Test 1- Week 2 Flashcards
Overweight/obese some concerns:
Cardiac output (CO) increased -↑ blood volume; contributes to volume overload with cardiac disease
↓ lung and chest wall compliance ↓*FRC excess fat and volume
impinging thorax
involved in gas exchange (↓PaO2)
Respiratory depression (low tidal vol; ↑CO2)
Mechanical ventilation using necessary
ASA Physical Status
Preparation Fasting guidelines (dog/cat)
Generally, 12 hr fast ( no food after 10 pm) but water always! ( some say fast 8 hrs)
may be longer if endoscopy or GI surgery
neonates/pediatrics should receive supplemental glucose containing liquids or soupy food- up to 4-6 hrs prior
Diabetics require adjustment in insulin dose
( usually half usual dosage) and procedure done early morning
Fasting large animals
Equine- no grain for 12 hr; most recommend no hay 8-12 hr but some will allow hay 4-6 hr ; water always
A full stomach needs to be avoided
Ruminants - no food 18-24 -hrs; no water 12-18 hr - smaller ruminants, calves - no food 12-18; no water 8-12hr
Why fast?
If patient vomits or regurgitates after/during
induction - pulmonary
aspiration of particulate
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material bad! ( liquid not good either)
regurgitated or refluxed liquid during anesthesia not uncommon
reason for intubation with a cuffed and adequately inflated endotracheal tube
Vomiting
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Vomiting- active process (retching) expulsion of stomach contents-very common only after premed opioid administration-
usually not a problem in healthy animals Avoid in animals at great risk for aspiration
ex. dilated esophagus; laryngeal paralysis; recumbent, somnolent
Fasting does NOT decrease
Fasting does NOT decrease incidence regurgitation or reflux
Regurgitation - passive process -material from esophagus (or stomach) into oral cavity
More common in animals with upper GI disease - and other less common disease processes- dilated esophagus; … rapid induction and intubation important!!
Regurgitation-during anesthesia-not uncommon- evident in mouth or on table
lavage esophagus with water then suction
Silent reflux ( into esophagus) ~38% healthy dogs reflux during anesthesia (detected with esophageal pH probe)- variety of drugs and fasting times
May result in esophagitis- ( or worse-esophageal stricture - but fortunately common)
Physical Signs to Assess Depth ofAnesthesia
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Physical Signs toAssess Depth ofAnesthesia
Presence/absence purposeful movement in response to stimuli-
• Potency of inhalants based upon this fact (MAC-minimal alveolar conc ( 50% subjects) to prevent movement
Muscle relaxation
• *Eyeball rotation; *Jaw tone; anal tone; abdominal mm tone;
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- Reflexes-
- *palpebral; corneal; anal pupillary light –(not helpful)
• Autonomic signs-changes in cardiovascular; respiratory parameters
What are the signs
Movement- purposeful movement to a noxious stimulus
Reflexes- gag, swallow, moving tongue, palpebral reflexes suggest too light plane of anesthesia CORNEAL REFLEX SHOULD ALWAYS BE PRESENT
Jaw tone- reliable sign of relaxation
Eye Position- we generally like to see the eyes rotated ventrally, see some sclera, probably has no palpebral reflex
Eyes- horse/ruminant eyes tend to roll forward; tearing is a sign of light anesthesia; pupil size- not very useful; HOWEVER, FIXED AND DILATED IS A BAD SIGN
At induction (if not profoundly sedate) animal usually
At induction (if not profoundly sedate) animal usually has more sympathetic activity( what mediators are being released?)
- Poss increased HR, Resp
- Avoid excessive excitation at induction
(why?- think about this)
As anesthesia progress, HR RR usually levels to more stable parameters
Ideal HR during anethesia
- Dogs
- small~70-120 • large ~50-100
Cats ~120 -180
Avoidbradycardiainpediatrics(why?)
Horse ~ 25 – 40
Calves, sheep, goats ~ 80- 120
Bovine–~60-90
Control of Heart Rate
Parasympathetic (vagal) –
Sinoatrial (SA), Atrioventricular (AV) nodes
Muscarinic receptors (M1)
Sympathetic – SA, AV,nodes;
ventricles
α1 (minimal) and β 1, 2 receptors
Causes of Bradycardia
**Increased parasympathetic
tone (Vagal stimulation)
Pressure on eyeball;
pulling on viscera
Drugs-( opioids; α2 agonists)
Possible profound depth of anesthesia ( lack of sympathetic tone)
High serum K+
SA nodal disease
Completeheartblock
Causes of Tachycardia
Increased sympathetic tone
Stimulation; pain
Hypovolemia ; Blood loss
Very elevated CO2;
Hypoxemia
Drugs ( ketamine ; inotropes)
Disease (pheochromocytoma; hyperthyroidism)
why is it important to monitor ECG?
