Anesthesia in the cardiac patient
Caleb D. Coursey, EMT-P
First and foremost, one must know a little anatomy and physiology to completely
understand what the “murmur” may mean and how it could affect anesthesia.
The patient that presents for elective procedures with know disease is treated
very similarly to a patient with suspected disease. While discussing every
possible cardiac process would be very valuable, it is beyond the scope of this
lecture, but one must understand a few basic (and more common) disease
processes.
Cardiomyopathies can be broken into two sections – dilated and hypertrophic.
Dilated cardiomyopathy is most commonly seen in certain large breed dogs. This
condition is characterized by elongation, weakening of the heart muscle, so that
chamber size is increased, but contractility is compromised. Stroke volume is reduced
and resulting in decreased blood pressure. Due to the increased size of the chamber,
communication between cardiac cells may be compromised leading to atrial and
ventricular arrhythmias. Ideally these patients would be controlled with medical
management for elective procedures. Digitalis and digoxin are positive inotropes that
increase the concentration of calcium within the myocardial cells thus increasing the
force of contractions and decreasing heart rate. A relatively new addition to
management is pimobendan, which elicits calcium sensitization of the myofilaments.
Anti-arrhythmic such as procainamide, quinidine or mexiletine may be used if indicated.
Calcium channel blockers and beta-blockers may be used to help control
supraventricular arrhythmias. Diuretics such as furosemide are used for decreasing
circulating blood volume. ACE inhibitors cause relaxation of the blood vessels, thereby
decreasing systemic vascular resistance.
Hypertrophic cardiomyopathy is most commonly seen in feline patients, but can be
rarely seen in canines. Feline hypertrophic cardiomyopathy is common complication of
hyperthyroidism, but generally, its etiology is not considered genetic. The disease is
considered a disease of diastole and is characterized by inability of the heart to fill
adequately with blood, thickening of the left ventricular wall and decreased chamber
size. Relaxation of the heart muscle during diastole and decreased filling due to
chamber size is affected thereby reducing cardiac output.
Hypertrophic cardiomyopathy may also occur independent of hyperthyroidism. In these
cases, increased wall thickness and decreased chamber size are still an issue. It is
important to maintain heart rate within normal range in order to maintain cardiac output
in the face of decreased stroke volume. Relaxation of the heart during diastole is
important to promote optimal chamber filling, as well as perfusion to the heart muscle so
that it may receive as much oxygen as possible to meet its increased demands.
Mitral valve disease is one of the most common processes in canine patients. A normal
mitral valve will close during ventricular contraction, thereby causing all blood to move
forward to systemic circulation. A defective valve will allow some blood to be pumped
back into the left atrium. This reduces forward flow, and thus cardiac output and
systemic blood pressure. In addition, pressure in the left atrium will increase, making it
more difficult for blood to enter it from the lungs. Resulting backpressure in the lungs
may lead to pulmonary edema. Compensatory mechanisms in response to lowered
blood pressure will increase the total fluid volume in circulation and cause
vasoconstriction. This, however, results in an increase in resistance against which the
left ventricle must pump. Over time, the left ventricular muscle will may enlarge due to
this “workout”, but its efficiency continues to decline. Eventually, if left untreated, leftsided heart failure will result in life threatening pulmonary edema and inadequate tissue
perfusion. Treatment for significant mitral valve dysfunction consists of medications that
cause relaxation of the blood vessels, such as ACE inhibitors, or other vasodilators
making it easier for the left ventricle to pump blood forward. Diuretics (e.g. furosemide)
are administered in order to reduce the volume load for the heart to pump, and remove
fluid causing pulmonary edema. In addition, positive inotropes (e.g. digitalis) will
increase contractility of the heart by increasing the concentration of calcium in heart
muscle cells. When anesthetizing a patient with mitral valve disease, one must be
careful since the vasodilator effects of many anesthetics may be exaggerated by the
patient’s existing medication. On the other hand, untreated mitral valve disease may
benefit from the vasodilation effects of anesthetics. When pressors are needed, pure
alpha agonists such as phenylephrine that cause vasoconstriction may exacerbate the
backpressure and may result in pulmonary edema. Beta agonists such as dobutamine
may be used to improve contractility. Fluids must be administered conservatively, to
avoid overload and pulmonary edema. However, because these patients may have
been on diuretics and also have the same issues a normal patient with regard to fluid
needs, there is a balance that must be achieved. Currently, the most effective way to
monitor this balance is by measuring central venous pressure (which approximates the
pressure of the blood entering the right atrium). Maintaining heart rate within the normal
range for these patients is important. Tachycardia should be avoided, as it will increase
the oxygen needs of the heart, so an anticholinergic is usually not recommended
prophylactically as in a pre-med. However, low doses can be used if indicated by
bradycardia that is causing hypotension. Opioids, benzodiazepines, and etomidate are
considered good choices in an anesthesia protocol for these cases. Ketamine is usually
avoided as it increases myocardial oxygen needs. Propofol should be avoided or used
with extreme care due to its vasodilation and hypotensive effects. IV administration of
an opioid/benzodiazepine combination immediately prior to induction with Propofol can
greatly reduce the amount of propofol required to capture the airway thus allowing the
anesthetist to use this agent while avoiding the majority of the myocardial depressive
effects.
