5.1 Medical-Surgical Nursing Care & Acute Conditions

5.1 Medical-Surgical Nursing Care & Acute Conditions

Cardiovascular Emergency Care: ACS & Heart Failure

Acute Coronary Syndrome (ACS)

Acute Coronary Syndrome (ACS) encompasses a spectrum of clinical conditions resulting from acute myocardial ischemia, ranging from unstable angina and non-ST-segment elevation myocardial infarction (NSTEMI) to ST-segment elevation myocardial infarction (STEMI). When an adult presents with acute chest pain, pressure, or dyspnea, registered nurses in New Zealand acute care settings must immediately initiate the ACS pathway. A 12-lead electrocardiogram (ECG) must be acquired and interpreted within 10 minutes of patient arrival. Diagnostic markers include ST-segment elevation ≥1 mm in two contiguous leads for STEMI, or ST depression and T-wave inversion for NSTEMI/unstable angina. Serial cardiac troponin (I or T) testing at baseline and 3 hours post-onset differentiates NSTEMI from unstable angina. Immediate nursing interventions include maintaining oxygen saturation between 94–98% (or 88–92% in patients at risk of hypercapnic respiratory failure), administering sublingual glyceryl trinitrate (GTN) 400 mcg spray every 5 minutes (up to 3 doses if systolic blood pressure remains >90 mmHg and the patient has not ingested phosphodiesterase-5 inhibitors), loading with oral aspirin 300 mg chewable, and administering IV opioids (morphine 2.5–5 mg or fentanyl 25–50 mcg) for severe unrelieved pain. Nurses must continuously monitor cardiac telemetry for lethal dysrhythmias (ventricular fibrillation, ventricular tachycardia) and prepare for immediate primary percutaneous coronary intervention (PCI) within 90–120 minutes or fibrinolytic therapy (tenecteplase) if PCI is unavailable within 120 minutes.

Heart Failure (HF) Management

Heart Failure (HF) management in acute medical wards requires systematic assessment of fluid volume status and cardiac output. Left-sided heart failure presents primarily with pulmonary congestion, including exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, bibasalar crackles (crepitations), and an S3 gallop. Right-sided heart failure leads to systemic venous congestion, characterized by jugular venous distension (JVD) >4 cm above the sternal angle, peripheral pitting edema, hepatomegaly, and ascites. Essential nursing management includes positioning the patient in high-Fowler's with legs dependent to reduce venous return (preload), administering high-flow oxygen, enforcing strict fluid restriction (typically 1.5–2.0 L/24 hours), maintaining an accurate fluid balance chart, and obtaining daily weight measurements using the same scale at the same time each morning. A weight increase of >1.5 kg over 48 hours or >2 kg in a week signifies acute fluid retention and warrants immediate medical notification. Pharmacological care centres on IV loop diuretics (furosemide 20–80 mg IV bolus or continuous infusion), monitoring serum potassium to prevent diuretic-induced hypokalemia, and titrating ACE inhibitors/ARBs, beta-blockers, and mineralocorticoid receptor antagonists (spironolactone) as hemodynamics stabilize.

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Respiratory Nursing & Acute Oxygen Therapy

COPD Exacerbation & Asthma Emergencies

In chronic obstructive pulmonary disease (COPD) exacerbations, airways become acutely obstructed due to bronchospasm, mucosal edema, and hypersecretion of mucus. Patients present with severe dyspnea, tachypnea, wheezing, and prolonged expiration. Hypoxic drive plays a critical role in chronic hypercapnic patients; excessive unguided oxygen administration can suppress ventilation, leading to severe carbon dioxide retention (hypercapnia) and respiratory acidosis. Targeted oxygen therapy via a Venturi mask or low-flow nasal cannulae must aim for a target SpO2 of 88–92%. Arterial blood gas (ABG) analysis is essential: typical decompensated COPD ABGs reveal uncompensated or partially compensated respiratory acidosis (pH <7.35, PaCO2 >45 mmHg, HCO3- >26 mmol/L). First-line pharmacological management involves nebulized short-acting beta-2 agonists (salbutamol 2.5–5 mg) combined with anticholinergics (ipratropium bromide 500 mcg) driven by compressed air (not oxygen) if hypercapnic, along with systemic corticosteroids (oral prednisolone 40 mg daily for 5 days or IV hydrocortisone). Non-invasive ventilation (NIV/BiPAP) is indicated for persistent hypercapnic respiratory acidosis despite optimal medical therapy.

Acute severe asthma is a medical emergency. Clinical warning signs of impending respiratory failure include a "silent chest" (absence of wheezing due to severe airflow limitation), inability to speak in full sentences, cyanosis, paradoxical thoracoabdominal movement, and peak expiratory flow rate (PEFR) <33% of predicted. Unlike COPD, acute severe asthma requires immediate high-flow oxygen targeting SpO2 94–98%, continuous nebulized salbutamol, IV hydrocortisone 100 mg, and IV magnesium sulfate 2 g infusion over 20 minutes to relax bronchial smooth muscle.

Pneumonia Nursing Management

Pneumonia management requires prompt risk stratification using the CURB-65 score (Confusion, Urea >7 mmol/L, Respiratory rate ≥30/min, Blood pressure <90 systolic or ≤60 diastolic, Age ≥65). Nursing care focuses on obtaining blood and sputum cultures prior to initiating empirical IV antibiotic therapy, encouraging deep breathing and coughing exercises, chest physiotherapy, maintaining hydration to liquefy secretions, and elevating the head of the bed to 30–45 degrees.

