MODULE 6: ANAESTHETIC CONSIDERATION IN CARDIAC ANAESTHESIA

Q1: Abbreviate NYHA

Answer:NYHA = New York Heart Association

The New York Heart Association functional classification system used for assessing heart failure severity and functional capacity in cardiac patients:

Functional Classification:

Class I:

• No symptoms with ordinary physical activity
• No limitation of physical activity
• No evidence of heart failure

Class II:

• Slight limitation of physical activity
• Comfortable at rest, but ordinary activity produces symptoms
• Mild limitation of physical activity

Class III:

• Marked limitation of physical activity
• Comfortable at rest, but less than ordinary activity produces symptoms
• Moderate limitation of physical activity

Class IV:

• Unable to carry out any physical activity without discomfort
• Symptoms of heart failure at rest
• Severe limitation of physical activity

Clinical Significance:

• Risk Stratification: Higher class indicates greater anesthetic risk
• Anesthetic Planning: Guides monitoring and management decisions
• Prognosis: Higher class associated with worse outcomes
• Medication Optimization: May require preoperative adjustment

Q2: Define arrhythmia

Answer:

Arrhythmia is any disturbance in the normal rhythm or rate of the heart, characterized by abnormalities in the formation or conduction of electrical impulses through the cardiac conduction system.

Types of Arrhythmias:

By Rate:

Bradyarrhythmias (Rate <60 bpm):

• Sinus bradycardia
• Heart blocks (1st, 2nd, 3rd degree)
• Junctional rhythm

Tachyarrhythmias (Rate >100 bpm):

• Sinus tachycardia
• Atrial fibrillation/flutter
• Supraventricular tachycardia
• Ventricular tachycardia
• Ventricular fibrillation

By Origin:

Supraventricular:

• Originate above the ventricles
• Atria or AV node
• Usually less life-threatening

Ventricular:

• Originate in ventricles
• More serious and potentially life-threatening
• Require immediate attention

Causes:

• Ischemic heart disease: MI, coronary artery disease
• Electrolyte imbalances: K+, Mg++, Ca++
• Medications: Antiarrhythmics, digitalis toxicity
• Autonomic imbalance: Sympathetic overactivity
• Structural heart disease: Cardiomyopathy, valvular disease

Clinical Significance:

• Hemodynamic compromise: Reduced cardiac output
• Embolic risk: Stroke, systemic embolism
• Anesthetic complications: Increased perioperative risk

Q3: What is the choice for premedication in cardiac patients

Answer:

Premedication choices for cardiac patients must prioritize cardiovascular stability while providing adequate anxiolysis and amnesia.

Preferred Premedicants:

Benzodiazepines (First Choice):

Midazolam:

• Dose: 0.05-0.1 mg/kg IV/IM
• Advantages: Rapid onset, short duration, minimal cardiovascular effects
• Mechanism: GABA receptor modulation

Lorazepam:

• Dose: 0.05 mg/kg PO
• Advantages: Longer duration, excellent anxiolysis
• Use: Oral premedication, sustained anxiety relief

Opioids (Selective Use):

Morphine:

• Dose: 0.05-0.1 mg/kg IM
• Indications: Severe pain or anxiety, myocardial infarction
• Cautions: Respiratory depression, hypotension

Fentanyl:

• Dose: 0.5-1 mcg/kg IV
• Advantages: Short-acting, minimal cardiovascular effects
• Use: Balanced anesthesia protocols

Medications to Continue:

• Beta-blockers: Continue unless contraindicated
• ACE inhibitors/ARBs: Continue until surgery
• Calcium channel blockers: Continue as scheduled
• Antiplatelet agents: Continue based on cardiac risk

Avoid or Use with Caution:

• Atropine/Glycopyrrolate: Only for bradycardia
• High-dose benzodiazepines: Risk of hypotension
• Phenothiazines: Cardiovascular depression

Special Considerations:

• Heart failure patients: Avoid heavy sedation
• Recent MI: Minimize sympathetic stimulation
• Elderly: Reduce doses, monitor closely

Q4: Define EF of heart

Answer:

EF (Ejection Fraction) is the percentage of blood pumped out of the left ventricle with each heartbeat, calculated as the fraction of end-diastolic volume ejected during systole.

Normal Values:

• Normal EF: 55-70%
• Mild dysfunction: 40-54%
• Moderate dysfunction: 30-39%
• Severe dysfunction: <30%

Calculation:

EF = (EDV - ESV) / EDV × 100

Where:

• EDV = End-diastolic volume
• ESV = End-systolic volume

Types of EF:

Left Ventricular EF (LVEF):

• Most commonly measured
• Predicts perioperative risk
• Guides anesthetic management
• Standard for heart failure classification

Right Ventricular EF (RVEF):

• Less commonly measured
• Important in pulmonary hypertension
• Correlates with right heart function

Measurement Methods:

1. Echocardiography: Most common, bedside assessment
2. Nuclear Medicine: MUGA scan, precise measurement
3. Cardiac MRI: Gold standard for accuracy
4. Cardiac Catheterization: Most accurate but invasive

Anesthetic Implications:

Low EF (<40%):

• Increased perioperative mortality
• Higher risk of heart failure
• Requires careful fluid management
• May need inotropic support
• Extended monitoring required

Normal EF:

• Standard anesthetic approach
• Standard monitoring
• Normal fluid management

Limitations:

• Load dependent: Affected by preload and afterload
• Measurement variability: Inter-observer differences
• Diastolic function: Does not assess diastolic dysfunction

Q5: Define angina

Answer:

Angina Pectoris is chest pain or discomfort caused by temporary myocardial ischemia due to inadequate coronary blood flow relative to myocardial oxygen demand.

Pathophysiology:

• Imbalance: Between myocardial oxygen demand and supply
• Coronary atherosclerosis: Most common cause
• Fixed stenosis: Reduced coronary flow reserve
• Transient ischemia: Reversible without myocardial damage

Classification:

Stable Angina:

• Predictable pattern with exertion or stress
• Duration: 2-10 minutes
• Relief: Rest or nitroglycerin
• Frequency: Consistent over time

Unstable Angina:

• New onset or worsening pattern
• Occurs at rest or minimal exertion
• Duration: >10 minutes
• Risk: High risk of myocardial infarction

Variant (Prinzmetal) Angina:

• Caused by coronary artery spasm
• Often at rest, early morning
• ST elevation during attack
• May occur without atherosclerosis

Clinical Features:

Location:

• Substernal chest pressure
• May radiate to left arm, jaw, neck, back
• Can be epigastric

Quality:

• Pressure, squeezing, burning
• Heaviness or fullness
• Dull ache or sharp pain

Associated Symptoms:

• Dyspnea
• Diaphoresis
• Nausea
• Fatigue
• Sense of impending doom

Risk Factors:

• Age >45 (men), >55 (women)
• Family history of CAD
• Smoking
• Diabetes mellitus
• Hypertension
• Hyperlipidemia
• Obesity
• Sedentary lifestyle

Canadian Cardiovascular Society Classification:

• Class I: No angina with ordinary activity
• Class II: Angina with strenuous activity
• Class III: Angina with minimal activity
• Class IV: Angina at rest

Management:

Acute:

• Oxygen
• Nitroglycerin
• Aspirin
• Beta-blockers
• Calcium channel blockers

Long-term:

• Risk factor modification
• Medications (statins, antiplatelet agents)
• Revascularization (PCI or CABG)
• Lifestyle changes

Q6: What are the investigation orders in PAC for cardiac patients

Answer:

Pre-anesthesia clinic investigations for cardiac patients focus on risk stratification, optimization, and guiding anesthetic management.