Arrhythmias are common during the anesthesia period even in animals with no pre-existing cardiac disease
Most are benign requiring no treatment – as long as they do not cause hemodynamic compromise
Some may progress to a potential serious outcome – and warrants close observation with or without treament
What will tell you that the rhythm is abnormal?
EKG
How do we measure Cardiac Output?
CO= hr X SV
These are hard to measure, so we measure BLOOD PRESSURE
Why do we want good BP?
For perfusion of tissues
In health, most organs are autoregulated over wide range of pressure to maintain flow
But when MAP < 80 flow (perfusion) decreases
Best to maintain MAP >60 mmHg to maintain renal perfusion
How do we measure BP?
Indirect ( non-invasive)
Doppler ultrasonic flow
Oscillometric
Direct ( invasive)
With arterial catheter and transducer recording system or fluid filled tubing to a sphygmomanometer
Oscillometeric
Automated inflation of cuff then deflation until machine senses flow (oscillations- blood flow ) under the cuff
Direct ( invasive) blood pressure
Arterial catheter (dorsal pedal coccygeal or radial artery)
not always easy- esp very small dogs and cats
BP usually displayed with transducer + monitor
How do we fix low blood pressure?
- Evaluate patient depth AND evaluate quality of pulse
a) Check cuff (transducer) position properly placed?
Blood pressure
- Reduce inhalant if possible 3. Evaluate HR
- Need volume?
- Increase inotropy
- Or ↑SVR ( de- vasodilate)
Causes of hypotension
Bradycardia
Vasodilation Drugs
Anesthetics;sedatives cardiac, renal meds
Poor cardiac function- disease or drug induced or dysrhythmia
Hypovolemia/shock/sepsis
Causes of hypertension
Light anesthesia
Pain
Drugs – catecholamines/ketamine/
Disease processes
↑intracranial pressure Renal, adrenal diseases pheochromocytoma
Causes of Bradycardia
**Increased parasympathetic
tone (Vagal stimulation)
Pressure on eyeball;
pulling on viscera
Drugs-( opioids; α2 agonists)
Possible profound depth of anesthesia ( lack of sympathetic tone)
High serum K+
SA nodal disease
Completeheartblock
Causes of Tachycardia
Increased sympathetic tone
Stimulation; pain
Hypovolemia ; Blood loss
Very elevated CO2;
Hypoxemia
Drugs ( ketamine ; inotropes)
Disease (pheochromocytoma; hyperthyroidism)
Anesthesia and Hypothermia
Decreasesmuscularactivity;metabolismandhypothalamic thermostatic activity
Evaporativeheatloss
Open body cavities, surgical scrub solutions
Non-insulatedsurfaces;infusedcoldsolutions
Anesthesiainducedvasodilationduringinduction produces core to peripheral redistribution of body heat
may drop 1-1.5 C ( 2-3 F) first hour
Decreases linearly as heat loss to environment > metabolic heat
production
Core temp stabilizes over time ( ~3 hr)
Significance of Hypothermia
Down to 96-97 F (36 C): minimal – some shivering may occur in recovery
Shivering increases O2 consumption and can be bad in patients with cardiac and pulmonary diseases
Down to down to 92-94 F (33-34 C) decreases anesthestic requirement ; prolongs anesthetic recovery- too low to shiver in recovery
89-90 F (32-33 C)– HR ; CO decreases – may not respond to treatment( drugs); Significantly reduces anesthetic requirements; blood viscosity increases; may interfer with wound healing mechanisms
Respiration
The uptake of oxygen and elimination of CO2
Requires adequate lung function
Elimination of CO2
requires adequate respiratory rate and tidal volume
Hypoventilation
Hypoventilation = High PaCO2 (hypercarbia)
Hyperventilation
Hyperventilation = Low PaCO2 ( hypocarbia)
Normal arterial CO2 (PaCO2 )
Normal arterial CO2 (PaCO2 ) = ~ 35-45 mmHg
Carbon Dioxide
Is a product of metabolism in tissues
Production minus elimination = PaCO2
Usually, hypercarbia is due to inadequate elimination
But sometimes due to hypermetabolism
Malignant hyperthermia
Production> elimination
Increased PaCO2
**Hypoventilation
Increased metabolism
Hyperthermia; seizure Malignant hyperthermia
Equipment failure/error leading to rebreathing CO2
1 way valve problem
Exhausted CO2 sodalime
Inadequate O2 flow rate ( non- rebreathing sys)
Decreased PaCO2
Hyperventiation
over ventilation with ventilator
Unusual with spontaneous breathing unless very light
Hypothermia
What is the main stimulus for breathing?
