4.2 Ventricular Arrhythmias & Cardiac Arrest Management

Premature Ventricular Contractions (PVCs) in Ischemic Heart Disease

Premature Ventricular Contractions (PVCs) are ectopic impulses originating from irritable focus points within the ventricular myocardium or Purkinje fiber network prior to the next expected sinus beat.

ECG Characteristics

1. Wide QRS Complex: Duration ≥ 120 ms (0.12 seconds) with aberrant, slow cell-to-cell ventricular conduction.
2. ST-T Wave Discordance: The ST segment and T wave are directed opposite to the main deflection of the QRS complex.
3. Full Compensatory Pause: The interval surrounding the PVC (pre-PVC RR + post-PVC RR) equals exactly two normal sinus RR intervals, as the ectopic impulse usually fails to penetrate retrogradely into the SA node.

Clinical Significance in Acute Myocardial Ischemia

While isolated PVCs are common in healthy individuals, their presence during acute myocardial infarction (AMI) or severe ischemic heart disease signifies severe electrical instability. Ischemia alters resting membrane potentials, impairs Na+/K+-ATPase pumps, and creates border zones of slow conduction that foster ectopic automaticity and re-entry.

• High-Risk PVC Patterns:
  • Frequent PVCs: > 30 per hour or > 10-15% total daily burden.
  • Multiform/Multifocal PVCs: Differing QRS configurations arising from multiple distinct ventricular foci.
  • Couplets & Triplets: Two consecutive PVCs (couplet) or three consecutive PVCs (triplet / non-sustained VT).
  • R-on-T Phenomenon: A PVC falling precisely on the vulnerable repolarization peak of the preceding T wave. This can instantly trigger chaotic, self-sustaining polymorphic VT or Ventricular Fibrillation.
• PVC-Induced Cardiomyopathy: Chronic high PVC burden (> 10-15% of total beats) causes progressive LV dilation and systolic heart failure due to dyssynchronous ventricular contraction. Suppression with beta-blockers, antiarrhythmics (amiodarone), or radiofrequency catheter ablation can completely reverse LV dysfunction.

---

Monomorphic vs. Polymorphic Ventricular Tachycardia

Ventricular Tachycardia (VT) is defined as three or more consecutive premature ventricular complexes occurring at a rate > 100 bpm (typically 150-250 bpm).

Monomorphic Ventricular Tachycardia

• ECG Features: Uniform QRS morphology beat-to-beat, regular RR intervals, and consistent conduction axis.
• Pathophysiology: Usually caused by a fixed, anatomical re-entrant circuit revolving around localized ventricular scar tissue (e.g., prior transmural MI or surgical scar).
• Hemodynamic & Clinical Management:
  • Pulse Present & Hemodynamically Stable: Administer IV Antiarrhythmics. Amiodarone (150 mg IV over 10 minutes, followed by 1 mg/min drip for 6 hours) or Procainamide (20-50 mg/min IV until arrhythmia suppressed, hypotension ensues, QRS widens > 50%, or max dose 17 mg/kg reached).
  • Pulse Present & Hemodynamically Unstable: (Hypotension, acute pulmonary edema, altered mental status, severe angina) → Immediate Synchronized Direct Current Cardioversion starting at 100 Joules biphasic.
  • Pulseless VT: Managed according to the ACLS Cardiac Arrest Algorithm (High-energy unsynchronized defibrillation).

Polymorphic Ventricular Tachycardia

• ECG Features: Continuously changing QRS morphology, amplitudes, and conduction axes beat-to-beat.
• Pathophysiology & Classification:
  • Ischemic Polymorphic VT (Normal QTc): Driven by acute ongoing myocardial ischemia or infarction. Baseline QTc interval is normal (< 460 ms). Treated aggressively with revascularization (emergency PCI), IV Beta-Blockers, IV Amiodarone, and Intra-Aortic Balloon Pump (IABP) support.
  • Torsades de Pointes (Prolonged QTc): Polymorphic VT occurring in the setting of a prolonged baseline QTc interval.

---

Torsades de Pointes (TdP) Pathophysiology & Management

Torsades de Pointes ('Twisting of the Points') is a unique subtype of polymorphic VT characterized by QRS complexes that continuously twist their points around the isoelectric baseline.

   Torsades de Pointes ECG Pattern:
   /
  / \      /\      /\        /\          /\        /
 /   \    /  \    /  \      /  \        /  \      /
      \  /    \  /    \    /    \      /    \    /
       \/      \/      \  /      \    /      \  /
                        \/        \  /        \/
                                   \/

Pathophysiology & Risk Factors

TdP is initiated by Early Afterdepolarizations (EADs) occurring during Phase 2 or Phase 3 of the action potential when ventricular repolarization is abnormally prolonged (QTc > 500 ms or QTc lengthening > 60 ms above baseline).

Emergency Management of Torsades de Pointes

1. Intravenous Magnesium Sulfate: The absolute first-line therapy. Administer 1 to 2 grams IV diluted in 10 mL D5W over 15 minutes in a conscious patient, or as a rapid IV push if pulseless or in active TdP. Magnesium influx inhibits L-type calcium channels and abolishes EADs.
2. Repletion of Potassium: Aggressively replete serum potassium to a high-normal target of 4.5 to 5.0 mEq/L.
3. Overdrive Pacing / Increasing Heart Rate: Increasing the underlying heart rate shortens the ventricular action potential duration and repolarization phase (QTc). Options include:
   • Temporary Transcutaneous or Transvenous Pacing set at a rate of 90 to 110 bpm.
   • Isoproterenol Infusion: Non-selective beta-1/beta-2 agonist (the beta-2 vasodilation lowers diastolic pressure) (drip 2-10 mcg/min) to increase heart rate (contraindicated in acute MI).
4. Discontinue Precipitating Agents: Immediately stop all QT-prolonging medications.

