Exam 3 Flashcards
Blood Gas Analysis Lecture
- Explain the physiology behind how an animal maintains acid- base balance
- Describe the pathology associated with acidosis and alkalosis in a patient
- Discuss why a blood gas sample is analyzed and what it determines
- Explain how and where to obtain an arterial sample in the different species
- Interpret a primary blood gas disturbance in a case example (you MUST know normal value ranges to do this)
- List the factors that affect the accuracy of the arterial sample
- Calculate the arterial oxygen content equation
- Explain the physiology behind how an animal maintains acid- base balance
what are the three principal mechanisms to buffer H?
What is the solubility coefficient?
Homeostasis
Carnivores produce CO2 and excess H precursors
Herbivores produce CO2 and excess HCO3 precursors
-Liver metabolizes protein, generating 1mmol H/kg daily
-Kidney excrete H and reabsorb HCO3
-Lungs eliminate CO2
-Gut modulates acid, base, and water excretion
Buffering mechanisms
- Chemical:
-extracellular HCO3 works within seconds,
-phosphate, hemoglobin and proteins are intracellular buffers work within 2-4hrs - Respiratory: chemoreceptors changes in pCO2 and [H+] works within minutes
- Renal: increased excretion of H+ works within hours to days.
Solubility coefficient
[0.0301]
-Henderson-Hasselbalch Equation: many approaches to acid/base disturbances diagnosis and treatment are based on this equation.
-Solubility coefficient
[0.0301]
-Relationship between pH and [H+] is exponential.
-pKa = pH at which 50% of an acid or base is in the ionized state.
-pKa of H2CO3 is 6.1
-Ideal HCO3:pCO2 ratio is 20:1
Mixed disturbances
-Two separate primary disorders occurring in a patient at the same time.
-pH change in opposite direction of the expected for primary disorder.
-Disorders can have a neutralizing or additive effect on pH.
-A triple disorder can be caused by metabolic acidosis, metabolic alkalosis, and either respiratory acidosis or alkalosis.
- Describe the pathology associated with acidosis and alkalosis in a patient
What are the four primary disturbances and the expected compensatory response?
Causes of Respiratory Acidosis
-Anesthetic drugs and equipment dead space.
-Pneumothorax
-Severe pulmonary disease
-Upper airway obstruction
-Neurological disease
-Malignant hyperthermia
Respiratory Alkalosis
-Overzealous IPPV
-Fever/hyperthermia
-Pain, fear, anxiety, stress
-Sepsis or SIRS
-Pulmonary thromboembolism
-Hypoxemia
-Severe anemia
-Hypotension
-Low cardiac output
Metabolic acidosis causes
-Vomiting, diarrhea
-Renal loss of HCO3 or retention of H
-IV nutrition
-Dilutional acidosis
-Ammonium chloride
-Hypomineralochorticism
Metabolic Alkalosis
-Vomiting due to pyloric obstruction
-Hypochloremia and hypokalemia
-Furosemide
-Hypermineralocorticism
-Contraction alkalosis
Consequences of Acid-Base disturbances
Acidosis
-Impair cardiac contractility and response to catecholamines
-Decrease CO, decreased renal and hepatic blood flow.
