Anesthesia Considerations (CV)

Normal Cardiovascular Physiology

  • Pathway of Blood Flow:

    • Pulmonary Vein → Left Atrium → Left Ventricle → Aorta → Peripheral Arteries → Arterioles → Capillaries → Venules → Veins → Inferior/Superior Vena Cava → Right Atrium → Right Ventricle → Pulmonary Artery → Lungs → Back to Pulmonary Vein

Anatomical Awareness

  • Myocardial Oxygen Supply: The myocardium receives oxygen from hemoglobin (Hgb).

  • When oxygen demand increases, the heart compensates by increasing blood flow through dilation of the coronary arteries and an increase in heart rate (HR).

  • Cardiac Output (CO):

    • Definition: The amount of blood ejected from the left ventricle in one minute.

    • CO = SV x HR

    • Measured in liters per minute (L/min).

  • Stroke Volume (SV): The amount of blood ejected from the left ventricle with each heartbeat.

    • Preload: The tension or pressure applied by blood volume on the heart wall during blood flow from the left atrium to the left ventricle, or during the atrial kick.

    • Afterload: The tension or pressure from blood volume on the heart wall that is required for ejecting the stroke volume.

  • Adequate Blood Flow: If there’s no compromise in heart contractility and HR, CO is usually sufficient, ensuring reliable venous return and adequate blood flow throughout the body and back to the heart.

Surgical Considerations

  • Surgical Stimulation Response: Surgical stimulation triggers a cardiovascular response that necessitates careful management.

  • Blood Pressure Management:

    • Optimizing control of blood pressure within the normotensive range prior to the procedure enhances stability during the perioperative and postoperative course and reduces the risk of cardiovascular morbidity.

    • Goal: Maintain blood pressure within 20% of the normal range during induction and maintenance of general anesthesia.

  • Airway Manipulation:

    • Laryngoscopy and tracheal intubation stimuli can trigger hypertension (HTN).

    • Recommended to reduce airway manipulation to ≤ 15 seconds.

  • Pre-Induction Medications:

    • Administer β Blockers, Lidocaine, and Fentanyl prior to induction.

    • Provide deeper sedation using inhaled anesthetics.

  • Anesthesia-Related Hypotension (HypoTN):

    • Strategies include:

      • Using a fluid bolus preoperatively before neuraxial/general anesthesia or during induction/maintenance. NOT FOR HTN

      • Gradual titration of general anesthesia induction agents as prophylaxis against HypoTN. NOT FOR HTN

      • Administering vasopressors if previous interventions do not produce an adequate response.

  • Post-Operative Hypertension:

    • HTN may occur upon termination of anesthesia and due to pain.

    • Immediate administration of antihypertensive agents and pain management is necessary after surgery.

Hypertension & Cardiovascular Compromise

Hypertension Facts

  • Prevalence: Approximately 1 out of 3 individuals in the U.S. are affected by hypertension, many of whom are asymptomatic but may already have atherosclerosis or organ damage prior to diagnosis or initiation of antihypertensive therapies.

  • Long-term Effects of Chronic Hypertension:

    • Chronic, uncontrolled hypertension leads to damage of target organs, including: Heart, Brain, and Kidneys

    • It exacerbates and accelerates changes in atherosclerotic vessels, contributing to conditions such as: Coronary Artery Disease (CAD), Myocardial Infarction (MI), Stroke, Kidney impairment

    • It is noted as a significant contributing factor to Congestive Heart Failure (CHF) and cardiomyopathy.

  • Hydration Status of Hypertensive Patients: Many patients with hypertension exhibit hypovolemia due to chronic vasoconstriction, renal impairment, and diuretic use in treatment.

Pathophysiology

  • Mechanical Changes in Coronary Arteries: Stenosis of coronary arteries implies they are maximally dilated, thus reducing blood flow during times of increased oxygen demand, which escalates the risk of ischemia in the heart muscle.

  • Cardiac Demand Dynamics: Increased preload raises myocardial demand. If this demand is excessive, the myocardium will reach a “cap” leading to compromised myocardial performance relative to demand.