Routine Investigations:

Basic Laboratory Tests:

• Complete Blood Count (CBC): Hemoglobin, WBC count, platelet count
• Basic Metabolic Panel: Electrolytes, creatinine, BUN, glucose
• Coagulation Studies: PT/INR, aPTT (especially if on anticoagulants)
• Urinalysis: Kidney function, proteinuria

Electrocardiogram (ECG):

• Timing: Within 30 days of surgery
• Findings: Arrhythmias, ischemia, conduction blocks, hypertrophy
• Significance: Baseline for intraoperative comparison
• Additional: May need 12-lead ECG if new symptoms

Specialized Investigations:

Echocardiogram:

• Indications: Known or suspected heart disease, unexplained dyspnea
• Parameters: EF, wall motion abnormalities, valve function
• Timing: Within 6 months if stable
• Information: Valvular disease, pericardial disease, pulmonary hypertension

Stress Testing:

• Indications:
  • Intermediate risk patients
  • Poor exercise tolerance
  • Asymptomatic with high cardiac risk
• Types: Exercise stress test, pharmacologic stress
• Purpose: Assess functional capacity, detect inducible ischemia

Cardiac Catheterization:

• Indications:
  • Recent MI or unstable angina
  • High surgical risk with known CAD
  • Abnormal stress test results
• Information: Coronary anatomy, pressure measurements
• Timing: Within 6 months for high-risk patients

Additional Tests (Based on Clinical Indication):

Cardiac Biomarkers:

• Troponin: If recent cardiac event suspected
• BNP/NT-proBNP: Heart failure assessment

Pulmonary Function Tests:

• COPD patients
• Assessment of perioperative respiratory risk

Holter Monitor:

• Frequent arrhythmias
• Syncope evaluation

Age-Based Guidelines:

Age <50, ASA I-II:

• ECG only if symptomatic
• Basic labs if indicated

Age 50-64, ASA I-II:

• ECG required
• Basic labs
• Consider stress test if multiple risk factors

Age >65 or ASA III-IV:

• ECG required
• Comprehensive lab work
• Stress test if indicated
• Consider cardiology consultation

High-Risk Features Requiring Further Investigation:

• Recent MI (<6 months)
• Unstable angina
• Severe valvular disease
• Heart failure with reduced EF
• Complex arrhythmias
• Syncope
• Poor exercise tolerance

Timing Guidelines:

• Stable CAD: Testing within 12 months
• Recent MI: Within 6 months
• Heart failure: Within 3-6 months
• Valve disease: Within 3 months

Integration with Anesthetic Plan:

• Results guide monitoring requirements
• Determines need for invasive monitoring
• Influences medication management
• Guides fluid management strategy

Q7: Write any 2 PAC orders for cardiac patients undergoing major surgeries

Answer:

PAC orders for cardiac patients undergoing major surgeries must address preoperative optimization, medication management, and specialized monitoring.

1. Medication Management Orders:

Continue Cardiac Medications:

Beta-blockers:

• Continue until surgery: Metoprolol, atenolol, carvedilol
• Do not discontinue abruptly: Risk of rebound tachycardia
• Hold only if: Severe bradycardia (<50 bpm) or hypotension

ACE Inhibitors/ARBs:

• Continue until morning of surgery: Captopril, lisinopril, losartan
• Exception: May hold if hypotensive
• Rationale: Reduce perioperative hypertension and cardiac stress

Statins:

• Continue indefinitely: Atorvastatin, simvastatin, rosuvastatin
• Benefits: Plaque stabilization, reduce perioperative cardiac events

Adjust Preoperative Medications:

Diuretics:

• Hold morning dose: Furosemide, hydrochlorothiazide
• Rationale: Avoid intraoperative hypovolemia and electrolyte imbalance
• Monitor: Daily weights, urine output, electrolytes

Antiplatelet Agents:

• Aspirin: Continue if recent stenting or high cardiac risk
• Clopidogrel: Continue if recent stenting (consult cardiology)
• Warfarin: Bridge with heparin if indicated

2. Monitoring and Assessment Orders:

Vital Signs Monitoring:

Blood Pressure:

• Frequency: Every 4 hours while awake
• Target: Maintain <160/100 mmHg, >90/60 mmHg
• Special: Orthostatic BP if on antihypertensives

Heart Rate:

• Target: 60-80 bpm (adjust for heart failure)
• Monitor: Rhythm and rate continuously
• Alert: Bradycardia <50 bpm, tachycardia >100 bpm

Laboratory Monitoring:

Daily Basic Metabolic Panel:

• Electrolytes: Especially K+ (4.0-5.0 mEq/L), Mg++ (2.0-2.5 mg/dL)
• Kidney function: Creatinine, BUN
• Glucose: Maintain 140-180 mg/dL

Daily CBC:

• Hemoglobin: Monitor for anemia
• Hematocrit: Assess volume status
• Platelets: Important for surgical planning

Specialized Tests:

• PT/INR: Daily if on warfarin
• Cardiac biomarkers: If recent cardiac events
• BNP/NT-proBNP: For heart failure assessment

Specialized Monitoring:

ECG Monitoring:

• Continuous: For unstable patients
• Daily 12-lead: If symptomatic
• Monitoring: ST-segment changes, arrhythmias

Daily Weights:

• Purpose: Assess volume status
• Time: Same time each morning, same scale
• Alert: Weight gain >2 lbs in 24 hours

Additional Preoperative Orders:

Preoperative Instructions:

NPO Guidelines:

• Clear liquids: 2 hours
• Breast milk: 4 hours
• Light meal: 6 hours
• Heavy meal: 8 hours

IV Access:

• Large bore IV (16-18G): For potential resuscitation
• Central line: Consider if severe heart failure
• Arterial line: For major surgery or hemodynamic instability

Emergency Preparation:

Emergency Medications:

• Epinephrine: For anaphylaxis, cardiac arrest
• Atropine: For bradycardia
• Lidocaine: For arrhythmias
• Adenosine: For SVT

Equipment:

• Defibrillator: Readily available
• Emergency cart: Within easy reach
• Portable monitor: For transport

Communication Orders:

• Consult cardiology: If abnormal findings or high risk
• Notify anesthesiologist: Of any changes in condition
• Family discussion: End-of-life care if appropriate
• Documentation: All findings and consultations

Q8: Define preload and afterload

Answer:

Understanding preload and afterload is fundamental to cardiac anesthesia as they determine ventricular function and guide fluid management and drug therapy.

PRELOAD:

Definition: The degree of stretch or tension on myocardial fibers at the end of diastole, just before contraction begins.

Clinical Measures:

• Left ventricular end-diastolic volume (LVEDV): Primary measure
• Left ventricular end-diastolic pressure (LVEDP): Invasive measure
• Central venous pressure (CVP): Right heart estimate
• Pulmonary capillary wedge pressure (PCWP): Left heart estimate

Normal Values:

• CVP: 2-6 mmHg
• PCWP: 8-12 mmHg
• LVEDV: 70-120 mL/m²

Determinants of Preload:

Blood Volume:

• Total circulating volume
• Venous return
• Distribution between compartments

Venous Tone:

• Venoconstriction → increased preload
• Venodilation → decreased preload

Heart Rate:

• Faster rate → less filling time → decreased preload
• Slower rate → more filling time → increased preload

Valve Function:

• Mitral regurgitation → increased preload
• Tricuspid regurgitation → increased preload

Clinical Assessment:

• Physical examination: Jugular venous distension, peripheral edema
• Imaging: Echocardiogram, chest X-ray
• Hemodynamic monitoring: CVP, PCWP, echocardiography

Anesthetic Implications:

• Fluid management: Guided by preload assessment
• Vasodilators: Reduce preload (nitroglycerin)
• Inotropic agents: May improve contractility
• Positioning: Trendelenburg increases preload

AFTERLOAD:

Definition: The resistance the heart must overcome to eject blood during systole, primarily determined by systemic vascular resistance.

Clinical Measures:

• Systemic vascular resistance (SVR): Primary measure
• Arterial blood pressure: Indirect estimate
• Mean arterial pressure (MAP): More accurate than systolic/diastolic

Calculation of SVR:

SVR = (MAP - CVP) / CO × 80

Where:

• MAP = Mean arterial pressure (mmHg)
• CVP = Central venous pressure (mmHg)
• CO = Cardiac output (L/min)
• Normal SVR: 800-1200 dynes/sec/cm⁻⁵

Normal Values:

• SVR: 800-1200 dynes/sec/cm⁻⁵
• MAP: 70-100 mmHg
• Pulmonary vascular resistance (PVR): 100-200 dynes/sec/cm⁻⁵

Determinants of Afterload:

Arterial Tone:

• Sympathetic nervous system activity
• Medications (vasodilators, vasoconstrictors)
• Endothelial function

Blood Viscosity:

• Hematocrit levels
• Plasma proteins
• Temperature effects

Vessel Compliance:

• Arterial stiffness
• Age-related changes
• Pathological conditions

Valve Function:

• Aortic stenosis → increased afterload
• Aortic regurgitation → increased afterload

Clinical Assessment:

• Blood pressure: Indirect measure
• Hemodynamic monitoring: SVR calculation
• Physical examination: Pulse quality, perfusion

Anesthetic Implications:

• Vasodilators: Reduce afterload (nitroprusside, nicardipine)
• Inotropic support: Overcome increased afterload
• Monitoring: Beat-to-beat BP assessment
• Goals: Maintain adequate coronary perfusion pressure

Frank-Starling Relationship:

• Increased preload → increased stroke volume (within limits)
• Increased afterload → decreased stroke volume
• Optimal function: Balance between preload and afterload

Clinical Integration:

Heart Failure:

• Reduced contractility: Requires optimal preload
• Mitral regurgitation: Afterload reduction beneficial

Hypertension:

• Increased afterload: Requires careful reduction
• Avoid rapid changes: Risk of organ hypoperfusion

Shock States:

• Hypovolemic: Decrease afterload, optimize preload
• Cardiogenic: Support contractility, cautious afterload reduction

Monitoring and Management:

Intraoperative Monitoring:

• Arterial line: Continuous BP monitoring
• CVP: Right heart filling pressures
• PAC: Comprehensive hemodynamic assessment
• TEE: Real-time cardiac function

Pharmacological Management:

Increase Preload:

• IV fluid boluses
• Trendelenburg positioning
• Vasoconstrictors (minor effect)

Decrease Preload:

• Diuretics
• Venodilators (nitroglycerin)
• Positioning (head-up)

Decrease Afterload:

• Vasodilators (nitroprusside, nicardipine)
• ACE inhibitors
• Afterload reduction improves cardiac output

Increase Contractility:

• Inotropic agents (dopamine, dobutamine)
• Calcium
• Digitalis (rarely used acutely)

This comprehensive understanding of preload and afterload is essential for optimal cardiac anesthetic management and patient outcomes.

