Week 6-7 - ECC Flashcards
Potassium mainly resides (inside/outside) the cell.
Potassium mainly resides INSIDE the cell.
Potassium is mainly responsible for maintenance of _____________.
resting membrane potentials
Signs of hyper and hypo-kalemia tend to be ________ or __________.
cardiac or neuromuscular
(Hyper/Hypo)-kalemia is an EMERGENCY due to __________
Hyperkalemia,
Potassium supplementation should be done at a (slow/fast) rate to ensure safety.
SLOW
Intracellular cation = _____
Extracellular cation = _____
Intra = Potassium, K+
Extra = Sodium, Na+
Normal PLASMA [K+] is _______ mEq/L
Is [K+] slightly higher in serum or plasma?
3-5 mEq/L
[K+] is higher in SERUM
How is potassium eliminated?
Potassium elimination by the kidney – enhanced by aldosterone.
What CAUSES HYPERkalemia? (3)
- inadequate excretion
-kidney failure, esp. acute
-post-renal causes = inability to physically eliminate potassium
–urethral/ureteral obx
–ruptured urinary tract with urine accumulation in cavity
-Addison’s disease
-Chronic body cavity effusions - Excessive intake: iatrogenic - never from diet/orally
- Shift from intracellular site: crushing or reperfusion injury
When is HYPERkalemia a concern?
[K+] ≥ 6.0 is a concern, just outside the interval
What generalized issues can hyperkalemia cause?
cause neuromuscular signs such as weakness, but these signs are usually overshadowed by importance
of the cardiac arrhythmia
so neuromuscular and cardio signs
IT IS AN EMERGENCY
What are the 5 EKG changes for HYPERkalemia? see Lecture 48-49, slide 8
- Tall, tented T waves
- Loss of P waves, with bradycardia
- Slowing of heart rate
- Widening of QRS complex
- Asystole or ventricular fibrillation: non-circulatory
rhythms (death)
How do you TREAT HYPERkalemia?
- Cardioprotection: IV Calcium gluconate
-Does not drop plasma [K+]!!!
-Ca resets resting potential -> BUYS time to do other things - Elimination: IV fluid therapy
-Increases GFR, leads to renal K+ elimination
-still give fluids therapy to patient with urethral obx as it will also dilute the [K] – and also quickly deal w obx
-also helps with dehydration - Drugs to shift K+ into cells (and push Na+
-Dextrose, +/- insulin - only give insulin if NOT hypoglycemic already
–when glucose is shuttled into a cell, a K goes with it
-Sodium bicarbonate – efficacy questioned, try to use only if metabolic acidosis (acidemia/acidosis)
-Terbutaline, other sympathomimetics - harness sodium potassium ATPase - makes it run faster
What causes Pseudohyperkalemia?
-false increase in potassium concentration on bloodwork
-lab error
- thrombocytosis (only in serum sample that has allowed to clot)
-Platelet degranulation leads to K+ release into serum
-thus a serum-to-plasma difference in [K+] - Hemolysis in Japanese Breeds (Akita, Shiba Inus)
-Na-K ATPase on RBCs, so hemolysis during blood sampling or handling causes pseudohyperkalemia
What CAUSES HYPOkalemia?
not as life threatening as HYPERkalemia
essentially anything that causes PU/PD
- Kidney failure, especially chronic (CKD)
- Diuretics, many other causes of PU/PD such as DM
- Diarrhea, vomiting, decreased intake
- Toxin – beta agonist (rare)
CS of HYPOkalemia
- Muscle weakness
-CERVICAL VENTROFLEXION is classic - can’t hold head up, but still looking around with the eyes
-can be generalized
-Can cause hypoventilation requiring IPPV (rare) - mechanical ventilation – this is the EMERGENCY of hypokalemia - ECG changes:
-Diminished T waves, tall P waves
How do you TREAT HYPOkalemia
-very common but NOT usually an emergency
- Supplement with IV potassium in fluids
-If very severe, can use concentrated potassium solutions
-potassium is FATAL if you injected FAST, so concentrated K+ solutions only given by highly trained - Treat underling disease process
-Reduce diuresis if possible (such as better glycemic control in DM) - If severe, magnesium supplementation may be required
What is the maximum rate for potassium supplementation?
