Cardiovascular disease - Nursing Case Study

Pathophysiology

• Primary mechanism: Atherosclerosis - Fatty deposits or plaques gradually build up on the inner walls of arteries, causing them to harden and narrow. This restricts blood flow to the heart, potentially leading to angina or a heart attack.

• Secondary mechanism: Hypertension - Persistently high blood pressure damages the arteries, making them more susceptible to atherosclerosis. It also strains the heart, increasing the risk of heart failure.

• Key complication: Myocardial infarction - When an artery supplying the heart becomes blocked, parts of the heart muscle can die due to lack of oxygen. This can cause serious heart damage or death.

Patient Profile

Demographics:

67-year-old male, retired construction worker

History:

• Key past medical history: Diagnosed with hypertension and high cholesterol 10 years ago, history of tobacco use (quit 5 years ago), family history of cardiovascular disease.

• Current medications: Lisinopril for hypertension, Atorvastatin for cholesterol, Aspirin for heart health

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increased fatigue, shortness of breath, and occasional chest pain

• Key symptoms: Swelling in the legs and ankles (edema), difficulty performing everyday tasks due to fatigue, intermittent chest pain especially during physical activity

• Vital signs: Blood pressure 160/95 mm Hg, heart rate 88 bpm, respiratory rate 18 breaths per minute, body temperature 98.6°F, oxygen saturation 93% on room air

Section 1

Change in Patient Status:

Upon reassessment, the patient’s condition seems to have deteriorated. He is increasingly dyspneic, with a respiratory rate of 24 breaths per minute and oxygen saturation dropping to 88% on room air. He reports a pressure-like chest pain radiating to his left arm, rating it 8 out of 10 on the pain scale. His blood pressure is elevated at 170/100 mm Hg, and his heart rate is irregular at 92 bpm. The patient is diaphoretic and appears visibly distressed.

Initial physical examination reveals jugular vein distension, increased bilateral lower extremity edema, and crackles in lower lung fields bilaterally. The patient also complains of feeling lightheaded, with a brief episode of syncope while attempting to stand. These new symptoms suggest that his cardiovascular disease may be progressing to congestive heart failure, potentially exacerbated by an acute coronary syndrome.

Section 2

Change in Patient Status:

The patient’s condition continues to deteriorate, with his respiratory rate increasing to 28 breaths per minute and oxygen saturation dropping further to 85% on room air. Chest pain persists, now rating it 9 out of 10 on the pain scale. His blood pressure remains elevated at 175/105 mm Hg, with his heart rate increasing to an irregular 100 bpm. The patient appears increasingly anxious, and his skin feels cool and clammy to the touch.

Upon further assessment, the patient's lower extremity edema has worsened, with pitting noted up to the mid-calf. His jugular vein distension is more pronounced, indicating increased central venous pressure. Crackles are now heard throughout both lung fields, suggesting worsening pulmonary edema. The patient also reports increasing lightheadedness and says he almost fainted when he tried to stand up to use the bathroom. His worsening symptoms and increased distress may indicate a progression of his heart failure and possible impending cardiogenic shock, potentially triggered by his underlying cardiovascular disease and suspected acute coronary syndrome.

In response to the patient's deteriorating condition, the healthcare team urgently requests an electrocardiogram (ECG) and cardiac enzyme tests. The patient is placed on high-flow oxygen to improve his oxygenation and nitroglycerin is administered sublingually for his chest pain. He is also given a bolus of IV furosemide to decrease his fluid overload and started on a nitroprusside drip to reduce his afterload, hoping to decrease the workload of his heart.

Section 3

Change in Patient Status:

Despite the interventions, the patient's condition continues to worsen. His respiratory rate has increased to 32 breaths per minute, and his oxygen saturation has further decreased to 80% despite high-flow oxygen. The patient's blood pressure is now alarmingly high at 185/110 mm Hg, with his heart rate escalating to 120 bpm. His level of consciousness is decreasing, and his skin is now pale and cold to touch, suggesting poor perfusion.

New Diagnostic Results:

The results of the ECG show ST-segment elevations, indicative of a myocardial infarction. Furthermore, the cardiac enzyme tests also support this finding, with significantly elevated troponin levels. The worsening edema, along with the patient’s now elevated B-type natriuretic peptide (BNP) level, confirms progression of his heart failure. The healthcare team is now faced with managing an acute myocardial infarction in the context of worsening heart failure, a challenging clinical scenario requiring careful balancing of interventions. The patient’s deteriorating condition and the diagnostic results necessitate an urgent cardiology consultation and possible transfer to a higher level of care. The team must weigh the benefits of aggressive interventions against the potential risks, given the patient's advanced cardiovascular disease and deteriorating hemodynamic status.

Section 4

New Complications:

Increasingly, the patient is showing signs of cardiogenic shock, a severe condition often associated with a large, acute myocardial infarction, also known as a heart attack. His blood pressure has dropped significantly to 90/50 mm Hg, his heart rate is now 140 bpm, and the cardiac index from his pulmonary artery catheter is 1.7 L/min/m2, far below the normal range of 2.5-4.0 L/min/m2. The patient is also exhibiting signs of renal failure as his urine output has been less than 0.5 ml/kg/hr over the past 6 hours. The latest lab results show a sharp increase in creatinine (2.8 mg/dL) and a decrease in urine sodium concentration (less than 20 mEq/L), both indicative of acute kidney injury (AKI), likely due to decreased renal perfusion from the worsening heart failure.

The healthcare team must now manage the patient's heart attack, heart failure, and kidney injury concurrently, a complex task. The patient's advanced cardiovascular disease and deteriorating hemodynamic status pose a significant challenge to the team's efforts. The team is now tasked with stabilizing the patient's hemodynamic status, managing the acute kidney injury, and considering the possibility of initiating renal replacement therapy. Considering the patient's overall condition, the intensivist is consulted, and a multidisciplinary approach is needed to manage these complications. The team must also carefully monitor the patient for any other potential complications while balancing the benefits and risks of each intervention.

Section 5

Initial Assessment Findings:

On further assessment, the nurse finds the patient to be restless, with increased anxiety. His skin is cold and clammy, with mottling observed on his lower extremities, a sign of inadequate perfusion. His ECG shows ST-segment elevation in leads II, III, and aVF, indicative of an inferior wall myocardial infarction. His respiratory rate has increased to 24 breaths per minute, with a SpO2 of 90% on 4L of oxygen via nasal cannula. The nurse also notes decreased breath sounds on the right side of his chest, and the patient complains of increased shortness of breath. His urine output remains less than 0.5 ml/kg/hr despite fluid resuscitation, indicating persistent renal dysfunction. His latest arterial blood gas shows a pH of 7.30, PaCO2 of 50 mmHg, and HCO3 of 24 mEq/L, suggesting respiratory acidosis.

The nurse's assessment findings indicate a worsening of the patient's cardiogenic shock and heart failure, with the emergence of respiratory distress likely secondary to pulmonary congestion or possible pleural effusion. The team must now consider further interventions such as inotropic support, mechanical ventilation, or possibly intra-aortic balloon pump (IABP) to improve the patient's hemodynamic status while managing the ongoing renal injury. The risk of multi-organ failure is high, and the team must act quickly to prevent further deterioration. The nurse's ongoing assessment and monitoring will be critical in guiding the team's decisions and managing the patient's complex condition.