Chapter 14: Electrolyte Physiology/Pathology Flashcards
when cell becomes more positive than baseline
depolarization
when cell becomes more positive than threshhold
overshoot
when cell becomes more negative than baseline
hyperpolarization
When cell becomes negative from a positive potential
repolarization
What is the electrical charge of all cells (except neurons and Purkinje cells) at rest?
-90mv
What is the electrical charge of neurons and Purkinje cells at rest?
-70mv
What electrolyte always wants to move out of the cell and can move freely at rest?
K (potassium)
What is important about the Nerst number (electrolyte electrical charge) - (cell electrical charge at rest) usually electrolyte electrical charge - (-90)
The higher the number, the faster the conduction speed, but also have to consider concentration gradient and size of electrolyte. i.e. Mg and Ca have higher Nerst numbers but they cannot fit through Na channels that are opened.
What is used to depolarize every cell in your body (except atrium and thalamus)?
Na
What depolarizes atrium and thalamus?
Ca
How does Na enter a cell?
first slow leaking Na channels open and by concentration gradient Na comes inside slowly; by making cell more positive, it reaches threshhold and opens fast Na channels (voltage gated) Na rushes in until it reaches equilibrium with its driving force; then voltage gates close.
What repolarizes a cell?
K leaks out and makes cell more negative and Na/K/ATPase will put 3 Na out and pump 2 K back in to re-establish concentration gradient but not the membrane potential
What other pump is used to re-establish membrane potential?
Na/Ca exchange (3 Na in/1 Ca out)
Every membrane’s action potential has phase 0,3,4: what happens during these stages?
Phase 0–depolarization–Na moves in
Phase 3–repolarization–K moves out
Phase 4–resetting–Na (in)/Ca out
What is the period during which no signal, no matter how large or strong, can depolarize the membrane?
absolute refractory period
What is the period after ARP in which some channels are reset; if the signal is strong enough, the membrane could depolarize but amplitude of depolarization will be lower:
relative refractory period
What is (TENS) transcutaneous electrical nerve stimulation unit
It is a pain relief therapy that uses the gate theory and keeps all nerve cells in the ARP, blocking all pain fibers of Spinothalamic tract
If there is increase in the depolarization of the brain, what will happen and how can we stop it?
seizures, use Na to stop it, use Na blockers like Phenytoin or Carbamazepine
If there is increase in depolarization of atrium, what will happen and how can we stop it?
atrial fibrillation or tachycardia; use Ca to stop it, need Ca blockers like Diltiazem or Verapamil
If there is increase in depolarization of the thalamus, what will happen and how can we stop it?
absence seizure, block Ca with Ethosuximide
Which agents can cause local anesthesia by blocking Na channels and stopping depolarization?
Lidocaine /Procainamide
Which drug is used for temporal lobe seizures?
carbamazepine
Which drug is used for mixed/myotonic seizures?
valproic acid
Which drug is used for febrile seizure?
acetaminophen (bring down fever)
Which drug is used for infantile spasm?
ACTH injections
Which drug is used for status epilepticus?
diazepam, lorazepam
What are the phases of AV node depolarization and what happens in each phase?
Phase 0–slurred curve due to slow Ca channels
Phase 1–Cl- in/ K out because of concentration gradient
Phase 2 plateau Ca (in)/K out because of concentration gradient (heart needs to “pause” for atrial contraction to fill up ventricles
Phase 3 K out (ARP)
Phase 4 automacity is less steep Na (in)/Ca (out)
What has the slowest conduction rate: SA, AV, or Purkinje?
AV
What controls the overall ventricular rate?
AV node
What has the fastest depolarization rate (atrium or ventricles) and why?
ventricles because they have Purkinje fibers
What are the phases of ventricular depolarization and what happens in each phase?
Phase 0: straight up due to fast Na channels
Phase 1 Cl (in)/K (out)
Phase 2 plateau Ca (in)/K (out)
Phase 3 K out
Phase 4 automacity is flat (Na in/Ca out)
If SA node depolarization is lost, what “takes over”?
AV node
If AV node depolarization is lost, what “takes over”?
