7.2 Cardiovascular & Respiratory System Disorders and Clinical Interventions

Cardiovascular & Respiratory System Disorders and Clinical Interventions

Clinical Core: Cardiorespiratory disorders represent leading contributors to global adult morbidity. Optimal bedside management demands acute clinical discernment to distinguish between arterial and venous pathologies, differentiate left- from right-sided ventricular failure, titrate targeted oxygen delivery in chronic carbon dioxide retainers, and execute complex antimicrobial regimens while anticipating toxicities.

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Cardiovascular Disorders: Hypertension, CAD & Heart Failure

Hypertension Classification and Pharmacotherapy

Thresholds differ by guideline. The American College of Cardiology/American Heart Association defines hypertension as $\ge 130/80\text{ mmHg}$ (2017, retained in 2025). WHO (2021), the International Society of Hypertension (2020) and many Caribbean programmes diagnose it at $\ge 140/90\text{ mmHg}$ on repeated readings. Management combines non-pharmacological interventions (the Dietary Approaches to Stop Hypertension [DASH] diet rich in fruits, vegetables, and low-fat dairy; sodium restriction to less than $2,000\text{ mg/day}$; regular aerobic exercise; weight loss; and alcohol moderation) with targeted pharmacotherapy:

• Angiotensin-Converting Enzyme (ACE) Inhibitors (e.g., lisinopril, enalapril): Block conversion of angiotensin I to the potent vasoconstrictor angiotensin II. Key adverse effects include hyperkalemia, angioedema (life-threatening airway compromise), and a persistent, dry, hacking cough secondary to bradykinin accumulation. If cough proves intolerable, clients are transitioned to Angiotensin Receptor Blockers (ARBs).
• Angiotensin Receptor Blockers (ARBs) (e.g., losartan, valsartan): Selectively block angiotensin II receptors, lowering vascular resistance without causing bradykinin accumulation.
• Calcium Channel Blockers (CCBs) (e.g., amlodipine, diltiazem): Inhibit calcium influx into vascular smooth muscle and myocardium, inducing systemic vasodilation. Notable adverse reactions include peripheral dependent edema, headache, flushing, and bradycardia (with non-dihydropyridines like diltiazem and verapamil).
• Thiazide Diuretics (e.g., hydrochlorothiazide): Inhibit sodium and chloride reabsorption in the distal convoluted tubule. Nurses must monitor for hypokalemia, hyponatremia, and hyperuricemia (which can precipitate acute gouty attacks).

Coronary Artery Disease & Acute Coronary Syndromes (ACS)

Coronary artery disease (CAD) progresses from stable angina (predictable substernal chest discomfort relieved by rest or sublingual nitroglycerin) to Acute Coronary Syndromes (unstable angina, Non-ST-Segment Elevation Myocardial Infarction [NSTEMI], and ST-Segment Elevation Myocardial Infarction [STEMI]).

• Emergency Nursing Interventions: The nurse immediately initiates the MONA protocol and rapid diagnostic triage upon presentation with ischemic chest pain:
  • Obtain a 12-lead electrocardiogram (ECG) within 10 minutes of client arrival to assess for ST-segment elevation, ST depression, or T-wave inversion.
  • Aspirin: Administer $162\text{ mg}$ to $325\text{ mg}$ of non-enteric coated chewable aspirin immediately to inhibit platelet aggregation.
  • Nitroglycerin: Administer sublingual nitroglycerin (0.4 mg) every 5 minutes up to a maximum of 3 doses, reassessing pain and blood pressure before each dose. Contraindications: SBP $<90\text{ mmHg}$, severe bradycardia ($<50\text{ bpm}$), right ventricular infarction, or concurrent use of phosphodiesterase-5 inhibitors (e.g., sildenafil within 24 hours, tadalafil within 48 hours) due to refractory, fatal hypotension.
  • Oxygen: Titrated only if oxygen saturation drops below $90\%$ or if the client is dyspneic.
  • Morphine: Intravenous morphine sulfate ($2\text{ mg}$ to $4\text{ mg}$) for persistent chest pain refractory to nitrates; dilates venous capacitance vessels and reduces myocardial preload and anxiety.
  • Cardiac Biomarkers: Serial Cardiac Troponin I and T measurements are the gold standard for detecting myocardial necrosis, rising within 3 to 4 hours post-infarction and persisting for up to 10 to 14 days.

Heart Failure: Left-Sided Versus Right-Sided Failure

Heart failure (HF) occurs when the heart cannot pump sufficient blood to meet metabolic tissue demands. The New York Heart Association (NYHA) functional classification categorizes impairment from Class I (no symptoms with ordinary physical activity) to Class IV (inability to carry on any physical activity without discomfort; symptoms present at rest).

