Anesthetic Management of Patients with Ischemic Heart Disease

Hemodynamic Goals of Induction and Maintenance of General Anesthesia

Core Pathophysiological Principle

Determinants of Myocardial O₂ Supply and Demand

• The left ventricle is perfused almost entirely during diastole
• Tachycardia disproportionately reduces diastolic time, simultaneously increasing demand and reducing supply - the most dangerous combination in IHD
• The right ventricle is perfused during both systole and diastole

HEMODYNAMIC GOALS

1. Heart Rate - THE MOST CRITICAL PARAMETER

• Tachycardia is the most common precipitant of perioperative ischemia; it increases demand and reduces supply simultaneously
• Disproportionate shortening of diastolic time at higher heart rates (diastolic time falls non-linearly with HR) directly limits coronary perfusion
• Bradycardia <45 bpm should also be avoided as it reduces cardiac output
• The most common hemodynamic abnormalities seen during ischemic episodes are hypertension and tachycardia - they are almost always the cause (not the result) of ischemia

• Adequate depth of anesthesia before laryngoscopy
• Opioid preloading (fentanyl 2-5 mcg/kg before intubation) to blunt laryngoscopy response
• Beta-blockers (esmolol 0.5-1 mg/kg IV) to treat intraoperative tachycardia
• Volatile agents (all have rate-lowering tendency at adequate MAC)
• Avoid anticholinergic tachycardia; if needed for bradycardia, use glycopyrrolate (less tachycardia than atropine)

2. Blood Pressure - Maintain in a Narrow Range

A. Hypertension

• Increases afterload → increases wall tension → increases O₂ demand
• Hypertension during laryngoscopy/intubation is one of the most dangerous moments
• Down-sloping/horizontal ST depression almost always accompanies severe hypertensive responses in IHD patients
• Management: adequate depth (volatile agent titration), iv fentanyl, β-blockers, nitroglycerin, nicardipine

B. Hypotension

• Reduces coronary perfusion pressure (Aortic DBP - LVEDP)
• Hypotension is a late and ominous manifestation of progressive ventricular dysfunction
• Higher diastolic pressures are preferable in patients with high-grade coronary occlusions
• The endocardium is most vulnerable to ischemia during hypotension (highest intramural pressures during systole)
• Management: vasopressors (phenylephrine preferred - pure α-agonist, does not increase HR; norepinephrine if cardiac output low); treat cause (hypovolemia, vasodilation from anesthetics, myocardial depression)

3. Preload (LVEDP / Filling Pressures)

• Excessive preload (fluid overload): Increases LVEDP → reduces coronary perfusion pressure (supply falls) AND increases ventricular wall tension (demand rises) - a double jeopardy
• Elevated LVEDP specifically reduces subendocardial perfusion
• Hypovolemia: Reduces preload → reduces cardiac output → hypotension → reduces coronary perfusion
• Optimal filling: guided by clinical assessment, arterial waveform variation, or TEE (LV chamber size)
• PAC-measured PCWP rises abruptly with ischemia (though PAC rarely used now)

4. Contractility

• Increased contractility = increased O₂ demand
• Excessive anesthetic-induced depression → low CO → hypotension → reduced perfusion
• Most volatile agents are mildly negatively inotropic - this is acceptable and even beneficial at moderate doses (reduce demand, reduce preload/afterload)
• Volatile agents also exert anesthetic preconditioning - activate ATP-sensitive K⁺ channels, reduce reperfusion injury, help "stunned" myocardium recover
• Avoid catecholamine surges (laryngoscopy, surgical stimulation) - they massively increase contractility and HR simultaneously

5. Systemic Vascular Resistance (Afterload)

• High SVR → increased wall tension → increased O₂ demand
• Low SVR → hypotension → reduced coronary perfusion pressure
• The goal is stable SVR within normal limits

6. Arterial Oxygen Content (CaO₂)

• Maintain adequate oxygenation and ventilation throughout
• Anemia → compensatory tachycardia → worsens supply-demand balance
• Most clinicians are reluctant to allow Hb <7 g/dL in CAD patients; transfusion decision is individualized
• Hypoventilation with resulting hypoxia and hypercarbia (both cause sympathetic stimulation and tachycardia) must be avoided

INDUCTION - SPECIFIC GOALS AND STRATEGIES

The Critical Period: Induction and Laryngoscopy

1. Anesthetic agents cause vasodilation/myocardial depression → risk of hypotension
2. Laryngoscopy causes intense sympathetic stimulus → tachycardia and hypertension

