CPR Flashcards
What are the three most common anesthetic complications?
hypoventilation (63%), hypothermia (53%), hypotension (38%)
Hemorrhage
Acute: hypovolemia, decreased d blood oxygen carrying capacity
Detectable at 10-20%, life-threatening circulatory failure if 30-40%
Clinical Signs of Hemorrhage
tachycardia, decreased pulse pressure/area under pulse arterial waveform, peripheral VC/pale MM
Treatment of Hemorrhage
Crystalloids 3x volume shed blood DT rapid extravasation of fluid
Dilution will occur: further dilute HCT, concentration of clotting factors/platelets, decreased oxygen carrying capacity, although improved CO
Likely will need blood +/- components
Most common arrhythmias seen in canine patients under GA?
o VPCs warrant treatment if: R on T, multifocal, >180bpm, perfusion
Traumatic Myocarditis
- Patient with traumatic myocarditis (trauma, HBC), arrhythmias, myocardial dysfunction peak ~ 24-48 hrs
RECOVER
Reassessment Campaign on Veterinary Resuscitation
Outcomes associated with CPR
100 patients undergo CPR: regardless of why experienced CPA, should get ROSC rate ~45%
Cats generally 42-44%, dogs 28-35%
Once CPA occurs, will lose 50% of patients best to prevent CPA
Survival to Discharge: Cause of CPA Matters
Perianesthetic 40-45% will survive to go home
ICU ~5-7%
o 20-90% of patients achieve ROSC in will die in PCA period
Risks Assoc with CPR
Rib fx – 1.6%
Muscle damage – 1.4%
Chest pain – 11.7%
Circulation Detection
Dorsal pedal palpable if MAP >60mm Hg
Apex beat: 4-6th ICS, lower 1/3 chest or elbow caudal to level of costochondral junction
Pulses should be palpated even if heart beat ausculted: apneic patients with inadequate contractility to generate blood flow sufficient to produce palpable pulses may still require chest compressions
No longer recommended to check pulses in apneic patients
DDX absence of pulses
o Severe shock
o Marked decreased contractility
o Pericardial effusion with tamponade
o Severe pleural space dz
Most Important Step when CPA Identified?
START BLS!!
preserve organ function
Promote circulation of RBCs oxygen delivery to tissues
Within 10’ of CPA, irreversible ischemic damage to tissues, decreases likelihood of successful ROSC
ALS techniques only applied once BLS perforated
At-Risk Patients for CPA
o 5 Hs: hypovolemia, hypoxia, hydrogen ions, hyperkalemia, hypoglycemia
o 5 Ts: toxins, tension pneumothorax, thromboembolism, tamponade, trauma
Main Cause of Canine, Feline CPA?
primary respiratory arrest more common with secondary cardiac arrest DT hypoxemia that develops from lack of ventilation
Horses: primary cardiac arrest
What are the most common arrest arrhythmias?
Pulseless electrical activity
Asystole
Doses of Emergency Drugs: epinephrine
High dose 0.1
Low dose 0.01mg/kg
Doses of emergency drugs: vasopressin
0.8U/kg
Doses of Emergency Drugs: Atropine
0.04-0.05mg/kg
Doses of Emergency Drugs: Amiodarone
5mg/kg
Doses of Emergency Drugs: Reversal Agents
Naloxone 10-40mcg/kg
Flumazenil 0.01mg/kg
Atipamezole 50mcg/kg
Defibrillation: monophasic, external
2-10J/kg
Defibrillation: monophasic, internal
0.2-1J/kg
Defibrillation: biphasic, external
2-4J/kg
Defibrillation: biphasic, internal
0.2-0.4J/kg
Components of BLS
Chest compressions
Ventilation
Components of ALS
–Monitoring
–Vascular Access
–Reversals
–Evaluation of ECG once monitoring
VF/Pulseless VT Algorithm
Continue BLS, charge defibrillator
Give one shock (or precordial thump)
If prolonged:
Amiodarone, lidocaine
epi, VP every other cycle
Increase defibrillation dose by 50%
Asystole/PEA Algorithm
-Low dose epi +/- VP every other BLS cycle
-Atropine every other BLS cycle
Prolonged >10’:
-High dose epi
-Bicarbonate therapy
Open Chest CPR Contraindications
contraindicated in small dogs <10kg, cats unless in sx DT size of chest cavity and difficulty assoc with cardiac massage in these patients
Importance of Good Compressions during CPR
o Only thing generating CO during arrest = compressions
o Ideal compressions: achieve 25-30% normal CO = without high-quality BLS, chances of ROSC minimal
Compression rate: 100-120/min, compression depth 1/3-1/2 width of thorax
Cycles = 2’
Consequences of compression rates >100-120bpm?
