Cardiovascular & Respiratory Disorders

Systemic medical-surgical nursing requires a deep understanding of hemodynamic stability, gas exchange, and rapid emergency intervention. Cardiovascular and respiratory conditions are the most time-critical emergencies encountered by nursing officers in acute clinical settings.

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1. Coronary Artery Disease & Acute Coronary Syndromes

Coronary Artery Disease (CAD) results from progressive atherosclerotic plaque accumulation in coronary arterial walls, impairing myocardial perfusion. When oxygen demand exceeds supply, myocardial ischemia develops.

Angina Pectoris Subtypes

• Stable Angina (Exertional): Predictable, episodic chest discomfort provoked by physical exertion or emotional stress. Relieved within 5 minutes by rest or sublingual nitroglycerin.
• Unstable Angina (Crescendo / Pre-infarction): Unpredictable pain occurring at rest, of increasing frequency, severity, or duration (> 20 minutes), and refractory to initial nitroglycerin doses. Represents an acute coronary syndrome (ACS) without immediate biomarker elevation.
• Prinzmetal (Variant) Angina: Caused by focal coronary artery vasospasm occurring almost exclusively at rest, often during early morning hours. Associated with transient ST-segment elevation that resolves when spasm terminates; treated with calcium channel blockers (amlodipine, diltiazem) and nitrates.

Myocardial Infarction (MI)

Myocardial infarction occurs when prolonged severe ischemia causes irreversible coagulative necrosis of myocardial tissue. It is classified into two major clinical entities based on initial 12-lead electrocardiography (ECG):

• ST-Segment Elevation Myocardial Infarction (STEMI): Complete, persistent occlusive thrombus resulting in transmural myocardial necrosis. Displays ST elevation ≥ 1 mm in two contiguous limb leads or ≥ 2 mm in precordial leads, or a new left bundle branch block (LBBB).
• Non-ST-Segment Elevation Myocardial Infarction (NSTEMI): Partial or intermittent occlusion resulting in subendocardial necrosis. Displays ST-segment depression or T-wave inversion without persistent ST elevation, confirmed by elevated cardiac biomarkers.

Cardiac Biomarkers & ECG Evolution

ECG Waveform Evolution in Infarction:

1. Hyperacute T waves: Tall, peaked, symmetrical T waves within minutes of occlusion.
2. ST-Segment Elevation: Indicates acute myocardial injury.
3. T-Wave Inversion: Reflects myocardial ischemia.
4. Pathological Q Waves: Width ≥ 0.04 seconds (one small box) or depth ≥ 25% of the ensuing R wave; indicates irreversible transmural necrosis and tissue electrical silence.

Acute Management: The MONA Protocol & Reperfusion

Emergency nursing stabilization follows the standard MONA regimen (administered based on clinical assessment, typically Oxygen-Aspirin-Nitroglycerin-Morphine):

• Morphine Sulfate: IV 2–4 mg titrated every 5–15 minutes. Decreases pain, anxiety, sympathetic outflow, and produces peripheral venodilation, reducing preload and myocardial oxygen demand. Naloxone must be immediately available.
• Oxygen: Administer via nasal cannula (2–4 L/min) only if hypoxemic (SpO2 < 90%) or in respiratory distress. Hyperoxia induces coronary vasoconstriction.
• Nitroglycerin (NTG): Sublingual tablet (0.4 mg) every 5 minutes up to 3 doses. Promotes coronary vasodilation and systemic venodilation. Contraindications: Systolic BP < 90 mmHg, heart rate < 50 bpm or > 100 bpm, suspected right ventricular infarction, or phosphodiesterase-5 inhibitor use (sildenafil within 24 hours, tadalafil within 48 hours).
• Aspirin (ASA): 162–325 mg non-enteric coated tablet chewed immediately to achieve rapid antiplatelet inhibition.