  • Valvular Heart Disease: Compromised heart function with elevated preload and afterload can lead to conditions such as cardiogenic shock or hypertrophy.

Anesthesia Considerations for Hypertensive Patients

  • Identifying hypertension in preop and typical maintenance

  • Continued Medication:

    • Patients should continue their antihypertensive medications through the day of surgery.

    • For newly diagnosed patients, antihypertensive therapies should not start HTN therapy in the preop setting if BP was maintained < 150/90 consistently.

  • Medication Regimen:

    • 1st Line in Non-African American Patients (Non A.A.): Hydrochlorothiazide (HCTZ) + Calcium Channel Blocker + ACE Inhibitor/Angiotensin Receptor Blocker (ACE/ARB)

    • 1st Line in African American Patients (A.A.): Hydrochlorothiazide (HCTZ) + Calcium Channel Blocker

    • For CAD Diagnosis: β Blockers + ACE/ARB + Statin

  • Timing for Initiation of Meds: If therapy initiation is needed, the patient must have stable, normotensive blood pressure under management for 2-7 days prior to any elective surgery.

    • Not sure which one is more accurate for test purposes (this or the highlighted point above)

Peri-operative Management

  • Pre-surgery Hydration: Adequate hydration is essential prior to surgery to mitigate hypovolemia and minimize the risk of HypoTN.

  • Anesthesia Considerations:

    • Antihypertensive treatment can be exacerbated under anesthesia.

    • Avoid the use of vasodilators if possible, as vessel stenosis may impede corrective blood flow increase intended from such medications.

    • Instead, utilize β Blockers to enhance blood supply and reduce demand, offering protection from myocardial ischemia.

  • Blood Pressure Goals:

    • Aim to maintain blood pressure within 20% of the normal range during induction and maintenance phases of general anesthesia.

    • Maintaining diastolic blood pressure (DBP) < 110 mm Hg is the minimum target.

  • Definition: Peripheral Vascular Disease is an inflammatory disorder primarily affecting arteries.

  • Causes: Atherosclerosis due to Uncontrolled hypertension, Diabetes, Smoking, Obesity, Hyperlipidemia, Age

  • Pathophysiology:

    • Blood flow to tissues decreases, unable to meet the oxygen (O2) demand, resulting in ischemia.

    • Arterial stiffness and plaque formation narrow the blood vessel lumen, further decreasing blood flow to surrounding tissues.

    • The presence of plaque induces an inflammatory response, attracting leukocytes to the affected area, which leads to a hypercoagulable state.

    • Interaction between leukocytes and platelets can result in:

      • Thrombosis (blood clot within the vessel)

      • Embolus (clot that travels to another location)

      • Aneurysm (dilation of weakened blood vessel wall)

Treatment of Peripheral Vascular Disease

  • Importance of Pre-Operative Assessment: Some treatments may need to be discontinued before surgery.

β Blockers

  • Function: Reduces the risk of cardiac ischemia by increasing blood supply and decreasing demand.

  • Therapeutic Goal: Target heart rate (HR) of 50-60 beats per minute (BPM).

  • Usage: Can be used until the day of surgery and continued post-operatively.

Statins

  • Function: Decrease vascular inflammation, thrombosis formation, and lipid concentration.

  • Therapeutic Goal: Start at least 30 days prior to surgery.

  • Usage: Should be administered up to the day of surgery and continued post-operatively.

Aspirin (ASA)

  • Type: Anti-coagulant therapy.

  • Administration: Taken orally daily for prophylaxis.

  • Considerations:

    • Effectiveness depends on how the patient is taking it, requiring review of Secondary vs. Primary ASA prophylaxis per the APSF article.

    • Physician/surgeon discretion is necessary depending on the type of surgery.

    • May continue to take ASA through the day of surgery and peri-operatively.

    • According to Nagelhout text:

    • Prevention Consideration: There is no clear benefit for preventing cardiac ischemia when taken peri-operatively.

    • Risk: Use poses a major hemorrhage risk.

    • Recommended to stop 5-7 days prior to surgery and can safely resume 8-10 days post-operatively.