Kmax = 0.5 mEq/kg/hr
has to be spread over the entire hour
will only exceed it based on continuous EKG and have arrhythmia
The (ionized/unionized) fraction of Ca++ accounts for most of its biochemical activity
IONIZED = unbound = active Calcium
bc Ca++ sticks to albumin and then doesn’t do much when bound
no reliable relationship between ionized and total calcium concentrations
Ca++ abnormalities CAN be emergencies
Calcium is involved in what?
- coagulation
- heart rhythm
- muscle contraction
What is the normal reference interval for Ca++?
Ionized: 1.1-1.45 mmol/L
Total: 9-11 mmol/L
What CAUSES HYPOcalcemia?
-more common as emergency condition
- “Eclampsia” (“puerperal tetany” or “puerperal hypocalcemia”)
-dogs
-seen only in female bc peri-natal issues
-no blood pressure issues, systemic other issues – just the Ca++ issues - Chronic kidney disease – high phosphorous state
-can’t eliminate phosphorus bc GFR is bad
-decrease in Calcitriol
-decrease in Ca++ resorption - so end up with HYPOcalcemia (not really seen in AKD) - Pancreatitis
- Critical illness - most likely from acid base abnormalities
- Iatrogenic –
-blood transfusion - blood has anticoagulant, binds Ca++
-sodium bicarbonate therapy (base) – leads to alkalization of blood, H+ come off albumin to normalize pH, thus more room on albumin molecules for Ca++
CS of Hypocalcemia
- None if Mild
-Clinical signs uncommon until iCa++ ≤ 0.8 mmol/L
-rare
-lethargic - Moderate = facial pruritus/rubbing, muscle tremors /“tetany”
- Severe = Seizure, obtundation,
What is ECLAMPSIA?
-Post-partum hypocalcemia
-Associated with greatest lactation demand: just prior to weaning
–not usually seen at parturition
-Smaller breeds, more or larger puppies
What are the CAUSES to HYPERcalcemia?
H – Hyperparathyroidism
A – Addison’s disease
R – Renal failure (acute)
D – Hypervitaminosis D
I – Idiopathic (especially cats)
O – Osteolytic diseases
N – Neoplasia
S – Spurious
remember younger animals also have higher normal ionized calcium concentration to due growth
CS of hypercalcemia
-PU/PD
-Poor appetite, lethargy
-Vomiting
-Causes acute kidney injury: azotemia common
-Often found during workup for the primary underlying problem (such as generalized lymphadenopathy)
pathologic potential with hypercalcemia is kidney injury (failure potential) and dystrophic mineralization in distant organs such as kidney and lung
How do you TREAT hypercalcemia?
-Indicated when iCa > 1.8 mmol/L or for hypercalcemia with azotemia - NOT COMMON
-concerned about phosphorus and Ca to form mineral and then deposit them in distant organs (generalized mineralization)
- Fluid therapy – 0.9% NaCl – rehydrate and diurese
-acidifying properties of NaCl help elimination at level of kidney - Furosemide – helps eliminate Ca in urine
- Glucocorticoids – try not to use prior to definitive dx (Pred, steroids)
- Treat underlying disease
________ is the most plentiful molecule dissolved in the extracellular water.
Sodium
How much of the proportion of water in your body is “extracellular”?
1/3
What is the normal [Na]?
140-160mEq/L
Dysnatremia is usually due to a _______ problem.
water
What is Hypernatremia?
- Excessive water loss - most common
-sole problem
-in combination with excess water loss (polyuria, GI losses) - Excess sodium intake
-playdough
-beef jerky
-saltwater
-sodium bicarbonate
What is Hyponatremia?
- Increased water retention
- Excess water intake
What CAUSES Hypernatremia?
- Excessive ELECTROLYTE-FREE water loss (H2O molecules)
-Diabetes insipidus (central or nephrogenic)
–not enough ADH from posterior pituitary
–kidney doesn’t respond correctly/not working correctly even though ADH is there as normal
-Excessive panting (uncommon)
-Rarely, diarrhea (usually not electrolyte-free)
*a lot easier to treat than hyponatremia
What CAUSES Hyponatremia?