---

Ventricular Fibrillation & ACLS Cardiac Arrest Algorithms

Ventricular Fibrillation (VF) represents chaotic, uncoordinated ventricular electrical depolarization with zero functional mechanical contraction, leading to immediate cessation of cardiac output, loss of consciousness, and clinical death within seconds.

High-Quality CPR Metrics

• Compression Rate: 100 to 120 compressions per minute.
• Compression Depth: 2 to 2.4 inches (5 to 6 cm) in adults.
• Full Chest Recoil: Allow complete chest wall recoil after each compression; avoid leaning on the chest.
• Chest Compression Fraction (CCF): AHA recommends a CCF of at least 60% (Class 2b); high-performance CPR programs target >80%, minimizing all interruptions in CPR to < 10 seconds.
• Ventilation: 30 compressions to 2 ventilations (unadvanced airway) or 1 breath every 6 seconds (10 breaths/min) with continuous compressions once an advanced airway (ET tube) is secured. Avoid hyperventilation (causes elevated intrathoracic pressure, decreasing venous return and cardiac output).

Shockable (VF / Pulseless VT) ACLS Algorithm

1. Recognize & Defibrillate Immediately: Deliver an unsynchronized shock (120 to 200 Joules biphasic or 360J monophasic). Resume CPR immediately for 2 minutes without delaying for rhythm or pulse checks.
2. Vasopressor Therapy: Administer Epinephrine 1 mg IV/IO push every 3 to 5 minutes, initiated immediately after the second shock.
3. Antiarrhythmic Therapy: Initiated after the third shock for refractory VF/pVT:
   • Amiodarone: First dose 300 mg IV/IO push; second dose 150 mg IV/IO push after an additional 3-5 minutes.
   • Lidocaine (Alternative): First dose 1.0 to 1.5 mg/kg IV/IO push; second dose 0.5 to 0.75 mg/kg IV/IO (max dose 3 mg/kg).

Non-Shockable (PEA / Asystole) ACLS Algorithm

• Interventions: High-quality CPR, Epinephrine 1 mg IV/IO push immediately (repeat q3-5 min), and systematic identification and rapid reversal of underlying causes (Hs and Ts):
  • Hs: Hypovolemia, Hypoxia, Hydrogen ion (Acidosis), Hypo/Hyperkalemia, Hypothermia.
  • Ts: Tension pneumothorax, Tamponade (cardiac), Toxins, Thrombosis (pulmonary / PE), Thrombosis (coronary / MI).

---

Post-Cardiac Arrest Care & Neuroprognostication

Following Return of Spontaneous Circulation (ROSC), structured critical care interventions are essential to prevent secondary organ failure and hypoxic-ischemic brain injury.

Targeted Temperature Management (TTM)

• Indication: Recommended for all adult patients who remain comatose (unresponsive to verbal commands) following ROSC.
• Target Core Temperature: Select and strictly maintain a constant core body temperature between 32°C and 36°C, OR strictly maintain normothermia avoiding fever (< 37.5°C) for at least 24 hours.
• Physiological Mechanism: TTM decreases cerebral metabolic rate of oxygen consumption (CMRO2 drops 6% to 8% for every 1°C drop in core temperature), inhibits free-radical generation, suppresses ischemic apoptotic pathways, and mitigates cerebral edema.
• Critical Nursing Interventions During Cooling & Rewarming:
  • Shivering Management: Shivering increases oxygen consumption and heat production. Treat step-wise using counter-warming blankets, sedatives (propofol, dexmedetomidine), opioids (meperidine, fentanyl), and neuromuscular blocking agents (cisatracurium continuous infusion).
  • Electrolyte Shifts: Cooling induces intracellular transport of potassium, causing hypokalemia. Avoid aggressive repletion during cooling because rewarming causes potassium to exit cells back into the vascular space, leading to severe hyperkalemia if over-repleated. Rewarm slowly at 0.25°C to 0.5°C per hour while monitoring for rewarming hypotension due to peripheral vasodilation.

Post-ROSC Hemodynamic & Ventilatory Targets

• Ventilation: Avoid hyperoxia. Titrate FiO2 to maintain SpO2 92% to 98% and PaO2 70 to 100 mmHg. Maintain normocapnia (PaCO2 35 to 45 mmHg) to prevent hypocapnic cerebral vasoconstriction.
• Hemodynamics: Maintain Mean Arterial Pressure (MAP) ≥ 65 to 70 mmHg or systolic blood pressure ≥ 90-100 mmHg using IV crystalloids, inotropes (dobutamine), or vasopressors (norepinephrine).

Multimodal Neuroprognostication Protocol

Prognostication of neurological recovery must never be performed prematurely. It must be multimodal and delayed until at least 72 hours after ROSC (or 72 hours post-rewarming to normothermia) to ensure complete clearance of residual sedatives, paralytics, and hypothermic metabolic delay.