-Ventricular arrythmias or fibrillation
-Arterial vasodilation and venous constriction centralized blood volume and causes pulmonary congestion
-Shifts oxygenated Hb curve to the right initially
-Hyperkalemia due to trans cellular shift
-Insulin resistance that impairs uptake of glucose
-Increased intracellular Ca
-CNS depression and coma
-Osteodystrophy and hypercalciuria
Alkalosis
-CNS signs (agitation, disorientation, stupor, coma)
-Seizures or tetany due to hypokalemia (rare)
-Hypokalemia due to trans cellular shifting causes muscle weakness, cardiac arrhythmias, GI motility disturbances, and altered renal function
-Shifts oxygen-hemoglobin curve to the left, which impairs oxygen release from Hb initially
Myocardial contractility decreased if pH <7.2
Respiratory and Metabolic Alkalosis
The problem with each
NAGMA: hyperchloremic
- Discuss why a blood gas sample is analyzed and what it determines
-Excellent tool for monitoring respiratory acid-base status
-Electrolytes can also be monitored
-Quick results = quick treatment
-Can be performed while awake or under using arterial or venous samples
Arterial gas vs. venous gas
Aterial sample
-Evaluation of respiratory gas
-Tells us what is happening on the respiratory side
-PaO2 = ~80-110 mmHg on room air
~ 500 mmHg if on 100% O2
-Bright red
-Pulsatile flow if catheter placed and arterial waveform present when attached to a pressure transducer
Venous sample
-Useful in determining acid-base status
-Slighter lower O2
-PvO2 = ~35-45 mmHg regardless of FiO2
PaO2 is 5 times the FiO2
ex: 100% oxygen to patient times 5 = 500 PaO2
-SvO2 65-75%
-Darker color of red
-No pulsatile flow from waveform present when attached to pressure transducer
- Explain how and where to obtain an arterial sample in the different species
Needed
-Clip and clean area
-Dry lithium heparin syringe or heparinize a 1-3 ml with a 22-25G needle, aspirate and expel before drawing blood.
-~ 1ml of blood
-No air bubbles
-analyze within 10 minutes or place rubber and store in ice up to 1 hour
-Apply pressure to sampling site to avoid hematoma
Small animals
-Dorsal pedal artery best
-Auricular, femoral, caudal artery, lingual artery
Large animals
-Facial artery, transverse facial, (horses, donkeys)
-lateral dorsal metatarsal artery, (horses donkeys)
-auricular artery (ruminants)
-lingual artery, femoral artery,
-medial artery (sheep)
Jugular vein acceptable
- Interpret a primary blood gas disturbance in a case example (you MUST know normal value ranges to do this)
Blood analyzers measure
-pH
-Partial pressure of oxygen (O2)
-Partial pressure of carbon of carbon dioxide (PCO2)
Blood analyzers calculate
-HCO3
-BE
-SaO2
Normal Blood Gas volumes
-pH: 7.35-7.45 (compatible with life 6.8-7.8 animals)
-FiO2: =0.21 at any altitude, but PB decreases with altitude.
-PaO2: 80-110 mmHg room air (95% SaO2)
Oxygen molecules dissolved in the plasma phase of arterial sample.
Mild hypoxia = 75-90 mmHg
Severe Hypoxia = < 60 mmHg
not bound to Hb. depends on the FiO2 (fraction of inspired oxygen)
-PaCO2: 35-45 mmHg
respiratory component of acid-base balance, used to determine if patient is hypocapnic, hypercapnia, or eucapnic. Inversely related to alveolar ventilation.
-SaO2: 95% (PaO2 = 80 mmHg)
The percentage of all available heme-binding sites saturated with oxygen from arterial sample calculated valued based on the position of the oxygen Hb dissociation curve.
-HCO3: 15-25 mmol/L (carnivore) 20-28 mmol/L (herbivores)
mainly responsible for regulating pH of bodily fluids. It acts as an immediate buffer when fixed acids enter blood. Also, facilitates the transport of CO2 from body tissues to lungs, bicarbonate-carbonic acid. Value is assessment of metabolic acid-base status. Most important buffer
-TCO2:
amount of carbon dioxide present in the plasma. 85% actually due to bicarbonate
-BE: 0 +/- 4 mmol/L
Base excess is a mount of strong acid or alkali required to titrate 1L of blood to a pH of 7.4 at 37C while the partial pressure of CO2 is constant at 40 mmHg
Excess = metabolic alkalosis
Deficit = metabolic acidosis
Used to calculate bicarbonate therapy
mEq to infuse = BE x kg x 0.3
Infuse sodium bicarbonate 1/3 over 20 minutes: if given too fast increased paCO2 will cross BBB and cause cerebral acidosis, vasodilation, and hypotension; hypernatremia = cerebral hemorrhage.
