Neuromuscular Blockers in Cardiac Anesthesia

In  patient on β-blockers, the choice of neuromuscular blockers (NMBs) is critical due to their potential cardiovascular effects. Here’s a detailed analysis of the implications of using fentanyl and various NMBs, particularly focusing on vecuronium and its effects.

Key Points on Fentanyl and β-Blockers

• Fentanyl:

  • Fentanyl is an opioid analgesic that can cause bradycardia due to its vagolytic activity. While it has minimal hemodynamic effects, the bradycardia it induces can be problematic, especially in patients already on β-blockers, which reduce heart rate and blood pressure.

• β-Blockers:

  • These medications reduce heart rate and blood pressure, which can compound the bradycardic effects of fentanyl. Therefore, careful consideration must be given to the choice of additional medications that may further depress cardiac function.

Vecuronium

• Effects:

  • Vecuronium is a non-depolarizing neuromuscular blocker that has minimal cardiovascular side effects when used alone. However, it can potentiate decreases in heart rate and cardiac index when administered after fentanyl.
  • The absence of positive chronotropic effects (unlike pancuronium) means that vecuronium does not counteract the bradycardia induced by fentanyl, leading to a higher risk of significant bradycardia and hypotension.

• Vagal Tone:

  • Vecuronium may enhance vagal tone, further predisposing patients to bradycardia. This is particularly concerning in patients on β-blockers, as the combination can lead to compounded cardiac depression.

Comparison with Other Neuromuscular Blockers

1. Pancuronium:

   • Vagolytic Action: Pancuronium has vagolytic properties that can help attenuate bradycardia and support blood pressure. It is often preferred in cardiac anesthesia for its more favorable hemodynamic profile compared to vecuronium.
   • Tachycardia: While it can induce tachycardia, this effect may be mitigated in patients on β-blockers, which can blunt the tachycardic response.

2. Atracurium:

   • Histamine Release: Atracurium can release histamine, leading to hemodynamic changes such as increased heart rate and decreased blood pressure. These effects can be minimized by slow administration of small doses.

3. Rocuronium:

   • Minimal Hemodynamic Effects: Rocuronium is generally associated with a lack of significant cardiovascular side effects, although occasional increases in heart rate have been noted.

4. Cis-Atracurium:

   • Cardiovascular Stability: Cis-atracurium does not have cardiovascular effects and does not release histamine, making it a safer option in terms of hemodynamic stability.

Cricothyroidotomy

Cricothyroidotomy is a surgical procedure that involves making an incision through the skin over the cricothyroid membrane, which is located between the thyroid and cricoid cartilages in the neck. This procedure is performed to establish an emergency airway in situations where intubation is not possible or has failed, such as in cases of severe airway obstruction, facial trauma, or anaphylaxis.

Indications

Cricothyroidotomy is indicated in the following situations:

• Acute Airway Obstruction: When there is a complete blockage of the upper airway due to swelling, foreign body, or trauma.
• Failed Intubation: When attempts to secure an airway via endotracheal intubation have been unsuccessful.
• Facial or Neck Trauma: In cases where traditional airway management is compromised due to injury.
• Severe Anaphylaxis: When rapid airway access is needed and other methods are not feasible.

Anatomy

• Cricothyroid Membrane: The membrane lies between the thyroid and cricoid cartilages and is a key landmark for the procedure.
• Surrounding Structures: Important structures in the vicinity include the carotid arteries, jugular veins, and the recurrent laryngeal nerve, which must be avoided during the procedure.

Procedure

Preparation

1. Positioning: The patient should be in a supine position with the neck extended to improve access to the cricothyroid membrane.
2. Sterilization: The area should be cleaned and sterilized to reduce the risk of infection.
3. Anesthesia: Local anesthesia may be administered, but in emergency situations, this step may be skipped.