Aortic stenosis is usually a congenital abnormality. Stenosis may be subvalvular,
valvular, or supravalular and is caused by the development of extra fibrous tissue
sometime during the first few months in life. This results in a partial obstruction of flow
from the left ventricle through the aortic valve and out the aorta to systemic circulation.
This obstruction causes increased left intraventricular pressure and subsequent
thickening of the left ventricular walls. Other issues include cardiac ischemia,
arrhythmias, aortic or mitral regurgitation, and left-sided congestive failure.
Diagnosis is usually made at an early age due to a murmur caused by the increased
turbulence of blood flow in the affected area, but the degree of disease may or may not
correlate with the loudness of the murmur. Mildly affected dogs may lead fairly long
lives, whereas severely affected animals develop CHF or may die suddenly of
ventricular arrhythmias. Medical management usually begins with the administration of
beta-blockers in order to limit myocardial oxygen consumption, prevent tachycardia and
ventricular arrhythmias. However, as heart failure ensues, increased heart rate is
necessary for maintaining cardiac output and beta-blockers become counterproductive.
As the heart walls thicken and the muscle becomes less compliant cardiac output is
dependent of adequate filling pressure. Thus, diuretics and venodilators must be used
with caution. ACE inhibitors, calcium channel blockers, or other arteriolar dilators may
also negatively affect the ability of the heart to produce adequate cardiac output due to
worsening of the obstruction. Positive inotropes may also exacerbate outflow
obstruction and ventricular arrhythmias.
Pharmacology Review:
Anticholinergic
Atropine / glycopyrrolate:
Will cause an increase in heart rate, contractility, cardiac output and myocardial
oxygen consumption.
Often there will be no change in blood pressure and a decrease in right atrial
pressure
Phenothiazine –
Acepromazine:
Main cardiovascular effect = peripheral vasodilation
Consequence – decreased blood pressure
Some boxers – fainting/syncope seen due to vasovagal response (bradycardia
and peripheral vasodilation)
Benzodiazepines
Midazolam / diazepam:
Cause little or no myocardial depressant effects
May see increase in heart rate due to excitation with inadequate use of
adjunctive agent (opioid)
When combined with an opioid as a CRI can be utilized to decrease MAC of
inhalant agent.
No analgesia provided
Alpha 2 agonist
Dexmedetomidine / Xylazine:
Significant cardiovascular effects
Vasoconstriction
Bradycardia
Decreased cardiac output
Mu opioids
Fentanyl:
Causes dose dependent bradycardia (increase in vagal tone)
Bradycardia is responsive to anticholinergic – atropine / glycopyrrolate
Hydromorphone:
Morphine like agonist primary activity at the mu receptors.
Cardiovascular effects: bradycardia due to central vagal stimulation,
Alpha-adrenergic depression causing peripheral vasodilation decreased
peripheral resistance baroreceptor inhibition.
Morphine:
No direct myocardial effect
Dose dependent bradycardia – responsive to anticholinergic
Mixed agonist/antagonist agents
Buprenorphine:
Partial mu agonist / antagonist. Slow onset of action, duration of 6-8 hours.
