hypertension - Nursing Case Study

Pathophysiology

• Primary mechanism: Increased systemic vascular resistance - Over time, factors like high sodium intake, obesity, and insulin resistance can cause the walls of the arterioles to thicken and narrow, increasing the force needed to pump blood through them, leading to high blood pressure.

• Secondary mechanism: Overactive renin-angiotensin-aldosterone system (RAAS) - In certain conditions, RAAS might become overactive, causing constriction of blood vessels and fluid retention, which elevates blood pressure.

• Key complication: End-organ damage - Chronic hypertension can lead to detrimental effects on various body organs, such as heart (causing left ventricular hypertrophy, heart failure), brain (stroke, dementia), kidneys (chronic kidney disease), and eyes (retinopathy).

Patient Profile

Demographics:

67-year-old male, retired mechanic

History:

• Key past medical history: Diagnosed with hypertension 5 years ago, Type 2 Diabetes Mellitus for 7 years, and mild COPD

• Current medications: Metformin, Lisinopril, Baby Aspirin, and an inhaler for COPD

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Persistent headaches, fatigue, and shortness of breath

• Key symptoms: Pain in the chest, irregular heartbeat, trouble with vision, difficulty sleeping

• Vital signs: Blood pressure 160/100 mmHg, pulse 90 bpm, respiratory rate 20 breaths per minute, temperature 98.6 °F, and blood glucose 180 mg/dL.

Section 1

New Diagnostic Results:

The patient's lab results return with an elevated creatinine level of 2.1 mg/dL and an estimated glomerular filtration rate (eGFR) of 40 mL/min/1.73m2, suggesting worsening renal function, possibly due to hypertensive nephropathy. His HbA1c is 8.5%, indicating poor glycemic control over the past 3 months. EKG findings show left ventricular hypertrophy, consistent with the chronic effects of hypertension on the heart. Additionally, an echocardiogram reveals an ejection fraction of 45%, suggesting a moderate decrease in left ventricular function, and the presence of diastolic dysfunction, both indicative of early heart failure.

Change in Patient Status:

In light of the new diagnostic results, the patient has progressed from complaining of persistent headaches, fatigue, and shortness of breath to experiencing increased dyspnea on exertion, occasional episodes of orthopnea, and swelling in his lower extremities. His blood pressure remains consistently high at 165/105 mmHg, despite adherence to his antihypertensive medication, Lisinopril. His blood glucose levels have also been fluctuating, with recent readings ranging from 150-200 mg/dL. The patient reports that he has been feeling more tired and weak, with decreased appetite.

Section 2

New Complications:

The patient's condition continues to deteriorate. He has developed proteinuria with a 24-hour urine test showing 2+ protein. The presence of protein in his urine is likely due to hypertension-induced glomerular damage, further suggesting the progression of hypertensive nephropathy. His serum potassium level has also increased to 5.7 mEq/L, a condition known as hyperkalemia, which could be an adverse effect of Lisinopril, an ACE inhibitor. In addition, his worsening renal function might also contribute to the elevated potassium level.

The patient has also begun to exhibit signs of fluid overload, with a weight gain of 4 lbs in the past week, jugular venous distention, and crackles in the lower lobes of his lungs on auscultation. His oxygen saturation has dipped to 90% on room air, and his respiratory rate has increased to 22 breaths per minute. These findings suggest that his heart failure may be worsening, possibly moving into a more advanced stage. The persistent hypertension, despite ongoing treatment, continues to place a heavy load on the patient's already compromised heart, contributing to the progression of his heart failure. At this point, the patient's multiple co-morbidities, including hypertension, diabetes, and renal dysfunction, are complicating his management and challenging his healthcare team's ability to stabilize his condition.

Section 3

Change in Patient Status:

The patient's condition takes a turn for the worse when he experiences a bout of severe chest pain radiating to his left arm, accompanied by diaphoresis and dyspnea. His oxygen saturation drops further to 86% on room air, and his heart rate increases to 110 beats per minute. These symptoms raise the suspicion of acute myocardial infarction (AMI), likely precipitated by the uncontrolled hypertension and worsening heart failure. The patient's ECG shows ST-segment elevation in leads II, III, and aVF, which further supports the diagnosis of an inferior wall MI.

In light of these new developments, the healthcare team initiates immediate interventions. The patient is started on oxygen therapy, aspirin, nitroglycerin, and morphine for pain. He is also scheduled for an urgent cardiac catheterization to assess the extent of coronary artery blockage and possibly perform a percutaneous coronary intervention if needed. As the healthcare team scrambles to manage this new crisis, it's evident that the patient's hypertension has led to a cascade of complications, making it crucial to gain control over his blood pressure to prevent further cardiac damage.

Section 4

New Diagnostic Results:

The results from the cardiac catheterization reveal significant blockage in the patient's right coronary artery, confirming the suspected inferior wall MI. His troponin levels are elevated at 2.5 ng/mL, further supporting the diagnosis of an acute myocardial infarction. The patient's blood pressure remains elevated at 170/95 mmHg despite medication, and his B-type natriuretic peptide (BNP) levels have increased to 900 pg/mL, indicating worsening heart failure.

Given these findings, the cardiology team decides to perform a percutaneous coronary intervention (angioplasty) to restore blood flow to the affected myocardium. Meanwhile, the nursing team must monitor the patient for signs of ongoing ischemia, arrhythmias, or hemodynamic instability. The patient's high blood pressure and elevated BNP levels also require aggressive management to prevent further cardiac strain and minimize the risk of further myocardial damage or heart failure decompensation. The team understands that the patient's uncontrolled hypertension has significantly complicated his condition, emphasizing the need for rigorous blood pressure management in preventing further cardiac events.

Section 5

Change in Patient Status:

During the night, the patient's blood pressure continues to rise, peaking at 180/105 mmHg, and his heart rate increases to 115 beats per minute. His oxygen saturation drops to 90% on room air, and he reports an increase in shortness of breath. Upon auscultation, crackles are heard in the lower lobes of both lungs. Electrocardiogram (ECG) shows new T-wave inversions, suggesting ongoing cardiac ischemia. The patient also complains of worsening chest pain, rated at 7/10 on the pain scale, despite the administration of nitroglycerin.

These changes in the patient's status indicate that the patient's heart failure is worsening and his myocardial ischemia is ongoing. The nursing team must reassess their interventions and work closely with the cardiology team to manage the patient's symptoms and prevent further deterioration. The new ECG changes and the patient's increased chest pain suggest that his myocardial infarction may be expanding, increasing the risk of life-threatening complications such as ventricular arrhythmias or cardiogenic shock. The patient's increasing dyspnea and lung crackles also suggest the development of acute pulmonary edema, a severe complication of heart failure that requires immediate intervention.