Anesthesia: Managing Complications
World Small Animal Veterinary Association World Congress Proceedings, 2013
Pablo E. Otero, DVM, PhD
Division of Anesthesiology and Pain Management, College of Veterinary Medicine, Buenos Aires University, Ciudad Autónoma de Buenos Aires, Argentina

Introduction

One of the major problems associated with the anesthetic procedure is the lack of tissue oxygenation. Hypotension, an adverse effect of anesthesia, increases the risk of morbidity and death as a result of diminished organ perfusion.

Hypotension is defined as systolic arterial blood pressure (SABP) < 80 mm Hg and is estimated to develop in 41% of anesthetized humans, in up to 32% of anesthetized dogs, and in up to 33% of anesthetized cats.

Strategies for correction of hypotension include IV administration of fluids, reduction or termination of anesthetic delivery, administration of adjunct anesthetic and analgesic agents to reduce the inspired volatile concentration, and administration of inotropes and other vasoactive drugs. However, every single therapeutic option should be preceded by a correct diagnosis of the problem.

For years the belief that fluid preload would prevent hypotension during anesthesia has been discharged. Throughout anesthesia, the origin of hypotension can be diverse. Mostly, the hypotension and thereby the lack of oxygen supply could be explained as a result of:

 Hypovolemia

 Lack of contractility

 Vasodilatation

 Arrhythmia


 

Diagnosis of the Origin of Hypotension During Anesthesia

The pulse oximeter provides a noninvasive window on several dynamic circulatory parameters. Although the pulse oximeter may indicate changes in perfusion for the tissues being illuminated, its waveform mimics an intraarterial pressure wave, despite its almost complete damping at the tissue level. The essential difference is that the peripheral pulse monitor reads local tissue blood volume change in transilluminated tissue (caused by blood flow), which is an indirect indicator of upstream pressure only. As flow cannot be quantified as exactly as pressure, changes in the pattern of the waveform, rather than its dimensions, become of prime importance.

Plethysmography

The plethysmogram essentially draws two curves.

 The pulse wave is a high-frequency curve that mimics the changes in intra-arterial pressure, becoming a mirror image of the arterial pressure waveform.

 The wave reflected, or respiratory changes, is a product of low-frequency curve of cyclical fluctuations promoted by changes experienced by the systolic discharge.

Changes in "High-Frequency" Pulse Wave

Amplitude

 The amplitude is the product of stroke volume and peripheral resistance.

 Increased resistance - the amplitude decreases and vice-versa.

 Interpretation of changes in amplitude of the pulse wave

 Increased amplitude

 Vasodilation

 Drugs

 Hyperthermia

 Anesthesia

 Decreased amplitude

 Vasoconstriction

 Hypovolemia

Area Under the Curve (AUC)

 Represents the blood volume scanned by the transducer into the tissue.

 Directly related to the stroke volume and vasomotor tone of the tissue.

 Interpretation of changes in AUC in the pulse wave

 Decreased AUC

 With vasodilation plateau time (width of the curve) is reduced and the curve becomes more "peaked."

 With hypovolemia and consequent vasoconstriction base is reduced and notch moves up.

Dicrotic Notch

 It is located in the descending section of the pressure or pulse trace and can be used as an indicator of vasomotor tone.

 Interpreting changes in the position of the dicrotic notch

 Vasodilation (decrease in the notch)

 As vasodilation progresses, peripheral veins are dilated, the pulse signal increases and the notch descends to the baseline diastolic pressure.

 Vasoconstriction (rise in the notch)

 The notch ascends to the apex of the pulse wave in relation to vasoconstriction.

Changes in "Low-Frequency" Pulse Wave

 ΔPS, ΔPp, ΔPpleth

Monitoring of Blood Pressure for Predicting Response to Volemic Reposition

 The starting point for hemodynamic resuscitation begins with the optimization of cardiac preload.

 Static indicators of preload, such as central venous pressure, heart rate, and blood pressure, have a number of limitations to recognize and consider the hypovolemia.

 Currently there is evidence that dynamic markers used to identify patient's "responders" to the supply of fluids provide useful information to determine the end-point of volemic resuscitation.

 The most studied dynamic indicators are those that quantify the observed variations in blood pressure (or components of the pressure curve) during positive pressure ventilation.

 Invasive

 ΔPS (systolic pressure variation)

 ΔPp (pulse pressure variation)

 Noninvasive

 ΔPpleth (plethysmographic variation)

The changes that occur on blood pressure as a result of positive pressure ventilation (PPV) are easily recognized on the monitor.

Changes Experienced by the Left Ventricle (LV) During PPV

 Changes experienced by the LV depend mainly on changes in intrathoracic pressure and lung volume

 During positive pressure inspiration:

 Increased preload due to increased lung volume and the resulting displacement of the pulmonary venous reservoir to the left circuit.

 Reduction of LV afterload by reducing the forces opposed to the ejection of the ventricle.

This combination of increased LV preload (LV volume before contraction) and decreased afterload (resistance to ejection) promotes an increase in systemic blood pressure.

Changes Experienced by the Right Ventricle (RV) During the PPV

 The increase in intrathoracic pressure causes a decrease in systemic venous return and preload of the RV.

 Increased lung volume increases pulmonary vascular resistance and RV afterload.

 These effects combine to reduce the RV ejection during inspiration.

The cyclic variation experienced by systemic blood pressure as a result of changes in intrathoracic pressure can be measured and quantified by dynamic markers such as:

 Systolic pressure variation (ΔPS)

 Pulse pressure variation (ΔPp)

 Plethysmographic wave amplitude variation (ΔPpleth)

 ΔPS

 The ΔPS is subdivided into a component of inspiration (Δ Up) and exhalation (Δ Down).

