【Anesthesia hotspot】Posterior vasopressin and resuscitation

Click on the blue word Follow us

Posterior vasopressin and resuscitation

Case form: Review of case analysis

The patient, a 75-year-old male, weighs 95 kg, has worsened abdominal pain for 4 days, suspected of perforation of duodenal ulcer, and is intended for emergency exploratory laparotomy
.
History of present life includes hypertension (valsartan 100 mg/day) and coronary artery disease
.
Coronary artery bypass graft was undergone at age 72, after which cardiac symptoms were relieved
.

Preoperative assessment in the emergency department showed that the patient was feeling significantly unwell, with a blood pressure of 100/60 mmHg, a heart rate of 110 breaths per minute, and a respiratory rate of 28 breaths per minute
.
Body temperature 39 ° C
.
Oxygen inhalation through nasal cannula 4L/min, pulse oxygen saturation 96%.

There has been no urine
since admission.
The laboratory results at the time of emergency admission were as follows: hemoglobin 150g/L, hematocrit 45%, serum potassium 4.
3mmol/L, sodium 140mmol/L, bicarbonate 18mmol/L, blood urea nitrogen 35mg/dl, creatinine 1.
0mg/dl
.
Echocardiography shows first-degree AV block with normal QRS waveform
.
The patient was taken to the operating room for exploratory laparotomy and routine ECG monitoring
.
Pre-administration of oxygen and pre-administration of cis-atracurium 2 mg followed by anesthesia induction
with propofol 100 mg.
Succinylcholine 160 mg is given for endotracheal intubation and smooth insertion of ID 8.
0 endotracheal tube
.
Shortly after induction, the patient's blood pressure dropped to 60/20 mmHg and his heart rate rose to 140 beats per minute
.
ST-segment depression
in the lower wall lead of the ECG on the body surface.
Immediate treatment includes intravenous norepinephrine 5 ug/min, gradually increased to 30 ug/min, 1500 ml of lactated Ringer solution and 500 ml
of 5% albumin.
Despite this, the patient's blood pressure continued to decrease until it became undetectable and the heart rate dropped to 55 beats per minute
.
With intravenous administration of epinephrine 1 mg, the patient's heart rate increased to 120 beats / minute, and blood pressure increased to 30/15 mmHg
.
After re-intravenous administration of 1 mg of epinephrine, the patient's heart rate increased to 160 beats per minute, and frequent ventricular prephase contractions occurred and caused ventricular tachycardia and ventricular fibrillation
.
DC cardioversion fails and cardiac arrest
occurs.
With intravenous administration of 40 U of posterior vasopressin, the patient developed spontaneous cardiac activity and blood pressure rose to 60/30 mmHg
.
Within 5 minutes, 500 ml of 5% albumin was infusion, and 0.
2 U/min
of posterior leaf vasopressin was continuously infused intravenously.
Subsequently, the patient's heart rate and blood pressure stabilized at 90 beats per minute and 100/50 mmHg
.

Case discussion

This case occurred during anesthesia in
an elderly patient with significant preoperative physiological dysfunction.
The causes of severe hypotension in clinical anesthesia are not always well understood, and the options for treatment are varied
.
The ideal approach is to identify the underlying cause of hypotension and take targeted measures
.
The goal of resuscitation is to ensure the perfusion and function
of vital organs.
In some cases, the established diagnosis is accurate, but the treatment measures are controversial
.
The debate revolves around the role of vasoconstrictors and volume supplementation in resuscitation: is one better than the other or is a combination better? Clinical studies
of cardiac arrest are difficult due to the large number of variables and the lack of control.
Although animal models of cardiac arrest and shock have been established, it is not known
whether the results can be applied to real patients.
The most commonly used vasopressors for cardiac arrest resuscitation are epinephrine and norepinephrine
.
Although the vasoconstrictive effect of posterior vasopressin has been known for more than a hundred years, it was not until the mid-90s of the 20th century that the role of posterior vasopressin in resuscitation attracted the attention
of the scientific community.

