Cardiomyopathy - Nursing Case Study

Pathophysiology

• Primary mechanism: Myocardial remodeling - Chronic pressure or volume overload results in hypertrophy and fibrosis of myocardial cells in an attempt to maintain cardiac output. This leads to dilated or hypertrophic cardiomyopathy, depending on whether it is predominantly eccentric or concentric remodeling.

• Secondary mechanism: Impaired contractility - Abnormalities in calcium handling, mitochondrial function, and energy production within cardiomyocytes impair cardiac contractility, resulting in systolic dysfunction and heart failure, common in dilated cardiomyopathy.

• Key complication: Arrhythmogenesis - Remodeling and impaired contractility can lead to electrical instability, causing arrhythmias. Ventricular arrhythmias are particularly dangerous, increasing risk of sudden cardiac death.

Patient Profile

Demographics:

73-year-old male, retired construction worker.

History:

• Key past medical history: Hypertension, Type II Diabetes Mellitus, Chronic Obstructive Pulmonary Disease (COPD), previous myocardial infarction.

• Current medications: Metformin, Lisinopril, Aspirin, Simvastatin, Salbutamol inhaler.

• Allergies: Penicillin, Sulfa drugs.

Current Presentation:

• Chief complaint: Severe chest pain, shortness of breath.

• Key symptoms: Persistent cough, swelling in the legs and abdomen, fatigue, rapid weight gain due to fluid retention, irregular heartbeat.

• Vital signs: Blood pressure 170/95 mmHg, pulse 120 beats per minute (irregular), respiratory rate 28 breaths per minute, O2 saturation 88% on room air, temperature 37.2 degrees Celsius.

Section 1

Change in Patient Status:

Over the next few hours, the patient's condition dramatically worsens. His O2 saturation drops to 84% despite supplemental oxygen via nasal cannula at 4 liters per minute, and his respiratory rate climbs to 32 breaths per minute. His blood pressure also spikes to 180/100 mmHg, and his pulse becomes even more irregular, increasing to 130 beats per minute. The patient reports increased difficulty breathing and his cough becomes more persistent and productive, producing frothy pink sputum. On auscultation, crackles are heard in both lung bases, indicating pulmonary edema. His level of consciousness also begins to fluctuate and he appears increasingly confused.

New Complications:

Shortly after, the patient's telemetry monitor alarms, showing a rapid onset of Ventricular Tachycardia. The patient becomes unresponsive and pulseless. CPR is immediately initiated and the patient is defibrillated, successfully converting him back to sinus rhythm. However, post-resuscitation, his BP remains unstable at 90/60 mmHg, his pulse is 110 beats per minute, and his O2 Saturation is 80%, despite being on high flow oxygen. Arterial blood gas analysis reveals a pH of 7.2, PaO2 of 60mmHg, PaCO2 of 60mmHg, and HCO3 of 22 mEq/L, confirming the presence of respiratory acidosis. The patient's rapid deterioration is indicative of Acute Heart Failure exacerbation complicated by a life-threatening arrhythmia and worsening respiratory status. A decision is made to intubate the patient and he is transferred to the Intensive Care Unit for further management.

Section 2

New Diagnostic Results:

Despite rapid intervention and transfer to the ICU, the patient's condition continues to deteriorate. Lab results return revealing an elevated B-type Natriuretic Peptide (BNP) level of 900 pg/mL, consistent with severe heart failure. His troponin level also comes back elevated at 0.9 ng/mL, suggesting myocardial damage. The patient undergoes an emergency echocardiogram, which reveals a severely dilated left ventricle with a low ejection fraction of 25%, indicative of dilated cardiomyopathy. The echocardiogram also shows evidence of mitral and tricuspid regurgitation, likely contributing to his pulmonary edema and respiratory distress.