- Increased water retention – requires ADH action (ADH works on kidney – tells kidney to resorb water)
-Inadequate effective circulating volume
–baroreceptors sense not enough volume is coming by them - so they shrink. That stimulates pituitary to release ADH, in attempt to maintain adequate circulating volume.
–chronicity aspect, this pathway takes time
-Diuretic therapy
-Addison’s disease - Excess water intake - not common
-Generally iatrogenic (water through feeding tubes) in animals with limited kidney function - overwhelm body’s ADH
CS of dysnatremias are ________
Neurologic!
Obtundation
Disorientation
Head pressing
Seizure
Coma
Death
will see CS fairly late, not acute signs
Sodium (can/cannot) cross cell membrane into the intracellular compartment.
CANNOT
What contributes to plasma osmolality?
-anything dissolved in solution (cannot be spun out)
-All molecules dissolved in plasma contribute equally, regardless of:
size / molecular weight
valence (charge)
shape
type (sugar vs. protein vs. mineral,
etc.)
Each individual molecule dissolved in plasma contributes equally to osmolality
What is the equation for Osmolarity calculated?
Osmo,calculated = (2 x Na+) + (BUN ÷ 2.8) + (BG ÷ 18)
Biggest contributor to osmolality is Na, then urea, then glucose
Which direction does water move?
Low to High OSMOLALITY
Why are neurons intolerable of cell size change?
Neuronal swelling (as could be seen in acute, severe hyponatremia or in the treatment of hypernatremic animals with water) leads to elevated intracranial pressure as soft tissue expands within a hard, un-pliable skull.
Neurons are also intolerant of volume loss (cell shrinkage, as can be seen with overzealous treatment for hyponatremia) because cell shrinkage disrupts the relationship between the neuron and its myelin sheath leading to “demyelination syndrome” (previously called “central pontine myelinolysis”).
Why must treatment of dynatremias must be SLOW?
Cells accommodate dysnatremias (changes in ECF
osmolality) by internal mechanisms to help retain proper size and shape.
Thus, treatment of dysnatremia must be careful and slow to minimize adverse neurologic events during therapy.
The adverse events during therapy can be as dangerous as the dysnatremia.
How do you TREAT STABLE Hypernatermia? This is when hypernatremia is an incidental finding. This also means there are not neuro signs/they are mentally normal.
Administer electrolyte-free water source: 3–7 mL/kg/hr with goal to return [Na+] to normal within 48 hours
Water deficit =
0.6 x (BW, kg) x [(current Na - ideal Na)/ideal Na]
Monitor [Na+] on a SINGLE machine q 2 – 6 hours
How do you TREAT hypernatremia when CS are present? This would mean neuro signs are present.
If neurologic signs present – Emergency
Administer electrolyte-free water source: 7–10 mL/kg/hr, 5% dextrose in water IV
Treat until neurologic signs resolve
Then treat for stable hypernatremia
What is SHOCK?
decrease in cellular energy production in form of ATP production
For cells to produce adequate energy, the following 3 things must occur
- Adequate delivery of substrates (oxygen)
* Intact cardiovascular system with adequate blood volume
* Good pulmonary/lung function - Ability to carry substrates (oxygen) to cells
* Adequate RBCs
* Functional RBCs - Ability for cells to convert substrate to energy
* Mitochondria
failure of any 3 will result in shock
What does RAAS stand for and what does it do?
Renin, Angiotensin, Aldosterone System
Goal: retain water via retaining sodium to increase blood volume
What perfusion parameters are used to recognize shock?
- mentation
- Mucous membranes (color and CRT)
- Heart rate
- temperature (rectal and periphery)
- peripheral pulses
What are the types of shock?
- Vasoconstrictive
-hypovolemic
-hemorrhagic
-obstructive
-cardiogenic - Vasodilatory
-septic shock
-anaphylactic - Metabolic
-hypoglycemia
-dyshemoglobinemia (something is wrong with Hb)
-histotoxic
-hypoxemia
-anemia
What is the Baroreceptor Reflex?
-barareceptors sense increase and decrease in BP
-when in shock, there is a decrease in BP, then you a decrease in firing of baroreceptors.
-the decrease in firing = increase sympathetic tone
-NE is released
-NE causes vasoconstriction > to shunt blood to brain and heart
What causes hypovolemia?