Reperfusion Benchmarks:

• Primary Percutaneous Coronary Intervention (PCI): Preferred strategy. Goal is door-to-balloon time ≤ 90 minutes (or ≤ 120 minutes if transferred to a PCI-capable center).
• Fibrinolytic / Thrombolytic Therapy: Indicated if primary PCI cannot be performed within 120 minutes. Goal is door-to-needle time ≤ 30 minutes using alteplase (tPA), tenecteplase, or streptokinase.
• Absolute Contraindications to Thrombolytics: Any prior intracranial hemorrhage, known structural cerebral vascular lesion (AVM), malignant intracranial neoplasm, ischemic stroke within 3 months (except acute ischemic stroke within 4.5 hours), active internal bleeding (excluding menses), and suspected aortic dissection.

Comparison: Angina vs. Myocardial Infarction

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2. Heart Failure (HF) & Hemodynamic Management

Heart failure is a complex clinical syndrome where structural or functional cardiac impairment prevents adequate ventricular filling or ejection of blood to meet systemic metabolic demands.

Left-Sided vs. Right-Sided Heart Failure

• Left-Sided Heart Failure (Forward Failure & Pulmonary Congestion): Increased pressure in the left ventricle backs up into the left atrium and pulmonary veins, causing pulmonary capillary fluid extravasation into alveoli. Key manifestations include:
  • Dyspnea on exertion, progressing to orthopnea (inability to breathe comfortably while lying flat; documented by number of pillows used).
  • Paroxysmal Nocturnal Dyspnea (PND): Sudden awakening 1–2 hours after sleep with suffocating breathlessness.
  • Bilateral inspiratory bibasilar crackles (crepitations), cough, and pink frothy sputum in acute pulmonary edema.
  • Third heart sound (S3 gallop), fatigue, oliguria from decreased renal perfusion.
• Right-Sided Heart Failure (Systemic Venous Congestion): Commonly caused by left-sided HF or severe chronic lung disease (cor pulmonale). Increased right ventricular pressure impairs venous return, resulting in systemic pooling. Key manifestations include:
  • Jugular Venous Distension (JVD) > 4 cm above the sternal angle at 45° bed elevation.
  • Dependent peripheral pitting edema (feet, ankles, pretibial, or presacral in bedbound patients).
  • Hepatomegaly, splenomegaly, right upper quadrant abdominal tenderness, and ascites.
  • Hepatojugular reflux, anorexia, nausea, and rapid involuntary weight gain (fluid retention).

NYHA Functional Classification

• Class I: Cardiac disease without resulting limitation of physical activity. Ordinary activity does not cause fatigue, palpitations, or dyspnea.
• Class II: Slight limitation of physical activity. Comfortable at rest; ordinary activity results in fatigue, palpitations, or dyspnea.
• Class III: Marked limitation of physical activity. Comfortable at rest; less than ordinary activity causes fatigue, palpitations, or dyspnea.
• Class IV: Inability to carry on any physical activity without discomfort. Symptoms of heart failure present even at rest; discomfort increases with any effort.

Pharmacotherapy for Heart Failure

1. ACE Inhibitors / ARBs (Enalapril, Ramipril, Losartan): First-line therapy to decrease afterload and preload, suppress the renin-angiotensin-aldosterone system (RAAS), and prevent ventricular remodeling. Monitor blood pressure, serum potassium (risk of hyperkalemia), and renal function. Persistent dry cough warrants switching from ACE inhibitors to ARBs.
2. Beta-Adrenergic Blockers (Carvedilol, Metoprolol Succinate, Bisoprolol): Reduce sympathetic stimulation, decrease heart rate, and improve long-term survival. Initiated when euvolemic. Withhold if heart rate < 60 bpm or symptomatic hypotension occurs.
3. Loop Diuretics (Furosemide, Bumetanide): Primary agents for rapid volume decongestion. Administer furosemide IV push over 1–2 minutes (max rate 20 mg/min) to prevent ototoxicity. Monitor for hypokalemia, hyponatremia, and dehydration; monitor intake and output and daily weights.
4. Cardiac Glycoside (Digoxin): Positive inotrope (increases myocardial contractility) and negative chronotrope (slows AV node conduction). Therapeutic serum range: 0.5–2.0 ng/mL.
   • Nursing Safety: Always auscultate the apical pulse for 1 full minute prior to administration. Withhold medication and notify the physician if apical pulse < 60 bpm in adults (< 90 bpm in infants).
   • Digoxin Toxicity Signs: Gastrointestinal (anorexia, nausea, vomiting, diarrhea), neurological (headache, confusion, fatigue), and visual disturbances (blurred vision, yellow-green halos around lights, photophobia). Cardiac dysrhythmias (PVCs, AV block, bradycardia).
   • Critical Trigger: Hypokalemia (< 3.5 mEq/L) potentiates digoxin binding to the Na+/K+ ATPase pump, dramatically precipitating life-threatening toxicity.