Induction Agents

• Propofol: Most commonly used; causes vasodilation and mild myocardial depression - titrate slowly to avoid sudden hypotension; use with opioid preloading
• Etomidate: Hemodynamically most stable (minimal CVS effects) - preferred when LV function is compromised; causes minimal change in HR, BP, and SVR; however does not blunt laryngoscopy response
• Ketamine: Generally avoided in IHD - sympathomimetic properties increase HR, BP, and O₂ demand; occasionally used when hemodynamics are very compromised
• Thiopental: Historically used, causes vasodilation and mild myocardial depression

Blunting Laryngoscopy Response

1. Opioid preloading - fentanyl 2-5 mcg/kg, remifentanil infusion
2. Lignocaine IV - 1.5 mg/kg given 90 seconds before intubation
3. Beta-blockers - esmolol 1-2 mg/kg bolus before laryngoscopy
4. Topical laryngeal analgesia - 4% lignocaine spray
5. Adequate depth - deep enough volatile anesthetic or propofol before laryngoscopy
6. Keep laryngoscopy brief - <15 seconds; use video laryngoscope

MAINTENANCE - SPECIFIC GOALS

Choice of Anesthetic Agents

• All are coronary vasodilators
• Reduce myocardial O₂ requirements
• Provide anesthetic preconditioning (cardioprotection via KATP channels)
• Reduce preload and afterload at moderate doses
• Caveat: Desflurane causes sympathetic stimulation during rapid increases in concentration → avoid rapid up-titration in IHD

• ACC/AHA Class IIa recommendation: either volatile or TIVA is reasonable (LOE: A)
• Propofol reduces preload and afterload but lacks preconditioning benefit

• High-dose opioid techniques provide excellent hemodynamic stability
• Fentanyl, sufentanil, remifentanil - blunt sympathetic responses, minimal direct cardiac depression
• Remifentanil infusion is particularly useful for moment-to-moment titration

• Vecuronium or rocuronium preferred (minimal cardiovascular effects)
• Avoid pancuronium (vagolytic - causes tachycardia)
• Avoid succinylcholine as primary agent if not needed urgently (fasciculations → transient increases in IOP and oxygen demand)

Maintaining Hemodynamic Stability During Surgery

• Increase depth of anesthesia
• Esmolol (short-acting β-blocker) or metoprolol
• Address pain/light anesthesia
• Ensure adequate analgesia

• Deepen anesthesia, increase volatile agent
• Nicardipine, labetalol, or GTN infusion
• Ensure adequate opioid analgesia

• Reduce anesthetic depth
• IV fluid bolus if hypovolemic
• Phenylephrine (if BP low, HR normal/high)
• Ephedrine (if BP low, HR low)
• Check ECG for new ischemia immediately

Temperature

• Maintain normothermia - hypothermia → shivering post-op → massive increase in O₂ demand; ACC/AHA Class IIb recommendation

MONITORING REQUIREMENTS

SUMMARY TABLE: Hemodynamic Goals in IHD

KEY EXAM POINTS TO REMEMBER

1. Tachycardia is the enemy - it simultaneously increases demand and reduces supply by shortening diastole
2. Coronary perfusion pressure = Aortic DBP - LVEDP - both sides of this equation matter
3. The myocardium cannot increase oxygen extraction (already near-maximal at rest) - supply must match demand
4. Volatile agents are cardioprotective via preconditioning (KATP channel activation) - this is a pharmacological advantage over TIVA
5. Hypotension is a late sign of ventricular dysfunction - by the time BP falls due to ischemia, significant myocardium is already compromised; the goal is to prevent this from happening
6. Induction and laryngoscopy are the highest-risk periods - use opioid preloading, adequate depth, and short laryngoscopy time
7. Etomidate is the hemodynamically most stable induction agent - preferred in compromised LV function
8. Pancuronium is contraindicated - vagolytic tachycardia
9. TEE > ECG for early ischemia detection (RWMA precede ST changes)
10. ACC/AHA: Either volatile or TIVA is acceptable (Class IIa, LOE A); prophylactic intraoperative nitroglycerin is not recommended (Class III: No Benefit)

Goldman's Cardiac Risk Index (CRI)

