Patients with COPD and chronic hypercapnia entering the operating room bring with them a unique neurophysiologic signature: a brain adapted to elevated PaCO₂ and reduced baseline arousal. Their respiratory mechanics—characterized by increased airway resistance, long expiratory time constants, dynamic hyperinflation, elevated intrinsic PEEP, and ventilation–perfusion mismatch—combine with impaired oxygen delivery due to reduced hemoglobin and chronic hypoxemia. This creates a fragile balance that can be rapidly disrupted by sedative–hypnotics.
In contrast, stress cardiomyopathy represents a state of myocardial vulnerability to both sympathetic surges and excessive anesthetic-induced hypotension. These patients frequently display transient LV dysfunction, labile hemodynamics, and abnormal responses to catecholamines. Both cardiac and pulmonary circuits must therefore be supported by precise anesthetic titration.
This chapter centers on a high-stakes clinical scenario:
A 54-year-old female with COPD, chronic CO₂ retention, and previous stress cardiomyopathy undergoing laparoscopic anterior resection + hysterectomy under general anesthesia with sevoflurane, dexmedetomidine, atracurium infusion, and a recently performed ESP block. Ten minutes prior to incision, she received a seemingly innocuous 30 mg propofol bolus—yet this bolus produced near burst suppression on EEG.
COPD + Stress Cardiomyopathy + Laparoscopy =
Highest-risk triad for anesthetic overdose.
COPD lowers EEG “activation tone” due to chronic hypercapnia, making EEG easier to suppress.
Stress cardiomyopathy mandates tight hemodynamic control, with myocardial ischemia risk if anesthesia is either too deep or too light.
Laparoscopy elevates intrathoracic pressure, increasing right heart load and decreasing venous return, amplifying the hemodynamic consequences of anesthetic-induced vasodilation.
Traditional anesthetic signs (BP, HR, MAC) are insufficient in such patients because:
They cannot mount strong sympathetic responses.
Opioids and dexmedetomidine blunt physiologic reactions.
ESP block reduces nociceptive input, masking surgical stimulation.
CO₂ pneumoperitoneum introduces hemodynamic artifacts.
Hypothermia alters anesthetic pharmacokinetics and EEG patterns.
EEG-derived parameters such as BIS, SEF, MF, and SR therefore become essential:
BIS tells you “how deep.”
SEF tells you “how fast the cortex is firing.”
MF tells you “where the power is distributed.”
SR tells you “how suppressed the brain actually is.”
Propofol hypersensitivity due to chronic CO₂ retention.
Even mild CNS depressant exposure can push such patients into suppression-level anesthesia.
Magnesium and dexmedetomidine synergy.
These agents reduce cortical excitability; combined with volatile agents, suppression risk increases dramatically.
ESP block’s timing (only 30 minutes pre-incision).
Partial block maturation reduces nociceptive drive and lowers cortical arousal, mimicking deep anesthesia even when hypnotic levels are normal.
Hypothermia at 33–33.2°C.
Hypothermia decreases MAC, reduces propofol clearance, and increases EEG suppression.
Stress cardiomyopathy vulnerability.
Deep anesthesia → hypotension → myocardial ischemia.
Light anesthesia →...
