Electrolytes imbalance and ECG changes presentation 2005

ECG
AND
ELECTROLYTES
IMBALANCE

PRESENTATION
by
DR.MUHAMMAD IDREES
DEPARTMENT OF
CARDIOLOGY ITTEFAQ
HOSPITAL LAHORE
23-06-2005

Case1. A 65-year-old man
known hypertensive and CRF,
presented with generalized
weakness, muscle cramps and
palpitation
O/E:
Pulse:100/m
B.P:180/90

This is classic hyperkalemia with tall peaked T waves, along with PR prolongation
and underlying LVH (patient has renal disease with hypertension). Potassium here
was 9.6mEq/L.
Not all tall positive T waves are "hyperacute." The latter term should be reserved
for increased T wave positivity secondary to transmural ischemia.

CAUSES OF HYPERKALEMIA
- renal failure
- hypoaldosteronism (Addisons disease)
- drugs
- ACE- inhibitors
- Potassium-sparing diuretics
- Beta blockers
- High-dose trimethoprim, digoxin, NSIADs,
cyclosporine.
- Heparin (prolonged use - greater than 3 days
use)
cont.

Continued. causes
- obstructive uropathy
- redistribution of potassium
- acidosis
- hyperkalemic periodic paralysis (familial)
- hypertonicity (mannitol, hyperglycemia)
- cellular damage - burns, crush injury
- severe physical exertion
- fasting in a dialysis patient

Pseudohyperkalemia
- hemolysis during blood sampling or
centrifuging
- excessively "tight" arm cuff +
"clenched fist"
- platelets > 1,000,000; leucocytes >
70,000
- family history of abnormal red blood
cell membrane permeability

ECG CHANGSES
ECG signs may be absent if the
onset of hyperkalemia is slow - as
seen in chronic renal failure - even
though the serum potassium is in the
range of 7 - 7.5meq/L; by contrast,
acute hyperkalemia can produce
ECG signs at much lower serum
potassium levels.

1. "Tenting" pattern with tall T waves
 Note the tall symmetrical T waves in the antero-
septal leads

2. "Thorn-like" T waves
ECG showing "thorn-like" T waves

3. "Sine" wave pattern
 Note the wide slurred QRS complex which
blends sinuously with the tall T wave into a
"sine" wave pattern

4. ECG mimicing an acute inferior
wall MI
 Note the elevated ST segments in two of the inferior
leads (S3 and AVF) suggestive of an inferior wall AMI,
and the reciprocal ST depression in leads S1, AVL and V
2 - 5 Clues that suggest hyperkalemia = absence of P
waves and the tall tented T waves in the chest leads

5. "Dumping" pattern
 Note the depression
of the ST segments
in leads V 2 - 6 - as if
something "heavy"
had been "dumped"
onto the ST segment
causing it to sink
down

6. "Z-fold" pattern
 Note the widening/slurring of the QRS
complex and how the ST segment
slopes straight up to the tall T wave
producing a "Z" pattern

Hyperkalemia (K+= 8.7 mEq/L) The ECG shows symmetrically peaked
("tented") T waves . The tracing also shows broad and flattened P waves
that precede frank sino-ventricular conduction seen with severe
hyperkalemia (i.e., conduction from the sinus node to the ventricles
through specialized inter-nodal tissue without atrial depolarization). This
conduction pattern may simulate a junctional rhythm. The narrow QRS
complex in this tracing is somewhat atypical for severe hyperkalemia.
case2. Elderly female on Dialysis presented with irritability

case3. The patient is an elderly man who presented to
the emergency ward with dizziness and new renal failure.
 Hyperkalemia (7.6 mEq/L) secondary to renal failure. widening of
the QRS complex. There is also peaking of the T waves with
prolongation of the PR interval and flattening of the P waves.

case4. 77-year-old female known HTN,CRF presented with irritability
 ECG shows sinus rhythm with LVH, and tall peaked T
waves with infero-lateral ST depressions. Also borderline
long QT (hypocalcemia). Putting it all together, the peaked
T waves indicate increased K+ (6.3 mEq/L) with LVH
suggesting renal failure associated with hypertension.

 Note the wide QRS complexes with no evident
P waves. CK was normal and ST elevations
were likely due to hyperkalemia.
case5. The K+ was 10.5 mEq/L in a patient with renal
failure.

 Hypothermia
Besides bradycardia, the most common finding is a prominent J
wave.
In addition, there may be delayed VAT , QRS prolongation, and
nonspecific T wave abnormalities, with QT prolongation.
Eventually, blocks, ventricular extrasystoles, and finally
ventricular fibrillation occurs, below 30oC.

Systemic hypothermia. The arrows (V3 through V6)
point to the characteristic convex J waves, termed
Osborn waves. Prominent sinus bradycardia is also
present.

case1. A 22 year old lady with prolonged vomiting.
This lady's serum potassium was 1.8 mmol/L.

Causes of Hypokalemia
 Inadequate intake
 diet very low in potassium
 geophagia - potassium-binding clay soil ingestion
 Excessive gastro-intestinal loss
 secretory diarrhea
 GIT fistula or small bowel enterostomy
 malabsorption syndrome
 excessive, voluminous vomiting
 laxative abuse cont.

