Hypotension....what to do? (Proceedings)


Mean arterial pressure (MAP) is the driving force for blood flow (perfusion) through capillaries that supply oxygen to organs and tissue beds of the body.

Why treat hypotension?

Mean arterial pressure (MAP) is the driving force for blood flow (perfusion) through capillaries that supply oxygen to organs and tissue beds of the body. Thus, when speaking of hypotension it is most important to focus on the MAP. In small animals, MAP < 60 mm of Hg result in compromised perfusion of visceral organs and peripheral tissues, potentially leading to whole organ or regional ischemia. In large animals perfusion of skeletal muscle (especially skeletal muscle in recumbent areas of the body) is compromised at MAP < 70 mm of Hg. In all species, MAP < 40 mm of Hg are associated with inadequate perfusion of vessel-rich organs such as the heart, lungs, and CNS. Clinically significant hypotension (i.e. mean arterial pressure less than 60 mm of Hg) can lead to renal failure, reduced hepatic metabolism of drugs, worsening of ventilation/perfusion mismatch and hypoxemia, delayed recovery from anesthesia, neuromuscular complications during recovery (especially large animals), and CNS abnormalities including blindness after anesthesia that may or may not resolve with time. Untreated, severe hypotension can lead to cardiac and respiratory arrest.

Estimation of MAP

Mean arterial pressure = diastolic pressure + 1/3(systolic pressure - diastolic pressure). Most indirect blood pressure monitors provide data for systolic pressure (e.g. doppler method) or systolic, diastolic, and mean arterial pressure (e.g. oscillometric devices). Roughly, the mean arterial pressure is 20 - 30 mm of Hg less than the measured systolic pressure on a doppler in most species. Thus, a doppler reading of 80 to 90 mm of Hg correlates with a mean arterial pressure that would be considered hypotensive. The exception to this rule is cats < 4 - 5 kg (and likely other small mammals) in which the doppler reading correlates most closely with mean arterial pressure.

What determines blood pressure?

Mean arterial pressure = cardiac output x systemic vascular resistance. In thinking about causes of hypotension, it is useful to break this equation down into its various components and then assess the effects of anesthetic drugs or the animal's physiologic state on each component. Cardiac output = heart rate x stroke volume. For example, a drug that reduces contractility (e.g. isoflurane) will lower stroke volume and can then contribute to a lower cardiac output, which may result in low mean arterial pressure if systemic vascular resistance has not increased.

Systemic vascular resistance

A reduction in systemic vascular resistance (SVR) will decrease mean arterial pressure. Many of the drugs commonly used for anesthesia will reduce systemic vascular resistance. These drugs include: acepromazine, thiobarbiturates, propofol, and, most importantly, inhalants. All of the above listed drugs decrease systemic vascular resistance in a dose-dependent fashion. Preexisting physiologic factors in a patient that presents for anesthesia (e.g. dehydration), or events that may occur as a result of surgical intervention (e.g. blood loss), will also decrease SVR. When possible, preexisting causes of reduced SVR should be corrected prior to general anesthesia. Examples include: hemorrhage, inadequate volume administration or replacement, dehydration, endotoxemic shock, overwhelming sepsis, cardiogenic shock, neurogenic shock, anaphylaxis, histamine release, severe hypercapnia.

Heart rate

A reduction in heart rate may or may not affect mean arterial pressure. If heart rate is low in the face of good contractility, then often the increase in end-diastolic ventricular volume (and associated increase in ejected stroke volume) will help to maintain cardiac output and therefore mean arterial pressure. If contractility is poor, however, as is often the case in patients receiving inhalant anesthetics, then stroke volume may not increase in response to a longer diastolic filling time and measured mean arterial pressure will be reduced. The following is a list of drugs or pre-existing conditions that may reduce heart rate: physiologic (athletic) bradycardia, hypothermia, increased vagal tone, high cervical cord compression, intracranial disease, electrolyte imbalances, opioids, alpha-2 agonists, inhalants, acetylcholinesterase inhibitors, anticholinesterases (transient, paradoxical; increase in heart rate usually follows; e.g. glycopyrrolate).