Short Note for MD Anaesthesia Exam

Introduction

The Nine Risk Factors and Their Point Values

Memory aid: "MI, S3, ECG, Age, Aortic stenosis, Poor status, Big surgery, Emergency" Point values (high to low): S3/JVP (11) > Recent MI (10) > PAC/non-sinus rhythm (7) = PVCs (7) > Age >70 (5) > Emergency op (4) > Aortic stenosis (3) = Big surgery (3) = Poor status (3)

Risk Classification and Cardiac Event Rates

• Class I and II = Low risk - proceed with surgery with standard precautions
• Class III = Intermediate risk - consider optimization and enhanced monitoring
• Class IV = High risk - surgery only if absolutely necessary; aggressive optimization; ICU care

Key Observations from the Original Study

1. Congestive cardiac failure (S3 gallop/raised JVP) carried the highest point value (11) - reflecting the importance of ventricular dysfunction as a risk determinant
2. Recent MI (<6 months) was the second highest risk factor (10 points). This gave rise to the classic teaching to defer elective surgery for 6 months following MI (now revised downward to 30-60 days with modern revascularization)
3. Arrhythmias - non-sinus rhythm and frequent PVCs were independent risk factors even without structural disease
4. Hypertension alone was NOT found to be an independent predictor of perioperative cardiac risk in this study (a surprising and controversial finding at the time)
5. Type of surgery mattered: major abdominal, thoracic, and aortic operations were higher risk than peripheral procedures

Limitations of the Original Goldman Index

1. Single-centre study - Massachusetts General Hospital; may not be generalizable
2. Small sample size (1,001 patients) with relatively few outcome events
3. Dated - does not include modern risk factors such as diabetes, renal insufficiency, or cerebrovascular disease
4. Does not account for functional capacity (METs) - a powerful predictor now incorporated in modern guidelines
5. Does not include type of anaesthesia or quality of intraoperative management
6. 6-month MI rule has been revised - with modern PCI, elective surgery may be considered at 30-60 days post-MI with appropriate precautions
7. Aortic and vascular surgery population was poorly represented - performs less well in vascular patients
8. No provision for echocardiographic or stress testing data

Subsequent Modifications and Evolution

Detsky Modified Cardiac Risk Index (1986)

• Modified Goldman's index to incorporate unstable angina (class III/IV), pulmonary oedema, and suspected critical aortic stenosis
• Applied as a pretest probability combined with a nomogram based on surgery type
• Was the preferred index in American College of Physicians guidelines

Revised Cardiac Risk Index - RCRI (Lee et al., 1999) - THE CURRENT STANDARD

• Score 0: ~0.4%
• Score 1: ~1%
• Score 2: ~2.5%
• Score ≥3: ~5-11%

ACS-NSQIP / MICA Calculator (2011, Gupta et al.)

• Uses 5 variables: type of surgery, dependent functional status, abnormal creatinine, ASA class, and age
• Better discrimination than RCRI, especially for vascular surgery
• Provides numerical probability (%) rather than class

Historical Significance and Exam Points

1. First multifactorial index - moved preoperative assessment from subjective impression to objective scoring
2. S3 gallop/JVP = highest-weighted single sign (11 points) - reflects overt CCF
3. Recent MI (within 6 months) = 10 points - led to "6-month rule" (now replaced)
4. Hypertension NOT a risk factor in Goldman's original study - controversial
5. Total = 53 points across 9 variables
6. Class IV (≥26 points) = 56% cardiac mortality
7. RCRI is the current preferred index - simpler (6 equal-weight variables), better validated in modern surgical populations
8. The Goldman index established the principle that preoperative optimization of CCF (the highest-weighted factor) reduces perioperative risk - a principle that remains valid today
9. The index is not designed for cardiac surgery patients - applies only to non-cardiac operations
10. Goldman's study also showed that elective surgery in the context of recent MI should be deferred whenever possible

Quick Comparison Table

Part 1: Common Problems Encountered During Anaesthesia for Geriatric Patients

Introduction

A. Cardiovascular Problems

Physiological Changes

• Decreased arterial elasticity (medial fibrosis) → increased afterload → left ventricular hypertrophy → diastolic dysfunction
• Elevated systolic blood pressure with widened pulse pressure (once pulse pressure ≥80 mmHg, associated with increased all-cause mortality)
• Resting systolic function is preserved even in octogenarians in the absence of disease - but diastolic filling is impaired
• Decreased adrenergic receptor sensitivity and decreased β-receptor responsiveness
• Decreased maximal heart rate (declines ~1 beat/min/year after age 50) - limits chronotropic response to stress
• Decreased baroreceptor reflex → poor compensation for hypotension
• Fibrosis of conduction system and loss of sinoatrial node cells → increased incidence of arrhythmias (AF, sick sinus syndrome, heart block)
• Ischemic preconditioning is diminished or absent from ~age 65 onwards