Cont. CAUSES OF HYPOKALEMIA
 Excessive urinary loss
 hyperaldosteronism - primary or secondary
 osmotic diuresis
 diuretic drugs
 renal tubular diseases
 high urinary concentrations of anions eg.
penicillin
 renal toxins eg. amphotericin B, gentamicin,
toluene

Cont. CAUSES OF HYPOKALEMIA
 Redistributional
 acute insulin administration during DKA => rapid
potassium uptake by the cells
 beta-sympathomimetic therapy
 hypokalemic periodic paralysis - familial or
associated with thyrotoxicosis
 transfusion of large amounts of refrigerated red
cells, which "sponge-up" plasma potassium when
infused
 excessive sweating or skin loss secondary to
extensive burns

Pseudohypokalemia
 occurs in acute myelogenous leukemia
when the large number of leucocytes in
the blood specimen (stored at room
temperature) sponge-up the extracellular
potassium => artefactually low serum
potassium reading

Determining the cause of the hypokalemia
 Drug-induced
hypokalemia
 beta agonists
 theophylline
 caffeine
 verapamil intoxication
 insulin overdose
 thiazides
 furosemide
 Mineralocorticoids
 aminoglycosides (Gentamycin)
 chewing tobaccos
 glucocorticoids
High dose antibiotics
 penicillin
 ampicillin
 carbenicillin
Diuretic therapy is the most common cause of hypokalemia
in ED patients
Alcoholism is also a common cause of hypokalemia in ED
patients

ECG changes in hypokalemia
 1. Flattened T waves and prominent U waves
(apparent QT interval prolongation)
Note the prominent U wave in leads V3 and V4 giving the
conjoined T-U wave the appearance of a "camel's hump"

2. Prominent U waves combined with depressed ST
segments and flattened T waves ("roller-coaster effect")
 - note the depressed ST
segments with
flattened/equiphasic T waves
in leads V4 and V5 and V6
 - note the small flattened T
wave in leads V2 and V3 and
how the ST segment dips
down slightly (just after the
flattened T wave) before
rising to the prominent U
wave (that has merged with
the following P wave)
creating a "roller-coaster"
effect

case2. 30-yr-old man, not on medication, he had severe hypokalemia
(1.5 mEq/L) due to diarrhea. Calcium and magnesium were normal.
 There are very (!) prominent U waves with Q-T(U) prolongation.
 this acquired-type long-QT(U) syndrome puts subject at risk for torsade

case3. 31-year-old woman with ECG simulating ischemia.
What metabolic abnormality should you suspect?
 K+ here was 2.2mEq/L.
 Very severe hypokalemia can cause ST depressions and T-
wave inversions as seen here, mimicking ischemia. But also note large
U wave (positive deflection after ST-T and before P).

Normal tracing with a juvenile T wave inversion pattern in
leads V1, V2, and V3, as well as early repolarization pattern
manifested by ST segment elevation in leads I, II, aVf, V4, V5,
and V6.

A 71-year-old woman in the ER with end stage renal disease
developed mental status changes and had this ECG.
 "CVA-T wave pattern," especially with intracranial bleeds
 This ECG shows massive diffuse, very broad T wave inversions
with marked QT or QT-U prolongation (see lead V1).

HYPERCALCEMIA
 Hpercalcemia is defined as a serum
calcium > 10.5 mg/dl and severe
hypercalemia is defined as a serum
calcium > 14 mg/dl (> 3.5 mmol/L)

ECG CHANGES IN
HYPERCALCEMIA
 - an ECG may demonstrate a shortened
QT interval and bradyarrhythmias

case1. 49-year-old man who presented with
progressive muscle weakness, paresthesias, and
constipation.
 Very short ST segment with a consequently short QT interval; and
prominent U waves (esp. in V3). These changes are very suggestive of
hypercalcemia.
 This patient's serum calcium was 16 mg/dl. He was found to
have hyperparathyroidism.

case2. 35-yr-old: If you could only obtain one lab test what
would it be?
 Classic (!) ECG for hypercalcemia (13.9 mg/dl here).
Note the very abbreviated ST segment such that the T
wave looks like it takes off directly from QRS in some
leads.

Risk factors for hypercalcemia
 Hyperparathyroidism
 Malignancy
 Granulomatous disease
 Non-parathyroid endocrine disorders
hyperthyroidism
adrenal insufficiency
pheochromocytoma
cont.

Cont. Risk Factors for Hypercalcemia
 Vitamin D intoxication
 Vitamin A intoxication
 Mild alkali syndrome
 Chronic renal insufficiency, or dialysis patients
taking vitamin D replacement therapy
 AIDS
 Drugs
 lithium
 aminophylline
 thiazide diuretics

ECG CHANGES
 Prolongation of the QT interval (ST
segment portion) is typical of hypocalcemia.

Case1.If you could do only one lab test, what would it be in
this case?
 Check the calcium (and yes, of course albumin). It was low here at 8.2 mg/dl
with minimally low albumin in patient post thyroidectomy. ECG shows QT
prolongation. Most important is that QT is long in this case because the ST
segment is stretched out.

CAUSES OF HYPOCALCEMIA
1.It may be consequence of thyroid or
parathyroid surgery.
2.If phosphate raised then either:
Chronic renal failure
Hypoparathyroidism or
pseudoparathyroidism.
3. If phosphate is normal or low then either:
Osteomalacia or
pancreatitis

SYMPTOMS OF HYPOCALCEMIA
 - symptoms include muscle cramping or
carpopedal spasms, distal extremity
paresthesia, positive Chvostek's and
Troussaeau's sign
 - smooth muscle contraction can cause
laryngeal stridor, dysphagia and
bronchospasm
 - altered mental status or seizures may
occur

Digitalis effects on ECG
 shortened QT interval
 characteristic down-sloping ST depression,
reverse tick appearance.
 dysrhythmias
– ventricular / atrial premature beats
– paroxysmal atrial tachycardia with variable AV block
– ventricular tachycardia and fibrillation
– many others


Electrolytes imbalance and ECG changes presentation 2005

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