Heart failure - Nursing Case Study

Pathophysiology

• Primary mechanism: Heart failure often starts with damage or injury to the heart, resulting in weakened or stiffened heart muscles. This prevents the heart from filling up with or pumping blood effectively, leading to the heart's inability to supply sufficient blood flow to meet the body's needs.

• Secondary mechanism: In response to reduced blood flow, the body releases adrenaline and noradrenaline, which initially helps to increase heart rate and contractility. Over time, however, this response stresses the heart and further weakens the heart muscles, worsening heart failure.

• Key complication: Fluid overload is a central complication in heart failure. As the heart's pumping action is impaired, blood can back up in the veins that return blood to the heart, causing fluid to build up in the body's tissues, including the lungs, leading to symptoms such as edema and breathlessness.

Patient Profile

Demographics:

72-year-old male, retired construction worker.

History:

• Key past medical history: Hypertension, Type 2 Diabetes Mellitus, previous myocardial infarction 10 years ago.

• Current medications: Metformin, Lisinopril, Aspirin.

• Allergies: Penicillin.

Current Presentation:

• Chief complaint: Shortness of breath, especially when lying flat.

• Key symptoms: Fatigue, rapid weight gain, swollen ankles and feet, decreased appetite, persistent cough with white or pink phlegm.

• Vital signs: Blood pressure 145/90 mmHg, pulse 110 bpm, respiratory rate 22 breaths per minute, temperature 98.6°F, oxygen saturation 88% on room air.

Section 1

Change in Patient Status:

Over the next 24 hours, the patient's condition notably deteriorates. His oxygen saturation drops to 81% on room air, requiring supplemental oxygen at 2 liters via nasal cannula to maintain saturation above 90%. His blood pressure also increases to 160/95 mmHg, while his pulse rate rises to 120 bpm. The patient experiences a worsening of his shortness of breath, now at rest, and his ankle edema extends upwards to include both lower legs.

The patient also reports a new onset of severe, crushing chest pain radiating to his left arm. He rates his pain as an 8 out of 10 on a numeric pain scale. His skin is cool and clammy to touch, and he appears anxious and restless. These symptoms suggest the possibility of a worsening heart condition, potentially a new myocardial infarction, which could be complicating his already diagnosed heart failure. Further diagnostic tests, including an electrocardiogram and cardiac enzymes, are urgently needed to confirm this. This situation also necessitates immediate intervention to manage his symptoms and prevent further cardiac damage.

Section 2

New Diagnostic Results:

The patient's electrocardiogram (EKG) results show significant ST-segment elevation in leads II, III, and aVF, suggesting an inferior wall myocardial infarction. His cardiac enzyme levels also confirm this diagnosis. His troponin level is elevated at 3.0 ng/mL (normal: <0.05 ng/mL), and his creatinine kinase-MB (CK-MB) level is at 40 ng/mL (normal: <5 ng/mL). The patient's complete blood count shows a slightly elevated white blood cell count of 12,000/µL (normal: 4,500-11,000/µL), possibly indicating a stress response or underlying infection.

The worsening of his heart failure symptoms, along with his new onset chest pain and EKG changes, support the diagnosis of acute myocardial infarction. The elevated cardiac enzymes confirm the presence of cardiac muscle damage. The increase in his blood pressure and pulse rate are likely compensatory mechanisms due to the decrease in his cardiac output from the failing heart and myocardial infarction. Given these new findings, immediate medical intervention is crucial to preserve the remaining heart function and prevent further damage. This could potentially involve medications, such as nitroglycerin and morphine for pain management and relief of cardiac workload, and antiplatelet therapy to prevent further clot formation.

Section 3

New Complications:

After a few hours, the patient's condition deteriorates. He becomes increasingly short of breath even at rest, and his blood pressure drops to 90/60 mmHg. His heart rate also increases to 110 bpm. On auscultation, there are new crackles heard at the bases of both lungs, suggesting pulmonary edema. His oxygen saturation drops to 88% on room air, and he appears to be in respiratory distress. His urine output has also decreased to 20 mL/hour over the last four hours, indicating that his kidneys may also be affected by the decrease in cardiac output.

These new complications suggest that the patient's heart failure is progressing, and he may be developing cardiogenic shock, a serious condition where the heart can't pump enough blood to meet the body's needs. The pulmonary edema is likely due to the backup of fluid in the lungs as the heart's pumping ability worsens. The low urine output could suggest that the kidneys are not receiving sufficient blood flow, which could potentially progress to acute kidney injury if not addressed promptly. Immediate interventions to stabilize the patient's condition are necessary, likely involving the use of intravenous diuretics to reduce fluid overload, oxygen therapy or even mechanical ventilation to address the respiratory distress, and possibly vasopressor medications to support his blood pressure. The team should closely monitor the patient's vital signs, respiratory status, and urine output.

Section 4

Change in Patient Status:

Over the next few hours, the patient's respiratory distress continues to worsen, with increasing difficulty in breathing and labored respirations. His oxygen saturation drops further to 82% on 4L of oxygen via nasal cannula. His blood pressure continues to remain low at 85/55 mmHg and his heart rate spikes to 125 bpm. His urine output remains low at 15 mL/hour. The patient also becomes increasingly lethargic and confused, indicating possible decreased cerebral perfusion.

These signs are concerning for further decompensation and worsening of the cardiogenic shock. The persistent hypoxia despite supplemental oxygen, worsening hypotension, and tachycardia suggest that the heart is unable to adequately perfuse the body's organs, including the brain. The persistent low urine output is concerning for ongoing poor renal perfusion, increasing the risk of acute kidney injury. The patient's altered mental status may be a sign of decreased cerebral perfusion due to the low cardiac output. Immediate escalation of care is necessary, including increasing oxygen delivery possibly via non-invasive ventilation or intubation, and considering more aggressive measures to support his blood pressure such as the introduction of a second vasopressor. The patient's worsening condition should be communicated to the critical care team for potential ICU transfer.

Section 5

New Diagnostic Results:

The patient's arterial blood gas (ABG) report shows a pH of 7.28, PaCO2 of 50 mmHg, PaO2 of 58 mmHg, HCO3 of 22 mEq/L, and SaO2 of 88%, indicating a mixed respiratory and metabolic acidosis. This supports the clinical findings of worsening respiratory distress and organ hypoperfusion. The patient's serum lactate level is also elevated at 4.2 mmol/L, suggesting tissue hypoxia and anaerobic metabolism. Troponin levels are found to be high at 0.8 ng/mL, indicating ongoing myocardial injury, possibly due to the worsening heart failure and low perfusion. His B-type natriuretic peptide (BNP) level is also significantly elevated at 900 pg/mL, further confirming the diagnosis of heart failure.

These findings suggest that the patient is in severe cardiogenic shock with multiple organ hypoperfusion. The mixed acidosis, combined with the elevated lactate level, could be the result of both poor oxygen delivery due to the compromised cardiac output and poor ventilation due to the respiratory distress. The elevated troponin and BNP levels underscore the severity of the heart failure. These findings warrant immediate and aggressive interventions, such as intubation and mechanical ventilation, inotropic support, and possibly consideration of intra-aortic balloon pump (IABP) or other mechanical circulatory support if the patient does not respond to initial interventions. The patient's family should also be updated about his critical condition and potential outcomes to assist in making informed decisions about his care.