Purkinje
What happens if ectopic sites take over?
arrhythmias
If pt is symptomatic and decompensating from arrhythmias, what do you do?
defibrillate! shock the heart will pause all cells so SA can reprogram
What does P wave indicate?
atrial depolarization, Ca in , Phase 0
What does PR segment indicate?
AV node pause or atrial contraction
What does PR interval indicate?
total conduction time from SA to AV to ventricle
What does QRS indicate?
ventricular depolarization, Na in , ventricular phase 0, Q is septum, R anterior and S posterior wall
What does ST segment indicate?
Ca in, ventricular contraction
What does T wave indicate?
ventricular repolarization, K out, ventricular phase 3
What does U wave indicate?
ventricular automacity, Na in/Ca out
What does QT interval indicate?
one complete ventricular cycle
On EKG what do width and height indicate?
width is duration (time); height is voltage
If atrium is small how will its P wave be? If atrium is large how will its P wave be?
small, large
If P wave is wide then what could that mean?
takes longer to depolarize; low Ca or Ca channel blocker
If QRS is wide, what could that mean?
Ventricle takes longer to depolarize; ventricle may be dilated or they are on Na channel blocker
If the ventricle is hypertrophied, how will the QRS look like on EKG?
tall and narrow
If ventricle is dilated, how will the QRS look like on EKG?
tall and wide
What is it called when one atrium depolarizes slower than the other (for example: one is dilated), and they don’t depolarize at exactly the same time, what will it show on EKG?
P mitrale
EKG “rabbit ears” on left lead QRS:
left bundle branch block
EKG “rabbit ears” on righ lead QRS:
righ bundle branch block
down ward on one side?
bundle block is on the opposite side
When does coronary blood flow happen: systole or diastole?
diastole
Which coronary artery supplies around 85 % of myocardium?
left main
left main branches into:
left anterior descending and left circumflex
left circumflex supplies
left atrium and gives off left lateral branch to supply lateral wall of left ventricle
LAD supplies:
anterior wall of ventricles including interventricular septum, and inferior 1/3 of posterior wall then anastomizes with posterior descending artery (RCA)
If you see sudden death, congested heart failure or recurrent ventricular arrhythmias, where is the infarct?
left coronary
What does Right Main coronary artery supply?
posterior wall of RA, SA nodal branch, AV nodal branch then divides into Right Posterior Descending (RPD) and Right Marginal
What area does Right Posterior descending supply blood?
posterior wall (and interventricular septum) of both ventricles, top 2/3 of posterior wall, anastomizes with distal LAD in the 1/3 of posterior wall
What area does right marginal branch supply blood?
lateral wall of right ventricle
What lead on EKG shows right marginal branch?
Lead II
Right coronary clue
heart block
Which leads on EKG see RA?
AVR and V1
Which leads on EKG see LA ?
I, aVL, V2
Which leads on EKG see right ventricle (right marginal)?
II
Which leads on EKG can see the apex?
aVF and V4
What are the anterior leads?
V1, V2, V3, V4
Which leads on EKG can see the left lateral wall?
III, V5, V6 (left marginal)
Which leads see LAD?
V3, V4
If QRS has positive deflection, but T wave is inverted, what does that mean?
repolarization of ventricles are going in same direction and may cause fibrillations or there is ischemia
If leads V2,V3,V4 have negative deflection, what does it mean?
anterior wall MI
If V5 and V6 are negative?
left ventricle MI
If lead II is negative?
right ventricle MI
fixed and prolonged P-R interval (more than .2 seconds–5 small boxes)?
first degree heart block (problem at the SA node or between SA and AV
What are some causes of first degree heart block?
CCB
beta blockers
adenosine which blocks cAMP
adriamycin
vasculitis
What is progressive lengthening of PR interval until QRS is dropped?
Mobitz 1: Wenkenbach’s
What kind of heart block PR is normal but QRS complexes are dropped erratically?
Mobitz 2 (Second degree heart block)
What causes Mobitz1?
Na/K ATPase pump stopped working, K leaks out making cell more negative until QRS is dropped
What causes Mobitz 2?
AV node has some cells more negative (early ischemia) and some positive (late ischemia because Na/Ca exchange is altered and Ca is trapped in cell), so if signal falls on negative, it will not fire, but falls on positive cell, it will fire.
