Chp. 23 Hypotension Flashcards
What are acceptable lower limits for BP in anesthetized small animals?
<60mm Hg –> compromised perfusion of visceral organs, peripheral tissues –> whole organ or regional ischemia (esp kidney)
What is MAP?
Mean Arterial Pressure
Driving force of blood (perfusion) through the capillaries to supply oxygen to organs and tissue beds of the body
What are acceptable lower limits for BP in anesthetized horses/large animals?
- Perfusion of skeletal m (esp skeletal m in recumbent areas of the body) compromised at MAP <70
- MAP <70 for extended length of time –> skeletal m ischemia –> post anesthetic myopathy
Consequences of MAP <40 mm Hg
-Inadequate perfusion of vessel-rich organs including heart, lungs, CNS
Anesthetic, post-anesthetic risks caused by hypotension
- Renal failure
- Reduced hepatic metabolism of drugs
- Worsening VQ mismatch, hypoxemia
- Delayed recovery from GA
- Neuromuscular complications during recovery (LA*)
- CNS abnormalities (blindness)
- Cardiac, respiratory arrest if left untreated
What defines hypotension?
To the anesthetist, hypotension defined as MAP <60mm Hg in small animals and <70mm Hg in large animals
What determines MAP?
MAP = CO x SVR (CO = SV x HR)
How can I estimate MAP from systolic?
MAP = diastolic P + 1/3(systolic-diastolic)
Most indirect BPs provide data for systolic pressure (Doppler) or SAP, DAP, MAP (oscillometric devices)
On a Doppler reading, how is systolic related to MAP?
Doppler –> provides info on systolic except in cats <4-5kg
-In most species, MAP is 20-30mm Hg less than measured systolic reading on a Doppler
What is true about Doppler readings in cats <4-5kg?
In cats smaller than 4-5kg (and likely other small mammals), Doppler corresponds most closely with MAP
Thinking about HR portion of CO - what factors influence HR?
SNS vs PNS tone
Drugs
Inotropes
Disease
What are the three components of stroke volume?
- Preload
- Contractility
- Afterload
What are the components of SVR?
- Blood volume
2. Vascular Tone
What factors into preload?
Venous blood volume
What factors into contractility?
SNS “tone”
Drugs
Inotropes
Disease
What factors into after load?
Arterial Tone
What are some commonly administered anesthetic drugs that decrease SVR, might cause hypotension?
- Acepromazine
- Thiobarbiturates
- Propofol
- Iso
- Sevo
- Des
- Halothane
- dose-dependent fashion*
- Injectable anesthetics decrease SVR transiently bc of rapid redistribution
What are some other factors that might reduce blood volume +/- vascular tone and lead to decrease in SVR in anesthetized patient?
- Hemorrhage
- Inadequate volume administration/replacement
- Dehydration
- Endotoxemic shock
- Overwhelming sepsis
- Cardiogenic shock
- Neurogenic shock
- Anaphylaxis
- Histamine release
- Severe hypercapnia
What are some physiological states that might decrease HR?
- Physiological bradycardia (eg athletic equine)
- High cervical disease
- Hypothermia
- Fasting (cattle only)
- Intracranial disease
- EL imbalances
What are some common anesthetic drugs that might decrease HR?
- Opioids
- alpha 2 agonists
- Inhalants
- ACh Inhibitors (edrophonium)
- Anticholinesterases (transient/paradoxical - increase in HR usually follows)
- usually dose dependent, more profound in animals with pre-existing bradycardia*
What are factors that reduce preload, and thus indirectly reduce SV?
- Reduction in venous blood volume from blood loss, dehydration, inadequate fluid replacement
- Vasodilation, “relative” hypovolemia from peripheral vascular pooling (eg inhalant anesthesia)
- Occlusion of vessels of venous return
How does PPV reduce preload?
- Common cause of reduced preload in anesthetized animals
- During inspiratory phase of PPV, peak airway pressure reflected as peak intrathoracic pressure -> may be high enough to transiently compress cranial/caudal VC as enter the thorax
- Results in reduced right atrial filling during inspiration -> lead to lower SV on subsequent ventricular systole
Afterload and SV are inversely related. What physiologic factors or drugs might increase afterload and thus reduce SV?