Posterior vasopressin, or antidiuretic hormone, is an endogenous nonapeptide synthesized by the hypothetamic brain and stored and secreted
by the neuropituitary gland.
Triggers posterior vasopressin release
when plasma osmolality rises, blood pressure drops, and heart filling decreases (hypovolemia).
Three receptors for posterior vasopressin have been identified: V1 receptors mediate vasoconstriction, V2 receptors act on the renal tubules to increase water retention, and V3 receptors mediate the release
of CNS adrenocorticotropic hormone.
V1 receptors that stimulate vascular smooth muscle cells can mobilize intracellular calcium ions and increase extracellular calcium aggregation, which in turn promotes vasoconstriction (Table 25.
1).

Posterior vasopressin passes V2 and V3 receptors mediate effects on metabolism and thus on
numerous physiological systems.
However, the effect of posterior vasopressin on metabolism in critically ill patients has not been extensively studied
.
Posterior vasopressin is known not to alter blood glucose, lactate, and electrolyte levels, possibly reducing aerobic demand and protecting pulmonary endothelial function
.
The posterior leaf vasopressin has a plasma half-life of 4~20 minutes
.
Terlipressin is an artisanally synthesized isomer of posterior vasopressin with a half-life of 6 hours
.
Posterior vasopressin has little
effect on blood pressure under normal physiological conditions.
However, when other compensatory mechanisms fail, posterior vasopressin becomes an important mechanism
for maintaining hemodynamic stability.
Metabolic acidosis attenuates the potency of catecholamines, while the vasoactive effects of posterior vasopressin are not affected by
acidosis.
Therefore, posterior vasopressin may be more appropriate
when acidosis is present or catecholamines are ineffective.
Low-dose posterior vasopressin dilates the vascular beds of coronary arteries and cerebral arteries and increases myocardial blood flow (Table 25.
2).

Table 25.
1 Posterior vasopressin receptors and effects

Table 25.
2 Posterior vasopressin doses

Posterior vasopressin may be effective in the following five situations: (1) cardiac arrest; (2) vasodilating shock; (3) anaphylactic shock; (4) hemorrhagic shock; (5) Liver transplantation
.

Cardiac arrest Although a small number of patients with posterior vasopressin have been successfully resuscitated from cardiac arrest as early as 1996, subsequent human and animal studies have not fully elucidated the mechanism
of action of posterior vasopressin in resuscitation.
Epinephrine has been used for decades
as the leading drug for the treatment of cardiac arrest.
Posterior vasopressin is beneficial in patients with cardiac arrest, and a combination of epinephrine (1 mg) and posterior vasopressin (40 units) may be superior to either agent
alone.
The current recommended regimen is that the use of posterior vasopressin (40 U) in cardiac arrest can replace the first or second dose of epinephrine
with 1 mg.
Out-of-hospital cardiac arrest has a poor prognosis, with a global survival rate of about 6%.

Proven ventricular fibrillation in out-of-hospital cases has been reported to have a survival rate of up to 74%.

This success depends on training in CPR for lay people and the availability of defibrillators
in the first place.
Patients in the operating room are closely monitored, and adverse events can be detected early and can be treated with strong
controllability.

Septic shock The cornerstone of treatment of septic shock is antibiotics, volume resuscitation, and catecholamines
.
For patients with septic shock, improving survival is focused on rapid intervention
.
Current recommended regimens for the treatment of septic shock include antibiotics and volume resuscitation to maintain central venous pressure of 8~12mmHg and mean arterial pressure of 65 mmHg or higher
.
If fluid therapy does not produce the expected hemodynamic effects, norepinephrine and dopamine are appropriate vasoactive agents of choice
.
When catecholamine tolerance in patients with septic shock or when the corresponding dose causes side effects such as tachyarrhythmias, posterior vasopressin can raise blood pressure and reduce the amount
of catecholamines.
High doses of posterior vasopressin can cause mesenteric vasoconstriction leading to gastrointestinal ischemia
.
At low doses, posterior vasopressin improves gastrointestinal blood perfusion
.
Continuous intravenous administration of posterior vasopressin is superior to intermittent single loading doses of terlipressin, which has a longer duration of action, thereby reducing the likelihood
of endoenteric vasoconstriction leading to gastrointestinal ischemia.