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3. Hypertension & Hypertensive Crises

According to standard clinical guidelines, blood pressure is categorized as follows:

• Normal: < 120 mmHg systolic and < 80 mmHg diastolic.
• Elevated: 120–129 mmHg systolic and < 80 mmHg diastolic.
• Stage 1 Hypertension: 130–139 mmHg systolic or 80–89 mmHg diastolic.
• Stage 2 Hypertension: ≥ 140 mmHg systolic or ≥ 90 mmHg diastolic.

Hypertensive Crisis: Urgency vs. Emergency

A hypertensive crisis is defined as a severe acute elevation in blood pressure with systolic BP > 180 mmHg and/or diastolic BP > 120 mmHg.

• Hypertensive Urgency (called severe hypertension in the 2025 AHA/ACC guideline): Severe blood pressure elevation WITHOUT acute progressive target organ damage (TOD). Managed with oral antihypertensive agents (captopril, labetalol, clonidine) to gradually lower blood pressure over 24 to 48 hours.
• Hypertensive Emergency: Severe blood pressure elevation WITH acute, life-threatening target organ damage (e.g., hypertensive encephalopathy, acute intracranial hemorrhage, acute pulmonary edema with left ventricular failure, acute aortic dissection, or acute renal failure).
  • Nursing & Medical Management: Requires immediate admission to an intensive care unit (ICU) and continuous intravenous titration of rapidly acting vasodilators (sodium nitroprusside, labetalol, nicardipine, hydralazine).
  • Target Reduction Rate: Do NOT lower blood pressure to normal immediately. Reduce mean arterial pressure (MAP) by no more than 20% to 25% within the first hour, or to approximately 160/100 mmHg over the first 2 to 6 hours. Excessive rapid reduction compromises cerebral, coronary, and renal perfusion, precipitating ischemic stroke or acute kidney injury.

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4. Chronic Obstructive Pulmonary Disease (COPD)

COPD is a progressive, largely irreversible airflow limitation characterized by chronic inflammatory changes in the airways and pulmonary parenchyma. It encompasses two primary pathological entities that frequently coexist:

Chronic Bronchitis vs. Emphysema

• Chronic Bronchitis ("Blue Bloaters"): Defined clinically as the presence of a chronic productive cough for at least 3 consecutive months in 2 successive years. Hyperplasia and hypertrophy of goblet cells and submucosal glands in the bronchi cause excessive mucus secretion and luminal narrowing. Chronic hypoxemia and hypercapnia induce polycythemia, cyanosis, and pulmonary hypertension leading to right ventricular failure (cor pulmonale and peripheral edema).
• Emphysema ("Pink Puffers"): Characterized anatomically by permanent, abnormal enlargement of airspaces distal to terminal bronchioles with destruction of alveolar walls and loss of elastic recoil. Breakdown of elastin leads to air trapping during expiration, hyperinflation, and increased anterior-posterior chest diameter (barrel chest with 1:1 AP-to-transverse ratio). Patients exhibit severe exertional dyspnea, use accessory muscles, and adopt pursed-lip breathing to create positive end-expiratory pressure, preventing dynamic airway collapse.

