04 Cardiovascular Assessment and ECG Interpretation

Cardiac circulation and conduction

The heart is a four-chamber pump. Systemic venous blood enters the right atrium, passes through the tricuspid valve to the right ventricle, and is pumped through the pulmonic valve to the lungs. Oxygenated blood returns to the left atrium, passes through the mitral valve to the left ventricle, and leaves through the aortic valve for systemic circulation. The left ventricle has the greatest muscle mass because it pumps against higher systemic resistance.

The coronary arteries supply the myocardium. The right coronary artery commonly supplies the right ventricle and inferior wall. The left main coronary artery divides into the left anterior descending artery, which supplies much of the anterior wall and septum, and the circumflex artery, which commonly supplies the lateral wall. Coronary anatomy varies, so an ECG territory suggests—but does not prove—which artery is involved.

Cardiac output equals heart rate multiplied by stroke volume:

Stroke volume is influenced by preload, contractility, and afterload. An electrical rhythm may be present without producing adequate perfusion, so assess the patient rather than relying on the monitor alone.

Electrical activity and ECG foundations

The sinoatrial (SA) node normally initiates each heartbeat. The impulse spreads through the atria, pauses briefly at the atrioventricular (AV) node, then travels through the His bundle, right and left bundle branches, and Purkinje network to depolarize the ventricles. The AV-node delay allows ventricular filling, while conduction through the His-Purkinje system coordinates ventricular contraction. Sympathetic stimulation generally increases heart rate and conduction; parasympathetic stimulation generally slows the SA and AV nodes.

An electrocardiogram (ECG) records electrical potential differences from multiple views. It does not directly measure mechanical contraction, cardiac output, or coronary blood flow. A standard 12-lead ECG uses 10 electrodes: six limb leads view the heart in the frontal plane, and six chest leads view it in the horizontal plane.

Correct electrode placement matters. Motion, poor contact, electrical interference, and lead reversal can create misleading patterns. Confirm the ECG’s calibration before measuring intervals or rate.

ECG waves and intervals

At a paper speed of $25\,\mathrm{mm/s}$, one small horizontal box represents $0.04\,\mathrm{s}$, and one large box represents $0.20\,\mathrm{s}$. The main ECG features reflect these electrical events:

• P wave: atrial depolarization; usually upright in lead II and under $0.12\,\mathrm{s}$ in duration.

• PR interval: conduction from the atria through the AV conduction system, including the AV-node delay; the common reference range is $0.12$–$0.20\,\mathrm{s}$.

• QRS complex: ventricular depolarization; usually under $0.12\,\mathrm{s}$.

• ST segment: the early period after ventricular depolarization; usually near the baseline, but interpreted in clinical context.

• T wave: ventricular repolarization; its shape and direction vary by lead.

• QT interval: spans ventricular depolarization and repolarization. It varies with heart rate, so consider the corrected QT (QTc).

Atrial repolarization is usually obscured by the QRS complex. The ECG describes electrical events; it does not by itself establish that the heart is producing a pulse or adequate circulation.

A systematic ECG reading method

Use the same sequence for every tracing:

1. Check quality and calibration. Verify patient identity, lead placement, paper speed, and artifact. Determine whether the tracing is a monitor strip or a diagnostic 12-lead.

2. Calculate rate. For a regular rhythm, estimate rate as $300$ divided by the number of large boxes between R waves, or $1500$ divided by the number of small boxes. For an irregular rhythm, count QRS complexes in a 6-second strip and multiply by $10$. These are estimates; use a longer strip when needed.

3. Assess regularity. Compare R–R intervals and, separately, P–P intervals. Identify whether irregularity is patterned or chaotic.

4. Inspect P waves and their relationship to QRS complexes. Check whether P waves are present and consistent in shape, whether one P wave precedes each QRS, and whether every P wave conducts.

5. Measure PR and QRS intervals. Note fixed, lengthening, short, or changing intervals; narrow versus wide QRS complexes; and dropped beats.

6. Assess axis and morphology. As a quick frontal-plane screen, a positive QRS in leads I and aVF generally indicates a normal axis. If the QRS is positive in lead I and negative in aVF, check lead II to distinguish borderline left axis from left-axis deviation. Interpret axis with the whole tracing and patient context.

