Comprehensive CPR Guide for Adults and Infants

Introduction

Cardiopulmonary resuscitation (CPR) is a lifesaving emergency procedure designed to maintain circulatory and respiratory function in patients experiencing cardiac or respiratory arrest until definitive care can be established. The technique has evolved over centuries, from early manual chest compressions described in the 8th century to modern algorithmic approaches endorsed by international resuscitation councils. The integration of pharmacologic agents such as epinephrine, amiodarone, and atropine into CPR protocols reflects the intersection between emergency physiology and drug therapy, underscoring the relevance of CPR to pharmacology and clinical medicine. This chapter aims to provide medical and pharmacy students with a comprehensive understanding of CPR, including theoretical foundations, procedural nuances, pharmacologic considerations, and practical application scenarios.

Learning objectives:

• Describe the historical evolution and current guidelines governing adult and infant CPR.
• Explain the physiological principles underlying chest compressions and airway management.
• Identify the key pharmacologic agents used during resuscitation and their mechanisms of action.
• Apply CPR techniques through case-based problem solving, integrating drug therapy where appropriate.
• Summarize critical procedural parameters and clinical pearls that enhance resuscitation success.

Fundamental Principles

Core Concepts and Definitions

CPR encompasses a combination of chest compressions, ventilations, and adjunctive pharmacologic support aimed at restoring adequate cerebral and coronary perfusion. The essential components include: (1) Chest compressions, delivering mechanical force to the thorax to generate blood flow; (2) Airway management, ensuring oxygen delivery to alveoli via bag‑mask ventilation or advanced airway devices; (3) Defibrillation, when indicated, to terminate life‑threatening arrhythmias; and (4) Pharmacologic therapy, administered as part of advanced cardiac life support (ACLS) protocols.

Theoretical Foundations

During cardiac arrest, the heart’s output falls to zero, necessitating external support to maintain perfusion. Chest compressions create a pressure gradient that forces blood through the aorta and into the coronary and cerebral circulation. The depth and rate of compressions directly influence stroke volume and cardiac output. For adults, a compression depth of 5–6 cm at a rate of 100–120 compressions per minute is recommended, whereas for infants, a depth of 2 cm or one‑third the anterior‑posterior diameter of the chest is prescribed at the same rate. Each compression cycle typically lasts 0.5–0.6 seconds, allowing for adequate recoil and venous filling.

The ventilation component facilitates oxygenation and carbon dioxide removal. A typical ratio of 30 compressions to 2 breaths (for adults) or 15 compressions to 2 breaths (for infants) is employed, aligning with the physiological need for oxygen delivery and ventilation support during arrest. Defibrillation is reserved for shockable rhythms such as ventricular fibrillation or pulseless ventricular tachycardia; the energy dose (e.g., 200 J biphasic) is calibrated to the patient’s size and clinical context.

Key Terminology

• Cardiac Output (CO): Volume of blood pumped by the heart per minute, calculated as Heart Rate (HR) × Stroke Volume (SV).
• Stroke Volume (SV): Volume of blood ejected during one compression.
• Compression Fraction: Proportion of time spent performing compressions during a cycle; higher fractions correlate with better outcomes.
• Compression Depth (CD): Measure of how far the sternum is depressed during a compression.
• Compression Rate (CR): Number of compressions delivered per minute.
• Ventilation Rate (VR): Number of breaths delivered per minute.
• Defibrillation Energy (DE): Electrical energy delivered to the heart; expressed in Joules (J).

Detailed Explanation

Mechanisms and Processes

Chest compressions generate intrathoracic pressure changes that drive blood flow. The initial compression elevates aortic pressure, while the subsequent recoil allows venous return. This cyclical process sustains perfusion to vital organs. The relationship between compression depth and stroke volume can be approximated by the equation: SV ≈ k × CD, where k represents a patient‑specific constant influenced by chest wall compliance and myocardial contractility. Although precise values vary, the guideline recommendation of a 5–6 cm depth for adults achieves an average SV of 30–40 mL per compression, sufficient to maintain cerebral perfusion for brief intervals.

