8.2 Cardiovascular & Pulmonary Pathophysiologies

8.2 Cardiovascular & Pulmonary Pathophysiologies

Cardiovascular and respiratory failure represent the leading causes of acute perioperative morbidity and mortality. Anesthesia technologists must possess a thorough technical grasp of coronary perfusion mechanics, electrophysiological dysrhythmias, obstructive and restrictive lung diseases, embolic phenomena, and airborne pathogen engineering controls.

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Ischemic Heart Disease, Myocardial Infarction & Coronary Hemodynamics

Ischemic heart disease (IHD) arises when myocardial oxygen demand exceeds coronary arterial oxygen delivery. Myocardial oxygen consumption (MVO2) is determined by four principal factors: heart rate (the single greatest determinant of MVO2), myocardial contractility, afterload (systolic wall stress), and preload (end-diastolic wall stress).

Coronary Perfusion Pressure (CPP) & Diastolic Perfusion

The physiological driving pressure for myocardial blood flow is defined mathematically as:

CPP = Aortic Diastolic Blood Pressure (Aortic DBP) - Left Ventricular End-Diastolic Pressure (LVEDP)

In the right ventricle, muscle mass is thin and intramyocardial pressures are low; right ventricular coronary flow occurs during both systole and diastole. However, in the thick-walled left ventricle, systolic contraction generates intramyocardial pressures that compress subendocardial capillaries, virtually halting blood flow. Consequently, left ventricular subendocardial perfusion occurs almost exclusively during ventricular diastole.

Three clinical variables dramatically threaten left ventricular CPP:

1. Tachycardia: At normal resting heart rates (60 to 70 bpm), diastole comprises approximately 60% to 65% of the cardiac cycle. As heart rate climbs above 100 bpm, diastole is shortened disproportionately (falling below 35% of the cycle). Tachycardia simultaneously decreases coronary perfusion time and escalates MVO2, precipitating severe subendocardial ischemia.
2. Systemic Hypotension (Decreased Aortic DBP): A drop in diastolic pressure directly decreases the upstream perfusion head.
3. Elevated LVEDP: Fluid overload, acute left ventricular failure, or myocardial ischemia stiffens the ventricle, raising LVEDP and opposing the inward driving pressure.

STEMI vs NSTEMI & Cardiac Biomarkers

Acute coronary syndromes (ACS) result from atherosclerotic plaque rupture and overlying thrombus formation:

• ST-Elevation Myocardial Infarction (STEMI): Reflects acute, complete, transmural coronary artery occlusion. The 12-lead ECG demonstrates new ST-segment elevation at the J-point in at least two contiguous leads (≥ 1 mm in limb leads, ≥ 1.5 to 2 mm in precordial leads) or a new left bundle branch block (LBBB). Requires emergent reperfusion (percutaneous coronary intervention [PCI] within 90 minutes).
• Non-ST-Elevation Myocardial Infarction (NSTEMI): Represents severe subendocardial ischemia and necrosis caused by partial occlusion or transient thromboembolism. The ECG shows ST-segment depressions, symmetrical T-wave inversions, or non-specific changes, accompanied by elevated cardiac biomarkers.
• Cardiac Biomarkers:
  • Cardiac Troponin I (cTnI) and Troponin T (cTnT): Highly sensitive and specific structural proteins of the cardiac contractile apparatus. Following myocardial necrosis, troponins begin rising in peripheral blood within 3 to 4 hours, peak at 18 to 24 hours, and remain elevated for about 1 to 2 weeks.
  • Creatine Kinase-MB (CK-MB): Rises within 4 to 6 hours, peaks at 24 hours, and normalizes within 48 to 72 hours; useful for detecting early re-infarction.

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Perioperative Cardiac Dysrhythmias & Conduction Disorders

Anesthesia technologists frequently assist in preparing defibrillators, pacing equipment, and antiarrhythmic infusions.

Atrial Fibrillation & Supraventricular Tachycardias

Atrial Fibrillation (AF) is characterized by disorganized, chaotic atrial depolarizations at rates of 350 to 600 bpm with an irregular ventricular response. Under general anesthesia, rapid ventricular response (RVR, heart rate > 120 bpm) impairs ventricular filling:

• Loss of Atrial Kick: In healthy hearts, coordinated atrial systole contributes 20% to 30% of left ventricular end-diastolic volume and stroke volume. In patients with left ventricular hypertrophy, aortic stenosis, or diastolic dysfunction, the loss of atrial kick causes a severe drop in cardiac output and precipitous systemic hypotension.
• Management: Pharmacologic rate control using IV beta-blockers (esmolol bolus 0.5 mg/kg or metoprolol 2.5 to 5 mg) or non-dihydropyridine calcium channel blockers (diltiazem 0.25 mg/kg IV). In the presence of acute hemodynamic instability, synchronized electrical cardioversion is performed immediately (AHA guidance for atrial fibrillation is an initial biphasic energy of about 120 to 200 J), synchronized to the R wave to avoid triggering ventricular fibrillation.