Surgical Considerations in Patients with PVD

  • Potential Complications: Risk of compounded hypotension (HypoTN) when combining β blockers with anesthetics.

    • Considering Regional or Neuraxial (Epidural) Anesthesia as an alternative to General Anesthesia to decrease the risk of cardiovascular morbidity.

  • Anti-coagulation Considerations: Evaluate between Heparin and Low Molecular Weight Heparin (LMWH) if anti-coagulation is indicated during hospitalization as alternatives to ASA.

  • Post-Operative Pain Management: Important in patients with PVD, as pain can increase the inflammatory response, potentially raising morbidity risks.

Textbook Notes

• Coronary Perfusion Pressure (CPP): Defined as Diastolic Blood Pressure (DBP) minus Left Ventricular End-Diastolic Pressure (LVEDP).

    ◦ Clinical Pearl: The Left Ventricle (LV) is perfused almost exclusively during diastole. Tachycardia is dangerous because it shortens diastole, reducing supply while simultaneously increasing metabolic demand.

• Autoregulation: Coronary blood flow remains constant between MAPs of 60 and 140 mm Hg.

    ◦ Hypertension: In chronic HTN, the autoregulation curve shifts to the right, meaning hypotension (and ischemia) can occur at "normal" MAPs (e.g., < 60 mm Hg might be ischemic). Basically, the patient will be hypo-perfusing at a normal BP, as this is not normal for them

• Coronary Anatomy:

    ◦ Dominance: Determined by which artery supplies the posterior descending artery (PDA). 50% of the population is Right Dominant (supplied by RCA); 10-15% are Left Dominant (supplied by Circumflex).

    ◦ Venous Drainage: The Coronary Sinus drains 85% of LV blood; it is the site for retrograde cardioplegia catheters.

II. Pressure-Volume (PV) Loops

• Phases:

    ◦ Isovolumetric Contraction: Steep rise in pressure, no change in volume (Mitral valve closes → Aortic valve opens).

    ◦ Ejection: Volume decreases as blood leaves LV.

    ◦ Isovolumetric Relaxation: Steep drop in pressure, no change in volume (Aortic valve closes → Mitral valve opens).

• Stroke Volume (SV): The width of the loop (EDV - ESV).

• Contractility: Represented by the slope of the end-systolic pressure-volume relationship. Increased contractility shifts the loop up and to the left (higher pressure, smaller ESV; basically a steeper slope of the same general shape).

• Bainbridge Reflex (Atrial Stretch):

    ◦ Stimulus: Increased blood volume (stretch) in RA/SVC.

    ◦ Response: Increased Heart Rate.

    ◦ Relevance: Autotransfusion after childbirth or rapid IVF bolus.

    ◦ This is different from baroreceptor reflex, which responds to pressure; high BP = decreased HR

• Aortic Stenosis (AS):

    ◦ Pathology: Pressure overload → Concentric LV hypertrophy (thick wall, small cavity). Compliance is poor; dependent on Atrial Kick.

    ◦ Triad: Angina, Syncope, Dyspnea (SAD).

    ◦ Anesthetic Goals: "Slow, Sinus, Tight, & Full"

        ▪ HR: Normal/low (60-80). Tachycardia causes ischemia (high demand, low supply).

        ▪ Rhythm: NSR is critical (loss of atrial kick = 40% loss of CO). Cardiovert immediately if AFib occurs.

        ▪ Afterload: Maintain or increase. Hypotension is lethal (coronaries rely on high driving pressure).

        ▪ Preload: Full (LVEDP needs to be high to fill stiff ventricle).

    ◦ CPR Note: Chest compressions are often ineffective due to fixed outflow obstruction.

• Aortic Regurgitation (AR):

    ◦ Pathology: Volume overload → Eccentric hypertrophy (dilation).

    ◦ Anesthetic Goals: "Fast, Forward, & Full"

        ▪ HR: Moderately high (80-100). Reduces diastolic time for regurgitation.

        ▪ Afterload: Decrease. Lowers resistance to forward flow.