Higher compression rates decrease CO bc do not allow full elastic recoil of chest –> decrease return of blood to heart –> decrease CO
Why are cycles 2’?
- Cycle = 2’ bc takes 1’ chest compressions for aortic BP to reach steady state that provides perfusion to heart/tissues
- Cycles <2min decrease perfusion bc steady state not achieved or maintained
Consequences of chest compressions in small dogs, cats
possible to overwhelm chest: overt chest trauma, myocardial contusion
Larger patients: large amount of force to obtain effective compressions
Abdominal Compressions
Must be coordinated with partner, alternate timing
Can increase venous return, with possible increases in CO
Medium sized dogs or greater
Normal Canine Cardiac Output?
100-200mL/kg/min
Normal Canine Stroke Volume?
1-2mL/kg
Cardiac Pump Theory
Direct compression of heart (LV/RV) generates blood flow
Key: forward flow of oxygenated blood to tissues accomplished via direct compression of heart
* Increased pressure in ventricles to close AV valves, prevent backflow of blood into atria
o Goal: provide maximum SV with each compression
How Heart Fills with Cardiac Pump Theory
- Elastic recoil to chest, heart btw compressions creates negative pressure within heart to allow ventricular filling for next compression
Patient Populations for Cardiac Pump Theory
Cats, small dogs, larger keel-chested dogs
* High thoracic compliance
* Narrow, triangular shaped chests
Heart right up against rib case, able to compress ventricles directly to generate blood flow
One or two handed technique depending on patient size
Limitation of Cardiac Pump Theory
Older or obese animals with less compliant chests: chest may be too stiff to employ cardiac pump theory DT normal aging changes or SQ fat
Thoracic Pump Theory
Key: forward flow of oxygenated blood to tissues accomplished via indirect compression of aorta increasing intrathoracic pressure
* Should maximally compress thorax
Change in intrathoracic pressure causes blood flow
Heart During the Thoracic Pump Theory
Heart = passive conduit
o MV, TV not closed during chest compressions – blood flowing passively through heart
* Drive intrathoracic pressure high to push blood out
Maximal change in thoracic volume = hands over widest part of chest
Patient Population for Thoracic Pump Theory
Medium, large round-chested dogs; unable to directly compress heart
heart filling with thoracic pump theory
Recoil of chest btw compressions causes negative pressure within thorax = draws blood into cr/cd VC, heart
Blood drawn into lungs during recoil phase DT expansion of highly compliant pulmonary vessels
Key points of Two Handed Technique
o Hips patient height or higher = step stool, climb on table, move patient to floor
o Heels of hands stacked with elbows over hands, shoulders over elbows
o Bend from hips only
o Overlap hands with fingers interlocked, heel of upper hand directly over heart
o DO NOT LEAN - Must allow chest to recoil
Which are the two shockable rhythms?
Pulseless VT
Ventricular fibrillation
Which recumbency is preferred for CPR per RECOVER guidelines?
