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
