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256 Cardiac Complications in Diabetic Ketoacidosis
• Drugs (cocaine) low levels of insulin. By 12 hours of treatment with
fluids and insulin , the extracellular potassium can
• Pregnancy
shift intracellularly causing hypokalemia. Serial ECG’s
DKA consists of the triad of hyperglycemia , keto- would be helpful in early detection of hypokalemia
sis and acidosis. Cardiovascular complications is or hyperkalemia.
increased in individuals with type 1 and type 2 DM. Hypokalemia is associated with ECG abnormalities
There has been little change in the mortality rate as- and cardiac arrhythmias. The most common and the
sociated with DKA despite great improvements in our earliest ECG finding in hypokalemia is a prominent U
understanding of its pathophysiology and treatment. wave. ST depression and T wave inversion can also
There are various cardiovascular complications in occur resembling myocardial ischemia. The most
DKA secondary to electrolyte disturbance and cate- common cardiac arrhythmias are atrial premature
cholamine release. DKA typically manifest as loss of contractions , atrial tachycardia with or without AV
5-8 litres of water , 400 -700 mEq of sodium, 250 block , SVT and ventricular premature contractions.
-700 mEq of potassium and 30-50 mEq of magne- Less common arrhythmias are AV junctional tachy-
sium.
cardia or escape rhythm and AV block.
The cardiovascular problems in DKA include : Hyperkalemia occurs in the initial stages of DKA. A
- Arrhythmia due to electrolyte imbalance potassium concentration of 5.5-7.5mEq/L , there is a
tall tent shaped peaked T wave which is often sym-
- Adverse effects of acidosis metrical with a narrow base and is best seen in leads
- Acute myocardial infarction ll ,lll and V2 to V5.
- Pulmonary oedema At potassium concentrations of 7.5 -10 mEq/L there
is a reduction in amplitude of P wave , prolongation
ARRHYTHMIAS IN DKA of PR interval . ST segment depression and disap-
pearance of P wave.
DKA results in electrolyte imbalance especially re-
duction in potassium , magnesium and phosphorus At leves above 10-12 mEq/L the QRS complex uni-
which can results in cardiovascular complications if formly widens. Potassium concentrations above 12
not carefully corrected. mEq/L , ventricular tachycardia or fibrillation, sine-
wave , slow ventricular escape rhythm or ventricular
Cardiovascular complications of electrolyte imbal- stand still occurs.
ance :
Intraventricular conduction defect is usually non spe-
Electrolyte Imbalance Potential Complications cific but patterns resembling RBBB , LBBB or LPHB
can also occur.
Hypokalemia Arrhythmia , cardiac arrest
ECG changes , ventricu- Occasionally in DKA , the ECG changes due to hy-
Hyperkalemia lar tachycardia, ventricular perkalemia can mimic acute myocardial infarction viz
fibrillation tall T wave , QRS widening and bundle branch block.
Treatment of hyperkalemia reverses these changes.
Decreased respiration thus
Hypomagnesemia low oxygen saturation ex- Magnesium levels should also be monitored close-
acerbating potassium loss ly. Hypomagnesemia can exacerbate potassium loss
causing persistent hypokalemia. Magnesium also
Altered mental status, hy- serves as muscle relaxant, hypomagnesemia can
Hypophosphatemia poventilation , cardiopul- result in decreased respiration and low oxygen sat-
monary arrest
uration which worsen the situation in individuals with
Potassium deficit is one of the most important elec- underlying asthma or COPD.
trolyte imbalance seen in DKA , as it can lead to fa- An additional electrolyte imbalance that may occur
tal arrhythmias. Normal serum range of potassium is elevated phosphorus levels. The normal levels of
is 3.5 to 5mEq/L. serum levels <3 mEq/L can result phosphorus are 2.5 to 4.5 mg/dl. Infact there have
in arrhythmias and cardiac arrest whereas levels been multiple case reports of complications due to
>5.5mEq/L can cause ECG changes with subsequent drastic reduction in phosphorus. Depleted phospho-
ventricular tachycardia or fibrillation. rus levels can also results in skeletal muscle weak-
Initially potassium levels elevated due to intracel- ness and hypoventilation, leading to cardiopulmo-
lular shift to the surrounding plasma secondary to nary arrest.
GCDC 2017

