Hypertension - Nursing Case Study

Pathophysiology

• Primary mechanism: Excessive vasoconstriction and high blood volume. Hypertension can occur when the blood vessels constrict excessively, increasing resistance to blood flow. Simultaneously, if the body retains too much salt and water, blood volume increases, leading to higher pressure against vessel walls.

• Secondary mechanism: Overactive renin-angiotensin-aldosterone system (RAAS). RAAS controls blood pressure by balancing fluid volume and vascular tone. In hypertension, RAAS may be hyperactive, leading to increased sodium and water retention, vasoconstriction, and eventually, high blood pressure.

• Key complication: Organ damage. Chronic hypertension can lead to damage to the heart, kidneys, brain, and eyes, potentially resulting in heart disease, kidney failure, stroke, and blindness. This highlights the importance of early detection and management of hypertension.

Patient Profile

Demographics:

54, Male, Office worker

History:

• Key past medical history: Mild hypertension diagnosed 5 years ago, family history of hypertension

• Current medications: Hydrochlorothiazide (25 mg daily)

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Frequent headaches, fatigue, and occasional chest pain

• Key symptoms: Blurred vision, nosebleeds, shortness of breath, and blood in urine

• Vital signs: Blood pressure 165/100 mmHg, Pulse 88 bpm, Temperature 98.6°F, Respiratory rate 16 breaths per minute

Section 1

Change in Patient Status:

Three weeks following the initial presentation, the patient returned to the clinic for a routine check-up. He reported worsening headaches and increased frequency of nosebleeds. Additional symptoms included persistent fatigue and occasional episodes of dizziness. He also voiced concern about his inability to maintain concentration at work and at home. The patient's blood pressure reading was now 175/105 mmHg, a significant increase from his previous visit. His pulse was 90 bpm, and respiratory rate was 18 breaths per minute.

The patient's worsening symptoms and increased blood pressure suggest his current treatment regimen may not be adequately managing his hypertension. The increased frequency of nosebleeds and persistent fatigue could indicate damage to the blood vessels and heart due to the elevated pressure. The episodes of dizziness and lack of concentration may point to decreased blood flow to the brain. These escalating symptoms necessitate a review of the patient's medication regimen and further diagnostic evaluation to assess for potential organ damage. This case underscores the importance of regular monitoring and prompt intervention in patients with chronic conditions like hypertension.

Section 2

Change in Patient Status:

A week after his routine check-up, the patient was brought into the emergency room experiencing severe chest pain that radiated to his left arm. He was also experiencing shortness of breath. The pain started while he was at work and it did not subside after an hour of rest. His current blood pressure reading was 190/110 mmHg, pulse was 100 bpm, and his respiratory rate was 24 breaths per minute. An EKG was performed immediately, which showed ST-segment elevation suggestive of myocardial infarction.

This new event indicates that the patient's hypertension has now led to coronary artery disease, which has resulted in a heart attack. The high blood pressure has likely caused damage to the coronary arteries, leading to a blockage and subsequent heart muscle damage. This could explain the patient's fatigue, as the heart has been working harder to pump blood through the body. The chest pain and shortness of breath are classic symptoms of myocardial infarction. The patient's significantly elevated blood pressure and heart rate upon admission further underscore the serious nature of his condition. This development necessitates immediate intervention to restore blood flow to the heart, and a thorough reassessment of the patient's hypertension management plan.

Section 3

Response to Interventions:

The patient was immediately started on nitroglycerin and aspirin to relieve the chest pain and prevent further clotting. He was then taken to the catheterization lab for an emergency percutaneous coronary intervention (PCI) where a stent was successfully placed in the left anterior descending artery. After the procedure, the patient's blood pressure dropped to 150/90 mmHg and his heart rate stabilized at 80 bpm. His chest pain subsided and his respiratory rate decreased to 18 breaths per minute.

However, the following day, the patient reported feeling lightheaded and dizzy. His blood pressure was noted to have fallen further to 110/70 mmHg and his pulse was irregular at 88 bpm. A subsequent EKG showed new onset atrial fibrillation. These findings suggest that the patient is now experiencing complications post-PCI, specifically hypotension and arrhythmia. His antihypertensive medications may need to be adjusted and anticoagulants may need to be added to his management plan to prevent thromboembolic events related to atrial fibrillation. This new development warrants careful monitoring and further evaluation.

Section 4

Upon further assessment, the patient continued to report feeling lightheaded and dizzy. His blood pressure remained low at 110/70 mmHg with an irregular pulse at 88 bpm. He was started on warfarin for anticoagulation due to the new onset atrial fibrillation. The patient's antihypertensive medications were adjusted, with a decreased dose of nitroglycerin.

Two days later, the patient developed a cough and reported feeling increasingly short of breath. His oxygen saturation dropped to 92% on room air, lower than the normal levels of 95-100%. On auscultation, crackles were noted in the lower lobes of the lungs bilaterally, indicating possible fluid accumulation. A chest x-ray was ordered, which confirmed the presence of pulmonary edema, a complication that can occur post-PCI due to left ventricular dysfunction. The patient was immediately started on supplemental oxygen and furosemide, a loop diuretic, was added to his regimen to help remove the excess fluid.

These new symptoms and the chest x-ray findings prompted the healthcare team to consider heart failure as a possible complication in this patient. Further diagnostic tests, including a B-type natriuretic peptide (BNP) level, were ordered to evaluate the patient's heart function. The patient's deteriorating condition requires careful monitoring and adjustments in treatment to manage the complications. This case calls for clinical reasoning to understand the patient's evolving condition and to plan for his ongoing care.

Section 5

The next day, the patient's B-type natriuretic peptide (BNP) results came back significantly elevated at 900 pg/mL, normal range being less than 100 pg/mL. This confirmed the suspicion of heart failure. His echocardiogram showed a decreased ejection fraction of 35%, indicating a reduced ability of the heart to pump blood effectively. The patient's condition deteriorated further, with his blood pressure dropping to 100/60 mmHg and his pulse becoming more irregular at 95 bpm.

In response to the new diagnostic results, the healthcare team decided to start the patient on an angiotensin-converting enzyme (ACE) inhibitor and a beta blocker, both of which are standard treatment options for heart failure. The nitroglycerin dose was further decreased to avoid lowering his blood pressure too much. The patient's condition and response to the new treatment plan required close monitoring. His vital signs, oxygen saturation, and fluid balance were checked regularly. The healthcare team also paid attention to the patient's urine output and weight, as these could indicate whether the diuretic was effectively removing excess fluid. This stage of the patient's journey required careful clinical reasoning and adjustments in treatment to manage the developing heart failure and its complications.