• B-Type Natriuretic Peptide (BNP): Released by ventricular myocytes in response to stretching and elevated filling pressures. A serum BNP $>100\text{ pg/mL}$ confirms heart failure as the primary etiology of acute dyspnea, distinguishing it from primary pulmonary disorders.
• Loop Diuretics (e.g., Furosemide): Administered to reduce preload and pulmonary congestion. Nurses must monitor for hypokalemia ($K^+ <3.5\text{ mEq/L}$), hypotension, and ototoxicity if administered too rapidly via IV push (maximum rate $20\text{ mg/min}$). Clients are instructed to record daily morning weights after voiding; a weight gain of $\ge 2\text{ to } 3\text{ lbs (0.9 to 1.4 kg)}$ in 24 hours or $5\text{ lbs (2.3 kg)}$ in one week indicates acute fluid decompensation requiring provider notification.
• Digoxin Therapy and Toxicity: Digoxin provides positive inotropic (increases contractility) and negative chronotropic (slows heart rate) effects. It has a narrow therapeutic range, traditionally quoted as 0.5 to 2.0 ng/mL. Heart failure guidance now aims for about 0.5–0.9 ng/mL.
  • Nursing Imperative: The nurse must auscultate the apical pulse for a full 60 seconds prior to administration; the dose is withheld if the apical pulse is $<60\text{ bpm}$ in adults (or $<70\text{ bpm}$ in children).
  • Toxicity Manifestations: Early gastrointestinal signs include anorexia, nausea, vomiting, and diarrhea. Neurological signs include fatigue, headache, and confusion. Visual disturbances are pathognomonic: photophobia, blurred vision, and yellow-green halos around lights. Cardiac toxicity produces dangerous bradydysrhythmias and ventricular ectopic beats.
  • Electrolyte Warning: Hypokalemia drastically potentiates digoxin toxicity because potassium and digoxin compete for identical binding sites on the myocardial cell membrane $Na^+/K^+$-ATPase pump. The nurse must check serum potassium before giving digoxin; antidote for life-threatening toxicity is Digoxin immune Fab (Digibind).

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Peripheral Vascular Disease: Arterial Versus Venous Insufficiency

Differentiating peripheral arterial disease (PAD) from peripheral venous disease (PVD) is essential to avoid catastrophic nursing errors, such as elevating an ischemic arterial limb or dangling a venous stasis leg.

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Respiratory System Disorders: COPD, Asthma, Pneumonia & Tuberculosis

Chronic Obstructive Pulmonary Disease (COPD) and the Hypoxic Drive

COPD is characterized by persistent, progressive airflow limitation comprising two overlapping phenotypes:

1. Emphysema: Abnormal, permanent enlargement of air spaces distal to terminal bronchioles with alveolar wall destruction and loss of lung elastic recoil. Clients present as "pink puffers" with tachypnea, cachexia, a barrel chest (anteroposterior-to-transverse thoracic diameter ratio 1:1), and use pursed-lip breathing (which generates positive end-expiratory pressure, staving off premature airway collapse during expiration).
2. Chronic Bronchitis: Clinically defined as a chronic, productive cough for at least 3 consecutive months in 2 consecutive years. Characterized by goblet cell hyperplasia and mucus hypersecretion. Clients present as "blue bloaters" with cyanosis, chronic hypoxemia, hypercapnia, secondary erythrocytosis (elevated hematocrit), and peripheral edema from secondary right-sided heart failure (cor pulmonale).

• The Hypoxic Drive Clinical Nuance: In healthy individuals, central brainstem chemoreceptors regulate ventilation primarily in response to arterial carbon dioxide tension ($PaCO_2$). In clients with severe, end-stage chronic hypercapnia, central chemoreceptors become desensitized to elevated $CO_2$. Consequently, respiratory drive shifts partially to peripheral chemoreceptors in the carotid and aortic bodies, which respond to arterial hypoxemia (hypoxic drive). Administering uncontrolled, high concentrations of oxygen eliminates this hypoxic stimulus, causing hypoventilation, severe $CO_2$ retention ($CO_2$ narcosis), respiratory acidosis, and lethargy. The nurse provides controlled, low-flow oxygen via nasal cannula (1 to 2 L/min) or a precise Venturi mask, titrating oxygen to maintain an $SpO_2$ of 88% to 92%. Current physiology attributes much oxygen-induced hypercapnia to worsening ventilation-perfusion mismatch and the Haldane effect, not only to loss of hypoxic drive. Either way, the target range is the same.

Asthma: Pathophysiology, Exacerbations & Peak Flow Tracking

Asthma is a chronic inflammatory disorder characterized by bronchial hyperresponsiveness, reversible bronchospasm, mucosal edema, and thick mucus production.