Q9: Define hypoxia and hypoxemia

Answer:

Understanding the distinction between hypoxia and hypoxemia is crucial in cardiac anesthesia as they represent different aspects of oxygenation problems with distinct causes and treatments.

HYPOXEMIA:

Definition: Abnormally low partial pressure of oxygen in arterial blood (PaO2 <60 mmHg).

Normal Values:

• PaO2: 80-100 mmHg (at sea level)
• SaO2: >95%
• SpO2: >94%

Causes of Hypoxemia:

1. Hypoventilation:

• Mechanism: Reduced alveolar ventilation → increased PaCO2
• Examples: CNS depression, neuromuscular disease, chest wall pathology
• Response: Decreased O2 intake despite normal lungs

2. Low Inspired Oxygen (FiO2):

• Mechanism: Reduced oxygen fraction in inspired air
• Examples: High altitude, equipment malfunction, anesthesia machine failure
• Response: Globally reduced oxygen delivery

3. Right-to-Left Shunt:

• Mechanism: Blood bypasses ventilated alveoli
• Examples:
  • Pulmonary edema
  • Pneumonia
  • Atelectasis
  • Right-to-left cardiac shunt
• Response: Mixing of oxygenated and deoxygenated blood

4. Ventilation/Perfusion (V/Q) Mismatch:

• Mechanism: Poorly ventilated but perfused lung units
• Examples:
  • COPD
  • Asthma
  • Pulmonary embolism
  • Heart failure
• Response: Reduced gas exchange efficiency

5. Diffusion Impairment:

• Mechanism: Thickened alveolar-capillary membrane
• Examples:
  • Pulmonary fibrosis
  • Interstitial lung disease
  • ARDS
• Response: Delayed oxygen diffusion

Clinical Signs:

• Cyanosis: Central cyanosis when PaO2 <50 mmHg
• Tachypnea: Increased respiratory rate
• Tachycardia: Compensatory response
• Altered mental status: Confusion, agitation
• Hypotension: Severe cases

Treatment:

• Oxygen supplementation
• Treat underlying cause
• Mechanical ventilation if needed
• Bronchodilators for V/Q mismatch

HYPOXIA:

Definition: Inadequate oxygen delivery to tissues, regardless of arterial oxygen content.

Types of Hypoxia:

1. Hypoxemic Hypoxia (Hypoxic Hypoxia):

• Low arterial PaO2
• Same causes as hypoxemia
• Examples: High altitude, lung disease

2. Anemic Hypoxia:

• Reduced oxygen-carrying capacity
• Causes:
  • Anemia
  • Carbon monoxide poisoning
  • Methemoglobinemia
• Response: Normal PaO2, reduced oxygen content

3. Stagnant (Circulatory) Hypoxia:

• Reduced blood flow to tissues
• Causes:
  • Heart failure
  • Shock
  • Vascular disease
  • Thrombosis
• Response: Normal PaO2 and content, inadequate delivery

4. Histotoxic Hypoxia:

• Cells unable to utilize oxygen
• Causes:
  • Cyanide poisoning
  • Hydrogen sulfide
  • Severe sepsis
• Response: Normal delivery, utilization failure

Clinical Signs:

• Lactic acidosis: Anaerobic metabolism
• Altered mental status
• Organ dysfunction:
  • Kidney: Acute kidney injury
  • Heart: Myocardial ischemia
  • Liver: Hepatic dysfunction
• Skin changes: Cyanosis, mottling

Treatment:

• Address underlying cause
• Improve circulation
• Support organ function
• Antidotes for toxins

Key Differences:

Feature	Hypoxemia	Hypoxia
Definition	Low arterial PaO2	Inadequate tissue oxygenation
Measurement	Arterial blood gas	Tissue perfusion markers
Treatment	Oxygen therapy	Varies by cause
Examples	Lung disease, altitude	Shock, heart failure, toxins

Clinical Significance in Cardiac Anesthesia:

Risk Factors:

• Pre-existing lung disease
• Cardiac failure
• Anemia
• Shock states
• High oxygen consumption

Monitoring:

• SpO2: Continuous pulse oximetry
• ABG analysis: PaO2 and SaO2
• Lactate levels: Tissue hypoxia marker
• Mixed venous O2 saturation: Global oxygen delivery

Prevention:

• Preoxygenation
• Adequate ventilation
• Oxygen supplementation
• Maintain hemoglobin
• Optimize cardiac output

Management:

1. Identify type: Hypoxemia vs. hypoxia
2. Treat cause: Specific therapy
3. Support oxygenation: Ventilation, oxygen
4. Monitor response: Clinical and laboratory
5. Prevent complications: Organ dysfunction

This distinction is crucial for appropriate treatment and preventing serious complications in cardiac surgical patients.

Q10: Write conduction system of heart

Answer:

The cardiac conduction system is a specialized network of cells that generates and conducts electrical impulses, coordinating the heart's mechanical contractions. Understanding this system is essential for cardiac anesthesia.

Components of the Conduction System:

1. Sinoatrial (SA) Node:

Location: Right atrial wall, near the superior vena cava opening

Characteristics:

• Rate: 60-100 bpm (normal sinus rhythm)
• Function: Primary pacemaker of the heart
• Innervation:
  • Sympathetic stimulation: Increases rate
  • Parasympathetic stimulation: Decreases rate

Mechanism:

• Automatic depolarization
• Spontaneous phase 4 depolarization
• Fires at regular intervals unless inhibited

2. Atrioventricular (AV) Node:

Location: Lower right atrium, near the septal leaflet of tricuspid valve

Characteristics:

• Rate: 40-60 bpm (if overriding pacemaker)
• Function: Conducts impulses from atria to ventricles
• Delay: 0.1 seconds (allows atrial contraction)

Properties:

• Decremental conduction: Progressive slowing
• Refractory period: Prevents rapid atrial rates
• Bidirectional block: Can block in either direction

3. His Bundle (Atrioventricular Bundle):

Location: Interventricular septum

Function: Main conduction pathway from atria to ventricles Rate: 40-60 bpm (if overriding) Characteristics: Specialized conducting tissue

4. Bundle Branches:

Left Bundle Branch:

• Location: Left ventricular septum
• Function: Conducts to left ventricle
• Branches: Anterior and posterior fascicles

Right Bundle Branch:

• Location: Right ventricular septum
• Function: Conducts to right ventricle

Rate: 20-40 bpm (if overriding)

5. Purkinje Network:

Location: Ventricular myocardium Function: Rapid conduction throughout ventricles Rate: 20-40 bpm (if overriding) Characteristics: Fastest conduction velocity

Normal Conduction Sequence:

1. SA node fires: 60-100 times per minute
2. Atrial depolarization: Spreads through atria
3. Atrial contraction: Atrial kick
4. AV node delay: 0.1 seconds
5. His bundle activation: Conduction to ventricles
6. Bundle branches: Rapid spread
7. Purkinje network: Final ventricular activation
8. Ventricular contraction: Systole

Electrophysiology:

Action Potential Phases:

Phase 0: Rapid depolarization

• Sodium influx
• Fast upstroke
• Creates QRS complex

Phase 1: Initial repolarization

• Potassium efflux
• Brief reversal

Phase 2: Plateau

• Calcium influx
• Sustained contraction
• Creates ST segment

Phase 3: Repolarization

• Potassium efflux
• Returns to resting potential
• Creates T wave

Phase 4: Resting potential

• Sodium-potassium pump
• Automaticity in pacemaker cells

Ion Channels:

• Fast Na+ channels: Phase 0
• Ca2+ channels: Phase 2 (plateau)
• K+ channels: Phases 1 and 3
• HCN channels: Pacemaker cells (phase 4)

Clinical Significance:

Arrhythmias by Mechanism:

Automaticity:

• Enhanced normal automaticity
• Abnormal automaticity
• Triggered activity

Re-entry:

• Circus movement
• Requires: Two pathways, unidirectional block, sufficient conduction time

Conduction Block:

