3.1 Cardiovascular & Respiratory Nursing Management

Cardiovascular Nursing Management

Acute Coronary Syndrome and Myocardial Infarction

Acute Coronary Syndrome (ACS) encompasses a spectrum of clinical conditions ranging from unstable angina to non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI). The primary pathophysiology involves the rupture of an atherosclerotic plaque, leading to thrombus formation and partial or complete occlusion of a coronary artery. Immediate nursing assessment and intervention are critical to preserving myocardial tissue and preventing life-threatening arrhythmias, such as ventricular fibrillation.

Electrocardiogram (ECG) Changes and Ischemia

Early recognition of ECG changes is vital.

• T-wave inversion or ST-segment depression indicates myocardial ischemia.
• ST-segment elevation (STEMI) indicates transmural myocardial injury and requires emergent reperfusion therapy.
• The development of pathologic Q waves indicates irreversible myocardial necrosis. Nurses must rapidly obtain a 12-lead ECG within 10 minutes of patient arrival for any chest pain presentation.

Diagnostic Lab Thresholds

• Troponin I/T: Highly specific to myocardial injury. Levels rise within 3-4 hours, peak at 10-24 hours, and can remain elevated for 10-14 days. Normal Troponin I is typically < 0.03 ng/mL. Any elevation above the 99th percentile indicates myocardial necrosis.
• CK-MB: Rises in 4-6 hours, peaks at 18-24 hours, and returns to baseline in 48-72 hours. Useful for detecting early re-infarction because it clears faster than Troponin.
• Myoglobin: Early marker, rises within 1-3 hours, but lacks cardiac specificity. It is primarily used to rule out an MI if levels remain negative.
• BNP (B-type Natriuretic Peptide): Indicator of heart failure and ventricular stretch. Normal is < 100 pg/mL; > 400 pg/mL strongly suggests heart failure.
• Lipid Panel: Total cholesterol < 200 mg/dL, LDL < 100 mg/dL (or < 70 mg/dL in high-risk patients), HDL > 40 mg/dL (men) or > 50 mg/dL (women), Triglycerides < 150 mg/dL.

Nursing Priority Interventions (MONA-B)

1. Oxygen: Administer if O2 saturation is < 90% or if the patient is in respiratory distress. Over-oxygenation in non-hypoxic patients may cause paradoxical coronary vasoconstriction.
2. Aspirin: Administer 162-325 mg (chewed for rapid absorption) immediately to inhibit platelet aggregation and prevent further thrombus expansion.
3. Nitroglycerin: Administer sublingual tablet (0.4 mg) every 5 minutes up to 3 doses for relief of ischemic chest pain. Monitor for hypotension. It is strictly contraindicated if phosphodiesterase inhibitors (e.g., sildenafil) were used within the last 24-48 hours.
4. Morphine: Administer IV for pain unrelieved by nitroglycerin. It reduces pain, decreases anxiety, and acts as a venodilator, reducing preload, afterload, and myocardial oxygen demand.
5. Beta-Blockers: Initiate cardioselective beta-blockers (e.g., Metoprolol) within 24 hours to decrease heart rate, contractility, and blood pressure, significantly reducing myocardial oxygen demand and the risk of fatal arrhythmias.

Heart Failure (HF)

Heart failure is a clinical syndrome characterized by the heart's inability to pump adequate blood to meet the body's metabolic demands. It is classified into Left-Sided (pulmonary symptoms) and Right-Sided (systemic symptoms) failure. Understanding the hemodynamics of HF is essential for effective nursing care.

Pathophysiology and Compensatory Mechanisms

When cardiac output drops, the body activates compensatory mechanisms that initially help but eventually worsen HF. The Sympathetic Nervous System (SNS) increases heart rate and vasoconstriction. The Renin-Angiotensin-Aldosterone System (RAAS) causes fluid retention (increasing preload) and severe vasoconstriction (increasing afterload), leading to cardiac remodeling and hypertrophy.