Factors that reduce preload (end diastolic ventricular volume) and thus indirectly reduce stroke volume include: reduction in venous blood volume from blood loss, dehydration, inadequate fluid replacement, vasodilation and "relative" hypovolemia from peripheral vascular pooling (e.g. inhalant anesthesia), occlusion of vessels of venous return. A common cause of reduced preload in anesthetized animals is positive pressure ventilation. During the inspiratory phase of positive pressure ventilation, peak airway pressure is reflected as peak intrathoracic pressure which may be high enough to transiently compress the cranial and caudal vena cavae as they enter the thorax. This results in reduced right atrial and ventricular filling during inspiration and will lead to lower stroke volume on the subsequent ventricular systole.


Stroke volume and afterload are inversely related. Some physiologic factors in patients presenting for anesthesia and anesthetic drugs can increase afterload and thus reduce stroke volume. These include high sympathetic tone, pheochromocytoma, hyperthyroidism, cardiac outflow tract stenosis (e.g. pulmonic stenosis, heartworm disease), exogenous epinephrine administration, phenylephrine, alpha-2 agonists, ketamine, tiletamine (telazol).


Reduced contractility is one of the most common causes of hypotension in anesthetized patients. This is because the inhalants are potent negative inotropes, yet are a necessary (almost always) component of general anesthesia. Physiologic factors that reduce contractility should be corrected, if possible, prior to administration of anesthetic drugs. The following is a list of peri-anesthetic factors that impair contractility: inhalants (isoflurane=sevoflurane>desflurane), thiobarbiturates, propofol, alpha-2 agonists, intrinsic cardiac disease (e.g. dilated cardiomyopathy), pericardial disease, severe sepsis or endotoxemia, electrolyte imbalances, severe acidemia, beta blocking drugs (e.g. propranolol, esmolol), profound hypothermia. Drug related reductions in contractility are dose-dependent. Among the commonly administered anesthetic drugs, inhalants probably have the most profound effect on contractility, with reductions of up to 50% at surgical planes of anesthesia. The induction drugs listed also reduce contractility, but their effect is more transient and less profound than that seen with the inhalants.

In summary, the major players in hypotension are reductions in SVR, heart rate, stroke volume, and contractility. Thus, when developing treatment approaches for hypotension one should consider these 4 major players and rule in/out factors that affect them in the anesthetized animal.

Treatment of hypotension

Low systemic vascular resistance

Almost by definition an animal anesthetized with inhalants (especially isoflurane and sevoflurane) will have some reduction in SVR. Premedication with acepromazine further reduces SVR. One approach is to "fill the space" with aggressive administration of IV crystalloids. Before doing this, however, one must assess the animal's anesthetic depth, since reducing the administered dose of inhalant will help to increase SVR. In inhalant-anesthetized patients with normal cardiac and renal function a standard crystalloid administration rate before hypotension develops is 10 - 20 ml/kg/hour. This allows for filling of the increased vascular volume caused by inhalant mediated vasodilation. If further increases in vascular volume are deemed necessary, and the patient has normal cardiac and renal function, one can increase the crystalloid rate to 50 -70 ml/kg/hr (cats) and 70 -90 ml/kg/hr (dogs) for 15 minutes and then assess the response to treatment. In other words, run a shock dose of crystalloids for 15 minutes so that the animal receives 1/4 of an hour's worth of shock fluids. This can safely be done 2-3 times unless the animal is at risk for pulmonary edema (e.g. mitral valve insufficiency) or is anemic or hypoproteinemic (dilutional effect). If mean arterial pressure has not increased at this point then one should return to the algorithm. When administering aggressive fluid therapy, it is advisable to monitor PCV/TP, electrolyte status, acid-base balance, and auscult lung sounds in order to recognize and prevent pulmonary edema.