Common Pathology in Geriatric Population

• Atherosclerosis, coronary artery disease, essential hypertension
• Congestive heart failure (especially diastolic), aortic stenosis, atrial fibrillation

Anaesthetic Implications

• Haemodynamic instability during induction - very sensitive to preload reduction (diastolic dysfunction requires adequate filling)
• Hypotension with induction agents (reduced dose required; use etomidate if cardiac reserve poor)
• Blunted tachycardic response to hypotension - bradycardia may be the predominant response to hypovolaemia
• High prevalence of undiagnosed or underdiagnosed cardiac disease
• Systolic murmurs in elderly must raise suspicion of aortic stenosis
• Continue beta-blockers and statins perioperatively
• Invasive arterial monitoring for major procedures

B. Respiratory Problems

C. Renal Problems

Physiological Changes

• Decreased renal blood flow and renal plasma flow (~1% per year after age 40)
• Decreased glomerular filtration rate (GFR declines ~10 mL/min per decade from age 40)
• Decreased renal mass (25-30% reduction by age 80)
• Impaired tubular function → impaired sodium handling, impaired concentrating and diluting ability
• Serum creatinine may be normal despite reduced GFR because lean muscle mass (creatinine source) also decreases - creatinine is therefore an unreliable marker; use eGFR

Anaesthetic Implications

• Predisposed to both dehydration AND fluid overload (narrow therapeutic window for fluid management)
• Prolonged drug elimination (renally excreted drugs: morphine-6-glucuronide, pancuronium, neostigmine, digoxin)
• Avoid NSAIDs (nephrotoxic), aminoglycosides, high-contrast loads
• Careful fluid management: avoid under- and over-hydration
• Electrolyte imbalances (hyponatraemia, hyperkalaemia) more common

D. Central Nervous System (CNS) Problems

Physiological Changes

• Brain mass decreases (~10% by age 80); cerebral blood flow decreases
• Loss of neurons, reduction in neurotransmitters (dopamine, acetylcholine, serotonin)
• Decreased cerebrovascular autoregulation range
• Reduced MAC (minimum alveolar concentration) - declines ~6% per decade after age 40; a 80-year-old may require only 50-60% the MAC of a young adult

Key Anaesthetic Problems

1. Postoperative Delirium (POD)

• Incidence: 15-50% in elderly surgical patients; higher after orthopaedic and cardiac surgery
• Characterised by acute fluctuating confusion, disorientation, agitation or hypoactivity
• Risk factors: pre-existing cognitive impairment, anticholinergic drugs, meperidine, benzodiazepines, sleep deprivation, pain, immobility, urinary catheters
• AGS guidelines: Avoid meperidine, anticholinergics, and benzodiazepines; employ non-opioid analgesia where possible

2. Postoperative Cognitive Dysfunction (POCD) / Perioperative Neurocognitive Disorder (PND)

• Detectable in 10-15% of patients >60 years old at 3 months after major surgery
• Short-term memory most affected
• Multifactorial: drug effects, pain, hypothermia, metabolic disturbance, inflammatory response, emboli
• Animal studies suggest anaesthesia alone (without surgery) can impair learning for weeks
• Greater risk in inpatients vs outpatients; higher after cardiac and major orthopaedic procedures

3. Increased Sensitivity to CNS Drugs

• Lower dose requirements for propofol, etomidate, opioids, benzodiazepines, and barbiturates
• Particularly sensitive to centrally acting anticholinergics (scopolamine, atropine)
• Slower emergence and recovery from general anaesthesia

E. Thermoregulatory Problems

• Elderly patients are highly prone to hypothermia perioperatively
• Impaired vasoconstriction response to cold
• Decreased heat production (lower basal metabolic rate)
• Anaesthetic agents (inhalational, propofol, alfentanil) lower the threshold for vasoconstriction/shivering by ~4°C; ageing adds an additional ~1°C impairment
• Consequences of hypothermia: myocardial ischaemia, coagulopathy, wound infection, prolonged drug metabolism, delayed emergence
• Shivering (if it occurs) places severe metabolic stress on borderline cardiac/pulmonary reserve
• Management: active warming devices (forced-air blankets), warm IV fluids, temperature monitoring throughout