Lateral
Pulseless Ventricular Tachycardia
Contractions very fast, no time for ventricular filling
regular, repeated electrical activity with ventricles contracting in coordinated fashion but very fast rate (>200bpm) without palpable pulses
Ventricular Fibrillation
- Both ventricles quivering in, out of sync: no effective ctx of heart
- Aberrant, uncoordinated mechanical activity of muscle cells of ventricles
- Ineffective mechanical activity, no forward flow of blood
- ECG: random, irregular activity
What are the two non-stockable rhythms?
- Asystole
- Pulseless electrical activity
Asystole
- Complete cessation of electrical, mechanical heart activity
- ECG: flatline
Pulseless Electrical Activity
- No effective mechanical activity of the heart, no palpable pulses
- ECG: continue to show [normal] electrical activity but no mechanical activity of heart
Consequences of Hypovenilation
Dilation of peripheral blood vessels, pooling of blood in periphery = decreased perfusion to core organs (brain, heart, lungs)
Cerebral vasculature extremely sensitive to [CO2] in arterial blood
Cerebral vasodilation secondary to hypoventilation can lead to increased ICP, further decreasing cerebral perfusion
Consequences of Hyperventilation
- Cerebral VC: increased resistance to blood flow to brain, compromising CPP
- Excessive PPV leads to increased mean intrathoracic pressure = compression of VC, decreased preload to heart = decreased CO
- Low PaCO2 decreases ventilatory drive, decreases likelihood that patients spontaneously ventilate if ROSC achieved
Ventilation Parameters
Do not interrupt compressions for intubation or breaths
10bpm, 1s duration, ~10mL/kg VT
Goal: minimize time thoracic pressure possible, opposing venous return
Mouth to Snout Breathing
30:2 compression:breath ratio
Close mouth
Extend neck to align snout with spine, open airway as completely as possible
Blow firmly into nares to inflate chest until normal chest excursion accomplished, inspiratory time <1s
Limitations of Mouth to Snout breathing
cannot be performed simultaneously with chest compression
* When chest compressed, increased intrathoracic pressure prevents air from entering lungs
* Air diverted into esophagus, stomach
Components of ALS
o Vascular Access
o Drugs
ALWAYS: vasopressors, reversals
MAYBE: atropine, bicarbonate, electrolytes
o Defibrillation
Drug Administration During CPR
ETT
IV - use most central catheter
IO
Without CO, need large volume of flush to push drugs in: 5-15mL in dogs, 3-5mL in cats
ETT Drug Administration
o Absorption is variable, use 2-3x standard dose except epi
o NAVEL: naloxone, atropine, vasopressin, epi (high dose), lidocaine
o Place red rubber tube down ET tube, give drug, flush
Vasopressor Therapy in ALS
o All cases of CPA, impt to shunt blood to central circulation
o Every other BLS cycle ~4’
o Epi = vasopressin: can give one or other every other cycle or together (equivalent in 2012 guidelines)
Epinephrine
a1 activity: VC
a1 activity: increased contractility, HR,
* Leads to myocardial oxygen demand, maybe bad in PCA
Receptors inactive with acidemia
* Dead = acidemia due to CO2, lactate
Low dose 0.01mg/kg = 0.1mL/10kg
High dose 0.1mg/kg – last resort, after 2-3 rounds with low dose = high ROSC, lower survival to discharge UNLESS giving via ET
Reversal Agents during CPR
o Atipamezole IV for 2s, flumazenil for benzos, naloxone for opioids
o TURN OFF THE VAPORIZER AND FLUSH SYSTEM!!!
Atropine
No more than every other BLS cycle
Bc more dogs, cats die from vagal arrests, more useful than in people?