• Mitral Stenosis (MS):

    ◦ Pathology: LV is underloaded; LA is overloaded (Pulm HTN).

    ◦ Anesthetic Goals: "Slow & Full"

        ▪ HR: Slow. Tachycardia reduces diastolic filling time across the tight valve.

        ▪ Preload: Maintain.

• Mitral Regurgitation (MR):

    ◦ Anesthetic Goals: "Fast & Forward"

        ▪ Afterload: Decrease (promotes forward flow).

        ▪ HR: Normal to high (prevents ventricular overdistention).

• Hypertrophic Cardiomyopathy (HCM):

    ◦ Obstruction: Dynamic LV outflow tract obstruction (SAM - Systolic Anterior Motion of mitral valve).

    ◦ Worsened by: Increased contractility, decreased preload, decreased afterload.

    ◦ Treatment: Phenylephrine (increases afterload/stents open outflow), Beta-blockers, Fluids.

    ◦ Contraindicated: Ephedrine (increases contractility), Nitroglycerin (decreases preload/afterload).

• Tamponade:

    ◦ Beck's Triad: Hypotension, JVD, Muffled heart sounds.

    ◦ Pulsus Paradoxus: >10 mmHg drop in SBP during spontaneous inspiration.

    ◦ Induction: Ketamine is preferred (preserves SNS). Avoid propofol/thiopental (myocardial depression). maintain "Fast, Full, and Tight".

• Abdominal Aortic Aneurysm (AAA)

    ◦ Law of Laplace: T=P×r (Wall tension = Pressure × radius). As the radius increases, wall tension increases, increasing rupture risk.

    ◦ Rupture Risk: Increases dramatically at > 5 cm.

    ◦ Aortic Cross-Clamping (Hemodynamics):

    ◦ Proximal to Clamp: Hypertension, increased afterload, increased myocardial wall tension/O2 demand.

    ◦ Distal to Clamp: Hypotension, tissue ischemia, anaerobic metabolism.

    ◦ Renal: Infrarenal clamping still decreases renal blood flow by 40%.

• Unclamping (Declamping Shock):

    ◦ Mechanism: Release of sequestered blood, vasodilation from metabolites (lactate, adenosine), and reactive hyperemia causing profound hypotension.

    ◦ Management: Volume load prior to release, gradual release, vasoconstrictors.

• Spinal Cord Ischemia (Thoracic/AAA repair)

    ◦ Blood Supply: Artery of Adamkiewicz, Major supplier of the anterior spinal cord (motor). Variable origin, usually T8–L12.

• Carotid Endarterectomy (CEA)

    ◦ Surgical Indications: Symptomatic stenosis > 70%.

    ◦ Cerebral Perfusion Pressure (CPP): CPP=MAP−ICP. Since ICP is low, MAP primarily drives perfusion.

• Monitoring Ischemia:

    ◦ EEG: Gold standard. Signs of ischemia = loss of beta-wave (fast) activity, emergence of delta-wave (slow) activity.

    ◦ Stump Pressure: Pressure in carotid distal to clamp. < 40-50 mmHg indicates hypoperfusion and need for a shunt.

• Anesthetic Management:

    ◦ MAP Goals: Maintain close to baseline (often high). During cross-clamp, MAP may need to be > 20% above baseline to perfuse via collaterals (Circle of Willis).

    ◦ Ventilation: Normocapnia. Hypocapnia constricts cerebral vessels; Hypercapnia causes "steal" phenomenon.

• Postoperative Complications:

    ◦ Hematoma: Airway emergency. If stridor/deviation occurs, evacuate hematoma immediately (may need to open wound at bedside).

    ◦ Nerve Injury:

        ▪ RLN: Hoarseness/stridor.

        ▪ Hypoglossal: Tongue deviates toward the side of injury.

    ◦ Chemoreceptors: Bilateral CEA can denervate carotid bodies → loss of ventilatory response to hypoxemia.

    ◦ Cerebral Hyperperfusion Syndrome: Headache, seizure, edema due to loss of autoregulation in a chronically ischemic vascular bed.