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Endocrine Crises: Diabetes Mellitus, DKA & HHS

Hypoglycemia Protocol

Hypoglycemia is defined as a capillary blood glucose level <4.0 mmol/L. Symptoms are categorized as autonomic (sweating, tremors, palpitations, anxiety, hunger) and neuroglycopenic (confusion, dizziness, blurred vision, seizures, loss of consciousness). Nursing management follows the "Rule of 15": for conscious patients, administer 15–20 g of fast-acting oral carbohydrates (e.g., 150–200 mL of fruit juice, 3–4 jelly beans, or 3 glucose tablets), recheck blood glucose in 15 minutes, and repeat if glucose remains <4.0 mmol/L. Once normalized, provide a long-acting complex carbohydrate snack (e.g., a slice of toast or glass of milk) to prevent recurrent hypoglycemia. For unconscious or nil-by-mouth patients, establish IV access and administer 100 mL of 10% Dextrose (or 20–50 mL of 50% Dextrose IV push), or administer 1 mg Glucagon IM/SC if IV access is unavailable.

Diabetic Ketoacidosis (DKA) vs Hyperosmolar Hyperglycemic State (HHS)

Diabetic Ketoacidosis (DKA) predominantly affects patients with Type 1 diabetes and is characterized by the triad of severe hyperglycemia (>14 mmol/L), metabolic acidosis (venous pH <7.30, serum bicarbonate <18 mmol/L), and ketonemia (blood ketones ≥3.0 mmol/L or heavy urine ketones). Patients present with Kussmaul breathing (deep, rapid respirations to blow off CO2), fruity acetone breath odor, dehydration, abdominal pain, nausea, and vomiting. Initial nursing priority is aggressive fluid resuscitation: administer 0.9% Sodium Chloride 1 L in the first hour, followed by titrated fluid replacement to restore intravascular volume. Continuous fixed-rate IV insulin infusion (0.1 units/kg/hour) is commenced ONLY after initiating fluid resuscitation. Potassium levels must be monitored hourly; if serum potassium is <3.3 mmol/L, insulin must be withheld and potassium replaced to prevent lethal ventricular arrhythmias. Glucose is added to IV fluids (5% Dextrose) once blood glucose drops below 14 mmol/L to allow continued insulin administration for ketone clearance without inducing hypoglycemia.

Hyperosmolar Hyperglycemic State (HHS) occurs primarily in elderly patients with Type 2 diabetes. It is defined by profound hyperglycemia (>30 mmol/L), high serum osmolality (>320 mOsm/kg), and severe dehydration without significant ketoacidosis or Kussmaul breathing. Treatment focuses on gradual rehydration with 0.9% NaCl over 24–48 hours, low-dose IV insulin, and monitoring for osmotic demyelination syndrome caused by rapid osmolality shifts.

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Acute Kidney Injury (AKI) & Neurological Care

Acute Kidney Injury (AKI)

Acute Kidney Injury (AKI) is an abrupt decline in renal function occurring over hours to days. It is classified into Prerenal (hypovolemia, shock, renal artery stenosis), Intrinsic/Renal (acute tubular necrosis from ischemia or nephrotoxins like NSAIDs, aminoglycosides, contrast dye), and Postrenal (urinary tract obstruction from BPH, kidney stones, neurogenic bladder). KDIGO staging defines Stage 1 AKI as serum creatinine 1.5–1.9 times baseline or urine output <0.5 mL/kg/hour for 6–12 hours; Stage 2 as creatinine 2.0–2.9 times baseline or urine output <0.5 mL/kg/hour for ≥12 hours; Stage 3 as creatinine >3.0 times baseline or anuria for ≥12 hours. Nursing management requires hourly urine output measurement via indwelling catheter, strict fluid balance recording, daily weights, avoiding nephrotoxic drugs, and monitoring for hyperkalemia (serum potassium >5.5 mmol/L). ECG changes in hyperkalemia include tall peaked T waves, flattened P waves, and widened QRS complexes; immediate treatment involves IV Calcium Gluconate 10% 10 mL to stabilize cardiac membranes, followed by IV short-acting insulin with 50% Dextrose to drive potassium into cells, and oral/rectal calcium resonium.

Acute Neurological Assessment & Stroke Care

Acute Stroke management begins with rapid screening using the FAST tool (Face drooping, Arm weakness, Speech difficulty, Time to call emergency services). Upon arrival at an acute stroke unit, the nurse calculates the National Institutes of Health Stroke Scale (NIHSS) score (0–42). A non-contrast head CT scan must be completed within 20 minutes to differentiate ischemic stroke from hemorrhagic stroke. Ischemic stroke patients who present within 4.5 hours of symptom onset and meet eligibility criteria may receive IV thrombolysis with Alteplase (0.9 mg/kg) or Tenecteplase. Blood pressure must be maintained below 185/110 mmHg prior to thrombolysis and below 180/105 mmHg for 24 hours post-thrombolysis. Strict neurological observations (GCS, pupil reactivity, limb strength) are conducted every 15 minutes during thrombolysis infusion. Oral intake is completely withheld until a formal nurse-led or speech-language therapy dysphagia screen is passed to prevent aspiration pneumonia.