It is rarely necessary to increase SVR with drugs. Usually, in hypotensive patients that do not respond to fluid therapy, the cause can be found in stroke volume or, less often, heart rate. However, occasionally ephedrine is used to increase SVR when other parameters in the algorithm have already been addressed. Ephedrine increases vascular tone by indirectly stimulating alpha-1 receptors in vascular smooth muscle through release of norepinephrine. The recommended dose of ephedrine is 0.03 - 0.07 IV as a slow bolus. Since the drug's mechanism of action is indirect it can take 20 - 30 minutes to induce a response.


Bradycardia can be friend or foe when dealing with hypotension. On the one hand, a slow heart rate allows for generous right atrial and ventricular filling, which in turn provides optimal diastolic filling and stroke volume on the subsequent systole. Since coronary blood flow (and myocardial oxygenation) occur during diastole, bradycardia and a long diastolic period help to optimize myocardial oxygen supply. However, if bradycardia is coupled with less than optimal contractility (either from anesthetic drugs or disease) it is sometimes necessary to increase the heart rate in order to treat hypotension.

Bradycardia is common in anesthetized patients, especially when systemic opioids are used concurrently for analgesia. The first approach to treating bradycardia is to reduce administered doses of inhalant, if possible. One can also consider reversal of systemic opioids, if present, with naloxone or butorphanol. Since opioids were likely given to provide analgesia, however, reversal may not be desirable for patient comfort and recovery. One should also ensure that the patient is normothermic, as bradycardia secondary to hypothermia will not respond to pharmacologic intervention. Finally, one should address electrolyte or acid-base abnormalities that may be contributing to bradycardia. If bradycardia is secondary to prior administration of alpha-2 agonist drugs (e.g. dexmedetomidine) then one should not attempt to increase the heart rate pharmacologically, but rather should consider reversal with atipamezole. This is because alpha-2 agonists increase afterload and the bradycardia is a physiologic response to the increase in afterload. Falsely raising the heart rate with alpha-2 agonists "on board" will dramatically increase myocardial work.

Anticholinergics such as atropine or glycopyrrolate will increase heart rate in all species. Atropine is more potent than glycopyrrolate, and as such is more likely to cause undesirable tachycardia. For this reason, atropine is more often used for life-threatening bradycardia. Both drugs can be given IV or IM. The dose for atropine is 0.02 - 0.04 mg/kg; glycopyrrolate is 0.005 - 0.01 mg/kg. Paradoxical bradycardia and AV block are occasionally seen soon after drug administration, especially with glycopyrrolate. This effect is usually overridden as the plasma concentration of glycopyrrolate reaches therapeutic levels.

Administration of anticholinergics can result in tachycardia. Severe tachycardia may worsen hypotension, since diastolic filling and stroke volume are compromised. However, if tachycardia develops after anticholinergic administration it usually resolves within 10 - 20 minutes. Other side effects of anticholinergic administration include ileus (especially in large animals), decreased salivation (which may or may not be desirable in a given patient), pupillary dilation, bronchodilation, and reduced mucociliary transport in the trachea.

Reduced preload

Reduced preload should be addressed first by eliminating factors that might mechanically cause it, such as positive pressure ventilation at high airway pressures, abdominal distension, etc. If this is not possible then preload can be increased with IV crystalloids as discussed with SVR. Occasionally, crystalloid administration is insufficient to increase preload, due to low oncotic pressure (e.g. hypoalbuminemia) or blood loss. Briefly, if the animal has reduced preload that has not improved with crystalloids, oncotic agents will help to maintain venous blood volume by reducing leakage of water into the interstitial spaces. Oncotic agents commonly used in anesthetized animals include fresh whole blood, plasma, hetastarch, and dextran 70. These agents are particularly useful in animals that are hypoproteinemic or have suffered blood loss. They should not, with rare exceptions, be used exclusively for volume replacement, but rather as an adjunct to crystalloids to enhance total venous blood volume. My preference is to give a bolus of hetastarch (5 ml/kg) over 15 minutes and assess the change in blood pressure. Hetastarch can be infused to a total volume of 20-40 ml/kg/day. Caution should be exercised in animals with myocardial or valvular disease and those with coagulopathies.