• SA node dysfunction
• AV node block
• Bundle branch block

Common Arrhythmias:

SA Node Dysfunction:

• Sinus bradycardia
• Sinus arrest
• Sick sinus syndrome

AV Node Block:

• 1st degree: Prolonged PR interval (>200 ms)
• 2nd degree: Intermittent AV conduction
• 3rd degree: Complete heart block

Bundle Branch Block:

• Left bundle branch block
• Right bundle branch block
• Hemiblock

Supraventricular Tachyarrhythmias:

• Atrial fibrillation
• Atrial flutter
• SVT

Ventricular Tachyarrhythmias:

• Ventricular tachycardia
• Ventricular fibrillation

Anesthetic Implications:

Preoperative Assessment:

• ECG evaluation: Baseline rhythm and conduction
• History: Previous arrhythmias, syncope
• Medications: Antiarrhythmic drugs

Intraoperative Management:

Monitoring:

• Continuous ECG monitoring
• ST-segment analysis
• Heart rate variability

Prevention:

• Maintain electrolyte balance (K+, Mg++)
• Avoid autonomic imbalance
• Minimize surgical stimulation
• Gentle handling of heart

Treatment:

• Bradycardia: Atropine, pacing
• Tachycardia: Beta-blockers, calcium channel blockers
• Arrhythmias: Antiarrhythmic drugs, cardioversion

Medications Affecting Conduction:

Positive chronotropes:

• Atropine
• Epinephrine
• Dopamine

Negative chronotropes:

• Beta-blockers
• Calcium channel blockers
• Digoxin

Antiarrhythmics:

• Class I: Sodium channel blockers
• Class II: Beta-blockers
• Class III: Potassium channel blockers
• Class IV: Calcium channel blockers

Diagnostic Tools:

Surface ECG:

• 12-lead ECG: Comprehensive assessment
• Rhythm strip: Continuous monitoring
• Event recorder: Intermittent symptoms

Invasive Studies:

• Electrophysiological study: Detailed mapping
• Programmed stimulation: Inducibility testing
• Mapping catheter: Ablation procedures

Implantable Devices:

• Permanent pacemaker: Sinus node dysfunction, heart block
• ICD: Ventricular arrhythmias
• CRT: Heart failure with conduction delay

Understanding the cardiac conduction system is fundamental for safe anesthetic management of cardiac patients and for managing perioperative arrhythmias.

Q11: Name cardiac stable induction agents and inhalational anesthetic

Answer:

Cardiac stable anesthetic agents minimize cardiovascular depression while providing adequate anesthesia. Selection depends on patient factors and surgical requirements.

Cardiac Stable IV Induction Agents:

Etomidate:

Dose: 0.3 mg/kg IV

Advantages:

• Minimal cardiovascular depression: Preserves hemodynamic stability
• Stable blood pressure: Maintains coronary perfusion pressure
• Preserved baroreceptor reflexes: Maintains autonomic responses
• Cerebral protection: Reduces intracranial pressure
• Bronchodilation: Beneficial for asthma/COPD

Mechanism:

• GABA receptor agonist
• NMDA receptor antagonist (minor)
• Alpha-2 receptor activation

Disadvantages:

• Myoclonus: Common but brief
• Adrenal suppression: Controversial for prolonged use
• Pain on injection: Requires lidocaine co-administration

Ideal for:

• Hemodynamically unstable patients
• Cardiac surgery
• Septic patients
• Elderly with cardiovascular disease

Ketamine:

Dose: 1-2 mg/kg IV

Advantages:

• Sympathetic stimulation: Increases blood pressure and heart rate
• Bronchodilation: Beneficial for reactive airway disease
• Analgesia: Superior pain relief
• Preserved reflexes: Maintains protective airway reflexes
• Cerebral protection: Increases cerebral blood flow

Mechanism:

• NMDA receptor antagonist
• Opioid receptor activation
• Sympathetic stimulation

Disadvantages:

• Emergence reactions: Hallucinations, agitation
• Increased secretions: May require anticholinergics
• Hypertension: May increase cardiac work
• Intracranial pressure: Contraindicated in some neurosurgical cases

Ideal for:

• Hypotensive patients
• Asthmatic patients
• Trauma patients
• Septic shock

Modified Propofol:

Dose: 1.5-2 mg/kg IV (reduced dose)

Advantages:

• Rapid onset and emergence
• Antiemetic properties
• Cerebral protection

Disadvantages:

• Dose-dependent cardiovascular depression
• Respiratory depression
• Pain on injection

Strategies for cardiac stability:

• Slower administration
• Pre-treatment: Ephedrine or phenylephrine
• Reduced dose: In combination with opioids

Cardiac Stable Inhalational Agents:

Sevoflurane:

MAC: 1.8-2.0%

Advantages:

• Minimal myocardial depression: Preserves contractility
• Maintained baroreceptor reflexes: Preserves autonomic control
• Non-pungent: Excellent for mask induction
• Bronchodilation: Beneficial for reactive airway
• Rapid induction and emergence
• Low arrhythmogenic potential

Mechanism:

• GABA receptor enhancement
• Potassium channel activation
• NMDA receptor modulation

Disadvantages:

• Metabolites: Compound A (nephrotoxicity debate)
• Cost: More expensive than isoflurane

Ideal for:

• Cardiac surgery
• Mask induction
• Outpatient surgery
• Patients with cardiovascular disease

Isoflurane:

MAC: 1.2-1.5%

Advantages:

• Cardiovascular stability: Preserved cardiac output
• Bronchodilation: Beneficial for asthma
• Cerebral protection: Reduces metabolic rate
• Cost-effective: Less expensive option
• Established safety profile

Disadvantages:

• Pungent odor: Poor for mask induction
• Respiratory irritation: May cause coughing
• Coronary steal phenomenon: Theoretical concern

Ideal for:

• Maintenance anesthesia
• Long procedures
• Patients with cardiovascular disease

Desflurane:

MAC: 6-7%

Advantages:

• Extremely rapid emergence: Quick recovery
• Low solubility: Fast onset and offset
• Hemodynamic stability
• Excellent for outpatient surgery

Disadvantages:

• Very pungent: Cannot use for mask induction
• Respiratory irritation: May cause coughing, breath-holding
• Sympathetic stimulation: May increase heart rate
• High cost

Ideal for:

• Short procedures
• Outpatient surgery
• Patients requiring rapid emergence

Avoid in Cardiac Patients:

Halothane:

• Significant myocardial depression
• Arrhythmogenic potential
• Hepatotoxicity risk
• Coronary steal phenomenon

Enflurane:

• Cardiovascular depression
• Proconvulsant properties
• Higher arrhythmogenic potential

Combinations for Balanced Anesthesia:

Propofol + Fentanyl + Sevoflurane:

• Propofol: Induction, then low-dose infusion
• Fentanyl: Analgesia, reduces inhalational agent requirements
• Sevoflurane: Maintenance, excellent hemodynamic profile

Etomidate + Fentanyl + Isoflurane:

• Etomidate: Induction for unstable patients
• Fentanyl: Balanced analgesia
• Isoflurane: Cost-effective maintenance

Monitoring Requirements:

Basic Monitoring:

• ECG: Continuous rhythm monitoring
• Blood pressure: Frequent measurements
• SpO2: Oxygen saturation
• EtCO2: End-tidal CO2

Advanced Monitoring:

• Arterial line: Continuous blood pressure
• TEE: Real-time cardiac function
• PAC: Comprehensive hemodynamics
• Bispectral index: Depth of anesthesia

Drug Selection Guidelines:

High-Risk Cardiac Patients:

• Induction: Etomidate or modified propofol
• Maintenance: Sevoflurane or isoflurane
• Analgesia: Fentanyl or remifentanil

Hemodynamically Unstable:

• Induction: Etomidate or ketamine
• Maintenance: Ketamine or etomidate infusions
• Avoid: Propofol boluses

Rapid Sequence Intubation:

• Induction: Etomidate + succinylcholine
• Alternative: Ketamine + rocuronium

Adjunct Medications:

Vasopressors:

• Phenylephrine: Pure alpha-agonist
• Ephedrine: Mixed alpha/beta agonist
• Epinephrine: Cardiac arrest, anaphylaxis

Inotropes:

• Dopamine: D1, beta, alpha effects
• Dobutamine: Pure beta-1 agonist
• Milrinone: Phosphodiesterase inhibitor

The selection of cardiac stable agents should be individualized based on patient factors, surgical requirements, and institutional protocols.

Q12: Classify induction agents & muscle relaxants

Answer:

Understanding the classification of anesthetic drugs helps in selecting appropriate agents for different clinical scenarios, especially in cardiac anesthesia.

