Electrolytes abn

Question 1

Effect hyperK on AP

Answer 1

• ↑ resting membrane potential = more positive value → ↓ slope of phase 0
• Shortening of AP duration: ↑ activity of channels responsible for IKr
  o IKr: sensitive to extra levels of K+ → ↑ conductance → ↑K+ efflux → ↑ slope of phase 2 and 3

Question 2

Phases of hyperK

Answer 2

o Initially: ↑ excitability since membrane potential is closer to threshold
o As [K+]↑: membrane potential > threshold → constant depolarized state
 Prevent formation of AP and ↓ conduction velocity

Question 3

Sensitivity of myocardial cells to hyperK

Answer 3

atrial myocardium > ventricular myocardium > conduction system

Question 4

ECG changes hyperK

Answer 4

o K+ > 6-6.5mmol/L: tented symmetrical T waves, short QT, P wave prolongation + ↓ amplitude

o K+ = 6.5-8.5mmol/L: sinus bradycardia, ↓P amplitude, broad QRS, prolonged PR, ST segment depression

o K+ = 8.5t10mmol/L: atrial standstill, sino-ventricular rhythm, no P waves

o K+ >10mmol/L: sine wave, asystole, Vflutter/fib

Question 5

Cats with hyperK+ from reperfusion injury

Answer 5

Initial alteration on ECG: RBBB pattern with R axis deviation and deep S wave

o Holters: cats die from ventricular asystole, not Vfib

Question 6

Effect of hypoK on AP

Answer 6

• ↓ resting membrane potential = more negative value → hyperpolarization
  o ↓  excitability/conduction velocity
  o Shorten effective refractory period
  o Prolong relative refractory period
  o ↑automaticity
• ↑ AP duration: impact activity of K+ channels (prolong phase 3)
  o Delay repolarization → U waves, ST segment deviation
   ↓K+ efflux during phase 3
• ↑ automaticity of Purkinje fibers

Question 7

What arrhythmia is promoted by hypoK

Answer 7

EAD

Question 8

ECG changes hypoK

Answer 8

↑ PQ interval, AVB, QRS duration
o Dip and rise pattern
o Flattening/inversion of T wave
o ↑ prominence of U wave
o ST segment depression
o ↑P wave amplitude/duration

Question 9

Effects of hyperCa on AP

Answer 9

Ca2+ >12mg/dL
o ↓AP duration → ↓ phase 2

o Positive inotropic effect , ↓ excitability, ↑ rate of diastolic depol

Question 10

Effects of hyperCa on ECG

Answer 10

o Shorter QT, ST segment depression
o Slowed conduction velocity and AVB reported

Question 11

Effects of hypoCa on AP

Answer 11

Ca2+ <6.5mg/dL
o ↑phase 2 plateau

o ↓ contractility and rate of diastolic depol, ↑ excitability

Question 12

Effects of hypoCa on ECG

Answer 12

o Prolong QT and ST segment
o Tachycardia, tall R waves, T waves abnormalities reported

Question 13

Effects of Mg on AP

Answer 13

• Interaction with Ca2+ and K+
  o ↑ intra [Ca2+]
  o Prevent accumulation of intra [K+]
• Prolongation of AP duration and conduction time

Question 14

Effects of Mg on ECG

Answer 14

o ↑ PQ, QT and QRS duration
o U wave may be apparent
* Can promote VPCs and provoke polymorphic Vtach

o HyperMg
 AV and intraventricular conduction disturbances (3AVB, asystole)
o HypoMg
 Potentiate pro arrhythmic effect of digoxin
 Predispose to SVT or Vtach

Question 15

Effects of hyperNa on AP

Answer 15

• Determine phase 0 of AP
  o Hypernatremia: ↑ phase 0

Question 16

Effects of hypoNa on AP

Answer 16

↓ phase 0

Question 17

Electrophysiologic role of K+

Answer 17

• 98% of total body K+ is intracell, 75% in skeletal muscle cell
  o Na+/K+ -ATPase = main mechanisms to maintain gradient

Question 18

Role of K+ in AP

Answer 18

• Outward K+ flow → main current responsible for repol
• Resting membrane potential → highly permeable to K+
  o Will be the main determining factor of resting value around -85mV
• Phase 1: Ito → transient efflux of K+
  o ↑ in atrial/Purkinje 
  o ↓ ventricular myocytes
• Phase 3: determines AP duration
  o K+ currents activated after delay: IKr (major contributor), IKs, IK1
   IKur: only in atrial myocytes → responsible for shorter AP duration
  o Closure of Ca2+ channels → stops Ca2+ influx
• Phase 4: resting membrane potential
  o IKir is the major determinant → absent in nodal cells

Question 19

Mechanism altering extracell concentration of K

Answer 19

o K+ intake

o K+ excretion
 90% kidneys by Na+/K+-ATPase exch in distal renal nephron
* ↓ renal perfusion/hypovolemia
* ↓Na+ levels
* ↑K+ levels
Trigger renin secretion → aldosterone release → ↑K+ excretion

 10% intestines → stools

o Transcell shift of K+ in/out the cells

Question 20

Causes of hyperK+

Answer 20

o Renal disorders
o cell lysis → release intracell K+ stores

Question 21

Pathophys of hyperK

Answer 21

o Sensitivity: atria > ventricles > His bundle > SA node > internodal tracts
o ↑membrane potential (less negative) → ↓ duration of AP
 From ↓ concentration gradient as extracell [K+] ↑
 ↓ upstroke velocity of phase 0
 ↓ conduction velocity btw adjacent cell

Question 22

Common ECG signs of hyperK

Answer 22

o 1st most common sign: tall, peaked T waves
o Atria affected → prolong PR → flat P waves → no P waves
o Ventricle affect → wide QRS
o Sine wave appearance
o Delayed AV conduction +/- AVB

Question 23

ECG changes: Mild hyperK 5.6-6.5mEq/L

Answer 23

 ↑ cell membrane permeability to K+
 Faster ventricular repol
* Shorter QT
* Tented T waves
 ↓phase 4 diastolic slope → sinus bradycardia

Question 24

ECG changes: moderate hyperK 6.6-7.5mEq/L

Answer 24

 ↓ conduction velocity in ventricles
 Wide QRS, low R wave amplitude

Question 25

ECG changes moderate to severe hyperK 7-8.5 mEq/L

Answer 25

 PR prolongation, small/absent P waves
 Prolonged QRS
 Tall T waves
 Sinoventricular rhythm → SA node creates impulse → internodal tracts w/o atrial depol → normal conduction through AV node → ventricular depol

Question 26

ECG changes severe hyperK >8.5 mEq/L

Answer 26

 Worsening of previous characteristics
 Can lead to cardiac arrest and Vfib