 After determining the systolic pressure during a period of apnea (baseline) ΔPS is determined as the sum of the upper (Δ Up) and lower (Δ Down) variations registered during controlled ventilation.

 In patients with mechanical ventilation, the normal value of ΔPS is 7 to 10 mm Hg and is composed of a Δ Up 2 to 4 mm Hg and Δ Down 5 to 6 mm Hg.

 The ΔPS is used as an early indicator of hypovolemia.

 In hypovolemic patients, positive pressure ventilation causes a dramatic increase ΔPS, particularly the component Δ Down.

 Increased ΔPS, especially Δ Down to predict hypovolemia, is useful even in patients in whom as a result of a compensatory vasoconstriction, arterial pressure is maintained near a normal value.

 ΔPS < 12 mm Hg fluids nonresponder

 ΔPS ≥ 12 mm Hg ΔPS fluids responder

 The ΔPS may not be the best indicator of change in stroke volume, because these variations can also occur as a result of changes in intrathoracic pressure.

 ΔPp

 The pulse pressure (Pp) is the difference between systolic and diastolic pressure.

 The ΔPp is defined as the maximum difference in arterial pulse pressure, measured during a respiratory cycle at positive pressure, divided by the average maximum pressure and minimum pulse.

 ΔPp (%) = 100 x (Ppmax - Ppmin) / [(Ppmax + Ppmin) / 2]

 The ΔPp is a more reliable indicator because, unlike the ΔPS, it is not subjected to changes in intrathoracic pressure.

 ΔPp ≤ 13 mm Hg fluids nonresponder

 ΔPp > 13 mm Hg fluids responder

 ΔPpleth

 It is determined noninvasively by analyzing the plethysmographic curve obtained by the pulse oximeter.

 Because the plethysmographic curve obtained by the pulse oximeter has no units, the change is calculated as a percentage of the baseline amplitude obtained during apnea (no positive intrathoracic pressure).  ΔPpleth(%) = 100 x (Pplethmax - Pplethmin)/[(Pplethmin + Pplethmax)/2]

 ΔPpleth > 9–15% fluids responder

 Important

 Dynamic Indicators used to define responders to fluid (ΔPS, ΔPp, ΔPpleth) cannot be used as reliable indicators in patients with cardiac arrhythmias, significant changes in the chest wall or lung compliance.

 All these measures have been validated only in patients (humans) with mechanical ventilation and are not applicable to subjects with spontaneous breathing.

Emergency Treatments During Anesthesia

 Always

 Provide oxygen

 Intubate and ventilate if necessary with 100% O2

 Seizure control

 Benzodiazepines (diazepam 0.25–0.5 mg kg-1 IV)

 Propofol (increments of 1 mg kg-1)

 Levetiracetam (Keppra®) 20 mg kg-1 IV TID

 If hypovolemic shock

 Intravenous fluids

 Crystalloids (Ringer lactate)

 Hypertonic saline (7.5%)

 Colloids (HES)

 Blood derivate

 If hypotension due to vasodilatation

 Vasopressors

 Phenylephrine (1–5 µg kg-1 IV) CRI 0.1–0.3 µg kg-1 min-1 IV)

 Vasopressin (0.003 UI kg-1) CRI 0.03 UI kg-1 h-1)

 Epinephrine (increments of 1 µg kg-1)

 Important

 Epinephrine is not recommended if bupivacaine toxicity occurs.

 The generation of serious ventricular dysrhythmias and lack of effectiveness on cardiac index and on cardiac relaxation may limit the use of epinephrine.

 As an alternative, amrinone should be used.

 If hypotension due to lack of contractility

 Inotropes

 Dobutamine (CRI 5–10 µg kg-1 min-1)

 Dopamine (CRI 5–10 µg kg-1 min-1)

 Noradrenaline (CRI 0.5–1 µg kg-1 min-1)

 If bradycardia

 Anticholinergics

 Atropine (0.02–0.05 mg kg-1 IV)

 Glycopyrrolate (0.005–0.01 mg kg-1)

 If ventricular fibrillation or sustained ventricular tachycardia with severe hypotension (MAP < 45 mm Hg)

 Cardiac massage

 Bretylium (5–20 mg kg-1 over 1–2 min)

 Magnesium (0.3–0.6 mEq kg-1 IV over 5 min)

 Defibrillation (0.5 J kg-1) may be considered

 If overdose

 Opioids: Naloxone incremental doses of 0.05 mg kg-1

 Alpha2 agonists: Atipamezole 0.2 mg kg-1

 Benzodiazepines: Flumazenil 0.2 mg kg-1

References

1.  Aarnes TK, et al. Effect of intravenous administration of lactated Ringer's solution or hetastarch for the treatment of isoflurane-induced hypotension in dogs. American Journal of Veterinary Research. 2009;70(11):1345–1353.

2.  Murray WB. The peripheral pulse wave information overlooked. Journal of Clinical Monitoring. 1996;12:365–377.

3.  Westphal GA, et al. Pulse oximetry wave variation as a noninvasive tool to assess volume status in cardiac surgery. Clinics (São Paulo, Brazil). 2009;64(4):337–343.

4.  Zimmermann M, Feibicke T, Keyl C, Prasser C, Moritz S, Graf BM, Wiesenack C. Accuracy of stroke volume variation compared with pleth variability index to predict fluid responsiveness in mechanically ventilated patients undergoing major surgery. European Journal of Anaesthesiology. 2010;27(6):555–561.

  

Speaker Information
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Pablo E. Otero, MV, PhD
Division of Anesthesiology and Pain Management
College of Veterinary Medicine
Buenos Aires University
Ciudad Autónoma de Buenos Aires, Argentina


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