• Pharmacological Distinction:
  • Rescue Bronchodilator: Short-acting beta2-agonists (SABA, e.g., albuterol) act within minutes to relax bronchial smooth muscle during acute attacks. Common side effects include tremors and tachycardia.
  • Maintenance Controller: Inhaled corticosteroids (ICS, e.g., fluticasone, budesonide) provide daily baseline anti-inflammatory control. Clients must rinse their mouth and gargle with water, spitting it out after every inhalation, to prevent oral candidiasis (thrush) and dysphonia.
• Peak Expiratory Flow Rate (PEFR) Monitoring: Clients use a handheld peak flow meter to establish a "personal best" and guide daily action plans:
  • Green Zone (80% to 100% of personal best): Good control; no symptoms present; continue routine daily maintenance medications.
  • Yellow Zone (50% to 79% of personal best): Caution; indicates airway narrowing or impending exacerbation. The client must take their prescribed inhaled SABA rescue medication and recheck peak flow.
  • Red Zone (<50% of personal best): Medical alert; severe airway obstruction. The client must immediately administer their rescue bronchodilator and seek emergency medical evaluation.
• Status Asthmaticus & The Silent Chest: An acute, severe asthma attack refractory to bronchodilators. If a client with loud wheezing suddenly exhibits a "silent chest" with diminished breath sounds and no audible wheeze, this is an ominous sign of impending respiratory arrest due to critical airway closure and exhaustion; immediate endotracheal intubation is indicated.

Pneumonia: Diagnostics, Collection & Nursing Management

Infectious inflammation of the lung parenchyma leads to alveolar exudative consolidation. Bacterial pneumonia (most commonly Streptococcus pneumoniae) manifests with abrupt fever, shaking chills, tachypnea, productive cough with rust-colored or purulent sputum, pleuritic chest pain, dullness to percussion, and bronchial breath sounds with inspiratory crackles.

• Sputum Specimen Collection Protocol: Sputum must be collected before initiating antibiotic therapy to ensure accurate microbiological identification. The nurse instructs the client to rinse their mouth with water (not mouthwash) to clear oral flora, take three deep breaths, and produce a deep, forceful cough from the bronchial tree into a sterile specimen cup upon awakening in the morning. Saliva is unacceptable.
• Bedside Interventions: Position client in semi-Fowler's to high-Fowler's position; maintain oral or IV hydration of 2 to 3 L/day to liquefy viscous secretions; assist with incentive spirometry 10 times hourly while awake; provide chest physiotherapy; and administer supplemental humidified oxygen.

Pulmonary Tuberculosis & The 4-Drug RIPE Regimen

Pulmonary tuberculosis (TB) is caused by Mycobacterium tuberculosis and transmitted via airborne droplet nuclei. Clinical manifestations include low-grade afternoon fevers, drenching night sweats, chronic productive cough lasting $>3$ weeks, hemoptysis, anorexia, and unexplained weight loss.

• Diagnostic Testing:
  • Mantoux Tuberculin Skin Test (PPD): $0.1\text{ mL}$ of purified protein derivative is injected intradermally, creating a 6 to 10 mm wheal. Read 48 to 72 hours later by palpating the transverse diameter of induration (firm swelling), not erythema.
    • $\ge 5\text{ mm}$ induration: Positive in HIV-infected individuals, immunosuppressed clients (e.g., organ transplant recipients, prednisone $\ge 15\text{ mg/day}$), or close contacts of active TB cases.
    • $\ge 10\text{ mm}$ induration: Positive in healthcare workers, immigrants from high-prevalence countries within 5 years, injection drug users, and clients with high-risk clinical conditions (diabetes, chronic renal failure).
    • $\ge 15\text{ mm}$ induration: Positive in all persons with no known risk factors for TB.
  • Confirmation: WHO recommends a rapid molecular test (such as Xpert MTB/RIF) as the initial test where available, because it also detects rifampicin resistance. Sputum smear for acid-fast bacilli (AFB) and culture are also used.
• The First-Line RIPE Regimen: For drug-susceptible TB, give all four drugs for a 2-month intensive phase, then isoniazid and rifampicin for a 4-month continuation phase (2HRZE/4HR). Doses are given as directly observed therapy to prevent resistance (Section 3.5):
  • R — Rifampin (RIF): Causes red-orange discoloration of bodily fluids (urine, saliva, tears, sweat); permanently stains contact lenses. Induces hepatic cytochrome P450 enzymes, significantly decreasing the efficacy of oral contraceptives, warfarin, and protease inhibitors. Baseline and periodic liver function tests (LFTs) required.
  • I — Isoniazid (INH): Potent bactericidal agent; carries a black-box warning for severe hepatotoxicity (monitor for jaundice, dark urine, elevated AST/ALT; instruct client to avoid alcohol). Causes peripheral neuropathy (paresthesias, numbness in hands/feet) by depleting pyridoxine (vitamin B6); co-administration of Vitamin B6 (pyridoxine, 25 to 50 mg daily) is mandatory for prevention.
  • P — Pyrazinamide (PZA): Inhibits renal uric acid excretion, causing hyperuricemia and precipitating acute gouty arthritis, along with hepatotoxicity. Monitor serum uric acid and liver enzymes.
  • E — Ethambutol (EMB): Bacteriostatic agent; major adverse effect is optic neuritis, causing decreased visual acuity, loss of red-green color discrimination, and central scotomas. Baseline and monthly visual acuity (Snellen chart) and color vision testing are required; the medication must be discontinued immediately if visual disturbances arise.