Felis ISSN 2398-2950

Perioperative complications: respiratory

Contributor(s): Teresa Dye

Introduction

  • Respiratory disease may occur in the surgical patient:
    • Secondary to the surgical procedure itself, ie laryngeal paralysis due to iatrogenic trauma to the recurrent laryngeal nerve.
    • As a direct complication of anesthesia, ie acquired atelectasis, aspiration pneumonia Pneumonia
    • As a complication or progression of the patients primary disease, ie thoracic wall injury, sepsis.
    • As an exacerbation of a pre-existing disease, ie cardiomyopathy.
  • Respiratory complications are relatively common in the perioperative period.
  • Hypoventilation and hypoxemia are two major respiratory complications and may result from a variety of causes.
  • Critically ill and postoperative patients may be less tolerant of respiratory impairment than healthy animals.
  • Hypothermia commonly occurs post-operatively and may cause shivering which increases tissue oxygen demand and can contribute to hypoxemia.
  • Surgical or traumatic blood loss and chronic illness can cause anemia and thus decreased blood oxygen content even at maximal hemoglobin saturation levels. For this reason, the packed cell volume Hematology: packed cell volume of critical patients with respiratory impairment should ideally be kept near 30% and should definitely not be allowed to fall <20%.
  • Decreased cardiac output due to concurrent cardiac disease or hypovolemia may cause decreased perfusion and thus further decrease tissue oxygenation.
  • Hypoventilation refers to decreased alveolar ventilation.
  • As a result of hypoventilation, arterial CO2 levels rise. Hypoventilation is defined as an arterial CO2 tension (PaCO2) >40 mm Hg. In general, end tidal CO2 measurements obtained via capnography  Anesthetic monitoring: respiratory system (capnograph) approximate or slightly underestimate the PaCO2. However, intermittent positive pressure ventilation (IPPV), thoracic surgery, and decreased perfusion can cause a significant underestimation of the CO2 tension with capnography.
  • Oxygen saturations may not be affected by mild hypoventilation, but hypoxemia may develop if hypoventilation is severe or prolonged.
  • Elevations in CO2 levels tend to cause centrally mediated increases in cardiac output and heart rate, but CO2 also acts directly to cause myocardial depression and arteriolar dilatation.The overall effect of hypercarbia tends to be mild increases in heart rate and blood pressure.
  • The catecholamine release associated with hypercarbia may predispose patients to cardiac arrhythmias Heart: dysrhythmia such as premature ventricular complexes Ventricular premature contraction.
  • Other electrocardiogram ECG: overview changes may include large T waves and reversed polarity of the T waves. Hypercarbia may also result in the development of respiratory acidosis Acid base imbalance.
  • Hypoventilation often occurs in the perioperative period.
  • Anesthetic drugs can cause respiratory depression by decreasing the sensitivity of the medullary respiratory centers to CO2. This is particularly seen in dogs which have been pre-medicated with opioids and then placed under gas anesthesia.
  • However, the respiratory depressant effects of opioids are less profound in small animals than in humans. Thiopental Thiopental and propofol Propofol often cause apnea following induction link. This effect tends to be dose and rate dependent. It may require several minutes for CO2 levels in these patients to rise enough to stimulate respirations, and positive pressure ventilation may be required following induction.
  • Pain may limit the movement of the thoracic wall in patients with fractured ribs or who have undergone thoracic surgery. Air flow can be restricted in patients with anatomic upper airway obstruction or if the endotracheal tube becomes occluded with blood or mucus or becomes kinked.
  • Diaphragmatic movement can be limited in patients with increased abdominal pressure (pregnancy, obesity, abdominal mass or effusion) or if the diaphragm is ruptured. Expansion of the lungs may be limited in patients with pneumothorax Pneumothorax, pleural effusion Pleural effusion, diaphragmatic hernia Diaphragm: hernia, or intrathoracic masses. Acquired atelectasis, pulmonary contusions Lung: pulmonary hemorrhage, or pulmonary edema Lung: pulmonary edema may result in a ventilation/perfusion mismatch Ventilation perfusion mismatching or shunting. Respiratory paralysis can occur due to neuromuscular blocking drugs (such as atracurium Atracurium) or epidural anesthesia.
  • Hypoxemia refers to an arterial blood oxygen tension (PaO2) <60 mm Hg and a blood oxygen saturation (SaO2) <90%. The oxyhemoglobin dissociation curve expresses the relationship between arterial hemoglobin saturation and the PaO2. At a PaO2 of 100 mm Hg, the hemoglobin is almost completely saturated (97.5%). Further increases in the PaO2 will barely increase the percent saturation. A SaO2 of 96% corresponds to a PaO2 of 80 mm Hg, and a SaO2 of 91% corresponds to a PaO2 of 60 mm Hg. The position of the oxyhemoglobin curve may shift due to changes in temperature, pH, CO2 levels, or erythrocyte 2,3 DPG levels causing changes in the relationship between SaO2 and PaO2.
  • Pulse oximetry Anesthetic monitoring: pulse oximetry is often used to monitor the SpO2 which provides an approximation of the SaO2. It is important to remember that hypothermia, shock, low cardiac output, anemia, and peripheral vasoconstriction can interfere with the accuracy of pulse oximetry readings. Additionally, the patients palpable pulse must match the rate indicated by the pulse oximeter for the reading to be accurate. For patients anesthetized with gas anesthesia, it is important to realize that the fraction of inspired oxygen (FIO2) is typically greater than 0.90 so the PaO2 in these patients is normally 400-500 mm Hg. At such a high PaO2, the SaO2 (and thus SpO2) should be 98-100%. Therefore, even a slight drop in the SpO2 below 98% in these patients represents a significant drop in the PaO2 and should be of concern. This fact makes pulse oximetry a weak assessment of ventilation in the anesthetized patient as the SpO2 will not decrease until severe or prolonged hypoventilation has occurred.
  • Patients who are hypoxemic may have mucus membranes which appear cyanotic, but cyanosis is not detectable until the SaO2 falls below 75% (a PaO2 of approximately 35 mm Hg). Cyanosis may be difficult to determine in patients who are anemic and when the patient is covered with surgical drapes and/or in poor lighting. Additionally some patients may have mucus membranes which appear white rather than cyanotic in the face of hypoxemia.
  • Initially, hypoxemia causes stimulation of the cardiovascular system resulting in tachycardia and hypertension. However prolonged or severe hypoxemia will cause bradycardia and hypotension. Electrocardiogram changes include reversed polarity of T waves with ST segment depression and slurring.
  • There are five major causes of hypoxemia. These are:
    • Hypoventilation.
    • Decreased fraction of inspired oxygen (FIO2).
    • Alveolar-capillary diffusion impairment (interstitial lung disease).
    • Right to left shunts (ventricular septal defects Ventricular septal defect and patent ductus arteriosus).
    • Ventilation/perfusion mismatch Ventilation perfusion mismatching (acquired atelectasis, pulmonary arterial thrombosis, pulmonary edema Lung: pulmonary edema).
    • Specific respiratory diseases are generally categorized anatomically as diseases of the upper airway, lower airways, pulmonary parenchyma, or pleural space.