Ventilations are essential to maintain oxygenation during arrest. The alveolar ventilation equation, V̇_A = (P_AO₂ × V_E)/P_atm, where P_AO₂ is alveolar oxygen partial pressure, V_E is tidal volume, and P_atm is atmospheric pressure, underpins the importance of adequate tidal volumes. In adult CPR, a tidal volume of 500–600 mL per breath is targeted, whereas in infants, 2–4 mL/kg per breath suffices. The timing of breaths is synchronized with compressions to prevent hyperventilation, which can increase intrathoracic pressure and impede venous return.

Mathematical Relationships

• Cardiac Output during CPR: CO_CPR = CR × SV. For example, with CR = 110/min and SV = 35 mL, CO_CPR ≈ 3.85 L/min.
• Compression Fraction (CF): CF = (Time spent compressing) ÷ (Total cycle time). A CF of ≥ 0.75 is desirable.
• Energy Delivered by Defibrillator: DE = Voltage × Current × Time. In biphasic defibrillators, the energy is calibrated to patient weight: DE ≈ 2 J/kg for initial shock.

Factors Affecting the Process

Several variables influence CPR efficacy: patient age, body habitus, underlying etiology of arrest, and presence of reversible causes (the H’s and T’s). Anatomical differences necessitate adjustments in compression depth and force; for instance, obese patients may require greater force to achieve adequate depth. The skill level of rescuers, fatigue, and interruptions (e.g., drug administration, airway placement) can diminish compression quality. Pharmacologic agents administered during CPR may also impact hemodynamics; for example, epinephrine increases systemic vascular resistance, potentially augmenting coronary perfusion pressure.

Clinical Significance

Relevance to Drug Therapy

Pharmacologic interventions are integral to advanced cardiac life support. Epinephrine, a potent α‑adrenergic agonist, is administered to increase aortic diastolic pressure and coronary perfusion; dosing typically involves 1 mg IV every 3–5 minutes during prolonged resuscitation. Amiodarone, an antiarrhythmic, is employed for refractory ventricular fibrillation or tachycardia, with initial doses of 300 mg IV followed by 150 mg IV. Atropine, an antimuscarinic agent, is indicated for symptomatic bradycardia, administered at 0.5 mg IV increments up to a total of 3 mg. The use of these agents is guided by rhythm analysis and clinical context, illustrating the interplay between pharmacology and resuscitation physiology.

Practical Applications

Understanding the pharmacokinetics of resuscitation drugs is essential for effective dosing. For example, the distribution of epinephrine during CPR is influenced by the reduced cardiac output; thus, the drug may remain within the central circulation longer, enhancing its efficacy. The clearance pathways of these agents, primarily hepatic metabolism for amiodarone and renal excretion for atropine, are less relevant during arrest but become critical during post‑resuscitation care, where drug accumulation may affect hemodynamics and organ function.

Clinical Examples

In cases of drug overdose leading to cardiac arrest (e.g., beta‑blocker toxicity), CPR combined with specific antidotes (e.g., glucagon) can restore rhythm. Similarly, in hypoxia‑induced arrest, high‑flow oxygen delivery and rapid airway management are paramount. These scenarios highlight the necessity of tailoring CPR to underlying etiologies, integrating pharmacologic therapy where appropriate.

Clinical Applications/Examples

Case Scenario 1: Adult Ventricular Fibrillation

A 55‑year‑old male presents with sudden collapse while exercising. No pulse is detected; palpable carotid pulse absent. An AED is applied, indicating ventricular fibrillation. The rescuer initiates CPR with 100–120 compressions per minute, achieving a compression depth of 5–6 cm. After 2 minutes of compressions, a 200 J biphasic shock is delivered. Rhythm reverts to sinus. Epinephrine 1 mg IV is administered, followed by amiodarone 300 mg IV due to recurrent VF. The patient is transported to the ICU, where intravenous lipid emulsion therapy is considered for suspected tricyclic antidepressant overdose.