Ventricular Tachycardia (VT) and Ventricular Fibrillation (VF)

• Ventricular Tachycardia (VT): Originates distal to the bundle of His, characterized by wide QRS complexes (>120 ms) at rates > 100 bpm. Monomorphic VT has identical QRS morphology, whereas polymorphic VT (e.g., Torsades de pointes associated with prolonged QTc intervals) features twisting QRS axes. Unstable VT with a pulse is treated with synchronized cardioversion (100 J biphasic).
• Pulseless VT and Ventricular Fibrillation (VF): Disorganized, chaotic ventricular quivering producing zero cardiac output. Demands immediate chest compressions, unsynchronized high-energy electrical defibrillation (120 to 200 J biphasic), intravenous epinephrine (1 mg IV q3-5 min), and amiodarone (300 mg IV first bolus, 150 mg second bolus). Torsades de pointes specifically requires magnesium sulfate (1 to 2 g IV).

Atrioventricular (AV) Blocks

Conduction blocks across the AV node or His-Purkinje system are classified into three degrees:

In Third-Degree Complete Heart Block, AV dissociation prevents atrial impulses from reaching the ventricles. Atropine is typically ineffective for infranodal complete block. The anesthesia technologist must immediately obtain and apply external defibrillator pads to initiate transcutaneous pacing (TCP) (set demand rate at 60 to 80 bpm; increase current in milliamps [mA] until consistent electrical capture—wide QRS followed by broad T wave—and a matching mechanical arterial pulse are verified). The provider may also initiate an infusion of isoproterenol, dopamine, or epinephrine while preparing for transvenous pacing (TVP) wire insertion.

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Congestive Heart Failure, Hypertension & Peripheral Vascular Disease

Heart Failure: HFrEF vs HFpEF

Congestive heart failure (CHF) is categorized by left ventricular ejection fraction (LVEF):

• Heart Failure with Reduced Ejection Fraction (HFrEF / Systolic Failure): LVEF is < 40%. Pathophysiology involves eccentric ventricular remodeling, chamber dilation, and impaired systolic contractility. Management aims to reduce afterload, maintain inotropy, and optimize preload without inducing pulmonary congestion.
• Heart Failure with Preserved Ejection Fraction (HFpEF / Diastolic Failure): LVEF is ≥ 50%. Pathophysiology involves concentric hypertrophy, marked ventricular stiffness, and impaired diastolic relaxation. Because the ventricular cavity is small and non-compliant, filling pressures are high. These patients are exceptionally dependent on atrial kick (sinus rhythm) and require adequate diastolic filling time; tachycardia or loss of sinus rhythm leads to acute pulmonary edema and cardiogenic shock.

Peripheral Vascular Disease (PVD)

Peripheral arterial disease is atherosclerotic narrowing of the aorta and limb arteries. It commonly presents with claudication, and an ankle-brachial index below 0.90 confirms the diagnosis. Its main anesthetic importance is that it signals widespread atherosclerosis, so these patients often have coronary artery disease, carotid disease, hypertension, diabetes, and renal impairment.

• Monitoring choices: Avoid blood pressure cuffs and arterial lines on limbs with severe disease, bypass grafts, or dialysis access; compare pressures in both arms, because subclavian stenosis can make one arm read falsely low.
• Positioning: Poorly perfused skin and nerves are vulnerable, so padding and pressure-point checks matter.
• Vascular surgery support: Expect heparin before arterial clamping with ACT monitoring (a common target range is about 200 to 250 seconds), invasive blood pressure monitoring, blood salvage for aortic cases, and hemodynamic swings at clamping and unclamping.

Acute Pulmonary Edema

When left ventricular end-diastolic pressure and left atrial pressure elevate acutely, pulmonary capillary wedge pressure (PCWP) exceeds plasma oncotic pressure (>18 to 20 mmHg). Transudation of fluid floods pulmonary interstitial and alveolar spaces, manifesting as severe hypoxemia, tachypnea, diffuse rales, and pink frothy secretions from the endotracheal tube. Treatment requires positive end-expiratory pressure (PEEP), diuresis (furosemide), afterload reduction (nitroglycerin), and inotropic support.