- Ongoing water losses
-Gastrointestinal (vomiting/diarrhea)
-Renal loss (renal disease/diuretics/hypoadrenocortism)
-Third-space losses (hypoproteinemia) - Hemorrhage
-Trauma, neoplasia, anticoagulant toxicity, thrombocytopenia
What is the goal of shock resuscitation? What does it entail?
to maximize O2 delivery to tissues
-O2, oxygen therapy
-vascular access (IVC as close to heart)
-intraosseous catheter
When would you use Isotonic Crystalloids? When would you not use it?
- Hypovolemic shock
- Obstructive shock
- Hemorrhagic shock
- Vasodilatory shock: septic shock, anaphylactic shock
-DO NOT USE for cariogenic shock
What’s the shock dose of isotonic crystalloids for a dog? A cat?
Dog: 80-90ml/kg
Cat: 40-60ml/kg
Shock doses are given in aliquots – how much of the shock dose should be given in a certain amount of time?
20-30ml/kg over 10-15 min
What is obstructive shock? Remember, it is a vasoconstrictive shock.
- Impedance to blood flow leading to
decreased venous return, preload or forward
blood flow
Common CAUSES:
* Gastric Dilation Volvulus
* Cardiac tamponade secondary to
pericardial effusion
* Tension pneumothorax
* Thrombus
* Space occupying lesions
What does hypertonic saline do to the body?
-it has a lot of sodium, thus it’s osmolality is higher
-it draws fluid into the intravascular space/into the blood FROM cells and the interstitial space
-helps by reducing amount of isotonic fluids used
What are the indications for Hypertonic Saline?
- Hypovolemic shock in large/giant breeds
- Evidence of cerebral edema with concurrent shock and traumatic brain injury
What are the contraindications for Hypertonic Saline?
- Cardiogenic shock
- Moderate to severe dehydration
- Hypernatremia
What is the dose and how fast do you want to give hypertonic saline?
4ml/kg over 5 minutes
Hypertonic saline has some additional benefits?
- Improvement in myocardial contractility
- Immunomodulatory effects
- Vasodilation and improvement in microcirculation
What are colloids/how do they work as fluids?
- Natural or synthetic colloids stays within vasculature to increase plasma oncotic pressure (Starling Eq)
*Hydrostatic pressure goes “out” of the vessel, Oncotic pressure goes “in” to the vessel
*INCREASE IN PLASMA ONCOTIC PRESSURE leads to ↑ retention of intravascular volume and ↑ in plasma
volume
Hydroxyethyl Starch is a synthetic colloid. What does the hydroxyl do? Indications for colloids?
-Hydroxyl prevents hydrolysis in vasculature, stays longer
INDICATIONS
* Hypovolemic shock
* Obstructive shock
* Septic shock (controversial)
* Shock with concurrent hypoalbuminemia
Contraindicaions for colloids?
- Cardiogenic shock
- Acute kidney injury or chronic renal failure
- Coagulopathy
When would NATURAL COLLOIDS be indicated? Remember, natural colloids are albumin.
Hemorrhagic shock due to coagulopathy
What is the hydroxyethyl starch doses + the time period that you should give them?
- Dog: 5 to 10 ml/kg over 10 to 15 minutes
- Cat: 5 ml/kg over 15 to 20 minutes
What is the max daily dose for HYDROXYETHYL STARCHES? (Hetastarch and Tetrastarch)
- Hetastarch: 20 ml/kg/day
- Tetrastarch: 50 ml/kg/day
What do Hydroxylethyl Starches do to coagulation?
HES coats proteins on platelets preventing them adhesion and aggregation. Interferes with vWF release and decrease Factors VIII.
What do Hydroxylethyl Starches do to kidneys?
HES filtered through kidneys. Causes osmotic nephrosis - cells get swollen, causes injury.
Can cause AKI.
What is cariogenic shock? It is a vasoconstrictive shock.
Inadequate cardiac output.
- Poor cardiac contractility
-Cardiomyopathy (DCM), Sepsis - Heart rate too low
-AV block, sinus arrest, sick sinus syndrome - Heart rate too high (inadequate filling during diastole)
-Tachyarrhythmias - Valvular insufficiency
-Myxomatous mitral valve degeneration (MMVD)
-Aortic valve insufficiency
Do you give fluids to cardiogenic shock?