F. Pharmacological Problems

Pharmacokinetic Changes

• Decreased total body water (↓ lean mass) → increased plasma concentration of water-soluble drugs
• Increased body fat → increased volume of distribution and prolonged effect of lipid-soluble drugs
• Reduced plasma albumin → more free (active) drug for albumin-bound drugs (barbiturates, benzodiazepines, opioids)
• α1-acid glycoprotein may be elevated (acute-phase reactant) → reduced free fraction of basic drugs (local anaesthetics)
• Reduced liver mass and hepatic blood flow → prolonged hepatic drug metabolism (Phase I reactions more affected than Phase II)
• Reduced renal clearance (as above) → prolonged elimination

Pharmacodynamic Changes

• Reduced MAC for volatile agents
• Increased brain sensitivity to CNS depressants
• Decreased β-adrenergic responsiveness → reduced response to beta agonists and antagonists
• Neuromuscular junction changes: morphological changes occur (NMJ lengthens, synaptic folds degenerate, Schwann cell invasion) but overall margin of safety is maintained; some NMBAs (vecuronium) have prolonged effect due to pharmacokinetic rather than pharmacodynamic changes; no evidence of succinylcholine-induced hyperkalaemia from NMJ changes alone

Practical Implications

• Reduce induction doses of propofol by 30-50%
• Titrate opioids carefully; start low
• Use short-acting agents where possible (mivacurium, atracurium, rocuronium with sugammadex reversal)
• Avoid pancuronium (tachycardia, prolonged block)
• Regional anaesthesia is often preferable to reduce CNS drug burden

G. Musculoskeletal and Airway Problems

• Sarcopenia - progressive loss of lean body mass and muscle strength
• Osteoporosis - risk of fracture from positioning; careful padding essential
• Arthritis - may limit neck extension, restrict mouth opening → difficult airway anticipated
• Degenerative cervical spine disease - limits neck extension and atlantoaxial mobility → risk of cord injury during intubation
• Skin atrophy - fragile skin susceptible to injury from adhesive tape, electrocautery pads, ECG electrodes
• Fragile veins - difficult IV access; easily ruptured by cannulae

H. Other Common Problems

• Multiple comorbidities and polypharmacy (drug interactions, withdrawal effects)
• Malnutrition and hypoalbuminaemia - impairs wound healing, alters drug binding
• Frailty (assessed by Fried criteria: shrinkage, weakness, exhaustion, low physical activity, slowness; 4-5 = frail) - independent predictor of poor surgical outcome
• Pre-existing cognitive impairment/dementia - impacts consent, postoperative recovery
• Impaired hepatic function → reduced drug metabolism, reduced coagulation factor synthesis
• Aspiration risk - impaired swallowing and laryngeal reflexes, reduced lower oesophageal tone, gastroparesis in diabetics
• Ethical issues - living wills, healthcare proxies, end-of-life discussions; one-third of elderly Medicare patients undergo surgery in their last year of life

Part 2: Pathological Changes in the Respiratory System in Old Age and Implications for Anaesthesia

Overview

A. Structural Changes in the Lung Parenchyma

1. Loss of Elastin (Decreased Lung Tissue Stiffness / Increased Lung Compliance)

• With ageing, elastin fibres are progressively lost from lung parenchyma. Unlike other tissues in the body, this elastin is not replaced by collagen - so the lung actually becomes easier to inflate (increased pulmonary compliance)
• This is fundamentally different from emphysema, where there is actual alveolar wall destruction, but the functional consequences are similar

2. Alveolar Changes

• Decreased alveolar surface area (alveolar enlargement, reduced alveolar wall count) - not destruction but reduction in total surface available for gas exchange
• Reduces diffusing capacity (DLCO declines with age)
• Contributes to an age-related decline in resting PaO₂

Anaesthetic Implication

• Reduced reserve for gas exchange - poorly tolerated periods of apnoea, atelectasis, or hypoventilation
• Even brief periods of desaturation during induction can be dangerous

B. Airway Changes - The Closing Capacity Problem

The Central Mechanism: Loss of Small Airway Tethering

• Small airways (<2 mm diameter) have no cartilaginous support; they remain open because of the outward tethering pull exerted by surrounding elastic lung tissue
• As lung elastin is lost, this tethering pull diminishes
• Small airways tend to close at a higher lung volume than before - this is reflected as an increase in Closing Capacity (CC)