Induced PEA in dogs: higher ROSC with atropine + epi
Calcium Gluconate
o Calcium Gluconate 1mL/kg SLOWLY IV if iCa <1.0, K >6-7
Essential for muscle ctx
Steroids per 2012 Guidelines
no benefit, likely harmful in hypoperfused patients
NaBicarb 1mEq/kg
Generates CO2, can worsen acidemia
Not routinely used, consider if prolonged CPR effort (>10’)
Intravenous Fluid Therapy
Detrimental in euvolemic patients: harder to pump circulation
Beneficial if known/suspected hypovolemia?
Blood loss, severe dehydration
TFAST to eval cardiac contractility
Coronary Perfusion Pressure
Diastolic blood pressure (DBP) – right atrial pressure (RAP)
Heart only gets blood during diastole, opposed by right atrial pressure
ECG with ALS
o Can only interpret during compressor change
o Non-shockable: asystole, PEA – 95% of CPR rhythms
o Shockable: vfib (course or fine) 5%, pulseless ventricular tachycardia <1%
Defibrillation
Goal = large current to depolarize all cells at once
Induce asystole, hopefully then SA node returns to normal activity
If used for non-shockable rhythms, will injure myocytes
Use least amt of energy possible
MUST PLACE IN DORSAL
Maximum Dose of Energy Used for Defibrillation?
10J/kg
MOA Defibrillator
Capacitor serves as “collection bucket” of continuous low current provided by wall outlet or battery: able to store then release when needed to provide brief, large electrical current
When potential difference applied across capacitor, excess positive charges on one side of plate, negative accumulate in other
To charge capacitor: charging system applies high voltage (via set up transformer) across capacitor based on energy level selected by operator
For capacitor to discharge, electrons need path to flow from one plate of capacitor to other: uses paddles and heart to accomplish
Hand Paddles
Opposite sides of thorax ~ over costochondral junction directly over heart
Allows maximal amt of current to pass directly through ventricles, increasing likelihood of successful defibrillation
Sufficient electrode gel or paste applied to paddles to ensure electrical contact - NO ALCOHOL
Posterior Hand Paddles
Flat paddle replacement for one hand of paddles
Can increase efficacy/safety of defibrillation by minimizing interruption to compressions, eliminating need to place in dorsal
Essentially placed under patient thorax
Traditional hand paddle used on up thorax
Pediatric Paddles
Consider for smaller patients
Directs more current through the heart
Monophasic Current
current only goes in one direction
- Inducer that slows current: lower peak, spread over longer period of time
Biphasic Current
current starts in forward direction, changes direction, goes in reverse direction
* Forward current stops before capacitor finished discharging (return to baseline)
Switching Interval
Truncation
Biphasic Current: Switching Interval
provides adequate time for forward current to properly switch off before reverse currents put on
o Otherwise, all four current switches would be on at same time
o Creation of short circuit: current returns back across switches, does not go through heart, dissipates as heat
Biphasic Current: Truncation
o If do nothing: gradual decrease returns to baseline gradually – problematic bc can induce fibrillation
o Truncation: cuts off tail end of biphasic waveform
What are the three phases of electrical defibrillator timing?