Classification of Induction Agents:

By Chemical Structure:

1. Phenols:

• Propofol (2,6-diisopropylphenol)
• Characteristics:
  • Rapid onset and recovery
  • Anti-emetic properties
  • Cardiovascular and respiratory depression
  • Pain on injection

2. Barbiturates:

• Thiopentone (Thiopental)
• Methohexital
• Characteristics:
  • Ultra-short acting
  • Cerebral protection
  • Cardiovascular depression
  • Accumulation with repeated doses

3. Imidazoles:

• Etomidate
• Characteristics:
  • Minimal cardiovascular effects
  • Adrenal suppression (controversial)
  • Myoclonus common
  • Pain on injection

4. Phencyclidines:

• Ketamine
• Characteristics:
  • NMDA antagonist
  • Sympathetic stimulation
  • Emergence reactions
  • Bronchodilation

By Duration of Action:

Ultra-Short Acting:

• Propofol: 5-10 minutes
• Thiopentone: 5-15 minutes
• Methohexital: 10-15 minutes

Short Acting:

• Etomidate: 3-5 minutes
• Ketamine: 10-15 minutes

By Cardiovascular Effects:

Hemodynamically Stable:

• Etomidate
• Ketamine

Hemodynamically Unstable:

• Propofol
• Thiopentone

Classification of Muscle Relaxants:

By Mechanism of Action:

1. Depolarizing Muscle Relaxants:

Succinylcholine:

• Mechanism: Acetylcholine receptor agonist
• Onset: 30-60 seconds
• Duration: 3-5 minutes
• Advantages:
  • Rapid onset and recovery
  • Excellent intubating conditions
  • No antagonism required
• Disadvantages:
  • Histamine release
  • Hyperkalemia risk
  • Malignant hyperthermia risk
  • Contraindications: Burns, neuromuscular disease

2. Non-Depolarizing Muscle Relaxants:

Aminosteroid Group:

• Vecuronium:

  • Dose: 0.08-0.1 mg/kg
  • Onset: 2-3 minutes
  • Duration: 20-30 minutes
  • Advantages: Minimal histamine release, cardiovascular stability

• Rocuronium:

  • Dose: 0.6-1.2 mg/kg
  • Onset: 60-90 seconds
  • Duration: 30-45 minutes
  • Advantages: Rapid onset, sugammadex reversal

• Pancuronium:

  • Dose: 0.08-0.1 mg/kg
  • Onset: 3-5 minutes
  • Duration: 60-90 minutes
  • Disadvantages: Tachycardia, long duration

Benzylisoquinolinium Group:

• Atracurium:

  • Dose: 0.5-0.6 mg/kg
  • Onset: 2-3 minutes
  • Duration: 20-30 minutes
  • Advantages: Hoffman elimination, minimal organ dependence

• Cisatracurium:

  • Dose: 0.15-0.2 mg/kg
  • Onset: 2-3 minutes
  • Duration: 30-40 minutes
  • Advantages: Minimal histamine release, Hoffman elimination

• Mivacurium:

  • Dose: 0.15-0.2 mg/kg
  • Onset: 90 seconds
  • Duration: 15-20 minutes
  • Disadvantages: Histamine release, short duration

By Duration of Action:

Ultra-Short: Succinylcholine (3-5 minutes)

Short: Mivacurium (15-20 minutes)

Intermediate:

• Vecuronium (20-30 minutes)
• Atracurium (20-30 minutes)
• Cisatracurium (30-40 minutes)
• Rocuronium (30-45 minutes)

Long: Pancuronium (60-90 minutes)

By Histamine Release:

Minimal Release:

• Vecuronium
• Rocuronium
• Cisatracurium

Moderate Release:

• Atracurium
• Succinylcholine (high dose)

High Release:

• D-tubocurarine
• Mivacurium

Reversal Agents:

Cholinesterase Inhibitors:

Neostigmine:

• Dose: 0.05-0.07 mg/kg (max 5 mg)
• Mechanism: Inhibits acetylcholinesterase
• Antagonist: Glycopyrrolate or atropine
• Duration: 30-60 minutes

Edrophonium:

• Dose: 0.5-1 mg/kg
• Mechanism: Rapid onset, shorter duration
• Use: Monitored anesthesia care

Pyridostigmine:

• Dose: 0.1-0.25 mg/kg
• Mechanism: Longer duration
• Use: Myasthenia gravis

Selective Relaxant Binding Agents:

Sugammadex:

• Dose: 2-4 mg/kg (depending on depth)
• Mechanism: Encapsulates rocuronium/vecuronium
• Advantages: Rapid, complete reversal
• Indication: Deep blockade, rapid sequence

Monitoring Requirements:

Train-of-Four (TOF) Monitoring:

TOF Ratio:

• <0.9: Insufficient recovery
• ≥0.9: Adequate recovery
• 100%: Complete recovery

Fade Pattern:

• Progressive reduction in responses
• Indicates non-depolarizing blockade
• Guides reversal timing

Clinical Assessment:

• Eye opening
• Head lift (5 seconds)
• Grip strength
• Tongue protrusion

Drug Selection Guidelines:

Rapid Sequence Intubation:

• First choice: Succinylcholine
• Alternative: Rocuronium

Malignant Hyperthermia Risk:

• Avoid: Succinylcholine
• Safe: All non-depolarizing agents

Myasthenia Gravis:

• Avoid: Depolarizing agents
• Use: Reduced doses non-depolarizing

Cardiac Patients:

• Preferred: Vecuronium, cisatracurium
• Avoid: Pancuronium (tachycardia)

Renal Failure:

• Preferred: Atracurium, cisatracurium
• Avoid: Pancuronium, vecuronium

Liver Disease:

• Preferred: Atracurium, cisatracurium
• Avoid: Pancuronium, vecuronium

Clinical Applications:

Short Procedures:

• Succinylcholine: Rapid onset/offset
• Mivacurium: Short duration

Long Procedures:

• Atracurium/Cisatracurium: Organ-independent elimination
• Pancuronium: Long duration

Cardiac Surgery:

• Vecuronium: Cardiovascular stability
• Avoid: Pancuronium (tachycardia)

Ambulatory Surgery:

• Rocuronium: Rapid onset
• Short-acting agents: Faster recovery

Understanding these classifications enables optimal drug selection for different clinical scenarios and patient populations.

Q13: Write down all the monitoring systems for cardiac patients & NYHA classification

Answer:

Comprehensive monitoring of cardiac patients is essential for detecting complications early and guiding therapeutic interventions. NYHA classification helps stratify risk and guide monitoring intensity.

Monitoring Systems for Cardiac Patients:

1. Basic Monitoring:

Electrocardiogram (ECG):

• Standard 3-lead: Basic rhythm monitoring
• 5-lead system: Enhanced monitoring, ST-segment analysis
• 12-lead ECG: Comprehensive assessment
• Monitoring parameters:
  • Heart rate and rhythm
  • ST-segment changes (ischemia detection)
  • PR interval and QRS duration
  • QT interval prolongation

Blood Pressure Monitoring:

• Non-invasive (NIBP):
  • Oscillometric measurement
  • Frequency: Every 5-15 minutes
  • Automatic cycling
• Invasive (Arterial line):
  • Continuous real-time monitoring
  • Beat-to-beat pressure assessment
  • Waveform analysis
  • Frequent sampling capability

Pulse Oximetry (SpO2):

• Continuous oxygen saturation monitoring
• Detection of hypoxemia
• Perfusion assessment
• Plethysmographic waveform analysis

2. Advanced Hemodynamic Monitoring:

Central Venous Pressure (CVP):

• Normal values: 2-6 mmHg
• Monitoring sites:
  • Internal jugular vein
  • Subclavian vein
  • Femoral vein
• Information:
  • Right heart filling pressures
  • Volume status assessment
  • Drug administration route

Pulmonary Artery Catheter (PAC):

• Parameters monitored:
  • Cardiac output (CO)
  • Pulmonary capillary wedge pressure (PCWP)
  • Mixed venous oxygen saturation (SvO2)
  • Systemic vascular resistance (SVR)
  • Pulmonary vascular resistance (PVR)
• Calculations:
  • Stroke volume and stroke volume index
  • Cardiac index (CI = CO/BSA)
  • Oxygen delivery and consumption

Transesophageal Echocardiography (TEE):

• Real-time cardiac imaging:
  • Ventricular function
  • Valve function
  • Wall motion abnormalities
  • Pericardial assessment
  • Volume status evaluation
• Advantages:
  • Immediate hemodynamic assessment
  • Direct visualization
  • Continuous monitoring

3. Neurological Monitoring:

Electroencephalogram (EEG):

• Depth of anesthesia monitoring
• Detection of cerebral ischemia
• Burst suppression patterns

Bispectral Index (BIS):

• Processed EEG analysis
• Anesthesia depth assessment
• Target range: 40-60 for general anesthesia

Cerebral Oximetry:

• Near-infrared spectroscopy
• Regional cerebral oxygen saturation
• Detection of cerebral hypoperfusion