Change in Patient Status:

Over the next 24 hours, despite being on a ventilator and receiving aggressive diuretic therapy, the patient's renal function begins to deteriorate, as indicated by an increasing creatinine level from 1.2 to 2.6 mg/dL and a decreasing urine output. His serum potassium level also rises to 5.8 mEq/L. His blood pressure remains persistently low, ranging from 80-90/50-60 mmHg despite vasopressor support. The patient's altered hemodynamics, combined with his worsening renal function, suggest the possibility of cardiorenal syndrome. This complicates his management further as it limits the use of aggressive diuretic therapy, which is needed to manage his pulmonary edema but may further compromise his renal function. This situation underscores the complexity of managing severe heart failure and calls for careful balancing of therapies to optimize both cardiac and renal function.

Section 3

New Complications:

In the subsequent 48 hours, the patient's condition takes a turn for the worse. His blood pressure continues to decline, now measuring on average 70/40 mmHg, despite escalating doses of vasopressors. He also develops a new onset of atrial fibrillation with a rapid ventricular response, likely secondary to his dilated cardiomyopathy and worsening hemodynamics, with a heart rate fluctuating between 130-150 beats per minute (bpm). Electrolyte panel reveals a further increase in his potassium level to 6.2 mEq/L, raising concern for hyperkalemia-induced arrhythmia.

Simultaneously, the patient's renal function continues to decline. His creatinine level now stands at 3.5 mg/dL, and urine output has decreased to less than 200 mL over 24 hours. His blood urea nitrogen (BUN) also increases to 45 mg/dL, indicating severe renal impairment. The progression of renal dysfunction in the setting of advanced heart failure suggests the patient has now developed Type 2 Cardiorenal Syndrome, characterized by chronic heart failure leading to kidney injury. This adds another layer of complexity to the patient's management, as many of the interventions aimed at improving his heart failure could potentially exacerbate his renal failure and vice versa.

Section 4

New Diagnostic Results:

Over the next several hours, the patient's condition further deteriorates. His blood pressure continues to drop, now at 60/35 mmHg, and his heart rate remains elevated at 150 bpm despite ongoing medical management. His respiratory status also begins to decline, with increased work of breathing and a declining oxygen saturation, now averaging 88% on a high-flow nasal cannula. Blood gas analysis reveals a worsening metabolic acidosis with a pH of 7.2, bicarbonate level of 15 mEq/L, and a pCO2 of 35 mmHg, indicating a compensatory respiratory response.

To further delineate the patient's status, a transthoracic echocardiogram is performed, which reveals a severely reduced ejection fraction of 20%, suggestive of worsening heart failure. Additionally, worsening renal function is evident, with a creatinine level now standing at 4.2 mg/dL, a BUN of 55 mg/dL, and minimal urine output. The patient's hyperkalemia persists at 6.6 mEq/L despite ongoing treatment, also suggesting worsening renal function. This rapidly progressive course signifies the patient has now entered a critical phase of his Cardiorenal Syndrome, where aggressive and carefully balanced interventions are required to prevent further deterioration.

Section 5

Change in Patient Status:

Throughout the night, the patient's condition worsens. His blood pressure drops further to 50/30 mmHg, and the heart rate increases to 160 bpm, showing refractory hypotension and tachycardia. His respiratory rate increases to 30 breaths per minute, and his oxygen saturation falls to 82% despite maximum oxygen support. He becomes increasingly lethargic, arousable only to painful stimuli. A repeat arterial blood gas analysis shows a pH of 7.1, bicarbonate of 12 mEq/L, and pCO2 of 30 mmHg, indicating a worsening metabolic acidosis with a failing respiratory compensation.

New Diagnostic Results:

Given the patient's rapidly deteriorating clinical status, a Swan-Ganz catheter is placed, revealing a cardiac output of 2.2 L/min and a cardiac index of 1.1 L/min/m^2, indicative of severe cardiac failure. His central venous pressure is elevated at 18 mmHg, suggesting significant fluid overload despite the low urine output. Repeat labs show a rise in creatinine to 5.8 mg/dL and BUN to 65 mg/dL, while the potassium level has increased to 7.1 mEq/L. The patient's worsening acid-base status, hyperkalemia, and renal function all point towards an escalating multi-organ dysfunction. This critical juncture calls for swift, judicious interventions to prevent catastrophic outcomes.