Critical Relationship: CC vs FRC

Anaesthetic Implication - THE MOST IMPORTANT RESPIRATORY CHANGE

• Induction of general anaesthesia further reduces FRC by 15-20% (supine position, loss of respiratory muscle tone, abdominal content pressure)
• In elderly patients where CC already exceeds FRC, induction causes extensive small airway closure → atelectasis, intrapulmonary shunt, hypoxaemia
• This is why elderly patients desaturate rapidly during induction and why PEEP is important during mechanical ventilation
• Pre-oxygenation before induction is absolutely mandatory and should be thorough (3-5 minutes of 100% O₂)

C. Lung Volume Changes with Ageing

D. Chest Wall and Respiratory Mechanics

1. Increased Chest Wall Stiffness / Barrel-Shaped Chest

• Calcification of costal cartilages and increased rib stiffness → reduced chest wall compliance
• The thorax becomes more barrel-shaped over time (kyphosis, loss of disc height increases AP diameter)
• Barrel-shaped thorax → flattening of the diaphragm → mechanical disadvantage: less diaphragmatic curvature reduces its ability to generate negative intrapleural pressure

2. Respiratory Muscle Weakness

• General sarcopenia affects respiratory muscles including the diaphragm and intercostals
• Increased work of breathing (stiff chest wall + weakened muscles)
• Decreased maximal breathing capacity
• Elderly patients are prone to respiratory fatigue when minute ventilation must be increased (sepsis, pain, airway obstruction, postoperative state)

Anaesthetic Implication

• Residual neuromuscular blockade is extremely dangerous in elderly patients - even small amounts of residual paralysis can precipitate respiratory failure
• Use objective neuromuscular monitoring (train-of-four with TOF ratio >0.9 before extubation)
• Weaning from ventilation may be prolonged
• Postoperative respiratory failure risk is high especially after thoracic and upper abdominal surgery
• Epidural analgesia can help by enabling deep breathing without pain

E. Ventilation-Perfusion (V/Q) Mismatch and Hypoxaemia

• Loss of elastic tethering makes ventilation less uniform - poorly ventilated regions continue to receive blood flow → V/Q mismatch and intrapulmonary shunt
• Reduced alveolar surface area
• Resting PaO₂ declines with age:
  • Formula: PaO₂ = 100 - (age/3) (approximate, in mmHg, breathing room air)
  • Or: PaO₂ (mmHg) ≈ 109 - 0.43 × age
  • A healthy 70-year-old may normally have PaO₂ of ~76-80 mmHg

Anaesthetic Implication

• Establish baseline ABG values preoperatively in elderly patients with significant respiratory disease
• Do not be reassured by a "normal for age" PaO₂ - it represents diminished reserve
• Supplemental oxygen in recovery is mandatory
• SpO₂ targets should be set conservatively

F. Ventilatory Control - Blunted Central Responses

Decreased Chemoreceptor Sensitivity

• ~50% decrease in the ventilatory response to hypercapnia with ageing
• Even greater decrease in ventilatory response to hypoxia - especially at night (nocturnal hypoxic episodes common)
• Generalized loss of muscle tone affects the hypopharyngeal and genioglossal muscles → predisposed to upper airway obstruction and obstructive sleep apnoea
• ~75% of people over 65 years may have some form of sleep-disordered breathing

Anaesthetic Implications

• Cannot rely on the normal hypercapnic or hypoxic drive to trigger spontaneous ventilation
• Respiratory depression from opioids, sedatives, and residual anaesthetics is poorly tolerated
• High risk of postoperative apnoea and hypoxia, especially in the first night postoperatively
• Sleep-disordered breathing increases risk of postoperative desaturation enormously
• CPAP may be needed postoperatively in at-risk patients
• Opioid-sparing techniques (NSAIDs cautiously, regional anaesthesia, paracetamol, dexmedetomidine) help

G. Impaired Cough and Aspiration Risk

• Decreased cough reflex - reduced velocity, less effective airway clearance
• Impaired swallowing (reduced coordination of pharyngeal muscles, laryngeal elevation)
• Aspiration is a significant cause of community-acquired and postoperative pneumonia in the elderly
• Reduced mucociliary clearance

Anaesthetic Implications

• Aspiration precautions for all elderly patients (treat as potentially at risk)
• Avoid excessive sedation that further impairs airway protective reflexes
• Consider RSI for any patient with reduced conscious level or known dysphagia
• Careful extubation only when fully awake with intact reflexes
• Postoperative physiotherapy and incentive spirometry

Summary Table: Respiratory Changes and Their Anaesthetic Implications