4. Respiratory Monitoring:

End-tidal CO2 (EtCO2):

• Normal values: 35-45 mmHg
• Capnography waveforms:
  • Ventilation adequacy
  • Airway patency
  • Circulation status
• Abnormal patterns:
  • Sudden drop: Air embolism, circuit disconnection
  • Gradual rise: Hypoventilation, rebreathing
  • Shaped changes: Airway obstruction

Respiratory Mechanics:

• Airway pressures
• Compliance measurements
• Resistance calculations

5. Temperature Monitoring:

Core Temperature Sites:

• Nasopharyngeal: Brain temperature
• Esophageal: Heart temperature
• Bladder: Core temperature
• Rectal: Less reliable

Peripheral Temperature:

• Skin temperature
• Temperature gradients
• Perfusion assessment

6. Laboratory Monitoring:

Point-of-Care Testing:

• ABG analysis:
  • pH, PaCO2, PaO2
  • Bicarbonate levels
  • Base excess
• Electrolytes: K+, Na+, Ca++, Mg++
• Hemoglobin/hematocrit
• Blood glucose
• Lactate levels
• Coagulation studies: PT/INR, aPTT, ACT

Cardiac Biomarkers:

• Troponin I/T: Myocardial injury
• CK-MB: Less specific
• BNP/NT-proBNP: Heart failure

NYHA Classification:

Functional Classification:

Class I:

• Symptoms: No symptoms with ordinary physical activity
• Physical activity: No limitation
• Examples: Asymptomatic heart disease
• Risk: Low anesthetic risk
• Monitoring: Standard monitoring adequate

Class II:

• Symptoms: Symptoms with ordinary physical activity
• Physical activity: Slight limitation
• Examples: Angina with exertion, mild heart failure
• Risk: Low to moderate risk
• Monitoring: Basic monitoring with vigilance

Class III:

• Symptoms: Symptoms with less than ordinary activity
• Physical activity: Marked limitation
• Examples: Comfortable at rest, symptoms with minimal activity
• Risk: Moderate to high risk
• Monitoring: Advanced monitoring recommended

Class IV:

• Symptoms: Symptoms at rest
• Physical activity: Unable to carry out any physical activity
• Examples: Severe heart failure, unstable angina
• Risk: High risk
• Monitoring: Comprehensive monitoring mandatory

Risk Stratification and Monitoring Guidelines:

Low Risk (NYHA I-II):

• Basic monitoring: ECG, NIBP, SpO2
• Laboratory: Basic metabolic panel, CBC
• Consider: Arterial line for major surgery

Moderate Risk (NYHA III):

• Advanced monitoring: Arterial line, CVP
• Laboratory: ABG, cardiac biomarkers
• Consider: PAC or TEE for major surgery

High Risk (NYHA IV):

• Comprehensive monitoring: PAC, TEE, continuous monitoring
• Laboratory: Frequent ABG, comprehensive metabolic panel
• Specialized: ICU-level monitoring

Specific Monitoring Protocols:

Cardiac Surgery:

• Mandatory: Arterial line, TEE, temperature monitoring
• PAC: For complex cases
• Specialized: Pulmonary artery pressures

Non-Cardiac Surgery (High Risk):

• Arterial line: Continuous BP monitoring
• CVP: Volume assessment
• Consider: PAC for unstable patients

Emergency Surgery:

• Rapid assessment: Basic monitoring initially
• Upgrade: Advanced monitoring as stable
• Backup: Emergency equipment readily available

Monitoring Complications:

Invasive Monitoring Risks:

• Arterial line: Bleeding, infection, thrombosis
• CVP: Pneumothorax, arrhythmias, infection
• PAC: Pulmonary artery rupture, arrhythmias
• TEE: Esophageal injury, hemodynamic compromise

Prevention Strategies:

• Aseptic technique
• Proper training
• Regular assessment
• Prompt removal when no longer needed

Integration with Anesthetic Management:

Data Interpretation:

• Trend analysis: Serial measurements
• Pattern recognition: Normal vs. abnormal
• Clinical correlation: Patient symptoms and signs

Therapeutic Decisions:

• Fluid management: Guided by hemodynamic parameters
• Drug therapy: Based on monitoring responses
• Intervention timing: Early detection and treatment

This comprehensive monitoring approach, combined with NYHA classification, ensures optimal care for cardiac patients throughout the perioperative period.

Q14: Define arrhythmia and explain them

Answer:

Arrhythmias are abnormalities in the heart's electrical rhythm, ranging from benign to life-threatening. Understanding their mechanisms and management is crucial for cardiac anesthesia.

Definition:

Arrhythmia is any disturbance in the normal rhythm or rate of the heart, resulting from abnormalities in the formation or conduction of electrical impulses through the cardiac conduction system.

Classification by Rate:

Bradyarrhythmias (Rate <60 bpm):

1. Sinus Bradycardia:

• Mechanism: Reduced automaticity of SA node
• Causes: Increased vagal tone, medications, hypothyroidism
• ECG: Regular rhythm, P waves present, PR interval normal
• Management: Atropine if symptomatic, pacing if persistent

2. Sinus Arrest:

• Mechanism: Failure of SA node to fire
• ECG: Absent P waves for variable periods
• Management: Atropine, temporary pacing

3. SA Exit Block:

• Mechanism: Blocked conduction from SA node
• ECG: Similar to sinus arrest but shorter pauses
• Management: Same as sinus arrest

4. AV Blocks:

First Degree AV Block:

• ECG: PR interval >200 ms (0.2 seconds)
• Significance: Usually benign
• Management: No treatment needed, monitor

Second Degree AV Block:

Mobitz Type I (Wenckebach):

• Mechanism: Progressive AV nodal delay
• ECG: Progressive PR prolongation, dropped QRS
• Management: Usually benign, monitor

Mobitz Type II:

• Mechanism: Block below AV node
• ECG: Constant PR interval, intermittent dropped QRS
• Management: Often requires pacing

Third Degree (Complete) AV Block:

• Mechanism: Complete dissociation between atria and ventricles
• ECG: No relationship between P waves and QRS complexes
• Management: Immediate pacing required

Tachyarrhythmias (Rate >100 bpm):

1. Sinus Tachycardia:

• Mechanism: Increased SA node automaticity
• Causes: Pain, anxiety, fever, heart failure, medications
• ECG: Regular rhythm, P waves present, normal morphology
• Management: Treat underlying cause

2. Atrial Fibrillation:

• Mechanism: Multiple reentrant circuits in atria
• ECG: No P waves, irregularly irregular rhythm, variable QRS
• Classification: Paroxysmal, persistent, permanent
• Management: Rate control, anticoagulation, cardioversion if indicated

3. Atrial Flutter:

• Mechanism: Single reentrant circuit in right atrium
• ECG: Sawtooth flutter waves, regular rhythm
• Management: Rate control, anticoagulation, cardioversion

4. Supraventricular Tachycardia (SVT):

• Mechanism: Reentry involving AV node or accessory pathway
• ECG: Regular narrow QRS tachycardia
• Management: Vagal maneuvers, adenosine, beta-blockers

5. Ventricular Tachycardia:

• Mechanism: Rapid ventricular rhythm
• ECG: Wide QRS complex (>120 ms), regular rhythm
• Classification: Monomorphic, polymorphic, sustained, non-sustained
• Management: Immediate cardioversion if unstable

6. Ventricular Fibrillation:

• Mechanism: Chaotic ventricular electrical activity
• ECG: Irregular, chaotic baseline
• Management: Immediate CPR and defibrillation

Classification by Mechanism:

Abnormal Impulse Formation:

Enhanced Automaticity:

• Mechanism: Increased rate of spontaneous depolarization
• Examples: Sinus tachycardia, atrial tachycardia
• Treatment: Beta-blockers, calcium channel blockers

Triggered Activity:

• Early afterdepolarizations: Long QT syndrome
• Delayed afterdepolarizations: Digitalis toxicity, catecholaminergic polymorphic VT
• Treatment: Antiarrhythmic drugs, pacing

Abnormal Impulse Conduction:

Reentry:

• Requirements: Two pathways, unidirectional block, sufficient conduction time
• Examples: AV nodal reentry tachycardia, atrial flutter, VT
• Treatment: Radiofrequency ablation, antiarrhythmics

Conduction Block:

• Mechanism: Interruption of normal conduction
• Examples: Bundle branch blocks, AV blocks
• Treatment: Pacing, treat underlying cause

Clinical Significance in Anesthesia:

Risk Factors:

• Pre-existing arrhythmias: History of arrhythmias
• Structural heart disease: Coronary disease, cardiomyopathy
• Electrolyte imbalances: K+, Mg++, Ca++
• Medications: Antiarrhythmics, digitalis toxicity
• Autonomic imbalance: Sympathetic stimulation

