ECG Interpretation and Cardiovascular Management Essentials

Posted on Mar 14, 2025 in Pharmacy

ECG Interpretation and Cardiovascular Management

ECG Lead Locations and Waveform Analysis

  • II, III, aVF: Inferior leads
  • V1 & V2: Septal leads
  • V3 & V4: Anterior leads
  • I, aVL, V5 & V6: Lateral leads

Electrode Placement

RA (White), LA (Black), V (Brown)

Intervals and Segments

  • PR Interval: 0.12-0.20 seconds
    • Shorter PR: Impulse from AV junction
    • Longer PR: First-degree AV block
  • QRS Interval: 0.06-0.12 seconds
  • QT Interval: 0.39-0.43 seconds (Predisposes to Torsades de Pointes, intensified by low calcium & magnesium)

ST Segment Abnormalities

  • ST Depression: Reciprocal changes, Digoxin toxicity, Ischemia

Cardiac Rhythms

Sinus Tachycardia

Rate: 101-150 bpm

Premature Atrial Contraction (PAC)

Early atrial beat, P wave and PR interval vary, pause after beat, P wave can be found in T wave.

Atrial Flutter

Ectopic foci in atria, “sawtooth” pattern (rate fast & regular, 250-300 bpm), no true P wave or PR interval, QRS normal unless distorted. Best seen in inferior leads.

Atrial Fibrillation

Erratic impulse of atria (no P wave, no PR interval), irregular ventricular rate.

Premature Ventricular Contraction (PVC)

Early ventricular beat, wide & bizarre (irregular), compensating pause, QRS >0.12 seconds, no P wave or PR interval. Caused by electrolyte imbalance, ischemia, hypoxia, drugs.

PVC Danger Signs
  • Frequent PVCs
  • Multifocal PVCs
  • 2+ PVCs in a row
  • R-on-T phenomenon (can lead to Ventricular Tachycardia or Ventricular Fibrillation)

Supraventricular Tachycardia (SVT)

Abrupt onset & termination, rate 150-250 bpm, regular.

Ventricular Tachycardia (VTach)

3+ PVCs, rate >100 bpm (150-250 bpm), wide QRS > 0.12 seconds. May or may not have a pulse.

VTach Treatment (with pulse)
  1. Amiodarone
  2. Lidocaine
  3. Cardioversion

Ventricular Fibrillation (VFib)

Chaotic & ugly waveform.

AV Blocks

First-Degree AV Block

Prolonged PR interval >0.20 seconds, same PR interval for each beat.

Second-Degree AV Block (Mobitz Type I/Wenckebach)

Progressive lengthening of PR interval until a QRS complex is dropped.

Second-Degree AV Block (Mobitz Type II)

Fixed PR interval with occasional dropped QRS complexes.

Third-Degree AV Block (Complete Heart Block)

No relationship between P waves and QRS complexes.

Pacemaker Malfunctions

Failure to Pace (“Fire”)

  1. Check connections
  2. Check battery
  3. Replace generator
  4. Remove magnet source

Failure to Capture

Spikes not followed by a beat.

  1. Reposition client to left side
  2. Increase output setting (mA) until capture occurs

Failure to Sense (“Undersensing”)

Not sensing client’s electrical activity, spikes occur after or unrelated to intrinsic rate.

  1. Increase sensitivity setting
  2. Replace & reposition

Failure to Sense (“Oversensing”)

Absence of pacing.

  1. Decrease sensitivity setting

Pacemaker Types

  • Demand/Synchronous: Picks up intrinsic beat (communicates with heart)
  • Fixed/Asynchronous: Set independent rate & fires when below set rate

Other Cardiovascular Conditions and Treatments

Ventricular Remodeling

Hypertrophy to compensate for lost heart muscle = normal.

Dressler’s Syndrome

Treated with corticosteroids.

Post-Cardiac Catheterization Care

Administer antiplatelet medications.

Transmural Infarction

Full thickness of heart.

Adenosine

Used to slow SVT.

Hemodynamic Parameters

Respirations

Normal range: 12-20 breaths per minute. 4 respirations over 8-12 seconds.