Mild +/- 5
Moderate +/- 10-15
Severe > 15
-Lactate: <2.0 mmol/L
How to interpret all this numbers?
Need to know the FiO2 and body temperature
Step 1
Determine if the sample is arterial or venous
-SaO2 >88% = Arterial
-SaO2 <88% = Mixed sample, venous or pulmonary disease
Step 2
Determine acid-base status of the patient
pH normal, acidic, basic
PCO2 normal, increased, or decreased
HCO3 normal, increased, or decreased
Step 3
Assess the ventilatory status (PaCo2)
-Hypoventilation = increased PaCO2
-Hyperventilation = decreased PaCo2
-Normal ventilation
Step 4 Assess how the animal is oxygenating
-Is the patient breathing room air?
Calculate Alveolar-arterial O2 gradient (A-a) to determine effect of hypoventilation
A= [(barometric pressure -47)*0.21 -(PaCO2/0.8)]
a= PaO2
A-a = the gradient between the alveoli and the arterial blood
A-a Gradient
-Normal 0-10
-Probably normal 11-20
-ARDS? 21-30
-ARDS >30
ARDS: Acute respiratory distress syndrome
If the patient is on an FiO2 >0.21
-Use PaO2:FiO2 ratio (used to compare arterial samples when the PaCO2 is stable)
Example: PaO2 = 450 mmHg FiO2 = 100% O2
PaO2 : FiO2 ratio = 450/1.00 = 450 normal function
PaO2:FiO2 ratios
>400 mmHg = normal pulmonary function
200-400 decreased pulmonary function
<200 severe pulmonary dysfunction
Step 5
Determine the Anion Gap
AG= (Na+K) - (Cl+HCO3) = UA(anions) - UC(cations)??
Law of electroneutrality: in reality there is no anion gap, just unmeasured anions.
Causes of increase: Ketoacids, Uremic acids, lactic acids, glycolic acid, and Salicylic acid.
Decrease: due to hypoalbuminemia usually
“emia” indicates changes in blood
“osis” indicates physiological process causing disturbances
The response to respiratory disorders occurs in two phases with two expected compensatory responses
1. Acute < 24hrs
2. Chronic > 48 hours
- List the factors that affect the accuracy of the arterial sample
-Air bubbles: increase PaCO2 and decreased PaCO2
-Excess heparin = decreased pH. Use specialized syringe and <0.1 ml of heparin in 2 ml of blood.
-Delay in analysis = decreased PaO2 and pH; increased PaCO2.
-Blood clot in sample; hemolysis, collecting from catheter
-Syringe type - glass preferred, plastic ok if analyzed within 10 minutes
-Temperature and barometric pressure
Hyperthermia - artificially lowers PaO2 and PaCO2
Hypothermia - artificially elevates PaCO2 and PaCO2
-Get rid of bubbles within 30 seconds
-Recommend PICO syringes (containing balanced sodium heparin that is lyophilized, so no danger of dilution effect)
Hypoxia vs. Hypoxemia
-Hypoxemia: decreased PaO2, SaO2, or Hb content. PaO2 <60 mmHg and/or SpO2 <90% severe hypoxemia
-Hypoxia: general term for impairment of oxygen delivery to tissue (DO2). Takes into account cardiac output (CO) and oxygen uptake at tissue level. So hypoxemia is one type of hypoxia.
Causes of Hypoxia
-Hypoxemia
-Reduced oxygen delivery to tissue (decreased CO - Left or right Shunt)
-Decreased tissue oxygen uptake (cyanide, CO, alkalemia)
Causes of Hypoxemia
-Ventilation/perfusion (V/Q) mismatch: The most common
-Hypoventilation
-Low FiO2
-Right to left shunt
-Diffusion impairment
What is V/Q mismatch?
