Monitoring and Complications Part 2 Flashcards
describe blood pressure
a marker of tissue perfusion
mean arterial pressure if the most valuable measurement as it represents average perfusion pressures
goals:
SA: MAP 60-150 mmHg
LA: MAP >70 mmHg
as you increase in size, this goal increases
-if patient >600kg MAP goal increases to >80 mmHg
describe MAP
cardiac output x systemic vascular resistance
CO: amount of blood pumped by heart during a period of time
SVR: the resistance the heart has to pump blood against (how vasodilated or vasoconstricted the vasculature is)
describe heart rate abnormalities
- bradycardia
-caused by anesthetic drugs, endogenous vagal tone
-management: goal is to speed up heart (work on SA node to increase electrical activity)
–anticholinergic: atropine or glycopyrrolate- most common!!
–sympathomimetic: ephedrine - tachycardia:
-diastolic filling time is compromised due to high heart rate
-management:
–fix underlying cause
–beta blocker: esmolol - arrhythmias: uncoordinated heart contraction affects diastolic filling time
-management:
–antiarrhythmic: lidocaine
–fix underlying cause
how do you determine is a patient’s preload is appropriate?
- preload is volume status, tells how much blood is returning to the heart
-potential causes of inappropriate preload: hypovolemia, hemorrhage, compression of vessels returning to the heart - ways of assessing:
-PCV/TS
-thoracic radiographs
-pleth variability index
-echocardiogram or central venous pressures - management: if inadequate
-first line: isotonic crystalloid fluid bolus
-hypertonic crystalloids, colloids, blood products
-fluid boluses should be avoided in patients with cardiovascular disease (can’t handle extra fluid usually!)
describe assessment of contractility
causes of inappropriate:
1. anesthetic drugs
2. existing cardiovascular disease
how to assess: echocardiography; unlikely to do during an anesthetic event = just assume it’s occurring
management:
1. reduce amount of inhalant being used
2. administer a positive inotrope
-increase inotropy by working at beta adrenergic receptors in the heart
describe how to assess if SVR is appropriate
causes of vasodilation:
1. anesthetic drugs
2. inflammatory cytokines
how to assess:
1. MAP is a surrogate measure (if hypotensive, have so component of vasodilation)
2. MM color: paler than would expect bc vessels vasodilated
3. CRT: slower then before anesthesia
4. toe web to core temp gradient
-if vasodilated, temp difference between inside and out much greater than normal
management:
1. decrease inhalant usage
2. administer a vasopressor
-drugs that increase SVR by working at alpha receptors causing vasoconstriction
describe inotropes and vasopressors
in general:
-alpha receptors: vasoconstriction
-beta receptors: increase contractility
- dopamine:
-alpha and beta agonist
-increase SVR and contractility
2 dobutamine:
-beta agonist
-increases contractility
-most common choice in large animal
describe and discuss relevant interventions for hypotension (LO)
- hypotension compromises delivery of oxygen to the tissues
-the result is ischemic injury and death - 4 big categories:
-bradycardia
-decreased prelaod
-decreased contractility
-vasodilation - common causes under anesthesia:
-anesthetic drugs: vasodilation, bradycardia, both
-hemorrhage: acute loss of preload
-hypovolemia: loss of preload
-sepsis: inflammatory mediators causing massive vasodilation
-inherent cardiovascular disease - what do:
-ensure heart rate is appropriate: anticholinergic like atropine if needed to correct bradycardia
-ensure volume status is normal: if not, fluid bolus
-use as little inhalant as possible: evaluate anesthetic depth (eye position, overall jaw and muscle tone)
-consider an inotrope or vasopressor: if all else fails to increase contractility or increase vasoconstriction
describe and discuss relevant interventions for hypertension (LO)
- not as common under anesthesia but can lead to over-perfusion
-leads to an increase in intracranial pressure, retinal detachment, hemorrhage - causes:
-patient too light an anesthetic plane: assess markers of anesthetic depth
–management: increase depth (increase vaporizer setting or give a bolus of an opioid or hypnotic)
-pain:
–anasthetic depth is adequate but surgeon is performing a painful manipulation, causing hypertension due to endogenous catecholamine release
–management: re-dose opioid, multimodal analgesic approach, think ahead because pre-emptive analgesia is better than giving after the fact
-drug effects:
–drugs that cause hypertension
1. alpha-2 agonists: hypertension usually tolerable and self-limiting
-if intolerable, reverse alpha-2 agonist with alpha-2 antagonist
2. vasopressors: decrease/discontinue the vasopressor
-physiologic reflexes: NOT TESTED ON
–cushing reflex: high intracranial pressure due to traumatic brain injury or space occupying mass; leads to compromised cerebral perfusion and massive release of catecholamine to increase blood pressure to perfuse the brain
-cushing triad: high blood pressure, low HR (reflex bradycardia), apnea/irregular breathing pattern
-management: immediate treatment for high intracranial pressure: hyperventilation, mannitol or hypertonic saline
describe hypoxemia
- occurs when the partial pressure of oxygen in arterial blood (PaO2) < 60mmHg
- compromises delivery of oxygen to tissues resulting in ischemic injury to vital organs and death, even if blood flow is perfect!