NO
What are the CS/findings for animals in cardiogenic shock?
- History of heart disease, breed-predisposition, syncope, toxin ingestion, systemic disease
- Mentation: Obtundation
- In respiratory distress?
- Arrhythmia: Tachyarrhythmia or bradyarrhythmia
- Thoracic auscultation: Pulmonary crackles, murmur (dogs), or gallop
- Pulses: Pulse deficits, poor pulse quality
- Mucous membranes: Pale, prolonged CRT
What are types of Vasodilatory Shock?
-sepsis
-anaphylaxis
What are the CS/findings for animals in vasodilatory shock?
- History: Bee sting, novel medications, transfusions, systemic infections, wounds
- Mentation: Obtundation
- Mucous Membrane: Often hyperemic, pale (anaphylactic shock)
- Fast capillary refill time (< 1 sec) or Undetectable
- Tachycardia or Tachyarrhythmia
- Bounding peripheral pulses
- Warm extremities
What is metabolic shock/what are some causes of metabolic shock?
- Hypoxemic
-Compromised pulmonary function
-Severe anemia - Hypoglycemia
- Cytopathic or Histotoxic shock
-Dyshemoglobinemia (esp in cats) – methemoglobinemia, carboxyhemoglobinemia
-Mitochondrial dysfunction – cyanide toxicity, sepsis
What is Heat Stroke?
- Life-threatening condition characterized by body Temp >40 °C (104 °F)
-CNS dysfunction
-Multi-organ derangements
What is the difference between hyperthermia vs. fever?
Hyperthermia: elevated temperature above hypothalamic set point (this is heat stroke)
Febrile/Fever: the body has reset the hypothalamic set point
What is the heat illness continuum?
- Heat cramps
-Muscle spasms secondary to sodium & water depletion - Heat exhaustion/prostration
-Fatigue, weakness, muscle tremors, vomiting, diarrhea - Heat STROKE
-CNS dysfunction
-Multiorgan failure
What are the different temps associated with heat stroke?
-Inadequate heat dissipation compared to production
- T < 106 °F - Heat stroke unlikely
- T > 107 °F -Cellular dysfunction begins
-May cause permanent brain damage
-Immediate cooling - T > 109 °F
-Severe organ damage
-Markedly increased mortality
What are the protective mechanisms to prevent heat injury?
Thermoregulation
* Controlled by hypothalamus
* Maintains balance between heat load &
heat dissipation
Normal heat dissipation mechanisms
* Radiation - more common in dogs/cats
* Convection - more common in dogs/cats
* Conduction
* Evaporation - can be more common with elevated temps
What’s the pathogenesis of heat stroke? There are two reasons with multiple causes.
- increased head load
-Environmental - Classic/non-exertional heat stroke (sitting in hot car)
-Metabolism/exercise - exercising too hard or prolonged seizure - decreased heat dissipation
* Confinement/poor ventilation
* Water deprivation
* Upper respiratory tract abnormalities
* Obesity
* Thick hair coat
* Lack of acclimatization
* Hypovolemia/poor cardiac output
* Drugs
Heat stroke leads to 3 things/The results of heat stroke are:
- heat injury to cells and proteins (direct cytotoxicity)
- associated severe systemic inflammation (mediated by cytokines and activated leukocytes and endothelial cells) (immune modulators)
- activation of coagulation cascades (coagulopathies)
These 3 things result in systemic inflammatory response, and then multiple organ dysfunction and death
What organ systems does heat stroke affect? (7)
- Coagulation
- CNS
- Cardiovascular
- Respiratory
- GI
- Renal
- Liver
How does heat stroke affect coagulation?
-heat affects coagulation factors and platelets
-hemorrhage, microthrombi, and coagulative necrosis
How does heat stroke affect the CNS?
-neuronal cells very sensitive to heat
-cerebral edema, hemorrhage, infarction, neuronal necrosis
How does heat stroke affect cardiovasculature?
-direct cytotoxicity > injury to cardiac myocytes
-vasoconstriction and hypoperfusion
How does heat stroke affect respiratory system?
-injury to lungs > aspiration pneumonia
-can progress to ARDS
How does heat stroke affect GI tract?