Intraoperative Triggers:

• Surgical stimulation: Sympathetic activation
• Hypoxia: Myocardial ischemia
• Hypotension: Reduced coronary perfusion
• Acidosis: Electrolyte shifts
• Temperature changes: Shivering, hypothermia

Anesthetic Management:

Prevention:

• Maintain normal electrolytes
• Avoid excessive sympathetic stimulation
• Gentle surgical technique
• Adequate analgesia
• Maintain hemodynamic stability

Monitoring:

• Continuous ECG monitoring
• ST-segment analysis
• Regular electrolyte checks
• Hemodynamic monitoring

Treatment Principles:

• Address underlying cause
• ABC (Airway, Breathing, Circulation)
• Specific antiarrhythmic therapy
• Pacing if indicated
• Defibrillation if needed

Emergency Management:

Stable Tachyarrhythmia:

• Assess hemodynamic stability
• Identify rhythm
• Treat underlying cause
• Consider antiarrhythmic drugs
• Cardioversion if refractory

Unstable Tachyarrhythmia:

• Immediate synchronized cardioversion
• Treat underlying cause
• Advanced life support

Bradyarrhythmia:

• Atropine 0.5-1 mg IV
• Temporary pacing if indicated
• Treat underlying cause
• Consider epinephrine

Antiarrhythmic Drugs:

Vaughan-Williams Classification:

Class I: Sodium channel blockers

• IA: Quinidine, procainamide
• IB: Lidocaine, mexiletine
• IC: Flecainide, propafenone

Class II: Beta-blockers

• Examples: Metoprolol, esmolol, labetalol

Class III: Potassium channel blockers

• Examples: Amiodarone, sotalol, ibutilide

Class IV: Calcium channel blockers

• Examples: Verapamil, diltiazem

Non-Antidote Agents:

• Adenosine: SVT, diagnosis of broad complex tachycardia
• Magnesium: Torsades de pointes, hypomagnesemia
• Digoxin-specific antibody: Digitalis toxicity

Prognosis and Outcomes:

Benign Arrhythmias:

• PVCs: Usually benign, no treatment needed
• Sinus arrhythmia: Normal variant
• First degree AV block: Usually benign

Serious Arrhythmias:

• Ventricular fibrillation: High mortality if not treated
• Sustained VT: Requires immediate treatment
• Complete heart block: Requires pacing

Factors Affecting Prognosis:

• Underlying heart disease
• Ejection fraction
• Duration of arrhythmia
• Response to treatment

Understanding arrhythmias and their management is essential for safe anesthetic care of cardiac patients and for managing perioperative complications.

Q15: Explain indications, procedure of ECG & Explain ABG technique, indications and complications

Answer:

ECG and ABG are essential monitoring tools in cardiac anesthesia, providing critical information about cardiac and respiratory status.

Electrocardiogram (ECG):

Indications:

Preoperative:

• Baseline assessment: All patients >40 years, cardiac risk factors
• Detection of: Previous MI, conduction abnormalities, arrhythmias
• Risk stratification: ASA classification, cardiac risk assessment
• Medication effects: Digitalis toxicity, antiarrhythmic therapy

Intraoperative:

• Continuous monitoring: All patients under anesthesia
• Ischemia detection: ST-segment changes
• Arrhythmia monitoring: Rate, rhythm, conduction
• Drug effects: Halothane, epinephrine, calcium

Postoperative:

• Complication detection: MI, arrhythmias
• Recovery monitoring: Return to baseline rhythm
• Medication effects: Residual drug effects

ECG Leads and Placement:

Standard Limb Leads:

• Lead I: Right arm (-) to Left arm (+)
• Lead II: Right arm (-) to Left leg (+)
• Lead III: Left arm (-) to Left leg (+)

Augmented Leads:

• aVR: Right arm (+), Left arm & leg (-)
• aVL: Left arm (+), Right arm & leg (-)
• aVF: Left leg (+), Right arm & Left arm (-)

Precordial (Chest) Leads:

• V1: 4th intercostal space, right sternal border
• V2: 4th intercostal space, left sternal border
• V3: Midway between V2 and V4
• V4: 5th intercostal space, midclavicular line
• V5: Horizontal level of V4, anterior axillary line
• V6: Horizontal level of V4, midaxillary line

Monitoring Leads for Anesthesia:

3-Lead System:

• Lead II: Most common, best for rhythm monitoring
• Lead I: Alternative rhythm monitoring
• Lead aVR: Can detect lateral ischemia

5-Lead System:

• Enhanced ST-segment monitoring
• Detection of: Anterior, inferior, lateral ischemia
• Better rhythm recognition

12-Lead System:

• Comprehensive assessment
• ST-segment analysis
• Detailed conduction assessment

ECG Interpretation:

Rate Calculation:

• 300 rule: 300 ÷ number of large squares between R waves
• 1500 rule: 1500 ÷ number of small squares between R waves

Rhythm Assessment:

• Regularity: R-R intervals
• P waves: Present, morphology, relationship to QRS
• PR interval: Normal 120-200 ms
• QRS duration: Normal <120 ms

ST-Segment Analysis:

• ST elevation: >1 mm above baseline
• ST depression: >0.5 mm below baseline
• Significance: Myocardial ischemia or injury

QT Interval:

• Normal: <440 ms
• Prolonged: Risk of torsades de pointes
• Shortened: Hypercalcemia

Arterial Blood Gas (ABG) Analysis:

Indications:

Preoperative:

• Baseline assessment: Severe COPD, diabetes, kidney disease
• Acid-base disorders: Metabolic or respiratory
• Oxygenation status: Severe lung disease

Intraoperative:

• Cardiac surgery: Comprehensive monitoring
• Major surgery: Extensive fluid shifts
• Respiratory complications: Hypoxemia, hypercapnia
• Acid-base monitoring: Complex cases

Postoperative:

• Ventilator management: Weaning decisions
• Acid-base disorders: Postoperative complications
• Oxygenation: Respiratory failure

ABG Technique:

Site Selection:

• Radial artery: First choice, collateral circulation
• Femoral artery: Alternative, larger vessel
• Brachial artery: Third choice
• Dorsalis pedis: Last resort

Equipment:

• Heparinized syringe: Prevents clotting
• 22-23 gauge needle: Minimizes trauma
• Ice bath: Preserves sample
• Bandage: Post-procedure care

Procedure:

1. Allen test: Assess collateral circulation (radial)
2. Aseptic preparation: Clean site with antiseptic
3. Palpate artery: Identify pulse
4. Insert needle: 45-degree angle to skin
5. Collect sample: 1-2 ml arterial blood
6. Apply pressure: 5-10 minutes to prevent hematoma
7. Label sample: Patient, time, site
8. Analyze immediately: Within 30 minutes

ABG Parameters:

Primary Measurements:

• pH: 7.35-7.45 (hydrogen ion concentration)
• PaO2: 80-100 mmHg (arterial oxygen tension)
• PaCO2: 35-45 mmHg (arterial carbon dioxide tension)

Calculated Values:

• HCO3-: 22-26 mEq/L (bicarbonate)
• Base excess: -2 to +2 mEq/L (acid-base status)
• SaO2: 95-100% (oxygen saturation)

Acid-Base Interpretation:

Primary Disorders:

Respiratory Acidosis:

• pH: <7.35
• PaCO2: >45 mmHg
• HCO3-: Normal initially, compensates with time

Respiratory Alkalosis:

• pH: >7.45
• PaCO2: <35 mmHg
• HCO3-: Normal initially, compensates with time

Metabolic Acidosis:

• pH: <7.35
• HCO3-: <22 mEq/L
• PaCO2: Compensates with hyperventilation

Metabolic Alkalosis:

• pH: >7.45
• HCO3-: >26 mEq/L
• PaCO2: Compensates with hypoventilation

Complications:

ECG Complications:

• Skin irritation: From electrode adhesive
• Electrical interference: From surgical equipment
• False alarms: Poor electrode contact
• Misinterpretation: Artifacts, lead placement errors

ABG Complications:

Local Complications:

• Hematoma: Most common, pressure needed
• Arterial spasm: Temporary reduction in flow
• Infection: Rare, sterile technique essential
• Nerve injury: Especially femoral approach

Systemic Complications:

• Ischemia: Inadequate collateral circulation
• Air embolism: Air bubbles in syringe
• Hemolysis: Excessive suction force

Quality Control:

ECG:

• Proper electrode placement
• Adequate skin preparation
• Regular calibration
• Artifact recognition

ABG:

• Proper heparinization
• Air-free collection
• Prompt analysis
• Temperature correction

Clinical Integration:

ECG Interpretation:

• Trend analysis: Serial comparisons
• Clinical correlation: Patient symptoms
• Medication effects: Antiarrhythmics, anesthetics
• Surgical factors: Cardiac manipulation

ABG Analysis:

• Acid-base status: Primary disorder identification
• Oxygenation: Adequacy of gas exchange
• Ventilation: CO2 elimination
• Compensation: Secondary responses

Both ECG and ABG analysis are integral components of comprehensive monitoring in cardiac anesthesia, providing essential information for safe perioperative management.

