardia, and shortness of breath. This is pericardial tamponade. Normally the pericardial elasticity can accommodate slow accumulations of fluid from conditions such as pericarditis, radiation therapy, uremia, or malignancy. When the elasticity of the pericardium is overwhelmed due to rapid fluid accumulation within the pericardial space, the right atrium and ventricles begin to be compressed. This leads to decreased end diastolic volumes in the right heart and ultimately hypotension. The decreased preload creates proximal venous engorgement and is demonstrated clinically as jugular venous distension. Patients may also have distended facial or scalp veins. Other clinical findings of pericardial tamponade include muffled heart sounds, a narrow pulse pressure, pulsus paradoxus (decreased systolic blood pressure with inspiration due to increased intrathoracic pressure causing decreased venous return), and respiratory distress. Electrocardiographic findings may include low voltage or electrical alternans (alternating high and low QRS voltage due to the heart swinging in the pericardium full of fluid). Bedside ultrasound is diagnostic and demonstrates anechoic (black) fluid between the hyperechoic pericardium and the myocardium. Right atrial or right ventricular collapse during diastole, leftward septal shifting during inspiration, and a swinging heart may be seen on ultrasound. Pericardiocentesis is the management of choice for pericardial tamponade.

The treatment of pulseless electrical activity (PEA) begins with initiation of advanced cardiac life support (ACLS). Common causes of PEA can be remembered by the Hs and Ts. This patient recently underwent an operative procedure and is at increased risk for developing a pulmonary embolism (PE). Therefore, lytic therapy with tissue plasminogen activator (t-PA) should be administered.

This patient presents with findings concerning for septic emboli secondary to endocarditis. Although rare, intravenous drug users are at the highest risk for endocarditis secondary to Pseudomonas species. They are also more likely to have right-sided endocarditis with tricuspid valve involvement. Patients should be treated with tobramycin and an extended spectrum beta-lactam antibiotic such as piperacillin-tazobactam, cefepime, or ceftazidime. Medical therapy with antibiotics can be attempted, but valve replacement is often needed for complete eradication of the underlying infection.
Ceftriaxone and vancomycin (B) do not cover Pseudomonas aeruginosa and therefore would be ineffective. The combination of gentamicin and nafcillin (C) or gentamicin and vancomycin (D) is not recommended. Although gentamicin does cover Pseudomonas species, a regimen with double coverage is more likely to be effective. Nafcillin has great coverage against non-methicillin resistant Staphylococcus aureus, and vancomycin is the treatment of choice for methicillin-resistant Staphylococcus aureus.

Myocarditis can be due to an infectious or non-infectious process, with most infectious etiologies caused by a viral infection, most commonly parvovirus B19, adenovirus, coxsackie B virus, and Echovirus. Trypanasoma cruzi (Chagas disease) is the most common etiology worldwide. Myocardial necrosis occurs likely as a result of direct invasion of the offending organism as well cytotoxic effects of the host’s immune system. Individuals develop flulike symptoms and in adults chest pain and shortness of breath. One of the hallmark signs of myocarditis is tachycardia out of proportion to fever. Depending on the time of presentation, patients may have symptoms of heart failure as the left ventricular ejection fraction is impaired as a result of the myocarditis. Troponin is often elevated as the disease progresses. The gold standard for diagnosis is endomyocardial biopsy. Management is supportive. ACE inhibitors help reduce myocardial inflammation.

Although most patients with infective endocarditis will exhibit a mumur at some point in their disease course, murmurs are often not present on initial presentation. Infective endocarditis often affects patients with underlying valvular abnormalities including rheumatic heart disease, calcific degenerative disease and patients with congenital heart defects. The incidence of infective endocarditis among intravenous drug users is particularly high. Symptoms of endocarditis are nonspecific. Most patients will report intermittent fevers (85%) and malaise (80%). Early in the disease, patients often will not have murmurs but one will almost always develop during the course of illness. Among intravenous drug users, less than 35% will present with a murmur. In patients with a moderate or high suspicion of endocarditis, an echocardiogram should be performed to establish the diagnosis.
Noninvasive cardiac monitors have been used in the ED to measure cardiac output, though they have yet to be proven to change measured clinical outcomes. A recent meta-analysis of 8 studies found that passive leg raise predicted fluid responsiveness as measured by an increase in descending aortic blood flow. The assessment was performed by transesophageal Doppler imaging in critically ill patients with a global area under the receiver operating characteristic curve of 0.95, indicating excellent sensitivity and specicity of these maneuvers in realtime clinical practice in the ED.

Ultrasonographic monitoring (transthoracic or esophageal), and arterial and venous pulse oximetry/plethysmography variation. While potentially promising as noninvasive means of monitoring cardiac output and providing information regarding the nature of a patient’s shock, further studies with clinical outcome data are needed to guide the use of these monitoring devices in the diagnosis and management of patients with shock.

Naloxone can safely be given to a pediatric patient in cardiac arrest via the endotracheal tube (ETT) if intravenous or interosseous access is not available. Endotracheal drug administration is infrequently used but has the potential to be therapeutic in patients without access. A number of medications can be given via ETT including atropine, naloxone, lidocaine and epinephrine.