-play an important role in pathogenesis of heat stroke
-injury to GI tract can also occur secondary to direct cytotoxic injury, GI hypoperfusion and
ischemia, and microthrombi, resulting in increased intestinal mucosal permeability > lead to absorption of endotoxin from GI tract and sepsis
How does heat stroke affect renal system/kidneys?
-common sequela of heat stroke
-AKI
-significant dehydration and hypovolemia resulting in
decreased perfusion, as well as thermal damage and hemorrhage or microthrombi
-
How does heat stroke affect the liver?
-Decreased synthesis of coagulation factors from the liver may compound coagulation
abnormalities
What is typical TPR for heat stroke?
T: could be low, normal, or high
P: usually tachycardic
R: usually tachypneic
What is typical TPR for heat stroke?
T: could be low, normal, or high
P: usually tachycardic
R: usually tachypneic
Would you have a slow or rapid CRT with heat stroke? What other cardiovascular CS?
RAPID CRT - vasodilation to get rid of heat
-hyperemic MM, weak pulses, ventricular arrhythmias
What are some respiratory CS you may see with heat stroke?
Stertor or stridor suggestive of upper airway abnormality
Pulmonary crackles
What are some CNS CS you may see with heat stroke?
Mentation changes
Tremors, ataxia, cortical blindness, seizures
What are some renal CS you may see with heat stroke?
↓ Urine output, pigmenturia
What are some GI CS you may see with heat stroke?
vomiting, diarrhea, melena
What are some coagulation CS you may see with heat stroke?
Petechiae, ecchymosis
Hematuria, bloody vomit/stools
What are some lab findings you may see on a CBC for heat stroke?
Hemoconcentration
↑ nRBCs!!!
-secondary to thermal injury and release from bone marrow – associated with worse prognosis
Thrombocytopenia
How do you TREAT heat stroke in general/what’s the first thing you want to do?
COOL!!
* Wetting entire patient w/ room temp water + fan
* IV fluids
* Wet patients at home!
-Prognosis related to degree & duration of hyperthermia (how high the temp and how long the temp has been high)
When cooling a patient for heat stroke, what do you NOT want to do?
- Ice water > peripheral vasoconstriction
- Whole body alcohol > noxious, defibrillation
- Foot pads alone > small surface area
- Internal conduction techniques > invasive,
complications
STOP cooling at 103 degrees
What other ways will you continue to treat heat stroke?
Cardio Support
* Fluid therapy for hypovolemia (mostly crystalloids; colloids controversial)
* Vasopressors if needed
* Reassess perfusion, BP, ECG if needed
Respiratory Support
* Oxygen supplementation
* SpO2 or blood gas monitoring
CNS Support
* Repeated neurologic exams
* Treat volume & metabolic abnormalities, supplement dextrose PRN
* Mannitol or hypertonic saline, elevate head
Renal support
* Correct perfusion/hydration deficits
* Monitor UOP
* Dialysis?
GI Support
* Supportive GI care (anti-emetics, PPIs, +/- sucralfate)
* Broad-spectrum antimicrobials? (if leukopenia, fever)
Coagulation support
* Coagulation monitoring
* Plasma as needed for evidence of significant bleeding
What CS of heat stroke do you find with poor prognosis? What lab findings would you find?
- Coma
- Seizures
- Ventricular arrhythmias
- Long delay (>90 min) until treatment
- Obesity
- Hypoglycemia
- ↓ Cholesterol or albumin
- ↑ Bilirubin
- Acute kidney injury
- Prolonged PT/aPTT
- ↑ #nRBCs
Mortality for heat stroke is _____% (for dogs)
50%
don’t know for cats – rarely develop heat stroke
What is primary and secondary hypothermia?
Primary (“accidental”) hypothermia
*Excessive exposure to low environmental temperatures
* Exacerbating factors may include immersion in water,
trauma, exhaustion
* Frostbite of extremities is commonly associated
Secondary hypothermia
* Caused by disease, trauma, surgery, drugs
* Result is altered heat production and thermoregulation
What is a MILD hypothermia and its CS?
90 – 99.5F
- Shivering, heat-seeking behavior
- Ataxia
- Vasoconstriction
What is a Moderate hypothermia and its CS?
82 - 90F
- Altered mentation (obtundation to stupor)
- Hypotension
- +/- Shivering
What is a SEVERE hypothermia and its CS?