7. Examine ST segments and T waves. Look for changes in contiguous leads, reciprocal changes, dynamic changes, and differences from prior ECGs.

8. State the interpretation and significance. Include rate, rhythm, conduction, QRS width, ischemic or injury patterns, and clinical stability. Review the tracing rather than accepting the machine interpretation without review.

At $25\,\mathrm{mm/s}$, an R–R interval of four large boxes estimates a rate of about $75/\mathrm{min}$; two large boxes estimate about $150/\mathrm{min}$. For an irregular rhythm, the 6-second method is more reliable than estimating rate from a single R–R interval.

Lead territories and ischemia

Contiguous leads view neighboring regions of the heart. The following territory map is approximate:

• Inferior: leads II, III, and aVF.

• Lateral: leads I, aVL, V5, and V6.

• Septal/anterior: leads V1–V4.

• Posterior: reciprocal ST depression and a tall R wave in V1–V3 may suggest posterior involvement. Additional posterior leads V7–V9 can help evaluate suspected posterior infarction.

• Right ventricle: consider right-sided leads, particularly V4R, when the clinical picture or an inferior ECG suggests right-ventricular involvement.

Acute coronary occlusion may produce ST elevation, reciprocal ST depression, hyperacute T waves, or other evolving changes. Ischemia may also appear as ST depression or T-wave inversion. A normal initial ECG does not exclude acute coronary syndrome. Interpret changes in contiguous leads alongside symptoms, serial ECGs, prior tracings, and the receiving system’s STEMI criteria.

Left bundle branch block and ventricular pacing complicate ST-segment assessment. Do not diagnose or exclude infarction from one isolated feature. Posterior and right-sided leads can reveal injury that is not well represented on the standard 12-lead.

Recognizing dysrhythmias

Classify a rhythm by rate, regularity, QRS width, atrial activity, and the relationship between P waves and QRS complexes. A narrow QRS usually indicates activation through the normal ventricular conduction system. A wide QRS may reflect ventricular origin, bundle-branch block, an accessory pathway, pacing, or metabolic or toxic effects. When uncertain, treat a wide-complex tachycardia as ventricular tachycardia (VT) until expert evaluation establishes otherwise.

Sinus, atrial, and supraventricular rhythms

• Sinus bradycardia: a regular rhythm with normal sinus P waves before each QRS and a rate below what is expected for the patient. It may be normal or reflect ischemia, hypoxia, medication effect, or another cause. Treat compromise, not the number alone.

• Sinus tachycardia: a regular, usually narrow rhythm with a sinus P wave before each QRS; the rate increases with a cause. Look for a driver such as hypovolemia, hypoxia, fever, pain, anxiety, or shock. The rate may be compensatory.

• Atrial fibrillation: no consistent discrete P waves and an irregularly irregular ventricular response. Assess perfusion and onset or history; consider ischemia, heart failure, and embolic risk in the broader care plan.

• Atrial flutter: repeating flutter waves, often with a sawtooth appearance; the ventricular response may be regular or variable. A regular ventricular rate near $150/\mathrm{min}$ can occur with 2:1 conduction, so do not assume sinus tachycardia.

• Regular narrow-complex supraventricular tachycardia (SVT): an abrupt-onset, usually regular narrow tachycardia. P waves may be hidden or occur just after the QRS. Assess stability first; follow protocol for vagal maneuvers or medication when appropriate. Unstable patients need prompt electrical treatment.

• Premature atrial or ventricular complexes: an early beat. A premature ventricular complex (PVC) is typically wide and has no preceding sinus P wave. Evaluate frequency, symptoms, perfusion, and whether the ectopy occurs with ischemia or other illness.

Atrioventricular blocks

• First-degree AV block: every P wave conducts, but the PR interval is prolonged and consistent. This is a conduction delay, not a dropped-beat rhythm; interpret it with symptoms and other ECG findings.

• Second-degree AV block, Mobitz I: the PR interval progressively lengthens until a QRS is dropped. It can be transient; assess symptoms and perfusion.

• Second-degree AV block, Mobitz II: PR intervals on conducted beats are generally constant, with intermittent dropped QRS complexes. It may progress to complete block; treat significant compromise urgently and consider pacing per protocol.