If poor contractility is suspected, one should first address, if possible, physiologic and pathologic causes as discussed above. For example, if the animal is severely acidemic that should be corrected prior to other manipulations to increase contractility. As mentioned previously, inhalants are the most common causes of poor contractility in normal, anesthetized animals. Thus, a logical approach to improving contractility is to reduce or eliminate the inhalant. However, eliminating the inhalant entirely is rarely feasible. One option is to reduce the required inhalant dose by supplementing with systemic opioids. For example, a patient anesthetized with isoflurane or sevoflurane can be given intermittent boluses of IV opioids such as oxymorphone or hydromorphone in order to reduce the delivered inhalant concentration while maintaining surgical anesthetic depth. Recommended doses for oxymorphone are 0.025 - 0.1 mg/kg; for hydromorphone 0.05 - 0.2 mg/kg; either drug can be given in this dosage range as needed to reduce the inhalant and thereby improve contractility. A "fine tuned" alternative is to deliver constant rate infusions of other analgesics, such as fentanyl (2.5 - 20 mcg/kg/hour [note units]), lidocaine (25-50 mcg/kg/min) or ketamine (2 – 10 mcg/kg/min). This can be accomplished using a syringe pump or buretrol. Constant rate infusions allow one to titrate the drug up or down to maintain adequate depth. With fentanyl doses of 10-20 mcg/kg/hour, especially in sick patients, anesthetic inhalant requirement maybe reduced by 100%. In other words, the MAC of isoflurane in a patient receiving fentanyl can be as low as 0.5%. The use of CRI's as adjunctive analgesics will be discussed in more detail in the "New and old approaches to treating acute peri-operative pain" lecture tomorrow morning.

Inotropes such as dopamine and dobutamine can be given to increase contractility. However, these drugs should not be used without attention to ensuring adequate vascular volume as well. Additionally, before administration of an inotrope, one should seek to minimize inhalant doses as described above. Dopamine and dobutamine stimulate beta-1 receptors in the myocardium, thus enhancing myofilament shortening and ventricular contractility. These drugs are given as infusions, at a dose range of 1 - 10 mcg/kg/min. Individual animal sensitivity varies greatly, so one should always start with the lowest recommended dose. The half life of these drugs is short (3 - 5 minutes) so their effect is short-lived once the infusion is discontinued. Do not bolus these drugs!

Dobutamine is a synthetic catecholamine, while dopamine is a precursor to epinephrine and norepinephrine. As such, these drugs exert effects similar to endogenous catecholamines. The most common side effect noticed in anesthetized animals when these drugs are given are tachycardia (especially with dopamine) and occasionally atrial and ventricular arrhythmias. Because the half-life of these drugs is short, termination of the infusion or reduction of the dose usually results in resolution of these complications.

Preventing hypotension

Plan ahead! Assess the patient's risk for hypotension prior to anesthesia. Ensure adequate volume status, correct underlying acid-base and electrolyte abnormalities, correct underlying pathologic states if possible, use the lowest possible dose required of acepromazine or alpha-2 agonists, or eliminate them altogether, premedicate with agonist opioids for preemptive analgesia and reduction of inhalant requirement, reduce induction drug requirements with IV benzodiazapines and opioids immediately prior to induction, consider supplemental opioids during anesthetic maintenance, as needed, look for alternative methods to provide analgesia and inhalant reduction for surgery, such as epidurals, local blocks etc., give IV crystalloids to all patients receiving inhalant anesthetics. Finally, monitor blood pressure! The best way to prevent hypotension is to detect reductions in blood pressure as soon as they occur!

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