What is target PaCO2 following achievement of ROSC?
Dog: 32-44 mmHg
Cat: 26-36 mmHg
Examples of static fluid responsive markers
CVP
MAP
IVC diameter
LVED (EED) area
- May have confounding factors to limit precision
Dynamic Markers of fluid response
- Try to determine patient’s location on curve by inducing short term change in preload (fluid bolus) & measuring magnitude of response
** Not volume status but fluid response!
LA:Ao, CVCd, CVCci
Type A hyperlactemia
(MC) occurs with clinical evidence of a relative (exercise, tremors, seizures) or absolute (hypoperfusion) tissue oxygen deficiency (more likely lactate >6 mmol/L)
Type B hyperlactemia
occurs in absence of clinical evidence of decreased O2 delivery–> Defective mitochondrial oxidative function and abnormal carbohydrate metabolism but adequate O2 delivery to tissues; usually associated with more mild to moderate increases in lactate (3-6mmol/L)
B1 : assd with underlying disease (Sepsis - A and B , SIRS, Shock)
B2: assd with drugs or toxins (prednisone, ethylene glycol, propylene gylcol -act charcoal, epinethrine)
B3 assd with congenital or hereditary metabolic defects
D Lactate
- Need specialty lab to measure
- Present in 1%-5% of L lactate
- In cats, DKA, propylene glycol intoxication and EPI with bacterial dysbiosis, cats with GI disease
- Consider a rare but possible cause for high anion gap in metabolic acidosis - once through whole checklist of acidosis and can’t find anything
What are the main neurohormonal compensatory mechanisms in shock states?
- Baroreceptor reflexes:
- Carotid sinus (IX) and aortic Arch (X) → NTS in Medulla (cardioregulatory and vasomotor centers)
- Decreased firing (due to dec BP) → decreases PSNS, increases SNS - Chemoreceptor reflexes
- Carotid bodies (IX) & Aortic Arch (X) → NTS of medulla
- Centrally sense pH and PaCO2; Peripherally pH and PaO2
- Decreased PaO2, increased PaCO2 and/or decreased pH → increased SNS to cardiac and vessels, decreased PSNS - Renin-angiotensin-aldosterone system
- ADH
- Counter-regulatory hormones
WHat is SvO2 vs ScvO2?
- SvO2: mixed venous hemoglobin saturation
SvO2 is reflective of the entire body’s oxygen utilization - ScvO2: central venous hemoglobin saturation
ScvO2 is reflective of the cranial portion of the body (head/neck) oxygen utilization - In health state; ScvO2 is greater thanSvO2 due to the increased oxygen utilization of the cerebrum
However, in shock states the relationship becomes reversed and ScvO2 is greater than Svo2 due to splanchnic hypoperfusion
What is coronary Perfusion Pressure?
CPP = aortic diastolic pressure - right atrial diastolic pressure
- higher compression rates improve CPP< HR above 120 decreases due to decreased time in decompressive phase
- Majority of myocardial perfusion happens during decompression phase of chest compressions & determined by coronary perfusion pressure (CPP). Higher CPP = better success of CPR
- takes 60 sec of continuous compressions before CPP reaches maximum
Well performed compressions only provide _______% of normal CO
30
Appropriate respirations for CPR
- 10 breaths/min
- inspiratory time of appx 1 sec
- tidal volume 10 ml/kg
- Avoid hyperventilation → dec arterial CO2→ cerebral vasoconstriction → dec cerebral blood flow
- Avoid high tidal volume: increased PPV→ dec venous return → decreased CPP
Epi dose for CPR
- Low dose (0.01 mg/kg) every other cycle = higher rates of survival to discharge. Recommended initially
- High dose epi (0.1 mg/kg IV) After prolonged CPR - higher rates of ROSC
- ET admin: 10x dose and dilute 1:1 with sterile water; administer with red rubber
*𝛂1: most beneficial during CPR, vasoconstrict periphery, but spare myocardial and cerebral vasculature
Vasopressin CPR
- 0.8 U/kg IV every other cycle of CPR
- Efficacious in acidic environments when 𝛂1 receptors unresponsive
- No 𝛃1 effects → no chronotropic or inotropic effects (which may worsen myocardial ischemia in epi cases)
**V1 receptors
WHen to use alkalinizing agents in CPR?
- CPA >10-15 minutes → acidemia
- Na bicarb 1 mEq/kg once dilutes IV may be considered if prolonged CPA and pH >7 of metabolic origin
**Acidosis usually resolves with ROSC
When should defibrillate in CPR?