The Hypoxic Drive Mechanism & Controlled Oxygen Delivery

In healthy individuals, the respiratory center in the brainstem (medulla oblongata) is primarily stimulated by central chemoreceptors sensitive to arterial carbon dioxide tension (PaCO2) and hydrogen ion concentration.

In severe end-stage COPD with chronic carbon dioxide retention, central chemoreceptors become desensitized. The primary stimulus for ventilation shifts to peripheral chemoreceptors located in the aortic and carotid bodies, which respond to hypoxemia (low PaO2)—known as the hypoxic drive.

Critical Nursing Consideration: If high concentrations of supplemental oxygen are delivered to a patient with chronic CO2 retention, the hypoxemic stimulus is abolished. Alveolar hypoventilation ensues, precipitating acute CO2 retention, carbon dioxide narcosis, somnolence, confusion, coma, and respiratory arrest.

• Target SpO2: 88% to 92%.
• Controlled Administration: Administer low-flow oxygen (1 to 2 L/min via nasal cannula) or precise fractional inspired oxygen (24% to 28% via a Venturi mask).

Comparison: COPD vs. Bronchial Asthma

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5. Bronchial Asthma & Status Asthmaticus

Asthma is a chronic inflammatory disorder of the airways characterized by bronchial hyperresponsiveness, reversible airway obstruction, mucosal edema, and excessive mucus plugging.

• Triggers: Environmental allergens (pollen, dust mites, animal dander), viral respiratory infections, exercise, cold air, emotional stress, and medications (NSAIDs, aspirin, non-selective beta-blockers).
• Clinical Triad: Dyspnea, wheezing (predominantly expiratory), and cough (frequently nocturnal or early morning).

Peak Expiratory Flow Rate (PEFR) Monitoring

PEFR measures the maximum airflow velocity achieved during forced expiration starting from total lung capacity, utilizing a handheld peak flow meter.

• Green Zone (80%–100% of personal best): Good control; maintenance therapy continued.
• Yellow Zone (50%–79% of personal best): Caution; acute exacerbation or airway narrowing; initiate rescue short-acting beta-2 agonist (SABA) per action plan.
• Red Zone (< 50% of personal best): Medical alert / emergency; severe bronchoconstriction; immediate rescue bronchodilators and emergency medical attention required.

Status Asthmaticus

Status asthmaticus is an acute, severe asthma exacerbation unresponsive to standard bronchodilator therapy. It is a life-threatening medical emergency.

• Ominous Warning Signs: "Silent chest" (complete absence of audible wheezing or breath sounds due to critical airflow limitation; indicates impending respiratory failure), pulsus paradoxus > 10–12 mmHg, inability to speak full sentences, central cyanosis, diaphoresis, and exhaustion.
• Emergency Treatment: High-flow humidified oxygen (titrated to SpO2 ≥ 92%), continuous or repetitive nebulization of SABA (albuterol / salbutamol) combined with anticholinergics (ipratropium bromide), IV systemic corticosteroids (hydrocortisone 100–200 mg or methylprednisolone) to reduce airway inflammation, and IV magnesium sulfate (1–2 g over 20 minutes) to induce bronchial smooth muscle relaxation.

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6. Pneumonia & Ventilator-Associated Care

Pneumonia is an acute inflammatory infection of the lung parenchyma characterized by alveolar exudate and consolidation.

• Community-Acquired Pneumonia (CAP): Acquired outside healthcare settings or diagnosed within 48 hours of hospital admission. Most common pathogen: Streptococcus pneumoniae.
• Hospital-Acquired Pneumonia (HAP): Develops ≥ 48 hours after hospital admission. Pathogens are frequently multidrug-resistant: Pseudomonas aeruginosa, Methicillin-Resistant Staphylococcus aureus (MRSA), and Klebsiella pneumoniae.
• Ventilator-Associated Pneumonia (VAP): Develops > 48 hours after endotracheal intubation. Prevention utilizes the VAP Bundle:
  1. Elevation of the head of bed (HOB) to 30°–45°.
  2. Daily "sedation vacations" and assessment of readiness to extubate.
  3. Peptic ulcer disease prophylaxis (H2 blockers / PPIs).
  4. Deep venous thrombosis (DVT) prophylaxis.
  5. Regular oral hygiene using 0.12% chlorhexidine gluconate oral rinse.
  6. Subglottic secretion drainage using specialized endotracheal tubes.