Hypertension & Hypertensive Crisis

According to ACC/AHA guidelines, systemic hypertension is defined as Stage 1 (SBP 130–139 or DBP 80–89 mmHg) and Stage 2 (SBP ≥ 140 or DBP ≥ 90 mmHg):

• Hypertensive Urgency vs Emergency: A hypertensive crisis occurs when SBP exceeds 180 mmHg or DBP exceeds 120 mmHg. It is classified as a Hypertensive Emergency only when there is evidence of acute, progressive target organ damage (e.g., encephalopathy, intracranial hemorrhage, acute coronary syndrome, aortic dissection, acute pulmonary edema, acute renal failure). Urgent reduction of BP with IV titratable agents (nicardipine, clevidipine, labetalol, nitroprusside) is required.
• Perioperative Hemodynamic Lability: Patients with chronic untreated hypertension exhibit chronically vasoconstricted vascular beds and contracted circulating plasma volumes. Upon anesthetic induction, peripheral vasodilation causes profound hypotension; subsequent laryngoscopy or surgical incisions elicit exaggerated hypertensive surges.

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Obstructive Airway Diseases: Asthma & Chronic Obstructive Pulmonary Disease

Asthma is characterized by chronic airway inflammation, bronchial hyperreactivity, and reversible airway obstruction. COPD encompasses chronic bronchitis and emphysema, featuring irreversible airflow limitation and loss of elastic recoil.

Bronchospasm Mechanics, Dynamic Hyperinflation & Intrinsic PEEP

Acute intraoperative bronchospasm involves smooth muscle contraction, mucosal edema, and secretions that increase airflow resistance during exhalation. Because exhalation is passive and resistance is high, the patient cannot fully exhale the tidal volume before the ventilator initiates the next breath:

1. Air Trapping and Dynamic Hyperinflation: Trapped air progressively accumulates in the alveoli at end-expiration.
2. Intrinsic PEEP (Auto-PEEP): The trapped gas generates positive alveolar pressure at end-expiration, which increases intrathoracic pressure, impedes venous return to the right atrium, compresses the vena cava, and precipitates severe systemic hypotension and barotrauma (pneumothorax).
3. Airway Pressure Profile: Bronchospasm causes a marked increase in Peak Inspiratory Pressure (PIP) while the Plateau Pressure (Pplat) remains normal, producing an abnormally wide PIP-Pplat gradient (>10 to 15 cmH2O). (In contrast, reduced lung compliance, such as tension pneumothorax or pulmonary edema, elevates both PIP and Pplat together).

VENTILATOR PRESSURE PROFILES IN OBSTRUCTIVE VS RESTRICTIVE PATHOLOGY:

NORMAL LUNG:          PIP ~20 cmH2O,  Pplat ~15 cmH2O  (Gradient ~5 cmH2O)
BRONCHOSPASM (Airway): PIP ~45 cmH2O,  Pplat ~16 cmH2O  (Gradient >25 cmH2O: Resistance)
PNEUMOTHORAX (Parenchyma): PIP ~45 cmH2O, Pplat ~40 cmH2O (Gradient ~5 cmH2O: Low Compliance)

Perioperative Ventilation & Pharmacology

• Mechanical Ventilator Adjustments: The technologist and provider must extend the expiratory time to allow complete exhalation. This is accomplished by lowering the respiratory rate (e.g., 6 to 8 breaths/min) and setting an Inspiratory-to-Expiratory (I:E) ratio of 1:3, 1:4, or 1:5. Tidal volume is maintained at 6 to 8 mL/kg of ideal body weight. The clinician permits permissive hypercapnia (allowing PaCO2 to rise to 50 to 65 mmHg provided pH remains > 7.20).
• Pharmacotherapy: Deepen volatile anesthesia (sevoflurane and isoflurane are potent bronchodilators); administer inhaled albuterol (6 to 10 puffs via an in-line MDI circuit adapter or nebulizer); administer intravenous epinephrine (10 to 50 mcg IV) for refractory bronchospasm.
• Drugs to Avoid: Histamine-releasing agents that trigger reflex bronchospasm, including morphine, codeine, and the benzylisoquinolinium muscle relaxant atracurium. Non-selective beta-adrenergic antagonists are also avoided.