-Pulmonary parenchyma disease such as pulmonary edema, pneumonia, pulmonary contusions and pulmonary neoplasia will lead to hypoxemia secondary to V/Q mismatch
- Calculate the arterial oxygen content equation
CaO2= (SaO2 x Hb x 1.34) + (PaO2 x 0.003)
Example:
Patient A
Hb = 7g/dL
SaO2 = 95%
PaO2 = 80 mmHg
Patient B
Hb = 15 g/dL
SaO2 = 85%
PaO2 = 55 mmHg
Patient A = 9.15 ml O2/100mL more hypoxemic
Patient B = 17.25 mL O2/100mL
Anesthesia Complications & Emergencies Dr. Kelley
What is the first rule of anesthesia?
How should you approach problems?
What should you do if you panic?
Do not panic
-Panic occurs when your ideas do not match outcomes
-If you panic, panic constructively: go back to the basics, Airway, Breathing, Circulation.
-Ask for help
Have a Plan checklist
-Plans will address the majority of problems that arise
-Plans are not always elaborate
-Be ready and willing to implement plan
Approaching Problems
- Identify that there is a problem: 5 minute sweeps
- I identify the problem
- Address the problem
- Follow up
What are some of the common and uncommon patient undesirable occurrences during anesthesia?
Common
Cardiovascular complications
Respiratory
Temperature regulation
Regurgitation and possible aspiration
Uncommon
Metabolic
Neuromuscular
Complications due to surgical or diagnostic procedure
Human error or patient idiosyncratic reaction
- Identify hypotension in an anesthetized patient
Which method is trusted most by Dr. Kelley?
Hypotension
Severe decrease in BP leads to decreased perfusion of optic nerve and kidneys - post-anesthetic blindness or renal failure (other organs will follow shortly)
What is too low BP?
-Systolic < 80 mmHg
What is normal/expected at LMU?
> or = 90 mmHg
Methods to determine BP
-Blood pressure cuff, droplet
-Oscillometric (Pulse detection by oscillometric machines depends on the amount of change in the volume of the arm with each pulse (small pulses are more difficult to detect) and on the regularity and rate of those pulses. With regular pulses and a relatively smoothly changing arm volume it is much easier for the microprocessor to estimate the systolic and diastolic BP)
-Arterial catheter “Gold Standard”
Droppler trusted the most
- Describe treatment of common causes of hypotension
What is the source of the low blood pressure?
-Pump (heart)
-Pipes (vasculature)
-Volume (blood)
Do they all respond to the same therapy?
Initial steps
-To identify
-To treat
Treatment
-Fluids
-Consider increasing the HR (pump)
-Consider decreasing inhalants (pipes)
-Consider fluid bolus (3-5 ml/kg over 10-15 minutes)
-Regardless look for UNDERLYING CAUSE
CV Supportive Agents
DoPamine
-Alpha 1, Beta 1
-CRI
DoButamine
- Alpha 1, Beta 1 predilection, Beta 2
-Caution: pre-existing arrhythmias
-Onset: 2 minutes
-IV, CRI
-Only in critical care settings
Ephedrine
-Alpha-1, Alpha-2, B-1, B-2 predilection.
-Bolus or CRI
Epinephrine
-Alpha-1 predilection, Alpha-2, Beta-1, Beta-2.
-Bolus
-First/bride treatment for equines, but can also be used SA
Review Receptors and Activation results
Alpha1: vascular smooth muscle = contraction = increase BP
Alpha2: Presynaptic adrenergic and cholinergic nerve terminals and GI tract = Inhibitory, negative feedback, activation leads to decrease of norepinephrine release from presynaptic terminals = High stimulation of sympathetic.
Beta1: Prominent in the heart, SA node, AV node = increased conduction in velocity, increased contractility in ventricular muscle. In salivary glands, adipose tissue, and kidney = promote renin secretion
Beta2: Vascular smooth muscle of skeletal muscle, walls of GI and bladder, and in bronchioles = relaxation or dilation.