<82F
- Loss of shivering
- Cardiac arrhythmias
- Severe mentation abnormalities
(stupor to coma)
What cardio effects does hypothermia have on the body?
- starts with tachycardia > bradycardia (non-responsive to atropine)
- starts with vasoconstriction > vasodilation
–this is bc vascular response is decreased to catecholamines
–sinus bradycardia develops that is not responsive to atropine administration
–thus, lower BP (hypotension) and lower cardiac output - ECG changes
–Osborn waves (J waves)
–Ventricular arrhythmias/fibrillation
How do you TREAT hypothermia?
REWARMING - technique depends on severity of hypothermia & stability of patient
Mild hypothermia
-Passive rewarming > augment patient’s heat/minimize heat loss
-Blankets
-Other insulation
-they will generate heat and can slowly rewarm themselves
Moderate/severe hypothermia - patients can’t shiver, can’t produce heat endogenously
-Active rewarming > apply exogenous heat (to skin or core)
-Warm air convection
-Warm water blanket or bottles
-Radiant heat
-Heated infusions
-Airway rewarming
-Peritoneal lavage with heated fluid
What complications can occur with rewarming with Hypothermia? How can you avoid these?
Rewarming shock
Surface rewarming > peripheral vasodilation >
relative hypovolemia and hypotension
Core temperature “afterdrop”
Cold peripheral blood returns to vital organs >
further decreases core body temp
Rewarming acidosis Lactic acid returns from periphery
Avoiding complications
* Apply external heat to trunk rather than extremities
* Steady rewarming rate: 2-4oF / hour
* Administer IV fluids
What is the pathophysiology of electrical and lightening injury?
1) Electrical injury – direct effects of electrical current
* May disrupt electrophysiologic activity and lead to…
* …Muscle spasms, cardiac arrhythmias, loss of consciousness, respiratory arrest
* Direct cellular injury > Electroporation (creates momentary holes in cells, passage of macromolecules across these membrane, resulting in osmotic damage to cells
2) Thermal injury – transformation of energy into heat
* Fluids become superheated
* Coagulation of proteins, thrombosis, degeneration of vascular walls
* Necrosis of tissues due to heat & ischemic injury
3) Mechanical injury – from blast effect
* Can occur with lightning
The severity of electrical and lightening injury depends on ______
1) Electrical resistance through body part
* Wet skin/mucous membranes have low resistance > max tissue damage
2) Nature of current
* Alternating (worse) vs. direct
3) Intensity of current
* Amperage
What are some CS and PE findings for electrical and lightening injury?
-Integument / mucous membranes
Surface burns
Oral trauma
Subsequent tissue necrosis
-Cardiac
Ventricular arrhythmias
Death from ventricular fibrillation, asystole
-Respiratory
Respiratory arrest when in contact with source
Common – tachypnea, cough, cyanosis
Crackles if neurogenic pulmonary edema
-Neurologic
Unconsciousness
Focal muscle tremors, seizures
Extensor rigidity / tetanic limb contraction
-Ocular
Cataracts
Visual impairment in cattle due to cerebrocortical
necrosis with lightning strikes
Respiratory stress is common with electrical and lightening injury. What are the mechanisms of respiratory distress?
- Facial/nasopharyngeal edema (not typically severe)
- Diaphragmatic tetany
- Neurogenic (non-cardiogenic) pulmonary edema
-CNS insult
–sympathetic outflow
–vasoconstriction/hypertension
–pulmonary edema
-typically caudodorsal alveolar infiltrates
-Often resolves in 18-24 hours
(CNS insult > increased sympathetic activity. A profound catecholamine surge results in marked vasoconstriction and hypertension in both the pulmonary and systemic circulation. This in turn leads to a marked elevation in left ventricular afterload, accumulation of blood in the pulmonary circulation, increased pulmonary capillary pressures, and subsequent pulmonary edema.)
How do you TREAT electrical and lightening injury?
first precaution is to prevent injury to rescuers! Turn off the source of electricity before touching
the victim!!
-Cardiovascular
CPR?
IV fluid therapy – with caution
Antiarrhythmics
-Respiratory
Oxygen
Intubation if upper airway obstruction
Furosemide? – controversial
-Neurologic
Anticonvulsants as needed
-Skin / mucous membranes
Analgesia
Standard wound care
Subsequent surgical debridement
What is the prognosis for electrical and lightening injury?