Case Scenario 2: Infant Sudden Cardiac Arrest

A 2‑month‑old infant collapses during feeding. Rescuer performs 15 compressions to 2 breaths, maintaining a compression depth of 2 cm. After 1 minute, a 2 J/kg biphasic shock is delivered. The infant regains spontaneous circulation. An atropine 0.01 mg/kg IV is given for transient bradycardia. Post‑resuscitation monitoring reveals an underlying congenital heart defect, prompting echocardiographic evaluation.

Case Scenario 3: Drug‑Induced Bradycardia

A 68‑year‑old woman on high‑dose beta‑blocker therapy experiences syncope. Cardiac arrest ensues with a pulse rate of 30 bpm. CPR is initiated; after 3 minutes, atropine 0.5 mg IV is given, resulting in a heart rate increase to 60 bpm. Subsequent administration of glucagon 5 mg IV yields a sustained sinus rhythm. The patient is stabilized and transferred for definitive management of beta‑blocker toxicity.

Problem‑Solving Approaches

When confronting a cardiac arrest of uncertain etiology, systematic assessment is vital. The H’s and T’s framework guides evaluation: hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, hypoglycemia, hypothermia, toxins, tamponade, thrombosis (pulmonary or coronary), traumatic injury, and tension pneumothorax. Each reversible cause necessitates targeted intervention, such as fluid resuscitation for hypovolemia or de‑airing for pneumothorax. Pharmacologic therapy is tailored accordingly, ensuring that drug selection aligns with the identified reversible factor.

Summary/Key Points

• CPR is a structured emergency intervention aimed at sustaining cerebral and coronary perfusion during cardiac or respiratory arrest.
• Adult CPR requires chest compressions of 5–6 cm depth at 100–120/min, plus 30 compressions to 2 breaths; infant CPR uses 2 cm depth at the same rate with 15 compressions to 2 breaths.
• Compression fraction should be ≥ 0.75 to maximize perfusion; interruptions should be minimized.
• Key pharmacologic agents include epinephrine (α‑agonist), amiodarone (antiarrhythmic), and atropine (antimuscarinic); dosing and timing are critical for efficacy.
• Defibrillation energy correlates with patient weight (≈ 2 J/kg for initial shocks) and is delivered when a shockable rhythm is present.
• Clinical scenarios illustrate the necessity of integrating CPR technique with pharmacologic therapy and etiologic assessment.
• Regular training, simulation, and adherence to guideline updates enhance CPR performance and patient outcomes.

Critical pearls: ensure adequate compression depth and rate; coordinate ventilations to avoid hyperventilation; maintain high compression fraction; administer epinephrine promptly in prolonged resuscitation; utilize the H’s and T’s framework to identify reversible causes; and document all interventions meticulously for post‑resuscitation analysis.

References

1. Walls RM, Hockberger RS, Gausche-Hill M. Rosen's Emergency Medicine: Concepts and Clinical Practice. 10th ed. Philadelphia: Elsevier; 2022.
2. Bennett PN, Brown MJ, Sharma P. Clinical Pharmacology. 12th ed. Edinburgh: Elsevier; 2019.
3. Waller DG, Sampson AP. Medical Pharmacology and Therapeutics. 6th ed. Edinburgh: Elsevier; 2022.
4. Feather A, Randall D, Waterhouse M. Kumar and Clark's Clinical Medicine. 10th ed. London: Elsevier; 2020.
5. Ralston SH, Penman ID, Strachan MWJ, Hobson RP. Davidson's Principles and Practice of Medicine. 24th ed. Edinburgh: Elsevier; 2022.
6. Loscalzo J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL. Harrison's Principles of Internal Medicine. 21st ed. New York: McGraw-Hill Education; 2022.
7. Trevor AJ, Katzung BG, Kruidering-Hall M. Katzung & Trevor's Pharmacology: Examination & Board Review. 13th ed. New York: McGraw-Hill Education; 2022.
8. Rang HP, Ritter JM, Flower RJ, Henderson G. Rang & Dale's Pharmacology. 9th ed. Edinburgh: Elsevier; 2020.