Steps

1. Identify the Cricothyroid Membrane: Palpate the thyroid and cricoid cartilages to locate the membrane, which is typically located about 1-2 cm below the thyroid notch.
2. Make the Incision: Using a scalpel, make a vertical incision through the skin over the cricothyroid membrane, approximately 2-3 cm in length.
3. Incise the Membrane: Carefully incise the cricothyroid membrane horizontally to create an opening into the airway.
4. Insert the Airway Device:
   • A tracheostomy tube or a large-bore cannula (e.g., a 14-gauge catheter) is inserted into the opening to establish an airway.
   • Ensure that the device is positioned correctly to allow for ventilation.
5. Secure the Airway: If using a tracheostomy tube, secure it in place to prevent dislodgment.

Post-Procedure Care

• Ventilation: Connect the airway device to a bag-valve-mask (BVM) or ventilator to provide oxygenation and ventilation.
• Monitoring: Continuously monitor the patient for signs of respiratory distress, oxygen saturation, and overall stability.
• Consider Further Intervention: Plan for definitive airway management, such as a formal tracheostomy or endotracheal intubation, once the immediate crisis is resolved.

Complications

While cricothyroidotomy is a life-saving procedure, it can be associated with several complications, including:

• Infection: Risk of infection at the incision site.
• Hemorrhage: Potential bleeding from surrounding vessels.
• Damage to Surrounding Structures: Injury to the recurrent laryngeal nerve, carotid arteries, or jugular veins.
• Subcutaneous Emphysema: Air escaping into the subcutaneous tissue.
• Tracheal Injury: If the incision is not made correctly, there is a risk of damaging the trachea.

Cardiovascular Effects of Sevoflurane, Halothane, and Isoflurane

• Sevoflurane:

  • Maintains cardiac index and heart rate effectively.

  • Exhibits less hypotensive and negative inotropic effects compared to halothane.

  • Cardiac output is greater than that observed with halothane.

  • Recovery from sevoflurane anesthesia is smooth and comparable to isoflurane, with a shorter time to standing than halothane.

• Halothane:

  • Causes significant decreases in mean arterial pressure, ejection fraction, and cardiac index.

  • Heart rate remains at baseline levels, but overall cardiovascular function is depressed.

  • Recovery from halothane is less favorable compared to sevoflurane and isoflurane.

• Isoflurane:

  • Preserves cardiac index and ejection fraction better than halothane.

  • Increases heart rate while having less suppression of mean arterial pressure compared to halothane.

  • Cardiac output during isoflurane anesthesia is similar to that of sevoflurane, indicating a favorable cardiovascular profile.

Inflammation is the respone of the body to an irritant.

Stages of Inflammation

1. General: Temperature Raised. In severe cases bacteremia or septicemia ,rigors may occur.

2. Local: classical signs of inflammation are due to hyperemia and inflammation exudate

i) Heat:  inflammed area feels warmer than the surrounding tissues.

ii) Redness

iii) Tenderness: Due to pressure of exudate on the surrounding nerves  If the exudate is  under tension, e.g. a furuncle (boil) of the ear, pain is severe.

iv) swelling

v) Loss of function.

The termination of Inflammation

This may be by:1. Resolution 2. Suppuration 3. Ulceration 4. Ganangren s. Fibrosis

Management

i. Increase the patients resistance., Rest,  Relief of pain by analgesics,  Diet: High protein and high calorie diet with vitamins,  Antibiotics,  Prevent further contamination of wound.

Surgical measures

1. Excision: If possible as in appendicectomy.

2. Incision and drainage: If an abscess forms.

Walsham’s Forceps

Walsham’s forceps are specialized surgical instruments used primarily in the manipulation and reduction of fractured nasal fragments. They are particularly useful in the management of nasal fractures, allowing for precise adjustment and stabilization of the bone fragments during the reduction process.

1. Design:

   • Curved Blades: Walsham’s forceps feature two curved blades—one padded and one unpadded. The curvature of the blades allows for better access and manipulation of the nasal structures.
   • Padded Blade: The padded blade is designed to provide a gentle grip on the external surface of the nasal bone and surrounding tissues, minimizing trauma during manipulation.
   • Unpadded Blade: The unpadded blade is inserted into the nostril and is used to secure the internal aspect of the nasal bone and associated fragments.

2. Usage:

   • Insertion: The unpadded blade is carefully passed up the nostril to reach the fractured nasal bone and the associated fragment of the frontal process of the maxilla.
   • Securing Fragments: Once in position, the nasal bone and the associated fragment are secured between the padded blade externally and the unpadded blade internally.
   • Manipulation: The surgeon can then manipulate the fragments into their correct anatomical position, ensuring proper alignment and stabilization.

