Patient Vasospasm Case Study

More blood, causing a high force within the Left Ventricle and left atrium. This weight backs up

If the perkinje fibers or the AV node becomes irritated, they can begin contraction of the ventricles at speeds well above normal. Other causes of ventricular tachycardia include heart disease and medications.

I. Description: Congestive Heart Failure is more of a syndrome than a disease. Heart failure may be classified according to the side of the heart affected, (left- or right-sided failure), or by the cardiac cycle involved, (systolic or diastolic dysfunction). (Schilling-McCann p. 176). The word "failure" refers to the heart's inability to pump enough blood to meet the body's metabolic needs. (Schilling-McCann p. 176). When the heart fails to deliver adequate blood supply edema may develop. (Cadwallader p. 1141). Where edema occurs depends on what side of the heart is failing.

The most common manifestation is chest pain (70% to 90%). Less common symptoms includes; dyspnea (20%) and pulmonary edema may be present. Acute heart failure, cardiogenic shock, and cardiac arrhythmias are uncommon.(9,10) About one third of patients with TCM have ECG

The patient may experience dyspnea, caused by pulmonary congestion. They may report orthopnea as blood is redistributed from the legs to the central circulation when the patient lies down a night, paroxysmal nocturnal dyspnea due to reabsorption of interstitial fluid when lying down, and reduced sympathetic stimulation while sleeping. Pulmonary congestion may also cause a non-productive cough. Later clinical manifestations of left sided heart failure include crackles due to pulmonary congestion and hemoptysis resulting from bleeding veins in the bronchial system caused by venous distention. On physical exam the patient may have cool, pale skin resulting from peripheral vasoconstriction, and may be restless and confused due to reduced cardiac

A diagnosis may start with routine bloodwork to rule out non cardiac conditions that could be triggering tachycardia. A chest x-ray may also be performed to see if there is any cardiomegaly present. In my case, and in most cases, it starts with a 12 lead ECG. According to Ellis and Rottman (Dec. 04, 2015) “the classic ECG features are as follows:

The patient is an 84-year-old gentleman who presents to the ED complaining of severe chest pain, mostly retrosternal, radiating to the left side essentially with shortness of breath. When first evaluated in the ED they felt he was in atrial fibrillation, however as the later EKGs revealed was really a sinus rhythm with multifocal atrial premature contractions. The patient also has a history of hypertension, dyslipidemia and some prostate issues. He is a smoker, continues smoke but has no alcohol history. On presentation initial blood pressure was 143/70 with pulse of 73, respirations of 14, is febrile and oxygenating well on room air. His laboratory work is essentially unremarkable. Initial troponins were 0.02, 0.03 and 0.026 with CK

Wolff-Parkinson-White syndrome (WPW) is a conduction disorder of the heart that is caused by pre accessory pathway resulting in tachyarrhythmias. Kesler & Lahham (2016) state, “Approximately 0.07% of the population often presents with the chief complaint of palpitations”. A diagnosis of WPW is made in conjunction with certain characteristics. Characteristics of WPW include: a short PR interval < 0.12 second caused by a faster electrical conduction through the accessory pathway than the atrioventricular node, upsloping of the QRS and a delta wave. The delta wave is indicative of rapid ventricular depolarization caused by the rapid conduction through the accessory pathway (Kesler & Lahham, 2016, p. 469).

Hypertrophic cardiomyopathy is characterized by interventricular septal hypertrophy (in absence of other cardiovascular conditions), causing decrease of left ventricle cavity and potentially leading to outflow obstruction. (1) (6) As a consequence of mutations in several genes encoding for thick and thin filaments which build the cardiac muscle, morphological changes occur leading to tangled, thickened myocardial fibers. It is an important cause of morbidity and mortality. Symptomatology varies a lot, from asymptomatic patients to those with severe cardiac function impairment. Some of the most common symptoms of HCM, which are not specific to this disorder may be: shortness of breath at rest or with exertion, fatigue, chest pain, arrhythmias, dizziness, but not only.

There is a wide splitting of the second heart sound heard, not sure about the early systolic ejection click or an S1 split. The precordium showed no abnormal impulse. There are no gallops.

Within 1 hour of chest pain onset, the patient will: Display vital signs within normal limits and display normal depth and rate of respirations

Hypoplastic left heart syndrome is characterized by hypoplasia of the left ventricle, aortic stenosis, hypoplasia of the ascending aorta, and coarctation (narrowing) of the aorta. In normal conditions the left side of the heart receives oxygenated blood from the lungs and pumps it into the systemic circulation. In patients with HLHS, the left ventricle and the aorta are underdeveloped. The

Blood tests will be done to assess troponin I, troponin T, creatine kinase (CK) and myoglobin which are classified as cardiac serum markers (Cardiac Emergencies, n.d.).

• Presents with shortness of breath, difficulty in breathing, anxiety, confusion, cyanosis, tachycardia, arrhythmia, tachypnea, and hypoxemia

Based on the laboratory test, electrocardiogram, and the patient’s presentation would lead the health care provider to believe that the patient is having a myocardial infarction or heart attack. A myocardial infarction is when suffienct blood flow to the coronary arteries is decreased or stopped which in turn leads to partial or complete failure of the cardiac muscles in that area of the heart (Abreu de Vargas, Riegel, de Oliverira Junior, Silveira Siqueira, & Oliveira Crossetti, 2017, p. 2804). When the cardiac muscle is not getting the blood flow and the oxygen that it needs the tissues start to become necrotic and release a chemical called troponin. A laboratory test that is performed on patient that complains of chest pain is a troponin,