Q16: Mention 4 major cardiac conditions which effect anesthesia and their management along with drugs used

Answer:

Several major cardiac conditions significantly impact anesthetic management. Understanding their pathophysiology and treatment is crucial for optimal outcomes.

1. Congestive Heart Failure (CHF):

Pathophysiology:

• Reduced contractility: Impaired systolic function
• Compensatory mechanisms: Neurohormonal activation
• Ventricular remodeling: Dilatation, hypertrophy
• Fluid retention: RAAS activation, ADH release

Anesthetic Implications:

Preoperative:

• Functional assessment: NYHA classification, exercise tolerance
• Medication optimization: ACE inhibitors, beta-blockers, diuretics
• Volume status: Avoid dehydration and overload
• Risk stratification: High perioperative risk

Intraoperative:

• Reduced cardiac reserve: Hemodynamic instability risk
• Sensitivity to fluid shifts: Careful volume management
• Arrhythmia risk: Electrolyte disturbances
• Medication interactions: Digitalis toxicity risk

Management Strategies:

Monitoring:

• Comprehensive: Arterial line, CVP, PAC if indicated
• TEE: Real-time cardiac function assessment
• Urine output: Target >0.5 ml/kg/hr
• Weight monitoring: Daily weights

Pharmacological Management:

Inotropic Support:

• Dopamine: 2-20 mcg/kg/min
  • Low dose: Renal vasodilation
  • Medium dose: Cardiac stimulation
  • High dose: Vasoconstriction
• Dobutamine: 2-20 mcg/kg/min
  • Beta-1 agonist
  • Increased contractility and CO
• Milrinone: 0.125-0.75 mcg/kg/min
  • Phosphodiesterase inhibitor
  • Inotropic and vasodilator effects

Diuretics:

• Furosemide: 20-40 mg IV bolus
• Continuous infusion: 0.1-0.4 mg/kg/hr
• Torsemide: Longer duration
• Aldosterone antagonists: Spironolactone

Vasodilators:

• Nitroglycerin: 0.1-0.4 mg/min
• Nitroprusside: 0.1-5 mcg/kg/min
• Nesiritide: 0.01-0.03 mcg/kg/min

Anesthetic Considerations:

• Induction agents: Etomidate, ketamine (hemodynamic stability)
• Maintenance: Sevoflurane, isoflurane (minimal depression)
• Opioids: Fentanyl, morphine (reduce sympathetic response)

2. Coronary Artery Disease (CAD):

Pathophysiology:

• Atherosclerotic plaque: Coronary artery narrowing
• Myocardial ischemia: Supply-demand imbalance
• Fixed stenosis: Reduced coronary flow reserve
• Acute coronary syndromes: Plaque rupture, thrombosis

Anesthetic Implications:

Preoperative:

• Risk stratification: Angina pattern, previous MI
• Stress testing: Functional capacity assessment
• Medication management: Beta-blockers, antiplatelet agents
• Monitoring preparation: ST-segment analysis capability

Intraoperative:

• Ischemia risk: Hemodynamic instability
• Supply-demand balance: Maintain heart rate, BP
• Arrhythmia risk: Electrolyte imbalance, hypoxemia
• Medication interactions: Beta-blocker withdrawal

Management Strategies:

Monitoring:

• ST-segment analysis: Continuous 5-lead ECG
• Arterial line: Continuous BP monitoring
• TEE: Wall motion abnormality detection
• Troponin monitoring: Postoperative ischemia

Pharmacological Management:

Anti-Ischemic Therapy:

• Nitroglycerin: 0.1-0.4 mg/min
  • Venous and arterial dilation
  • Reduced preload and afterload
• Beta-blockers: Metoprolol 2.5-5 mg IV
  • Reduce heart rate and contractility
  • Improve myocardial oxygen supply-demand balance

Antiplatelet Agents:

• Aspirin: Continue unless contraindicated
• Clopidogrel: Continue if recent stenting
• Heparin: Bridge therapy if indicated

Anesthetic Considerations:

• Induction: Etomidate, ketamine (stable hemodynamics)
• Maintenance: Sevoflurane, isoflurane
• Avoid: Tachycardia, hypertension, hypoxemia
• Temperature: Maintain normothermia

3. Valvular Heart Disease:

Aortic Stenosis:

Pathophysiology:

• Fixed obstruction: Reduced valve area
• Pressure overload: Left ventricular hypertrophy
• Reduced coronary perfusion: Increased wall stress

Anesthetic Implications:

• Fixed cardiac output: Cannot increase with demand
• Hypotension risk: Reduced stroke volume
• Arrhythmia risk: Hypertrophied myocardium
• Sudden death risk: Severe AS

Management:

• Maintain sinus rhythm: AV synchrony critical
• Avoid tachycardia: Decreased filling time
• Maintain preload: Adequate ventricular filling
• Vasopressors: Phenylephrine, norepinephrine
• Avoid: Vasodilators, inotropes (increase demand)

Mitral Regurgitation:

Pathophysiology:

• Volume overload: Left atrial and ventricular dilatation
• Forward flow reduction: Regurgitant fraction
• Pulmonary congestion: Elevated left atrial pressure

Anesthetic Implications:

• Afterload reduction beneficial: Decreases regurgitation
• Volume overload risk: Exacerbated by IV fluids
• Arrhythmia risk: Atrial dilatation

Management:

• Afterload reduction: Nitroprusside, nitroglycerin
• Heart rate optimization: 80-100 bpm optimal
• Careful fluid management: Avoid volume overload
• Inotropes: Dobutamine for forward flow

Tricuspid Regurgitation:

Management:

• Maintain sinus rhythm: Atrial contribution important
• Afterload reduction: Beneficial
• Careful fluid management: Avoid volume overload

4. Hypertension:

Pathophysiology:

• Elevated systemic vascular resistance
• Cardiovascular remodeling
• End-organ damage: Heart, kidneys, brain
• Autonomic dysfunction: Baroreceptor sensitivity

Anesthetic Implications:

Preoperative:

• Poor control risk: Perioperative complications
• Medication interactions: Beta-blocker withdrawal
• Volume status: Often dehydrated

Intraoperative:

• Labile blood pressure: Difficult to control
• Medication interactions: Enhanced drug effects
• Autonomic imbalance: Labile responses

Management Strategies:

Monitoring:

• Arterial line: Continuous BP monitoring
• Frequent measurements: Even non-invasive
• ST-segment monitoring: Coronary perfusion

Pharmacological Management:

Acute Hypertension:

• Labetalol: 10-20 mg IV bolus
  • Combined alpha/beta blockade
  • Smooth BP control
• Hydralazine: 5-10 mg IV
  • Direct vasodilation
  • Reflex tachycardia
• Nicardipine: 5-15 mg/hr infusion
  • Calcium channel blocker
  • Controlled BP reduction

Chronic Management:

• Continue medications: Until morning of surgery
• ACE inhibitors: May hold if hypotensive
• Beta-blockers: Continue (reduce perioperative risk)
• Diuretics: Hold morning dose

Anesthetic Considerations:

• Induction: Etomidate, ketamine
• Maintenance: Sevoflurane, isoflurane
• Avoid: Sudden BP changes
• Monitor: End-organ perfusion

General Principles for All Conditions:

Preoperative Optimization:

• Medication review: Continue beneficial drugs
• Functional assessment: Exercise tolerance, symptoms
• Risk stratification: NYHA classification, risk scores
• Patient education: Procedure explanation

Intraoperative Management:

• Comprehensive monitoring: Based on condition severity
• Hemodynamic stability: Avoid rapid changes
• Maintain supply-demand balance: For ischemic hearts
• Temperature control: Normothermia important

Postoperative Care:

• Continued monitoring: Extended observation
• Medication resumption: Gradual return
• Complication surveillance: Ischemia, arrhythmias
• Early mobilization: Gradual activity progression

Drug Selection Guidelines:

Avoid in All Cardiac Conditions:

• Halothane: Myocardial depression, arrhythmias
• High-dose propofol: Cardiovascular collapse
• Succinylcholine: Hyperkalemia (some conditions)

Preferred Agents:

• Etomidate: Hemodynamic stability
• Ketamine: Sympathetic stimulation
• Sevoflurane: Minimal cardiovascular effects

This comprehensive approach to major cardiac conditions ensures optimal anesthetic management and patient outcomes in cardiac anesthesia practice.

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This completes Module 6: Anaesthetic Consideration in Cardiac Anaesthesia. The module covers essential cardiac physiology, pathology, and anesthetic management principles crucial for safe care of cardiac patients.