Clinical Manifestation Table: Left vs. Right HF

Nursing Interventions for HF

• Fluid Balance: Restrict fluids (e.g., 1.5-2 L/day) and sodium (< 2g/day). Monitor daily weights (a gain of > 3 lbs in 2 days or 5 lbs in a week requires immediate reporting to the provider).
• Medications: Administer ACE inhibitors/ARBs (reduce afterload and prevent remodeling), Beta-blockers (improve ejection fraction over time), and Diuretics (reduce preload, e.g., Furosemide). Monitor potassium levels closely, especially with loop diuretics (hypokalemia risk) or potassium-sparing diuretics (hyperkalemia risk).
• Positioning: High-Fowler's position to maximize lung expansion, decrease venous return, and relieve dyspnea.
• Education: Teach patients about the MAWDS approach: Medications, Activity, Weight, Diet, and Symptoms.

Respiratory Nursing Management

Chronic Obstructive Pulmonary Disease (COPD)

COPD includes emphysema (alveolar destruction, loss of lung elasticity) and chronic bronchitis (airway inflammation, mucosal edema, and mucus hypersecretion). Patients with COPD often have chronic hypercapnia (retained CO2) and rely on a hypoxic drive to breathe. The progressive airflow limitation is not fully reversible, leading to air trapping and hyperinflation of the lungs (barrel chest).

Nursing Priority Interventions

• Oxygen Therapy: Administer low-flow oxygen (1-2 L/min via nasal cannula or a Venturi mask at 24-28%) to maintain SpO2 between 88-92%. Avoid suppressing the hypoxic drive. Continuously monitor for signs of CO2 narcosis (confusion, lethargy, somnolence).
• Breathing Techniques: Teach pursed-lip breathing (prolongs exhalation, prevents alveolar collapse) and diaphragmatic breathing to reduce the work of breathing.
• Nutrition: Provide high-calorie, high-protein, small frequent meals to prevent fatigue during eating. Carbohydrate metabolism produces more CO2, so a higher fat/lower carb diet may be beneficial. Provide rest periods before and after meals.
• Medications: Bronchodilators (beta2-agonists, anticholinergics like Tiotropium) are the mainstay of treatment, supplemented by inhaled corticosteroids for frequent exacerbations.

Asthma

Asthma is a reversible obstructive airway disease characterized by airway inflammation, hyperresponsiveness to triggers, and bronchospasm.

Disease Comparison: COPD vs. Asthma

Acute Asthma Exacerbation Management

• Assess: Respiratory rate, accessory muscle use, wheezing. The sudden absence of wheezing with severe distress indicates a "silent chest"—a medical emergency indicating complete airway obstruction and impending respiratory failure.
• Intervene: Administer short-acting beta2-agonists (SABA) like Albuterol via nebulizer, systemic corticosteroids (IV Methylprednisolone to reduce inflammation), and anticholinergics (Ipratropium).
• Monitor: Peak Expiratory Flow Rate (PEFR). Green zone (>80%), Yellow zone (50-80%), Red zone (<50% - emergency). Instruct patients to seek immediate medical attention if in the red zone.

Arterial Blood Gas (ABG) Interpretation

Understanding ABGs is essential for assessing acid-base balance and respiratory status in critically ill patients.

Normal Values

• pH: 7.35 - 7.45
• PaCO2: 35 - 45 mmHg (Respiratory parameter)
• HCO3-: 22 - 26 mEq/L (Metabolic parameter)
• PaO2: 80 - 100 mmHg
• SaO2: 95 - 100%

Interpretation Guide

1. Respiratory Acidosis: pH < 7.35, PaCO2 > 45. Causes: Hypoventilation (COPD, opiate overdose, chest trauma, neuromuscular diseases). Interventions aim at improving ventilation (CPAP, BiPAP, intubation).
2. Respiratory Alkalosis: pH > 7.45, PaCO2 < 35. Causes: Hyperventilation (anxiety, severe pain, hypoxia, fever). Interventions focus on treating the underlying cause of hyperventilation and calming the patient.
3. Metabolic Acidosis: pH < 7.35, HCO3- < 22. Causes: Diabetic ketoacidosis, renal failure, severe diarrhea (loss of base). May present with deep, rapid Kussmaul respirations as the lungs attempt to blow off CO2 to compensate.
4. Metabolic Alkalosis: pH > 7.45, HCO3- > 26. Causes: Severe vomiting, excessive gastric suctioning, diuretic use (loss of acid).

Note: Compensation occurs when the system not primarily responsible for the imbalance attempts to correct the pH. For example, in metabolic acidosis, the lungs will hyperventilate to blow off CO2 and raise the pH. If the pH returns to normal, it is fully compensated; if not, it is partially compensated.