Exam 2: Anesthetic Consideration in Cardiac, Neuro, Renal and Hepatic Patients Flashcards
What signs may point to a “cardiac” patient and what diagnostics should be run if suspected?
History, PE…
A history of lethargy, coughing, and syncope.
Minimum: auscultation, CBC, biochem, and chest radiographs.
ECG is good for conduction abnormalities, Echo for structural abnormalities.
Common premedications for patients with cardiac disease include** opioids and benzodiazepines, as these have minimal effects on the cardiovascular system**. Anticholinergics may be used if there is a concern that the opioid induced bradycardia would be deleterious. Agents with significant or profound cardiovascular effects such as acepromazine and dexmedetomidine should, in general, be avoided. Stress should also be avoided insomuch as possible, as it will
increase heart rate and myocardial oxygen demand in an already compromised patient.
How can you minimize changes in cardiac and vascular function and maximize cardiac output without significant changes in myocardial workload in a patient with mitral valve disease?
What drugs would you use during or before anesthesia?
Mitral valve disease is a common cardiac disease encountered in small and medium breed older dogs.
In this patient, you want to avoid fluid overload and maintain and appropriate heart rate. Vasoconstriction should be avoided and vasodilators can be used as therapy.
To AVOID: Alpha 2s cause vascoconstriction, so you want to avoid, can cause CHF.
OKAY to use: If you have to use something, opioids and benzos becasue they cause very little cardi changes. Acepromazine also decreases regurgitation because of its vasodilation properties.
Induction agents can be alflaxalone and propofol.
want vasodilation
Mitral valve disease causes eccentric hypertrophy of the left ventricle as well as retention of sodium and water to increase blood volume. Additionally, it causes premature atrial contractions or a-fib. It leads to pulmonary edema. Is often accompanied with tricuspid valve insufficiency where central venous pressures (as opposed to pulmonary) increases.
How can you minimize changes in cardiac and vascular function and maximize cardiac output without significant changes in myocardial workload in a patient with pulmonic stenosis?
In this case, acepromazine not helpful, hypovolemia bad thing. Benzos and opioids good.
Don’t forget to think about inhalants as drugs, inhalants biggest thing is they are vasodilators.
HELPFUL: Dexmedetomidine to undo changes from inhalant. Dex CRI in dog - undo vascular tone changes.
do not want vasodilation
Will see the ventricle expanding. Heart lifts off sternum in radiograph.
How can you minimize changes in cardiac and vascular function and maximize cardiac output without significant changes in myocardial workload in a patient with PDA?
Patent ductus arteriosis (PDA) usually always clinical (exercise intolerance, cyanosis)
Maintain circulatory, from systemic to pulmonary. Left to right.
Careful how you fix things in anesthesia so post-anesthesia isn’t worsened, want to watch volume… vascular tone is important here, do not want the shunt to reverse. Do not decrease SVR.
Once PDA is closed, no longer have to treat as cardio patient.
How can you minimize changes in cardiac and vascular function and maximize cardiac output without significant changes in myocardial workload in a patient with HCM?
thinking of cats here
NO: anticholinergics (judiciously)
YES: Etomidate. Can use alflaxalone IM if cat is difficult.
(vasopressor) Phenylephrine can help manage hypotension
a little dexmedetomidine is okay becasue maintains vascular tone and low heart rate
filling time (lusitropy) is important
dynamic outflow obstrution is the problem in HCM
avoid fluid overload
How can you minimize changes in cardiac and vascular function and maximize cardiac output without significant changes in myocardial workload in a patient with DCM?
dobermans, grain free diet
not really a cat problem
reach for dobutamine, causes little vasodilation and does not effect vascular tone.
opioids and benzos, not ketamine.
AVOID: alpha 2 agonists
dexmedetomidine is sometimes called “euthanasia lite”
What is the premedication, induction agent, and maintenance of anesthesia in a renal patient and why?
Premedication:
OKAY: Opioids (do not cause renal elimination, minimal cardio changes, and no impact to renal blood flow), benzos (provides sedation with minimal cardio effects), anticholinergics (if bradycardia induces decrease in CO or renal blood flow)
NO: Acepromazine (good sedation but causes vasodilation and hypotension and refractory to inotropes like dopamine and dobutamine.) Alpha 2 agonists like dexmedetomidine also causes isgnificant vasoconstriction and bradycardia reducing CO and renal blood flow.