- Organize an approach to manage hypoventilation
-Look for causes many are iatrogenic: drugs, positioning of patient, hypothermia, Pop-off closure, obesity
-Treat causes accordingly: alter protocols, positions, etc.
Capnography is the “Gold Standard” for ventilation monitoring
Normal: 35-45 mmHg for PaCO2
-Why can some hypoventilation be accepted while undergoing anesthesia? because of increased FiO2
-PaCO2 influence on oxygen is described by the alveolar gas equation
Alveolar Gas Equation
PAO2 = FiO2 (Patm-PH20) -(PACO2/0.8)
At 100% oxygen = 625 mmHg
At 21% oxygen (room air) = 61mmHg problems
Addressing Apnea
-Hand ventilation: there is not set rate that will work for every patient
-Supplementation vs Suppression
Addressing Hypoventilation
-Looking at minute volume using minute ventilation
MV= Respiratory Rate x Tidal Volume
Tidal volume (mL).
Example: (250 ml) x (12 RR) = 3000 ml/min
-Rate may be slow or fast
-Supplementation vs Suppression
-Monitor progress with Capnography
- Explain the common causes of hypoxemia
** If breathing 100% O2, pulse oximetry should read 94%**
NEAR
-Nearest to the patient first
-Equipement
-Adjustment
-Reassess
Oxygen Hb disassociation curve
SpO2 & PaO2
90 60
80 50
70 40
Major causes of Hypoxemia
- Hypoventilation
- Low fractional inspired oxygen (FiO2)
- Diffusion impairment
- Ventilation/perfusion mismatch (V/Q)
- Shunt
Each can have multiple causes
Low FiO2
-Check the flow meter: is it turned on, is the rate appropriate for the circuit type?
-Check the pressure gauge on the tank (if using portable)
-Is your machine/circuit appropriately connected?
-Is there a leak?
Diffusion impairment
-What would be the likely cause under anesthesia?
-How would you be able to determine this?
V/Q mismatch
-Species and underlying disease dependent (horses don’t like to be on their back)
-Can and does happen to all anesthetized patients to some degree
-How can it be managed?
-Maintain both sides of the equation as best and possible: ventilation, perfusion, cardiac output.
Right/Left Shunt
-How do you determine a shunt? not much can be done
Thermoregulation Complications
Hypothermia
-Taking to long in surgery is the number one cause
-Tiny patients get cold quickly
Hyperthermia
-Different than fever
-Causes: malignant hyperthermia
-Species differences
Regurgitation
Myopathy and Neuropathy
~ 1% up to 15% incidence in dogs
-Passive process: may only appear as nasal or oral discharge = silent
-Ensure airway patency
-Treat with copious lavage and suction +/- Bicarbonate
Myopathy and Neuropathy
-Myopathy caused by ischemic muscle damage due to prolonged compression or inadequate padding and or prolonged hypotension leading to under-perfusion of muscles
-Peripheral neuropathy caused by stretching, compression, ischemia, metabolic derangement, and surgical resection
-Prevention is better than treatment: adequate padding, short time in surgery, promptly treat hypotension.
-Treatment includes IVF for diuresis, analgesics, anti-inflammatory drugs, sedative if needed, and vasodilators.
-Rehabilitation therapy is also beneficial
- List potential common complications that could occur in an anesthetic episode
Hypotension
Hypothermia
Hyperthermia
Hypoventilation
Regurgitation
Hypoxemia
Preventable complications
-Human error: never walk away from the patient
-leaving pop-off valve closed
-Intracarotid or perivascular injection
-Tracheal tear from turning intubated patient attached to breathing system 90 degree rule of rotation
-Miscalculations in medications
-Equipment malfunction: oxygen tank runs out, improper use of machine or breathing system, hole in ETT cuff, etc.
Philosophical Anesthesia
Human error will happen
Always label syringes
Stabilize patient prior to anesthesia and continue to monitor into the recovery period
When complication does occur KEEP CALM and quickly communicate the problem to the peri-operative team.