What is third degree heart block?
complete AV dissociation; P waves and QRS have no relationship; need pace maker immediately!
If there is a wide QRS without a P wave before it and a longer pause afterwards, what is it?
premature ventricular complex (PVC)
What is it called when PVC every other beat?
bigeminy
What is it called when PVC every third beat?
trigeminy
Do you need treatment for PVC, bigeminy or trigeminy?
no, many times will correct itself and treatment may do more harm
What is it called when there are no recognizable QRS complexes?
v fib (ventricular fibrillation)
What is the treatment for v fib?
1 oxygen epinephrine or DDAVP to stimulate carotid reflex via vasoconstriction; shock with 360 joules; #2 (Na blocker) lidocaine, shock, #3 (K channel blocker)amiodarone or bretylium #4 IV magnesium (USE FIRST FOR TORSADES)
What is it called when pt has palpitations now and then?
PSVT paroxysmal supraventricular tachycardia
Where is the ectopic site located in atrial flutter?
between IVC and tricuspid valve
treatment for atrial flutter?
CCB and ablation
treatment for atrial arrhythmias?
- oxygen 2. adenoine 3.CCB (diltiazem/verapimil) 4. beta blocker 5 potassium channel blocker 6. digitalis
What kind of arrhythmia has the highest risk of thromboembolic stroke?
atrial fibrillation
Where do clots usually form during a fib?
atrial appendage
Where do most a fib form?
90% behind pulmonary veins of left atrium
treatment for a fib with artificial valves?
warfarin
treatment for a fib no artificial valves?
apaxiban, rivaroxiban
Who needs to be on warfarin the rest of their lives?
Women with CHADS2VaSc score more than 3
Men with CHADS2VaSc score more than 2
CHF=1
HTN (uncontrolled)=1
Age 65-75=1
greater than 75=2
DM (uncontrolled)=1
Stroke/TIA/thromboembolism=1
Vasculitis =1
Sex woman on estrogen/with vasculitis)=1
Problems with hypermagnesia (greater than 2.0mg)
less likely to depolarize (Mg competes with Na by blocking channel); affects Ca because up PTH; affects K due to co-transport in DCT of kidney; affects all kinases
treatment of hypermagnesia
normal saline IV and loop diuretic
Problem of hypomagnesia (less than 1.5)?
more likely to depolarize, down PTH, lowers K, and affects all kinases
treatment of Hypomagnesia?
magnesium sulfate IV
What is the problem with hypercalcemia (greater than 10.8)
less likely to depolarize, except in atria and thalamus (more likely to depolarize)
What about hypercalcemia in smooth muscle?
initially less likely (blocks nerve); then more likely because of upregulation of IP3-DAG
Treatment for hypercalcemia?
IV normal saline, loop diuretics; bisphosphonates (inhibit osteoclast activity); denosumab (more ab against osteoclasts); mithramycin (CALCIUM CHELATOR)
What is the sign of hypocalcemia?
tetany
Problems with hyperkalemia (more than 5.0)?
Initially m ore likely to depolarize but as K gets trapped in cells, less likely to depolarize. Prolonged QT intervals (peaked T waves) predispose to arrhythmias.
Treatment for hyperkalemia (mnemonic C BIG K) if 6.5 or greater and EKG changes:
Ca gluconate to protect SA node
Bicarbonate (induce alkaloses and K excretion in urine.Insulin and Glucose because insulin will push
excess K into surrounding cells and glucose
will prevent from hypoglycemia
Treatment for hyperkalemia (mnemonic C BIG K) if 6.5 or greater and EKG changes:
Ca gluconate to protect SA node
Bicarbonate (induce alkaloses and K excretion
in urine.
Insulin and Glucose because insulin will push
excess K into surrounding cells and glucose
will prevent from hypoglycemia
Kayexalate pull K out of GI tract–poop it out
last resort: hemodialysis
Problem with hypokalemia?
K will rush out of cell (concentration gradient) making cells less likely to depolarize; weakness/SOB; pancreas down release of insulin;
treatment for hypernatremia
IV normal saline, correct Na no more than 0,5meq/hr. because may cause central pontine demyelination
