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Anesthesia > Test 1- Week 2 > Flashcards

Test 1- Week 2 Flashcards

1
Q

Overweight/obese some concerns:

A

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

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2
Q

ASA Physical Status

A
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3
Q

Preparation Fasting guidelines (dog/cat)

A

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

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4
Q

Fasting large animals

A

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

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5
Q

Why fast?

A

If patient vomits or regurgitates after/during
induction - pulmonary
aspiration of particulate

•

•

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

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6
Q

Vomiting

A
  • -

-

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

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7
Q

Fasting does NOT decrease

A

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)

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8
Q

Physical Signs to Assess Depth ofAnesthesia

A

•

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;

•

  • Reflexes-
  • *palpebral; corneal; anal pupillary light –(not helpful)

• Autonomic signs-changes in cardiovascular; respiratory parameters

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9
Q

What are the signs

A

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

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10
Q

At induction (if not profoundly sedate) animal usually

A

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

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11
Q

Ideal HR during anethesia

A
  • Dogs
  • small~70-120 • large ~50-100

Cats ~120 -180

Avoidbradycardiainpediatrics(why?)

Horse ~ 25 – 40

Calves, sheep, goats ~ 80- 120

Bovine–~60-90

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12
Q

Control of Heart Rate

A

 Parasympathetic (vagal) –

 Sinoatrial (SA), Atrioventricular (AV) nodes

 Muscarinic receptors (M1)

 Sympathetic –  SA, AV,nodes;

ventricles

 α1 (minimal) and β 1, 2 receptors

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13
Q

Causes of Bradycardia

A

**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

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14
Q

Causes of Tachycardia

A

 Increased sympathetic tone

 Stimulation; pain

 Hypovolemia ; Blood loss

 Very elevated CO2;

 Hypoxemia

 Drugs ( ketamine ; inotropes)

 Disease (pheochromocytoma; hyperthyroidism)

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15
Q

why is it important to monitor ECG?

A

 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

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16
Q

What will tell you that the rhythm is abnormal?

A

EKG

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17
Q

How do we measure Cardiac Output?

A

CO= hr X SV

These are hard to measure, so we measure BLOOD PRESSURE

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18
Q

Why do we want good BP?

A

 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

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19
Q

How do we measure BP?

A

Indirect ( non-invasive)

 Doppler ultrasonic flow

 Oscillometric

 Direct ( invasive)

 With arterial catheter and transducer recording system or fluid filled tubing to a sphygmomanometer

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20
Q

Oscillometeric

A

Automated inflation of cuff then deflation until machine senses flow (oscillations- blood flow ) under the cuff

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21
Q

Direct ( invasive) blood pressure

A

Arterial catheter (dorsal pedal coccygeal or radial artery)

not always easy- esp very small dogs and cats

BP usually displayed with transducer + monitor

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22
Q

How do we fix low blood pressure?

A
  1. Evaluate patient depth AND evaluate quality of pulse
    a) Check cuff (transducer) position properly placed?

Blood pressure

  1. Reduce inhalant if possible 3. Evaluate HR
  2. Need volume?
  3. Increase inotropy
  4. Or ↑SVR ( de- vasodilate)
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23
Q

Causes of hypotension

A

Bradycardia

 Vasodilation  Drugs

 Anesthetics;sedatives  cardiac, renal meds

 Poor cardiac function- disease or drug induced or dysrhythmia

 Hypovolemia/shock/sepsis

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24
Q

Causes of hypertension

A

 Light anesthesia

 Pain

 Drugs – catecholamines/ketamine/

 Disease processes

↑intracranial pressure Renal, adrenal diseases  pheochromocytoma

25
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
26
Causes of Tachycardia
Increased sympathetic tone  Stimulation; pain  Hypovolemia ; Blood loss  Very elevated CO2;  Hypoxemia  Drugs ( ketamine ; inotropes)  Disease (pheochromocytoma; hyperthyroidism)
27
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)
28
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
29
Respiration
 The uptake of oxygen and elimination of CO2  Requires adequate lung function  Elimination of CO2  requires adequate respiratory rate and tidal volume
30
Hypoventilation
Hypoventilation = High PaCO2 (hypercarbia)
31
Hyperventilation
Hyperventilation = Low PaCO2 ( hypocarbia)
32
Normal arterial CO2 (PaCO2 )
Normal arterial CO2 (PaCO2 ) = ~ 35-45 mmHg
33
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
34
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)
35
Decreased PaCO2
Hyperventiation ## Footnote over ventilation with ventilator Unusual with spontaneous breathing unless very light  Hypothermia
36
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+
37
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+
38
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!!
39
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
40
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
41
What are the two types of capnographs?
42
Advantages and Disadvantages of the two capnographs
43
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)
44
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
45
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
46
ET tube in esphagus
47
Inadequate seal around ET tube
48
Rebreathing
49
Obstruction in Airway or breathing circuit
50
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
51
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
52
Pulse Oximetry (SPO2)
Is non-invasive; continuous- estimate of hemoglobin-O2 saturation
53
Hb-O saturation curve
54
How does the pulse ox work?
recognizes arterial from venous due to pulsatile flow
55
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 %
56
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
57
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 • • • • • • ! For HR? but there are better sources
58
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
59

Anesthesia (14 decks)

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