Generally GOOD for those that survive initial shock
What is drowning?
“Drowning is a process resulting in primary respiratory impairment from
submersion/immersion in a liquid medium.”
What is the process of drowning?
- 90% – “wet” (aspiration of fluid into lungs)
–Fills alveoli/gas exchange units
–Washes out surfactant - 10% – “dry” (intense laryngospasm)
- +/- Non-cardiogenic pulmonary edema
What is the effect of water temperature on drowning?
-Ice-cold water submersion
* Evidence for increased chance of survival
* “Dive reflex” in most mammals > occurs seconds after a victim’s face contacts cold water and is a reflex mediated by the trigeminal nerve that sends impulses to the CNS and results in preferential shunting of blood to the cerebral and coronary circulation. This is thought to be protective against hypoxia-induced injury (though there is some controversy over its role in human submersion). Hypothermia also causes decrease in metabolic demand, which may protect the brain from injury.
-Warm water submersion
* Hypothermia = negative prognostic indicator
How do you TREAT drowning?
- respiratory
* Oxygen + oxygenation monitoring (pulse ox, blood gas)
* Thoracic radiographs
* Antibiotics? Intubation & mechanical ventilation? - cardio
* Fluid therapy (avoid overload)
* ECG and antiarrhythmics as needed - CNS
* Serial neurologic exams à hypertonic therapy if persistently abnormal
* Maintain normal O2, CO2, glucose; avoid excessive rewarming
* Steroids not recommended - GI
* Evaluate gastric volume
* Pass NG tube & empty stomach if large
What is the general prognosis with drowning?
Better with minimal respiratory, neuro, CV abnormalities
3 factors associated with 100% mortality
1) Submersion >25 min
2) Resuscitation >25 min
3) Pulseless cardiac arrest at ER
What are the components of blood?
-Red blood cells
-Coagulation factors
-Platelets
-Proteins
transfusions center around the need for these blood components
What does fresh whole blood contain?
Fresh whole blood contains all
cellular and plasma components of blood.
What can fresh blood be split into?
we can split a whole unit donation into:
red cells
platelets
plasma
can further fractionate plasma into cryoprecipitate
and cryosupernatant
Why would you transfuse RBCs?
anemia
What are some transfusion triggers to consider with transiting RBCs for anemia?
- Degree of anemia
-Avg. trigger of PCV 20-22% - Ongoing loss
- Chronicity
- Clinical response to anemia (i.e. perfusion parameters)
- Underlying or concurrent disease
-Unstable CV patient: PCV 25%?
-IMHA: PCV 15-18%
-Lower if cardiac disease, volume overload - Resources available
In terms of storage and product – what components of blood are a part of fresh whole blood?
Depends if the fresh whole blood is stored for under 8 hours or under 24 hours
<8 = RBCs, plasma, platelets
<24 = RBCs, plasma
platelets do not last after 8 hours
After how many hours, when does fresh whole blood become stored whole blood?
After 24 hours, and must be used within 28 days
only RBCs
How long can packed RBCs be stored for?
28-42 days
What are the transfusion volumes for packed RBCs and whole blood?
pRBCs: 1-1.5 ml/kg to increase PCV 1%
Whole blood: 2 ml/kg to increase PCV 1%
What are the typical transfusion goals?
-Raise hematocrit to ~25% to maximize oxygen
delivery without increasing blood viscosity
-If hemodynamically unstable/currently losing
blood, may aim for higher PCV (~30%)
-If concerning comorbidities, may aim for lower
PCV (~20%)
What are some indications of Plasma transfusions?
- treatment of an acquired coagulopathy with serious bleeding:
-Anticoagulant rodenticide intoxication
-Liver failure
-Heat stroke
-DIC (controversial) - Treatment of bleeding or prevention of bleeding with an invasive procedure due to a congenital coagulopathy
-vWD
-Hemophilia
What is primary and secondary hemostasis?
- Primary hemostasis = formation of platelet plug (clinical signs typically small bleeds)
- Secondary hemostasis = stabilization of platelet plug with cross-linked fibrin, which requires coagulation factors (clinical signs typically large body bleeds)