Cardiovascular depression and respiratory depression not as with a profound as
pure mu agonists.
Butorphanol: partial agonist/antagonist. Similar to buprenorphine in
cardiovascular / respiratory effects. Quicker onset of action, shorter duration that
buprenorphine.
Recommended in multiple texts for premedication for cardiac patients due to
minimal cardiac effects.
Hypnotic / Amnestic
Etomidate: no direct myocardial depression.
Cardiovascular stability may be better due to maintained baroreceptor mediated
responses.
Propofol:
Does cause direct myocardial depression as well as decrease in systemic
vascular resistance
Decrease in contractility leads to increase in heart rate – will be transient –
lasting several minutes
Profound bradycardia has been noted (dose dependent)
Use cautiously in patients with heart disease and hypovolemia
Neurosteroidal Hypnotic / Amnestic
Alfaxalone
Minimal cardiovascular depression
Similar to etomidate without the unpleasant retching / coughing / gagging
Dissociative Agents
Ketamine:
Will indirectly stimulate the cardiovascular system by increasing sympathetic tone
causing an increase in heart rate, cardiac output, mean arterial pressure,
pulmonary arterial pressure and central venous pressure. Increase in rate
causes an increase in myocardial work and oxygen demand/consumption
Developing a protocol that will provide a smooth induction – good muscle
relaxation with analgesia, and allow the airway to be rapidly secured it critical.
This will help prevent undue stress (which will increase oxygen demand, heart
rate, and blood pressure), as well as help prevent aspiration of any gastric
contents.
Suggested protocols may include the following:
Pre-medication: should be given 20-30 minutes prior to induction time to allow adequate
onset of activity. Remember that this is for an elective procedure and not an emergency
induction.
Glycopyrrolate (0.011 mg/kg) or Atropine (0.02 – 0.04 mg/kg) given subcutaneously,
dependent on patient’s heart rate and needs
Hydromorphone (0.1 mg/kg) or Oxymorphone (0.05 mg/kg) given subcutaneously.
Should patients be of a brachycephalic breed where respiratory difficulties may be
present, Butorphanol (0.2 mg/kg) can be substituted for the Hydromorphone and the
patient will be observed for any signs of distress. Additional analgesics can be given
post intubation.
Pre-oxygenation should be performed for 2 – 3 minutes before induction.
Induction agents:
Diazepam / Midazolam (0.2 mg/kg) given IV followed by
Etomidate at 1-2 mg/kg given IV to effect to facilitate placement of the endotracheal
tube. This protocol can cause some distress if you are not comfortable with the use of
etomidate (regurgitation, difficult intubation, etc.)
Midazolam (0.2 mg/kg) given IV followed by
Propofol (2 – 5 mg/kg) given IV slowly to effect.
Midazolam (0.2mg/kg) given IV followed by
Alfaxalone (2 mg/kg) given IV to effect
Lidocaine (2 mg/kg) IV followed by
Midazolam (0.2 mg/kg) IV followed by
Etomidate (1 – 2 mg/kg) OR Propofol (2 – 4 mg/kg) OR Alfaxalone (2 mg/kg) IV. All are
given slowly and to effect.
Fentanyl can also be added (5 mcg/kg IV) at the start of the protocol to increase
sedation. In the debilitated animal, an “induction” drug may not be needed.
Anesthetic maintenanceInhalant gas anesthesia maintenance is often sevoflurane with oxygen, but this may not
be practical for every hospital. Bumps of Propofol should be avoided to prevent “rollercoaster” anesthesia, and in turn increase cardiac complication.
Fentanyl at 0.8 mcg/kg/minute and midazolam at 8 mcg/kg/minute combined may
be given IV via syringe pump as an anesthetic adjunct for a MAC sparing
effect. This will allow the vaporizer setting to be reduced to between 0.25-1% if
sevoflurane is the inhalant used. Other CRI’s can be added to further decrease
inhalant need (Lidocaine, Propofol, Alfaxalone). Depending on the procedure,
the use of local blocks / epidurals will also facilitate a reduction in the amount of
general anesthetics needed.