Central Venous Pressure (CVP)

Normal range: 2-8 mmHg, Pad 8-12.

  • Decreased CVP: Decreased Cardiac Output (CO)

Preload

Force of blood returning to the heart.

  • Vasodilating medications may decrease CVP; may need to administer fluid to maintain MAP.

Decreased Cardiac Output (CO)

Hypotension, bradycardia, dysrhythmias, elevated Systemic Vascular Resistance (SVR), cardiac tamponade, beta-blockers, Calcium Channel Blockers (CCB).

Increased Cardiac Output (CO)

Early sepsis, exercise, anxiety/stress, inotropes, dilators, hyperthyroidism, decreased SVR (Cardiac Index 2.2-4.0) = CO from left ventricle to Body Surface Area (BSA).

Pulmonary Artery Pressures

  • PA Systolic (Left CVP): 20-30 mmHg
  • PA Diastolic (Right CVP): 4-12 mmHg

Systemic Vascular Resistance (SVR)

  • Left Afterload: 800-1200 dynes/sec/cm-5
  • Right Afterload: 160-380 dynes/sec/cm-5

Electrolyte Imbalances

Potassium (K)

  • Hyperkalemia (H): Treat with D5W & Insulin, potential dialysis, Kayexalate, Calcium Chloride (CaCl)
  • Hypokalemia (L): Monitor for phlebitis at site & can always slow drip down

Magnesium before Potassium.

Magnesium (Mag)

  • Prolonged QT & PR intervals, may have U waves.
  • Causes of low magnesium: ETOH abuse, rapid administration of citrated blood products, malnourishment → Torsades can result
  • Hypermagnesemia (H): Renal impairment at risk

Calcium (Ca)

  • Hypocalcemia (L): Low albumin, low contraction, low CO & hypotension (prolonged QT) → Torsades can result
  • Hypercalcemia (H): Prone to heart block, can enhance Digoxin toxicity. Treatment: diuretics, bisphosphonates, dialysis

Cardioversion and Defibrillation

  • Cardioversion: 50-100, 200, 300, 360 Joules
  • Defibrillation: Biphasic 120-200 Joules, Monophasic 360 Joules

Implantable Cardioverter-Defibrillator (ICD)

Resets heart from abnormal rhythm.

Mixed Venous Oxygen Saturation (SVO2)

  • Normal range: 60-80%
  • Low SVO2: Low Hemoglobin (Hgb), low SaO2, CO is not high enough to meet tissue needs, O2 consumption has increased without an increase in O2 delivery (fever, sepsis)
  • High SVO2: Initial stages of sepsis

Medications to Manage Heart Rate and Contractility

  • To increase HR: Atropine & Pacemaker
  • To decrease HR: Beta-blockers & Calcium Channel Blockers (Diltiazem)
  • To increase contractility: Inotropes (Epinephrine, Dopamine, Dobutamine, Milrinone)
  • To decrease contractility: Hyperdynamic CO/CI (Fluids)

Medications to Manage Vascular Resistance and Fluid Volume

  • To increase Vascular Resistance (VR): Vasoconstrictors (Levophed, Vasopressin, Phenylephrine, Angiotensin II)
  • To decrease VR: Vasodilators (Nitroglycerin, Nicardipine, Clevidipine, Hydralazine)
  • To increase fluid volume: Blood products, Albumin, Crystalloids
  • To decrease fluid volume: Diuretics & Dialysis

Systemic Vascular Resistance (SVR) Explained

  • Normal range: 800-1200 dynes/sec/cm-5
  • Resistance to blood flow (“Afterload”)
  • Increased SVR: Hypothermia, aortic stenosis, cardiogenic shock, medications (Levophed, Vasopressin, Phenylephrine, Dopamine)
  • Decreased SVR: Anaphylactic & neurogenic shock, hyperthermia, sepsis, medications (Nitroglycerin, Nitroprusside, Nicardipine, Clevidipine)
  • Increased SVR will increase MAP & decrease CO (lower CO but high MAP) and high CO low MAP — for CO to remain same – contractility & HR must increase