- High sympathetic tone
- Pheochromocytoma
- Hyperthyroidism
- Cardiac outflow tract stenosis (PS, heart worm disease)
- Exogenous epi administration
- Phenylephrine
- Alpha 2 agonists
- Ketamine, tiletamine
What anesthetic drugs reduce contractility?
- Inhal (halothane > iso = sevo > des)
- Thiobarbiturates
- Propofol
- a2 agonists
- Beta blockers (propanolol)
What disease states reduce contractility?
- Intrinsic cardiomyopathy (DCM)
- Pericardial disease
- Severe sepsis, endotoxemia
- Electrolyte imbalances
- Severe acidemia
- Profound hypothermia
What is important to remember about anesthetic agents’ effects on cardiac contractility?
- Dose-dependent
- Inhal probably have most profound effect on contractility, with reductions up to 50% at surgical places of GA
Summarize the major players that reduce MAP and may lead to hypotension?
-Anything that reduces SVR, HR, or SV can contribute to hypotension
Can I treat a low SVR with crystalloids?
- Animal anesthetized with inhalants (esp sevo, iso) will have some degree of reduction in SVR
- Can fill the space with aggressive administration of IV crystalloids, but reducing inhalant will also increase SVR
When does bradycardia cause hypotension?
- Slow HR allows generous RA filling -> provides optimal diastolic ventricular filling, stroke volume on subsequent systole
- Coronary blood flow and myocardial oxygenation occur during diastole, bradycardia and long diastolic period help to optimize myocardial oxygen supply
- If bradycardia is coupled with less than optimal contractility, sometimes necessary to increase HR to tx hypotension
Options for increasing HR
- Reduce doses of inhalant, if possible
- Consider reversal of systemic opioids (naloxone, nalbuphine)
- Correct to/maintain normothermia -> bradycardia secondary to hypothermia will generally not respond to pharmacological intervention
- Address EL/AB abN that may be contributing
- Anticholinergics
- Positive inotropes
Are there risks to treating bradycardia with anticholinergics?
- Can result in tachycardia
- Severe tachycardia can worsen hypotension -> diastolic filling/SV compromised
- If tachycardia develops after anticholinergic administration, usually resolves within 10-20’
In addition to tachycardia, what are other SE of anticholinergics?
- Ileus (esp in LA)
- Decreased salivation
- Pupillary dilation
- Bronchodilation
- Reduced mucociliary transport in the trachea
What are treatment approaches for reduced preload?
- Addressed first by eliminating factors that might mechanically cause it -> PPV to high airway pressures, abdominal distention
- If not sufficient, can increase preload with IVF -> can be insufficient in cases of low oncotic pressure or blood loss
How can I increase preload with fluids other than crystalloids?
- Oncotic agents: fresh whole blood, plasma, hetastarch, dextran 40/70
- Agents particularly useful in animals that are hypoproteinemic or blood loss
- Should not be exclusively used for volume replacement, except in rare circumstances, but rather as an adjunct to crystalloids*
Oxymorphone Dose
0.025-0.05mgkg IV
Hydromorphine dose
0.05-0.1mgkg IV
Fentanyl CRI rate in mcg/kg/hr
- 5-20mcgkghr
* with doses of 20mcgkghr or higher, especially in sick patients, anesthetic inhalant requirement may be reduced by 100% so in a patient receiving fentanyl MAC of iso can be as low as 0.5%
What drugs will increase HR?
Anticholinergics (atropine, glycopyrrolate): increase HR in all species
Atropine = more potent than glycol, more likely to cause undesirable tachycardia.
- -IM or IV administration
- -Can see paradoxical bradycardia, AV block occasionally seen soon after drug administration -> effect usually overridden once plasma concentration reaches therapeutic levels
What drugs directly improve contractility?
- Inotropes = dobutamine, dopamine
- Ensure volume resuscitated, minimize inhalant doses
- Stimulation of beta 1 R in myocardium, thus enhancing myofilament shortening and ventricular contractility
- Short half life (3-5’) -> effect short lived once infusion discontinued
Are there risks associated with giving inotropes?
- Dobutamine = synthetic catecholamine
- Dopamine = precursor to NE, epi
- Most common SE = tachycardia (esp dopamine), atrial and ventricular arrhythmias
- Termination of infusion or reduction of dose usually resolves signs