Upper airway diseases

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Lower airway disease

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Pulmonary parencyhmal disease

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Pleural space diseases

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Summary

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Further Reading

Publications

Other sources of information

  • Brashers V L & Huether S E (2004)Structure and function of the pulmonary system and Alterations of pulmonary function.In: Huether S E, McCance K L (eds) Understanding Pathophysiology.3rd edn. Philadelphia:Mosby, Inc. pp 729-786.
  • Haskins S C (2004)Interpretation of blood gas measurements.In: King L G (ed) Respiratory diseases in Dogs and Cats.St Louis, Saunders. pp 181-192.
  • Perowski S I (2004)Anesthesia of the Patient with Respiratory Disease.In: King L G (ed) Respiratory diseases in Dogs and Cats.W B Saunders, St Louis. pp 253-261.
  • Fossum T W (2002)Surgery of the lower respiratory system: lungs and thoracic wall.In: Fossum T W (ed) Small Animal Surgery.2nd edn. St. Louis: Mosby, Inc. pp 761-787.
  • Fossum T W (2002)Surgery of the lower respiratory system: pleural cavity and diaphragm.In: Fossum T W (ed) Small Animal Surgery. 2nd edn. St. Louis: Mosby, Inc. pp 788-820.
  • Hedlund C S (2002)Surgery of the upper respiratory system.In: Fossum T W (ed) Small Animal Surgery. 2nd edn. St. Louis: Mosby, Inc. pp 716-759.
  • Bateman S W (2001)Medical management of respiratory emergencies. Proceedings 11th Annual ACVS Veterinary Symposium. Chicago. pp115-117.
  • Bateman S W (2001)Managing the acutely lung injured patient. Proceedings 11th Annual ACVS Veterinary Symposium.Chicago. pp 539-561.
  • Paddleford R (1999)Manual of Small Animal Anesthesia.2nd edn. W B Saunders, Philadelphia.
  • Greene S A & Harvey R C (1996)Airway Disease.In: Thurman J C, Tranquilli W J & Benson G J (eds) Lumb and Jones' Veterinary Anesthesia. 3rd edn.Williams & Wilkins, Baltimore. pp 807-811.
  • Lee L (1995)Postanesthetic recovery care.In: Taylor R, McGehee R (eds) Manual of Small Animal Postoperative Care.Media, PA, Williams &Wilkins, pp 88-101.
  • Kuehn N F (1993)Acute respiratory distress (primary pulmonary).In: Bojrab M J (ed) Disease Mechanisms in Small Animal Surgery. 2nd edn. Philadelphia: Lippincott, Williams, and Wilkins. pp 388-395.


ADDED