- Electrical Phase
- Circulatory Phase
- Metabolic Phase
Affects optimal timing for first electrical defibrillation attempt
Electrical Phase of Defibrillation
- 0-4min no circulation
- Minimal ischemia
Circulatory Phase of Defibrillation
- 4-10min
- Energy depletion, potentially reversible cell injury – insufficient oxygen
Metabolic Phase of Defibrillation
- > 10min
- Advanced ischemia, cellular injury
Witnessed or Monitored Arrest for Shockable Rhythm
<4min CPA: minimal ischemic injury
Heart capable of re-establishing perfusing rhythm quickly if VF/PVT terminated immediately
Perform BLS long enough to charge defibrillator: shock, 1 cycle BLS then check ECG
Unwitnessed CPA for Shockable Rhythm
> 4min
Complete full 2’ cycle BLS before defibrillation
Likely that entered circulatory or metabolic phase so full BLS cycle provides perfusion to heart, restoration of ATP stores and thus increasing likelihood of successful defibrillation
Shocking ischemic heart depleted of ATP unlikely to retire perfusing rhythm, creates additional myocardial injury
Other Features of Defibrillation
Lots of gel, NO ALCOHOL = burns, fire
Roll into dorsal, tape into place if two regular paddles
Avoid contact with pet, table: can kill someone but usually just knocks them out, can induce fibrillation in person
Person shocking responsible for group safety
After Electrical Defibrillation
–Restart BLS: resume chest compressions immediately after each defibrillating attempt, interpret ECG after 2’ cycle
–If VT/PVT persists: increase dose by 50%
–Repeat every BLS cycle
Precordial Thump
large forceful single manual compression to chest if no defibrillator
o Delivers only 5-10J of energy to heart
o Strike chest directly over heart
Med to large dogs: strike chest with as much force as possible
Small dogs, cats: careful not to overly traumatize heart
Post Cardiac Arrest Syndrome
Consequences to dying - brain injury, acute kidney disease, myocardial damage, severe vasodilation and coagulopathy, secondary to low blood flow and subsequent ischemia-reperfusion injury
Second arrest common in first 24hr after resuscitation
4 Main Features of Post Cardiac Arrest Syndrome
- Systemic ischemia, repercussion response: SIRS potenital, MODS
- Brain injury: seizures, altered mentation, death
- Myocardial injury, dysfunction: decreased CO, arrhythmias, hypotension, ongoing organ perfusion
- Persistant precipitating pathology: need to address why happened in the first place
Goal Parameters for Post Arrest Patient
BP normal to hypertensive with systolic >100, MAP 80-120 (settle for 60)
* Injured brain/organs cannot autoregulate perfusion well
* Must maintain normal perfusion from them
Central venous oxygen >70%
Lactate <2.5mmol/L – will take time to come down
Urine output >1mL/kg/hr
* <0.5mL/kg/hr suggestive of renal injury
Oxygenation in the Post Arrest Patient
Do not hyperoxygenate creation of more free radicals, particularly injurious to brain
May have pulmonary contusions from compressions
Cardiovascular Rhythm in the Post Arrest Patient
Caution treating
Sinus tachycardia may take a while to resolve: do not chase # for several hours
Ventilation in the Post Arrest Patient
Often hypercapnic from some period of time bc large build up from ischemic tissues that has to be cleared
* Hypovolemic, decreased vascular resistance
Goal = normocapnia
May take awhile to start ventilating well on own, may be painful when expanding chest
+/- MV for short period of time
Blood Glucose in Post Arrest patient
Blood glucose >80mg/dL
Typically high initially from catecholamine surge
If persistently high, consider insulin to maintain <180mg/dL, may worsen brain injury if persistently high
Permissive Hypothermia in the Post Arrest Patient
Practically withhold warming after arrest but warm if hypotensive, shivering
True hypothermia = core temp ~90F
* Mild hypothermia (~97F) seems to be safe target
* True target, speed of rewarming not established
Shivering increases myocardial oxygen consumption!