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Pulmonary Embolism (PE)

Pulmonary embolism is the mechanical occlusion of pulmonary arterial vessels by a detached thrombus (originating from deep vein thrombosis [DVT]), fat, amniotic fluid, or air.

Virchow's Triad & Hemodynamic Collapse

Risk factors follow Virchow's Triad:

1. Venous Stasis (prolonged immobility, surgical positioning, venous pooling).
2. Endothelial Vascular Injury (surgical trauma, orthopedic reaming, central venous cannulation).
3. Hypercoagulability (malignancy, oral contraceptives, inherited thrombophilias).

When a massive clot occludes a primary pulmonary arterial trunk, unperfused lung units are ventilated, creating massive alveolar dead space (VD/VT). Simultaneously, pulmonary vascular resistance (PVR) escalates acutely, producing acute cor pulmonale: the thin-walled right ventricle dilates, tricuspid regurgitation develops, the interventricular septum shifts leftward (flattening the left ventricle), left ventricular stroke volume collapses, and cardiogenic shock ensues.

Intraoperative Recognition Under General Anesthesia

Under general anesthesia, the classic awake symptoms of chest pain and dyspnea are masked. Recognition relies on distinct physiological monitors:

• Sudden, Precipitous Drop in End-Tidal CO2 (PetCO2): Because pulmonary capillary blood flow to ventilated alveoli is abruptly blocked, carbon dioxide cannot be delivered to exhaled gas. PetCO2 falls dramatically (e.g., from 40 mmHg down to 10 to 15 mmHg) despite constant mechanical ventilation.
• Refractory Hypoxemia (SpO2 drop): Arises from severe ventilation-perfusion (V/Q) mismatch and right-to-left intrapulmonary shunt.
• Acute Cardiovascular Collapse: Tachycardia, severe systemic hypotension, elevated Central Venous Pressure (CVP), new right bundle branch block (RBBB) or S1Q3T3 on ECG, and progression to Pulseless Electrical Activity (PEA) cardiac arrest.

Immediate management consists of 100% inspired oxygen, discontinuing nitrous oxide (which expands air emboli and worsens PVR), fluid resuscitation, inotropic support (norepinephrine, epinephrine), unfractionated heparin, and emergent transesophageal echocardiography (TEE) to confirm McConnell's sign (right ventricular free wall akinesis with sparing of the apex) followed by systemic thrombolysis or surgical embolectomy.

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Tuberculosis (TB): Infection Control & Facility Engineering

Mycobacterium tuberculosis is an acid-fast bacillus transmitted via aerosolized droplet nuclei (1 to 5 micrometers in diameter) generated when an infected patient coughs, speaks, or undergoes airway manipulation. These microscopic particles remain suspended in ambient air currents for hours.

Airborne Infection Isolation Room (AIIR) & OR Engineering

Operating rooms are kept at positive pressure to protect the sterile field, which works against containing airborne organisms. CDC guidance therefore calls for delaying elective surgery until the patient is no longer infectious (for example, after effective therapy and consecutive negative sputum smears). For urgent procedures, CDC recommends these measures rather than switching the operating room itself to negative pressure:

1. Room Selection and Traffic: Use an operating room with an anteroom if one is available, keep the doors closed, minimize traffic, and schedule the case when fewer staff and patients are present (often at the end of the day).
2. Airborne Infection Isolation Rooms (AIIRs) for Recovery and Induction When Possible: AIIRs are held at negative pressure relative to the corridor (at least about 0.01 inch of water, or 2.5 Pa) and provide at least 12 air changes per hour in new or renovated construction (6 in older rooms). Intubation and extubation can be performed there, and the patient recovers there rather than in an open PACU.
3. Exhaust Filtration: AIIR air is exhausted outdoors away from intakes or passed through High-Efficiency Particulate Air (HEPA) filters, which capture 99.97% of particles 0.3 micrometers in size.

Personal Protective Equipment & Anesthesia Circuit Isolation

• Respiratory Protection: Surgical masks do not protect the wearer from droplet nuclei. All personnel in the room must wear a fit-tested N95 or higher-level respirator, such as a Powered Air-Purifying Respirator (PAPR).
• Breathing Circuit Protection: To prevent Mycobacterium tuberculosis from contaminating the internal components, absorber, and transducers of the anesthesia workstation, the technologist must place a certified hydrophobic HEPA bacterial/viral breathing circuit filter directly between the patient's endotracheal tube and the circuit Y-piece, or on the expiratory limb prior to entering the machine. If contamination is suspected, the anesthesia workstation must undergo specialized technical decontamination.