• Third-degree AV block: atrial and ventricular activity are independent, with no consistent P-to-QRS relationship. The escape rhythm may be slow and unreliable; assess for instability and prepare for pacing when indicated.

Ventricular rhythms and arrest patterns

• Ventricular tachycardia: usually a wide-complex tachycardia that may be regular and monomorphic or vary in shape. Determine pulse and perfusion immediately. Pulseless VT is cardiac arrest; polymorphic VT requires immediate shock treatment under the resuscitation protocol.

• Ventricular fibrillation: disorganized ventricular activity without identifiable effective QRS complexes. It is a cardiac-arrest rhythm; begin resuscitation and defibrillation per protocol.

• Asystole: no meaningful ventricular electrical activity after checking leads and gain.

• Pulseless electrical activity (PEA): organized electrical activity without a palpable pulse. Asystole and PEA are nonshockable arrest rhythms; confirm the patient and pulse, then follow the cardiac-arrest algorithm.

An ECG rhythm does not establish that a pulse is present. Check responsiveness, breathing, and a central pulse as appropriate. Distinguish pulseless arrest from a perfusing rhythm before selecting an electrical or medication pathway.

Cardiovascular assessment and decisions

Assess the patient first

1. Primary survey: assess airway, breathing, circulation, mental status, skin signs, and overall perfusion. Identify cardiac arrest, respiratory failure, shock, or an immediate need for resuscitation. Support oxygenation and ventilation as indicated; oxygen is not automatically required for every patient with chest pain.

2. Assess stability: look for hypotension, altered mental status, signs of shock, ischemic discomfort, acute heart failure, syncope, or a rapidly worsening condition. Reassess after every intervention.

3. Obtain a focused history: use OPQRST for symptoms and SAMPLE for history, allergies, medications, and events. Ask about onset and duration, exertional or positional triggers, radiation, dyspnea, palpitations, diaphoresis, nausea, syncope, prior cardiac disease or procedures, and prescribed or recently taken drugs. Consider atypical presentations, especially in older adults and people with diabetes.

4. Examine and measure: obtain repeated vital signs, pulse rate and quality, blood pressure, respiratory status, oxygen saturation, and level of consciousness. Assess skin temperature and moisture, capillary refill where useful, work of breathing, lung sounds, jugular venous appearance, peripheral edema, and signs of poor perfusion. A single reassuring measurement does not rule out deterioration.

5. Monitor and obtain ECGs: apply cardiac monitoring and obtain a diagnostic 12-lead when indicated and available. Repeat the ECG if symptoms persist, recur, or change; obtain right-sided or posterior leads when indicated. Transmit or report critical findings early, and do not delay time-sensitive stabilization or transport solely to obtain additional tracings.

6. Consider causes and mimics: consider acute coronary syndrome, dysrhythmia, heart failure, pulmonary embolism, aortic catastrophe, hypoxia, anemia, electrolyte or metabolic disturbance, medication or toxin effects, and noncardiac causes. A rhythm may cause instability or may be a response to another emergency.

Link ECG findings to physiology and action

A regular rate of $150/\mathrm{min}$, for example, could be sinus tachycardia due to shock or a reentrant tachycardia. Abruptness of onset, P-wave pattern, symptoms, and the overall examination help distinguish them. A slow rhythm with hypotension may be causing poor cardiac output, but hypoxia, myocardial ischemia, medication effects, or metabolic problems may be the underlying driver. Treat life threats while looking for reversible causes, and follow medical direction and local protocols for interventions and destination decisions.

For tachycardia, signs of cardiopulmonary compromise include hypotension, acute altered mental status, shock, ischemic chest discomfort, or acute heart failure. The 2025 guidance recommends synchronized cardioversion for unstable tachyarrhythmia with a pulse; polymorphic VT is treated immediately with defibrillation.

Symptomatic bradycardia is a clinical diagnosis, not simply a heart-rate threshold. A typical bradyarrhythmia rate is below $50/\mathrm{min}$, but clinical compromise and reversible causes matter. For persistent compromise, follow the current local algorithm, which may include atropine and, if ineffective, transcutaneous pacing and/or an adrenergic infusion.