Advantages of Permissive Hypothermia
- Decreased cerebral O2 requirements, brain metabolic demand, excitatory NTs, inflammatory cytokines, and free radicals
Other Brain Protective Strategies
Elevate head 15-30*: do not kink neck, elevate front half of animal
Brain will slowly come back online: return of ventilation efforts, facial nerve responses
Impedance Threshold Device
Connected to ET tube, controls air entry into lungs - requires certain inspiratory threshold
Decompression phase of CPR: patients upper airway pressure decreases = closure of valve
* Recoil, valve opens
Enhancing negative intrathoracic pressure during recoil
Can augment venous return, increase CO; improves coronary perfusion pressure, aortic pressure
Negatives assoc with ITD
Cause pulmonary edema (increased transthoracic pressure (between intrathoracic and alveolar pressures), may favor leaky capillaries
Not recommended for patients <5 kg or cats
Contraindications of ITD
congestive heart failure, DCM, pulmonary hypertension, aortic stenosis, flail chest, chest pain, and shortness of breath
Lidocaine as Anti-Arrhythmic - Literature
Increases energy requirements to successfully electrically defibrillate dogs, humans, pigs
Decreases defibrillation threshold with biphasic defibrillation
Successful defibrillation at lower energies in patients with prolonged VF
Incidence of Perianesthetic Respiratory Problems
Resp problems implicated in up to 50% of canine, 66% of feline anesthetic related deaths
Causes of Unexpected Hypoxia
Endobronchial intubation, mucus occluded tube, kinking or cuff induced occlusion of ETT, presences of pleural fluid or undiagnosed pneumothorax
Hypoxia can be from airway obstruction secondary to laryngospasm
Acute Pneumothorax
defect in pleura that allows air leakage into pleural space causing partial or total lung lobe collapse but air does not continue expanding
Types of Pneumothorax
Spontaneous/simple
* Primary: without underlying lung disease
* Secondary: underlying lung disease
Traumatic: any kind of trauma
Iatrogenic: baro or volutrauma
Tension Pneumothorax
pleural injury acts as one way valve that allows air to enter pleural space during inspiration, unable to escape during expiration
Patient can tolerate volume of pleural air that 2.5-3.5x FRC (~45 ml/kg)
Consequences of Pneumothorax
maximal expansion of chest, inspiratory muscles can’t work
lung collapses, IttP increases vena cava collapses, even aorta = CV collapse
Clinical Signs of Pneumothorax
Rapid shallow breathing
Activation of accessory respiratory muscles, gasping inspiration
May be hyper-resonant on percussion
Diminished breath sounds, tachycardia, hypotension
Treatment Pneumothorax
If no intervention: cyanosis then arrest
Tx: thoracocentesis +/- chest tube placement
o Open pneumothorax, start IPPV until defect can be fixed – require gentle expansion of lung, no aggressive ventilation
Bronchospasm
o Drug reaction, physical intervention
o Cats, sheep = particularly sensitive
o Fluid instillation during broncho-alveolar lavage can initiate bronchospasm, often associated with oxygen responsive hypoxia
Clinical Signs of Bronchospasm
Difficulty maintain acceptable hemoglobin saturation, tachypnea, tachycardia, and increasing airway pressures (if being ventilated), shark fin wave form on capnograph, wheezing may be auscultated
Treatment of Bronchospasm
Bronchodilator: albuterol, terbutaline SQ or IV, atropine
Aspiration of ruminal or stomach contents, consider pulmonary lavage
* Non-ruminants = controversial
Most inhalants, ketamine = bronchodilation
Desflurane: airway irritation
Volutrauma, Barotrauma
Even brief periods of lung overinflation: air leak, extraalveolar air accumulation
Increases in endothelial, epithelial permeability = edema, severe ultrastructural damage
Can lead to fulminant pulmonary edema with tracheal flooding, severe hypoxemia, death
High airway pressures depend on species, comorbidities: lower in amphibians, ruminants
Tracheal Tears - Cats
dorsal, longitudinal trachealis muscle most common in cats
2-5 cm, most commonly at level of thoracic inlet
Interval from anesthesia and diagnosis = 4 hours to 14 day
RF: dentals (83% of cases), stylet, multiple positions
Dx, Tx Tracheal Tears
pneumomediastinum on AXR
1/2 of cats improve with conservative treatment
Oxygen therapy and cage rest
Progressive dyspnea is an indication for surgical intervention
Procedures Associated with Higher Risk for Asp Pneumonia
upper airway surgery, neurosurgery, laparotomy, thoracotomy, endoscopy
Closed APL Valve
volutrauma, pneumothorax, or failure of venous return = cardiac arrest
Tipped Vaporizer
Precision vaporizers tip, or even move > 45 degrees = super high vaporizer output