- Treatment for Pulseless V tach and V fib
- VF >4 min: one full cycle of CPR prior to defibrillating; this allow blood flow and O2 delivery to myocardial cells → generates ATP and restore normal membrane potentials → more likely to respond positively to defib
** VF less than 4 min –> IMMEDIATE defibrillation
- Biphasic: 2-4J/kg
- Monophasic: 4-6J/kg
** May increase dose by 50% up to 10, recommend doing this only once
Ventricular fibrillation phases
- Initial phase: VF </= 4 minutes → continue compressions only until defib can be charged, then defib immediately
- Circulatory phase: subsequent 6 minutes of VF: reversible ischemic injury due to depletion of cellular energy stores
- Metabolic phase: VF >10 min: potentially irreversible ischemic damage occurs
INdications for Open chest CPR
- Pleural space disease, pericardial effusion, penetrating thoracic injuries, intra-abdominal sx, thoracic sx
**Preferable in giant breed dogs with round or barrel chest conformation
Explain process of open chest CPR
- Left lateral thoracotomy at 4-5 intercostal space with patient in R lat recumbency
- Use care to not lacerate the internal thoracic vessel
- Finochetto retractors to open chest
- Pericardium may be removed to facilitate compressions (must be removed with effusions or pericardial disease
- Directly compress ventricles from apex to base (one hand or 2 hand technique acceptable)
- 2hand technique: RV cupped in L palm and LV covered by R fingers
- 1 hand technique: LV & finger of R hand in contact with heart compressed to sternum
Prognosis of CPR
- 47% in perianesthetic period
- Depends on underlying disease otherwise
- One study showed Cats 19% survival to discharge and 5x more likely to survive than dogs
What are the parts of post cardiac arrest Syndrome
- Systemic Ischemic - Reperfusion Injury (SIRS; hypercoagulable, impaired vasoregulation & adrenal function, increased susceptibility to infection, impaired DO2 and O2 utilization)
- Post cardiac arrest Brain injury (impaired cerebrovascular autoreg, cerebral edema, post ischemic neurodegeneration)
- Post cardiac arrest myocardial dysfunction (RV and LV dysfunction –> myocardial stunting)
- Persistent precipitating disease
Early hemodynamic optimization goals for post arrest care
- MAP: 80 - 120 mmHg (higher target than sepsis as risk of cerebrovascular autoregulation being absent PCA & perivascular edema or intravascular clot formation can compromise cerebral blood flow)
- Central venous O2 saturation [ScvO2] >70%
- Lactate <2.5 mmol/L (should be elevated due to having catecholamines administered)
- MM and CRT normalizations→ monitor for markers of vasodilation
- Echocardiographic determination of left ventricular function (dobutamine may help if present)
**GOAL: normoxemia PaO2 80-100 mmHg, SpO2 94-98% - avoid both hyper and hypoxemia for cerebral protection
Targeted temp management following ROSC
- Contraindication: arrhythmias, low BP
- Reducing core temp to 89.6 - 96.8 for 24-48 hours & inducing hypothermia ASAP
- Rewarming rate of normal temp at (0.25-0.5C/hr)0.5 - 0.9F degrees /hr
- Cooling methods: cooling blankets, ice packs, IV infusion of ice cold saline and endovascular cooling devices
- Side effects: shivering/increased muscle tone (BAD), changes in metabolism, acid/base, electrolytes, arrhythmias, drug elimination, coagulation and immune function
Cooling without sedation abolishes protective effects of TTM
Neurologic dysfunction following ROSC
Greatest cause of death
- Ischemia: Cerebral ATP depleted within 2 -4 min (20 to 40 min in intestines and myocardium)
- Once ATP depleted → cellular membrane potentials lost
- Large amts of Na, Ca and Cl enter cell → cell swelling → membrane disruption - Reperfusion: INcreased exposure to Ca, + oxidative stress + energy depletion → mitochondrial injury → increased ROS production at reperfusion → apoptosis and necrosis
- Control with mild hypocalcemia and avoiding hyperoxemia
- May take 72 hours following ROSC to really know whether neurologic assessment is indicative of prognosis
- May use modified glascow to monitor - not
- Good prognosis: Improvement of spontaneous vent, gag reflex and PLR are good
- Poor prognosis at 72 hrs: absent noxious stimuli, bilaterally absent PLRs and corneal reflexes, absent SSEP (somatosensory evoked potential)
Myocardial dysfunction after ROSC
- Characterized by increased CVP and pulmonary wedge pressure, reduced L & R sided systolic & diastolic ventricular function with increased end diastolic volume on both sides and reduced L ventricular ejection fraction & CO
- Myocardial stunting: term given to the reversibility due to absence of cell necrosis (resolved in 48 hrs typically)
Mechanisms myocardial dysfunction:
1. extent of myocardial ischemia and conditions on which reperfusion occurs (presence or absence of hypothermia/hyperoxia)
2. Lack of capillary blood flow: microvascular obstruction by endothelial cell activation and swelling, neutrophil-endothelial cell interactions, activation of the coagulation cascade, platelet aggregation, tissue blood flow impairment, post ischemic RBC tendency to form erythrocyte plugs (decreased deformability)
3. INtra-arrest administration of epinephrine and used of high energy monophasic waveform defibrillation
Give dobutamine!!