Hold a M&M rounds afterwards to discuss complication (s)
Development of a SOP to prevent or reduce future occurrences
Procedural Sedation
- Describe the difference between tranquilization, sedation, and general anesthesia.
- Discuss how you would change your approach for a patient that requires heavy sedation to accomplish a diagnostic or therapeutic procedure compared to providing premedication prior to induction of general anesthesia.
- Describe your technique or approach for a “difficult” or non-compliant patient requiring sedation.
- Classify commonly used veterinary drugs by their Schedule number and describe how this impacts your record keeping and the abuse potential of the drug.
- List the methods, according to the AVMA Guidelines for the Euthanasia of Animals, that are considered acceptable, conditionally acceptable and unacceptable methods of euthanasia. Describe what drugs are used, how to confirm death, and proper disposal of a body.
- Describe the difference between tranquilization, sedation, and general anesthesia.
Tranquilization
-Behavior changes and relief of anxiety
-Patient is calmed, stress is reduced, indifferent to minor pain
Immobilization
-wildlife/exotic anesthesia mostly
-Patient rendered incapable of movement
Sedation
-State characterized by central depression accompanied by drowsiness. Unaware of its surroundings but responsive to pain stimuli
General anesthesia
-Drug induced unconsciousness
-Controlled and reversible depression of CNS
-Patient not arouse by noxious stimuli.
Reasons for Sedation and General Anesthesia
-Safe surgical experience
-Restraint for examination, exotics, wildlife
-Safe transportation
-Diagnostics and therapeutic procedure
-Euthanasia
-Humane slaughter of food animals
- Discuss how you would change your approach for a patient that requires heavy sedation to accomplish a diagnostic or therapeutic procedure compared to providing premedication prior to induction of general anesthesia.
All depending on the practice and/or patient
Tech preference, etc.
Scenarios
Premedication prior to inducing general anesthesia
-Premedications may be given IM or IV
-An IM dose is generally 2 times the IV dose
-Neuroleptanalgesic approach is common but species and patient dependent.
-Example: Hydromorphone 0.1 mg/kg IM
-No “make them a rug” unless necessary
Heavy sedation required for a diagnostic or therapeutic procedure
-Neuroleptanalgesic approach commonly used
-Yes, “make them a rug” unless physical status warrants a more cautious approach
-Consider reversal for short procedure
- Describe your technique or approach for a “difficult” or non-compliant patient requiring sedation.
“White coat syndrome” BP is higher at a health care provider facility than at home. An owner could actually buy a white coat and conditioned the animal at home.
-Pre-existing conditions could be aggravated and induce pain: osteoarthritis, dental disease, otitis external, oncological pain, ophthalmic disease.
Non-pharmacological approach CAT
-Fear-free or low stress handling
-Separate waiting areas for cats and dogs
-Feliway diffuser or calming spray
-Meals or treats in carrier then short car rides while giving treats
-Avoid standing over the cat, directly making eye contact, and trying to touch the animal right away.
-Move cats into the exam room as quickly as possible or provide a towel to cover the carrier.
-Don’t let the cat wait too long
-Soothing music
If this approach is not working, then chemical restraint may be appropriate
-Distinguish between nervous and aggressive patient
-Body language is important
Non-pharmacological approach DOG
-Calm dog will interact socially, easy to approach. Wiggling tail/body
-Nervous dog may be hiding, or retreats, tense body language, yawing or licking noted.
-Gently offer treat and see if it is accepted
-Consider using pheromones (Adaptil)
Medications for owners to give at home
-Gabapentin: several hours prior to transport for cats (150 mg or 50mg depending on size). It may cause ataxia, so warn owner. It can last 12 hours. Dogs a higher dose than used for pain
-Selio (dexmedetomidine gel) for dogs with noise phobia, prior to transport
-Trazadone, for anxious dogs and cats, after surgery confinement use
-Alprazolam (Xanax) higher dose than used to treat anxiety
No diazepam oral for cats = hepatic necrosis
Be sure to warn owner of all potential complications