Sputum Examination Protocol: Sputum specimens must be collected early in the morning before breakfast, after the patient rinses their mouth with sterile water to minimize oral bacterial contamination. Specimen must represent a deep bronchial cough (not saliva) and be sent immediately to the laboratory prior to starting broad-spectrum antibiotics.

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7. Pulmonary Tuberculosis (TB)

Pulmonary tuberculosis is an infectious bacterial disease caused by Mycobacterium tuberculosis, an acid-fast bacillus (AFB) transmitted via airborne droplet nuclei (1–5 micrometers in diameter) expelled when an infected individual coughs, sneezes, or talks.

Diagnostic Evaluation

• Mantoux Tuberculin Skin Test (TST / PPD): Intradermal injection of 0.1 mL of Purified Protein Derivative (containing 5 Tuberculin Units) onto the volar forearm, producing a 6–10 mm wheal. Read 48 to 72 hours later by palpating and measuring the transverse diameter of induration (firm raised area), NOT erythema.
  • ≥ 5 mm Induration: Positive in HIV-infected individuals, close contacts of active TB cases, or immunosuppressed patients (organ transplants, prednisone ≥ 15 mg/day).
  • ≥ 10 mm Induration: Positive in immigrants from high-prevalence areas, healthcare workers, injection drug users, and residents of high-risk congregate settings.
  • ≥ 15 mm Induration: Positive in individuals with no known risk factors for TB.
• Sputum Smear Microscopy: Stained with Ziehl-Neelsen (ZN) acid-fast stain. M. tuberculosis retains carbol fuchsin dye despite acid-alcohol decolorization, appearing as bright red/pink slender beaded rods against a methylene blue background. Under India's NTEP, two sputum specimens (one spot and one early-morning) are examined by microscopy, and rapid molecular tests (CBNAAT/Truenat) are the preferred upfront diagnostic test.

First-Line Anti-TB Therapy & Adverse Effects

Under India's NTEP, the intensive phase uses four first-line drugs (HRZE, also remembered as RIPE) given daily as weight-band fixed-dose combinations:

1. Rifampicin (RIF): Potent bactericidal agent. Causes harmless red-orange discoloration of urine, sweat, saliva, and tears (educate patient not to wear soft contact lenses); potent hepatic cytochrome P450 inducer; causes hepatotoxicity.
2. Isoniazid (INH): Inhibits mycolic acid synthesis. Causes peripheral neuropathy due to competition with pyridoxine (Vitamin B6). Prophylactic Pyridoxine (10–25 mg daily) must be co-prescribed. Highly hepatotoxic (monitor AST/ALT).
3. Pyrazinamide (PZA): Inhibits urate excretion in renal tubules, leading to hyperuricemia and non-gouty polyarthralgia or acute gouty arthritis. Also hepatotoxic.
4. Ethambutol (EMB): Bacteriostatic agent. Causes dose-dependent retrobulbar optic neuritis, presenting as decreased visual acuity and red-green color blindness. Monthly visual acuity and Ishihara color testing required; used with caution (weight-band dosing) in young children who cannot report visual changes.

Infection Control Protocols

• Admit patient to an Airborne Infection Isolation Room (AIIR) with negative air pressure (minimum 6–12 air exchanges per hour) vented directly outdoors.
• Healthcare personnel must wear a properly fit-tested N95 particulate respirator mask prior to entering the room.
• The patient must remain in the room; if transport is mandatory, the patient must wear a standard surgical mask to contain respiratory droplets.