- delivered oxygen = cardiac output x content of oxygen in arterial blood
-DO2 = CO x CaO2 - measure PaO2:
-blood sample from arterial blood
-normal PaO2 in a healthy patient breathing room air is 90-100mmHg
-patients under anesthesia are breathing 100% oxygen, therefore expect to be much higher PaO2 (4-5x inspired oxygen content!!) - blood gas analysis is NOT continuous, have to keep poking and running to machine
- venous partial pressure of oxygen does NOT tell you if patient is hypoxemic
-use pulse ox: oxygen saturation of hemoglobin (SaO2) is correlated to PaO2
list the 5 causes of hypoxemia and relevant interventions for each cause (LO), for sure on exam
- decreased inspired fraction of oxygen
-administer 100% oxygen via endotracheal tube, mask, nasal insufflation, oxygen cage - alveolar hypoventilation
-evaluate ventilation status via blood gas analysis or noninvasively via capnography
-provide positive pressure ventilation: patient must be intubated and heavily sedated or anesthetized - right to left shunt:
-deoxygenated blood on right side of heart is shunted to the left side of the heart through a VSD or PDA; the deoxygenated blood enters systemic circulation, causing hypoxemia
-100% oxygen will NOT fix the problem, generally requires a surgical procedure - diffusion impairment:
-pneumonia or severe injury to blood gas barrier
-treatment dependent on severity, at minimum supplement oxygen! - ventilation/perfusion mismatch: most common cause in anesthetized patients!
-most commonly due to atelectic lung fields
–atelectasis: collapse of lung fields due to deflated alveoli, alveoli are perfused but not ventilated, pulmonary capillary blood returns to the systemic circulation without ever becoming oxygenated
-contributing factors: dorsal recumbency, pneumothorax, large animal patients, spontaneous ventilation
management: - positive pressure ventilation with 100% oxygen
- ventilator recruitment maneuvers
- positive end-expiratory pressure (PEEP valves)
- move to sternal recumbency
- bronchodilators
describe hypoventilation
- the partial pressure of carbon dioxide in the blood tells the brain you need to breathe, but many anesthetic drugs increase the threshold where this occurs
- therefore, patients under anesthesia may not have adequate respiratory rates and/or tidal volumes, leading to hypoventilation
- detected via an increase in PaCO2 on an arterial or venous blood gas or an increase in EtCO2
when do we care about hypoventilation?
- normal EtCO2 in an awake, healthy patient is 35-45 mmHg
- as CO2 increases in the body, there is a decrease in the pH of the blood
-patient has a respiratory acidosis leading to acidemia; measure pH through blood gas analysis - healthy patients often compensate for slight changes in pH therefore may allow “permissive hypercapnia”
-MAX EtCO2 accepted under anesthesia: 55-60 mmHg - if pass permissive hypercapnia threshold:
-ventilate them! must be intubated
-can be as simple as giving occasional manual breaths with the rebreathing bag on the anesthesia machine
-more complex would be use of a ventilatory to provide positive pressure breaths
interpret the results of a blood gas analysis (LO)
increase in PaCO2: hypoventilation
describe signs of hemorrhage and significant blood loss (LO)
- common adverse effect of surgery
- quantifying blood loss:
-environment: suction canister, saturated gauze and lap pads, blood on the floor
–4x4 gauze: 10-12 ml, lap sponge: 100ml when fully saturated
-patient: tachycardia, hypotension
-laboratory:
–PCV: interpret with caution: with acute blood loss, PCV may be normal or increased due to splenic contraction
–total protein: can decrease with large acute blood lodd
–lactate: severe hemorrhage decreases oxygen carrying capacity, so tissues go through anaerobic metabolism increasing lactate in the blood