Anaphylactic shock The recommended treatment regimen for anaphylactic shock is fluid therapy and the use of epinephrine
.
Posterior vasopressin has been shown to completely reverse histamine-mediated vasodilation, while epinephrine is only partially reversed
.
In the absence of further evidence, posterior vasopressin remains a suitable option
when epinephrine fails to maintain hemodynamic stability.

Hemorrhagic shock The goal of hemorrhagic shock resuscitation is to maintain effective circulating blood volume to maintain or improve vital organ perfusion and function
.
In animal model trials, there is growing evidence that volume resuscitation alone tends to have a poorer prognosis than limited volume therapy combined with
posterior vasopressin or norepinephrine.
However, the exact mechanism by which posterior vasopressin improves prognosis needs to be further elucidated, including posterior vasopressin-mediated vasoconstriction to reduce wound bleeding and increased postcirculating vasopressin levels
due to endogenous posterior vasopressin depletion.
Successful use of posterior vasopressin for resuscitation may be dose-related
.
Low-dose posterior vasopressin improves hemodynamic stability while avoiding harmful effects
such as organ ischaemia caused by high doses of posterior vasopressin.

Liver transplantation Patients with liver failure often have a variety of systemic diseases, and when hepatorenal syndrome develops, the prognosis is often poor
.
Low-dose intravenous infusion of posterior vasopressin may increase renal blood flow and has been successfully used to treat hypotension
in the immediate aftermath of liver transplantation.
At present, there are insufficient data to clarify the role of
posterior leaf vasopressin in patients with liver failure.

Intraoperative hypotension Patients treated with long-term angiotensin-converting enzyme inhibitors or angiotensin receptor blockers are prone to hypotension
during anesthesia.
This hypotension is often tolerated
to catecholamines or volume therapy.
The vasoconstriction of posterior vasopressin is independent of catecholamines and angiotensin receptors
.
Posterior vasopressin has been shown to be effective in the treatment of hypotension
in these patients.

The use of posterior vasopressin in patients with severe hypotension and shock is controversial
.
In a state of shock, vascular smooth muscle may be less sensitive or even tolerated
by catecholamines.
For patients with poor catecholamine reactivity, posterior vasopressin offers another treatment option
.
Further research
is needed to clarify the role of posterior vasopressin.

brief summary

Volume depletion and sepsis were the main causes of
intraoperative shock in this case.
Volume resuscitation does not always improve haemodynamic disturbances due to infectious or hemorrhagic shock
.
In fact, excessive fluid therapy can have a negative impact
on the patient's prognosis.
We don't always know how to maintain a balance of endogenous substances and intravascular volume to maintain hemodynamic stability
.
In this case, the amount of infusion, the type of fluid, as well as the vasoactive drug
must be determined.
Norepinephrine and epinephrine have been used for decades
to treat hypotension and shock.
Patients who respond poorly to these drugs may have a positive effect
offset by side effects when they are increased.
Posterior vasopressin is a naturally secreted vasoactive substance that may be relatively inadequate in some patients and require replacement therapy
.
Posterior vasopressin plus catecholamine use promotes hemodynamic stabilization and reduces catecholamine use
.
Initial enthusiasm for the use of posterior vasopressin for resuscitation tended to temper with further research
.
Compared to catecholamines, posterior vasopressin has a different mechanism of action at the cellular level, and these two different drugs may complement each other
.
If epinephrine does not have the desired effect, posterior vasopressin is the best choice
later.
Although the advantages of posterior vasopressin over other vasoactive agents in the treatment of shock are not well understood, the timing of interventions is decisive
.
The anesthesiologist can intervene in shock at an early stage and take effective treatment measures, thereby increasing the likelihood of
successful resuscitation.
Posterior vasopressin is often used in the operating room for the treatment of anaphylactic shock, postcardiopulmonary vasodilating shock, and intractable hypotension
in patients treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers.

Key information