CARDIOLOGY
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effect of pethidine administration, and to lesser
extent with morphine. Morphine induces vomiting (increases patient anxiety and stress) more
commonly compared to fentanyl and methadone. Therefore, pre-emptive treatment with an
antiemetic (e.g. maropitant) prior to morphine
administration is advised. Buprenorphine, a partial mu-agonist, should only be reserved for minor
painful procedures or as a post-surgical analgesic
when pain levels have subsided to a mild to moderate pain level (e.g. gonadectomy procedures).
Butorphanol, a mixed mu-antagonist-kappa-agonist, is usefully to partially antagonise undesirable
effects of pure-mu opioids (e.g. dysphoria, delayed recovery, hypoventilation) while maintaining some analgesia.
Induction agents that can be used include potent
opioids of the fentanyl group (e.g. fentanyl, sufentanil), propofol or alfaxalone. Patients suffering a
murmur of cardiac origin may have a decreased
cardiac output and thus the perfusion to the central nervous tissue may be decreased. Therefore,
careful titration of intravenous induction agents is
always advised as there will be a delay in the onset
of action. Volatile inhalation anaesthetics (isoflurane, sevoflurane) are the preferred maintenance
agents because they provide good myocardial
perfusion and rapid recovery.6, 11
The routine use of alpha2-adrenoceptor agonists
(xylazine, medetomidine, dexmedetomidine) are
contraindicated in most cardiovascular cases and
should only be used in cases where the pathophysiology of the disease process is well understood. These drugs cause a profound peripheral
vasoconstriction, increase in blood pressure and
reflex bradycardia during the initial phase of drug
administration. Once the drug moves more centrally (central nervous system) there is a decrease
in sympathetic tone which causes a decrease in
vasoconstriction and relative increase vagal tone
to the heart which maintains the bradycardia.8
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Figure 3: Maintaining normothermia with judicious use of blankets and heating devices.
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Both the initial peripheral and delayed centrally
mediated drug effects are not desirable in most
patients suffering cardiac disease due to alterations in the systemic vascular resistance and heart
rate. However, in certain cardiac pathologies
where a murmur may be heard, such as hypertrophic cardiomyopathy in cats, medetomidine
has been shown to decrease the dynamic outflow obstruction of the left ventricle and is useful
in maintaining cardiac output.
Making use of a familiar protocols to induce and
maintain general anaesthesia is considered safer
than using an unfamiliar protocol. However, there
are physiological derangements which manifest
from inappropriate drug selection which may be
detected over time, such as an early cardiac patient presenting with acute renal failure, a stable
patient rapidly deteriorating weeks after the general anaesthesia. Thus the immediate post- operative recovery for a poorly planned anaesthetic
does imply that no “harm” has been done to the
patient. Examples of less desirable anaesthetic
protocols would include: xylazine-atropine premedication, thiopentone induction and maintenance, and protocols with no-premedication or
analgesics.
Always provide enough analgesia during the procedure using a multimodal approach where possible. Maintenance agents are designed to keep
the patient asleep in an appropriate surgical plane
(or lighter for diagnostic investigations such as
radiographs). If the patient awakens often during
surgical stimulation it is indicated to increase the
analgesia and not the anaesthesia depth. In patients with cardiac disease a combination of opioids, local anaesthetics and judicial use of nonsteroidal-anti-inflammatory (NSAIDs) drugs are
preferred. Whereas healthy patients without other
organ failure, a combination of opioids, local anaesthetics and routine use of NSAIDs should suffice.7
Fluid management in patients with cardiac disease
requires titration to individual needs. Ensuring that
the intravascular volume is maintained throughout the general anaesthetic is important however
fluid overloading is a real post-anaesthetic risk in
patients suffering from cardiac disease. An early
indicator of fluid overloading is an increase in
the respiratory rate of at least 20% which is not
due to surgical stimulation or depth of general
anaesthesia. The effort of breathing will also be
increased and referred breath sounds can be auscultated due to the increased sound carrying capacity of the lung tissue due to interstitial fluid accumulation. Late indicators of fluid overloading
are jugular distension, increase in central venous
pressure, auscultating for changes in respiratory
sounds (crackles) and pleural effusions (especially
in cats).
A fluid rate of 10 mL/kg/hour could be started
just after induction and titrated downwards to 5
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