CO2 is the main stimulus to breathing
Normally, (conscious) the medullary centers of brainstem initiate breathing when CO2 is ~35-40mmHg
When medullary centers become injured or intoxicated (drugs) brainstem is less responsive to CO2
Actually H+
What are all anesthetics are?
All anesthetics are respiratory depressants
Brainstem becomes depressed with high concentrations of anesthetics and most sedatives
Reason apnea may occur after bolus of propofol; thiopental
The more profound depth anesthesia the more respiratory depression
The CO2 threshold that initiates breathing now higher - could be 50-60+
What is compliance?
..Is the slope of pressure volume curve
Less compliant lungs or thorax- need greater pressure to inflate to a given volume (flatter curve)
Pneumothorax; pulmonary edema;
Rigid chest wall
If it seems to be difficult to expand thorax- there is a problem!!
How do we assess ventilation?
Resp rate -~ 8-15bpm
Visuallyassessthedepth of breathing (tidal volume- TV)
Measure the tidal volume with respirometer
Minute volume (MV)= RR/min x TV
*Tidal vol = ~ 10-15 ml/kg
Capnometry
Non-invasive, breath by breath technique to measure exhaled CO2
Now is a standard component of anesthesia monitoring
In healthy small animals ( not horses) ETCO2 closely approximates the PaCO2
What are the two types of capnographs?
Advantages and Disadvantages of the two capnographs
ETCO2 is lower than….
ETCO2 is lower than PaCO2
PvCO2 > PaCO2> ETCO2
Normal PaCO2 35-45:
‘Normal’ PaCO2- ETCO2 difference =~3- 7 mmHg
Gradient will increase with abnormalities in pulmonary function
( V/Q mismatch- specifically dead space)
What is very bad in neurological pts?
High PCO2 is very bad in neurologic patients
PCO2 is a potent dilator of cerebral vessels – will increase cerebral blood flow and cerebral blood volume
In neurologic patients with intracranial lesions - increased intracranial pressure
Brainherniationcouldoccur
PaCO2 should be kept < 40 but >25 mmHg
Consequences of low PCO2
During anesthesia due to excessive ventilation; ventilator ( or bagging) is excessive
Low PaCO2 will result in higher pH –respiratory alkalosis -
If metabolic acidemia is present might help normalize the pH
ET tube in esphagus
Inadequate seal around ET tube
Rebreathing
Obstruction in Airway or breathing circuit
What is a predictor of circulation?
ETCO2- an important tool to predict adequate cirulation
When cardiac output is low, less blood and CO2 presented to lungs so ETCO2 is low ( large gradien)
ETCO2 during *CPR may predict outcome for return to spontaneous circulation (RTSC)
Studies in CPR in humans and veterinary patients find that Return to (RTSC) during CPR is unlikely when ETCO2 < 15 mmHg dogs; <20 cats
Pulse Oximetry
Provides HR and s%saturation
Plethysmographic waveform
represents pulse rate, rhythm and quality of signal
If quality of signal is not good will get erroneous values
Pulse Oximetry (SPO2)
Is non-invasive; continuous- estimate of hemoglobin-O2 saturation
Hb-O saturation curve
How does the pulse ox work?
recognizes arterial from venous due to pulsatile flow
What is normal SpO2 and when should we be worried?..
SPO2 > 97% = PaO2 >90 mmHg
91% significant desaturation – PaO2 <65mmHg (Steep part of curve)
Hypoxemia =< 80 mmHg Hypoxemia –severe <70
‘Healthy ‘Horses under anesthesia – may have sPO2 < 90 %
Causes of Hypoxemia
Pulmonary dysfunction affecting
O2 uptake in lungs Perfusion of lungs Atelectasis of lungs
Extra-pulmonary
Pneumothorax;hemothorax
** Respiratory depression without supplemental O2
When should we use pulse
oximetry
Most important for
patients at hypoxemia
Pulmonary disease Pneumothorax Thoracotomy Bronchoscopy
Healthy patients heavily sedated or anesthetized without supplemental oxygen
risk for
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For HR? but there are better sources
Does anemia effect the SPO2?
Oxygen content is significantly reduced
Less total Hb but what Hb is there can be well saturated
Shape of curve is same