Induction: propofol and alflaxalone is okay and has less effect than ketamine (large doses should be avoided in patients with significant renal compromise). inhalant inductions should be avoided as it causes vasodilation, myocardial depression and decreased CO.
Maintenance: sevofluorane produces compound A when in contact with CO2 absorbents which is toxic to kidneys. isofluorane and desofluurane is okay.
What should be monitored in a renal patient? What kind of care should be provided?
blood pressure and oxygen delivery specifically for the kidneys with a doppler, invasive pressure with arterial catheter. blood gases, hemoglobin and creatinine.
MABP should be maintianed at 60-70mmHg
Systolic BP should be 90-100mmHg
When urine output falls below .6ml/kg/hr, depth should be assessed (2ml in normal awake patient)
fluids shouldbe administerd JUDICIOUSLY to anuric or oliguric patients fo risk of volume overload and CHF.
Crystalloid therapy is good for maintenance of intravascular volume several hours PRIOR to anesthesia. Colloids should be used with catuion. HES known to accumulate in renal parenchyma.
Mannitol is okay as diuretic and dopamine to inrease renal blood flow, GFR and ruine output in dogs. In cats, fenoldopam.
What is the premedication, induction agent, and maintenance of anesthesia in a hepatic patient and why?
Premedication:
NO: acepromazine, metabolism is dependent on liver and concern for hypotension and vasodilation. All alpha 2 agonists cause vasoconstriction and bradycardia, decreasing CO and should be avoided if possible
YES with caution: Benzos (midazolam preferred) may exacerbate hepatic encephalopathy and are significantly metabolized by liver but is reversible with flumazenil.
YES: opioids, gold star
Induction:
NO: thiopental, significantly prolonged elimination and duration of effect
YES: propofol and alflaxalone, administered to effect and both rely on redistribution for termination.
MAintenance:
NO: Halothane, significant hepatotoxicity
YES:inhalant anesthetics (des, iso, sevo)
prolonged drug activity should be expected
drugs that can be reversed or are metabolized/eliminated by other routes should be given preference.
What should be monitored in a hepatic patient? What kind of care should be provided?
As with any patient: ECG, pulse oximetry, capnography, temperature, and BP
Crystalloid administration should be MINIMIZED
Synthetic colloids (hetastarch and vetstarch) and plasma good.
MONITOR blood glucose
What are some considerations for a CNS patient?
What are intervranial events or changes that can be involved?
Intra-Cranial Pressure (ICP)
CNS Metabolic Rate (CMR)
CNS Blood Flow (CBF)
Cerebral Perfusion Pressure (CPP) = MAP-ICP
Increased ICP should always be suspected in cases of head trauma or suspected intra-cranial pathology.
The Cushing’s Relfex is often a late marker of increased ICP, where MAP increases suddenly in the face of increased ICP to maintain CPP.
How can you prevent the increase of ICP?
maintain low normal PaCO2 (30-35 mmHg)
prevent signoificant hypoxemia
maintain adequate MAP
Prevent significant alterations in acid-base status
Increases in intrathoracic pressure (coughing or straining to breathe) can increase venous pressure and cause a back up (possibly into closed back space of the skull) and increasing jugular venous pressure by mechanical acclusion or inappropraite restrint will decrease venous outflow from cranium leading to an increased ICP, therefore a decreased CPP and mechanical or ischemic neurologic injury.
What are some pre-anesthetic considerations for the neuro patient?
avoid administering large volumes of crystalloid fluids, preoxygenate patients to alleviate the drop in PaO2, have sufficient IV access, patient’s head should be below the level of the heart, no sudden thoracic or abdominal compressions, monitor blood glucose, avoid large swings in blood pressure, monitor temp/ hypothermia can be useful, recovery should be slow and calm.
What drugs are contraindicated in the neuro patient? What works?
alpha 2 agonists such as dexmedetomidine, and ketamine are to be avoided.
inhaled anesthetics should be administered at MAC levels below 1.
Propofol (due to preservation of CBF/CMR coupling) is the agent of choice.
glucocorticoids are controversial, do not give in any head trauma
What are anesthetic considerations in the spinal/ PNS patient?
thiopental is drug of choice in spinal patients but hard to find currently. ketamine/diazepam (midazolam) is appropriate.
excessive bleeding is a probelm in surgery.
in the PNS, analgesia good, opioids, alpha 2 agonists, ketamine (also good for wind up), lidocaine.
