cardiac myopathy - Nursing Case Study

Pathophysiology

• Primary mechanism: Cardiac myopathies are primarily caused by alterations in the myocardial structure, causing the heart muscles to become thick, rigid, dilated, or weak. These structural changes lead to impaired contraction, reducing the heart's ability to pump blood efficiently, contributing to arrhythmias and heart failure.

• Secondary mechanism: The structural changes also disrupt the electrical signaling in the heart, leading to irregular heart rhythms (arrhythmias). This can result in inadequate blood supply to the body, causing symptoms like fatigue and shortness of breath.

• Key complication: Overtime, the inefficient pumping can cause the heart to enlarge (cardiomegaly), worsening the heart's function, and leading to complications such as heart failure, where the heart can't pump enough blood to meet the body's needs.

Patient Profile

Demographics:

54-year-old male, office worker

History:

• Diagnosed with hypertension and hyperlipidemia 10 years ago

• Current medications include Lisinopril (for hypertension) and Atorvastatin (for high cholesterol)

• Allergic to Penicillin

Current Presentation:

• Chief complaint: Increasing shortness of breath, especially during physical activity

• Key symptoms: Exercise intolerance, fatigue, swelling in the legs, ankles, and feet (edema), occasional chest pain

• Vital signs: Blood pressure 150/90 mmHg, Resting heart rate 98 bpm, Oxygen saturation 92% at rest, Respiratory rate 20 breaths per minute

Section 1

Change in patient status:

Over the next two days, the patient's condition worsened. He reported increasing fatigue, even with minimal activity, and his shortness of breath was now persistent, even at rest. His blood pressure increased to 160/100 mmHg and his resting heart rate rose to 105 bpm. Oxygen saturation dropped to 88% at rest, leading to an increase in his respiratory rate to 24 breaths per minute. On physical examination, the swelling in his legs, ankles, and feet had become more pronounced and pitting edema was now present. He also developed orthopnea, needing multiple pillows to breathe comfortably while lying down.

These physical findings suggested that the patient's cardiac myopathy was progressing rapidly, leading to worsening heart failure. The persistent shortness of breath, even at rest, could be due to pulmonary congestion caused by the heart's inability to pump out all the blood it receives from the lungs. The increased blood pressure and heart rate were likely compensatory mechanisms to maintain cardiac output. The worsening edema and development of orthopnea indicated that the patient was retaining fluid, a classic symptom of heart failure. These changes in the patient's status required immediate medical intervention to prevent further deterioration.

Section 2

New Diagnostic Results:

The patient's continued deterioration prompted a set of diagnostic tests. The results of these tests indicated a further decline in the patient's cardiac function. His B-type natriuretic peptide (BNP) levels had dramatically elevated to 1250 pg/mL, indicating severe heart failure. An electrocardiogram (EKG) showed an irregular heartbeat with signs of left ventricular hypertrophy, further confirming the worsening condition of the patient's heart. Interestingly, the patient's blood labs revealed an increase in creatinine levels to 2.5 mg/dL and a decrease in glomerular filtration rate (GFR) to 30 mL/min, suggesting that the patient's renal function was also declining.

These results raised a concern about the development of cardiorenal syndrome, where both the heart and kidneys are affected. The elevated BNP levels, irregular heartbeat, and signs of left ventricular hypertrophy pointed to a worsening of the patient's cardiac myopathy and heart failure. The increased creatinine levels and decreased GFR suggested that the patient's kidneys were also under stress, likely due to the reduced blood flow caused by the failing heart. This new complication added another layer of complexity to the patient's condition and required a careful re-evaluation of the treatment plan.

Section 3

Change in Patient Status:

Over the next few days, the patient's condition continued to deteriorate. His blood pressure consistently registered at 90/60 mmHg, indicating hypotension. This further supports the diagnosis of heart failure, as the heart is not efficiently pumping blood, causing a drop in blood pressure. His heart rate also increased to a tachycardic rate of 110 beats per minute, likely in an attempt to compensate for the low blood pressure.

Furthermore, the patient began to experience increasing shortness of breath, even at rest, and a persistent cough producing frothy, pink-tinged sputum - both indicative of pulmonary edema. On auscultation, crackles were noted in the lung fields. The patient's oxygen saturation levels dipped to 88%, revealing hypoxemia. These clinical signs suggested that fluid was building up in the patient's lungs due to the failing heart, causing respiratory distress. The clinical team must reevaluate the patient's treatment plan in light of this new information and consider aggressive interventions to manage the patient's heart failure and prevent further complications.

Section 4

Change in Patient Status:

In the following hours, the patient's condition took a turn for the worse. His blood pressure dropped further to 85/55 mmHg and his heart rate escalated to 120 beats per minute. His oxygen saturation levels continued to decrease, now registering at 84%. Additionally, the patient complained of worsening chest pain and fatigue, suggesting that his heart was working harder and still struggling to pump blood.

New Complications:

Notably, the patient's mental status began to change. He appeared confused and disoriented, likely due to low oxygen levels in the brain. His skin became cool, moist, and pale, suggesting poor peripheral perfusion. The patient's urine output decreased significantly to 20 ml/hour, far below the normal range of 30-50 ml/hour, indicating possible renal impairment caused by inadequate blood flow to the kidneys. The team ordered urgent lab tests, including a complete blood count, basic metabolic panel, and cardiac biomarkers, to further evaluate the patient's deteriorating condition. The healthcare team needs to intensify their interventions to manage the patient's worsening heart failure and address these new complications promptly.

Section 5

Response to Interventions:

Despite the team's efforts to manage the patient's worsening heart failure, his response to interventions was less than favourable. The patient was started on intravenous furosemide to facilitate diuresis, aiming to reduce fluid volume and decrease the workload on his heart. However, his urine output remained alarmingly low at 25 ml/hour, indicating that his kidneys were not responding optimally to the medication.

The team also administered supplemental oxygen to improve his oxygen saturation levels. While there was a slight improvement, his oxygen saturation remained suboptimal at 88%, suggesting continued inadequate oxygen supply to his tissues. The patient's blood pressure remained low at 88/56 mmHg and his heart rate continued to be elevated at 115 beats per minute. This could be suggestive of a compensatory mechanism by his body to maintain cardiac output. Both these factors indicated that the patient's cardiac function was not improving as expected and that his heart continued to struggle.

The team was faced with the challenge of revising their management plan to address the patient's persistent symptoms and deteriorating vital signs. They had to consider the possibility of more aggressive interventions such as inotropic support to improve cardiac output or even the need for mechanical circulatory support as a bridge to recovery or transplantation. Their clinical reasoning skills were put to the test to decide the next course of action in the patient's management.