3. Indications:

   • Walsham’s forceps are indicated for use in cases of nasal fractures, particularly when there is displacement of the nasal bones or associated structures. They are commonly used in both emergency and elective settings for nasal fracture management.

4. Advantages:

   • Precision: The design of the forceps allows for precise manipulation of the nasal fragments, which is crucial for achieving optimal alignment and aesthetic outcomes.
   • Minimized Trauma: The padded blade helps to reduce trauma to the surrounding soft tissues, which can be a concern during the reduction of nasal fractures.

5. Postoperative Considerations:

   • After manipulation and reduction of the nasal fragments, appropriate postoperative care is essential to monitor for complications such as swelling, infection, or malunion. Follow-up appointments may be necessary to assess healing and ensure that the nasal structure remains stable.

SHOCK

Shock  is  defined  as  a  pathological  state  causing  inadequate  oxygen  delivery  to  the peripheral tissues and resulting in lactic acidosis, cellular hypoxia and disruption of normal metabolic condition.

CLASSIFICATION

Shock is generally classified into three major categories:

1.    Hypovolemic shock

2.    Cardiogenic shock

3.    Distributive shock

Distributive shock is further subdivided into three subgroups:

a.    Septic shock

b.    Neurogenic shock

c.    Anaphylactic shock

Hypovolemic  shock  is  present  when  marked  reduction  in  oxygen  delivery results from diminished cardiac output secondary to inadequate vascular volume. In general, it results from loss of fluid from circulation, either directly or indirectly.
e.g.    ?    Hemorrhage
    •    Loss of plasma due to burns
    •    Loss of water and electrolytes in diarrhea
    •    Third space loss (Internal fluid shift into inflammatory exudates in
        the peritoneum, such as in pancreatitis.)

Cardiogenic shock is present when there is severe reduction in oxygen delivery secondary to impaired cardiac function. Usually it is due to myocardial infarction or pericardial tamponade.

Septic Shock (vasogenic shock) develops as a result of the systemic effect of infection. It is the result of a septicemia with endotoxin and exotoxin release by gram-negative and gram-positive bacteria. Despite normal or increased cardiac output and oxygen delivery, cellular oxygen consumption is less than normal due to impaired extraction as a result of impaired metabolism.

Neurogenic shock results primarily from the disruption of the sympathetic nervous system which may be due to pain or loss of sympathetic tone, as in spinal cord injuries.

PATHO PHYSIOLOGY OF SHOCK

Shock stimulates a physiologic response. This circulatory response to hypotension is to conserve perfusion to the vital organs (heart and brain) at the expense of other tissues. Progressive vasoconstriction of skin, splanchnic and renal vessels leads to renal cortical necrosis and acute renal failure. If not corrected in time, shock leads to organ failure and sets up a vicious circle with hypoxia and acidosis.

CLINICAL FEATURES

The clinical presentation varies according to the cause. But in general patients with hypotension and reduced tissue perfusion presents with:
•    Tachycardia
•    Feeble pulse
•    Narrow pulse pressure
•    Cold extremities (except septic shock)
•    Sweating, anxiety
•    Breathlessness / Hyperventilation
•    Confusion leading to unconscious state

PATHO PHYSIOLOGY OF SHOCK

Shock stimulates a physiologic response. This circulatory response to hypotension is to conserve perfusion to the vital organs (heart and brain) at the expense of other tissues. Progressive vasoconstriction of skin, splanchnic and renal vessels leads to renal cortical necrosis and acute renal failure. If not corrected in time, shock leads to organ failure and sets up a vicious circle with hypoxia and acidosis.

CLINICAL FEATURES

The clinical presentation varies according to the cause. But in general patients with hypotension and reduced tissue perfusion presents with:
•    Tachycardia
•    Feeble pulse
•    Narrow pulse pressure
•    Cold extremities (except septic shock)
•    Sweating, anxiety
•    Breathlessness / Hyperventilation
•    Confusion leading to unconscious state