hyperkalemia protocol presentation

20
Clinical Policy CLN 14-001 Treatment of Cardiac Arrest Patients with Confirmed Renal Failure

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Page 1: Hyperkalemia protocol presentation

Clinical Policy CLN 14-001

Treatment of Cardiac Arrest Patients with Confirmed Renal

Failure

Page 2: Hyperkalemia protocol presentation

Purpose:

This self learning program has been developed to in service CPHM EMS personnel on the new clinical policy in which goes into effect June 17, 2014.

Dr Janikas has noted the need for CPHM EMS staff to be able to readily access Dialysis Patient’s dialysis catheters in cardiac arrest.

It has also been recognized that many of these patients are in cardiac arrest directly due to Hyperkalemia and this policy allows for Paramedic level staff to administer Sodium Bicarbonate and Calcium Gluconate on standing orders.

Page 3: Hyperkalemia protocol presentation

Objectives

1. Review of Hyperkalemia

2 Accessing a Dialysis Catheter

3. Review of Policy CLN 14-001

Page 4: Hyperkalemia protocol presentation

Hyperkalemia

Hyperkalemia occurs when the extracellular potassium ion [K+] concentration is above the normal value. It is a potentially life-threatening emergency that can be corrected with treatment.

Page 5: Hyperkalemia protocol presentation

Potassium

It is essential for the normal functioning of the muscles, heart, and nerves. Potassium helps the body regulate activity of muscle, including the:

Smooth muscles

Skeletal muscles

Cardiac muscle

Potassium is very important for maintaining normal heart electrical rhythm as well as conduction for normal electrical signals in the nervous system.

Page 6: Hyperkalemia protocol presentation

Potassium levels

The normal potassium level in the blood is 3.5-5.0 milliEquivalents per liter (mEq/L).

Potassium levels between 5.1 mEq/L to 6.0 mEq/L are considered to be mild hyperkalemia.

Potassium levels of 6.1 mEq/L to 7.0 mEq/L are moderate hyperkalemia, and levels above 7 mEq/L reflect severe hyperkalemia.

Page 7: Hyperkalemia protocol presentation

Hyperkalemia

Excess potassium in the bloodstream can result from diseases of the kidneys or adrenal glands as well as from certain medications.

Hyperkalemia can also be the result of potassium moving out of its usual location within cells into the bloodstream.

Generally 98% of the body’s Potassium is in the cells, with 2% in the circulation.

There are many causes that can move the intracellular Potassium into the circulation.

Page 8: Hyperkalemia protocol presentation

Hyperkalemia Causes Chronically recurring hyperkalemia is most commonly

seen in patients with chronic kidney disease (CKD), as the decline of renal function compromises the kidney's ability to properly excrete K+.

Additionally, renin-angiotensin-aldosterone inhibitor therapy, the current standard of care for CKD and heart failure that has been proven to delay progression to end-stage renal disease, often exacerbates Hyperkalemia (Angiotension II receptor blockers).

Medications such as: NSAIDS, ACE inhibitors, and Succinylcholine.

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Hyperkalemia Causes

Any condition which there is massive tissue destruction can result in elevated levels of Potassium.

Trauma, burns, rhabdomyolysis, and destruction of red blood cells.

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Hyperkalemia Symptoms

Clinical presentation of hyperkalemia is highly variable with some pt’s with acute illness, and other who are aysmptomatic.

Symptoms do not become apparent until levels are very high, 6.5 and greater. Most symptoms are nonspecific:

Muscle weakness, tiredness, tingling sensations, or nausea.

Hyperkalemia does have an effect on the pt’s EKG.

Page 11: Hyperkalemia protocol presentation

Hyperkalemia and the EKG

Hyperkalemia causes rapid reduction in the resting membrane potential leading to increased cardiac depolarization & muscle excitability.

The classic criteria has been “Peaked T waves”.

Peaked T waves are best seen in the precordial leads, shortened QT interval, and sometimes ST segment depression.

Widening of the QRS complex (usually potassium level is 6.5 or greater). This frequently appears as in "non-specific intraventricular conduction delay" or IVCD which is characterized by a widened QRS complex of > 120 ms that does not meet the criteria for a left or right bundle branch block.

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Hyperkalemia

Page 13: Hyperkalemia protocol presentation

Hyperkalemia and the EKG

Decreased amplitude of the P waves, an increase in the PR interval, and bradycardia in the form of AV blocks occur as the potassium level exceeds 7.0.

Absence of the P waves and eventually a "sine wave" pattern (see below) which is frequently a fatal rhythm.

Page 14: Hyperkalemia protocol presentation

Hyperkalemia Symptoms

CLINICAL PEARLS:

Supportive measurements like fluids, pacing, and pressors do not work in the setting of hyperkalemia. You must treat the hyperkalemia first.

The ECG changes with hyperkalaemia do not consistently follow a stepwise, dose-dependent pattern. In reality, many patients have rapid changes in their ECG. The risk of arrhythmias increase with K+ values > 6.5 mmol/L and even small elevations in K+ above this concentration can lead to rapid progression from peaked T waves to ventricular fibrillation. The longer a patient has high K+ concentrations, the greater the risk of sudden deterioration.

Giving intravenous calcium is "cardioprotective" in the setting of hyperkalemia. Frequently instant reversal of all hyperkalemic ECG changes within seconds of administration (see example 4 below). Calcium does not decrease the potassium levels, so other therapy like bicarbonate or insulin is needed to do this. Calcium administration can be fatal when digoxin toxicity is causing the hyperkalemia and should be avoided.

Page 15: Hyperkalemia protocol presentation

Dialysis Catheters

Dialysis catheters are typically placed in the neck or upper chest.

Access ONLY one port.

Use strict aseptic technique (all connectors should be cleaned with Betadine or Chlorahexadine swabs).

Catheters are filled with a Heparin solution. You must withdraw 5-10cc of fluid/blood prior to attaching IV tubing. Then gently flush with normal saline bolus to confirm patency.



Page 16: Hyperkalemia protocol presentation

Dialysis Catheters

Catheters come in various shapes, sizes, and number of ports.

Remember access only one port at a time.

Only infuse through one port.

If Dialysis staff is present consider asking staff to access port for you.

Page 17: Hyperkalemia protocol presentation

Dialysis Catheters

Remember these catheters are directly into the great vessels. AVOID AIR EMBOLI at all costs. Clamp catheter (using only the clamp on the catheter) prior to taking caps off and attaching IV tubing.

Do not allow air to enter the central circulation due to any air in the IV tubing.

Don’t forget to unclamp the catheter once everything is attached!

Page 18: Hyperkalemia protocol presentation

Policy CLN 14-001

ON STANDING ORDER PER MD 420

Cardiac Monitor Defibrillate as appropriate

Access dialysis catheter if available If dialysis catheter is not available, initiate IV

access

Calcium Chloride 1 gram IV Bolus

Sodium Bi-Carbonate 50 mEq IV Bolus

Continue to appropriate cardiac arrest protocol based on patient’s underlying rhythm.

Page 19: Hyperkalemia protocol presentation

Policy CLN 14-001

This policy may ONLY be used while working as a Paramedic with Clifton Park Halfmoon EMS. It is not valid when working with any other agency.

Calcium and Bicarb may take time to have an effect on the patient. The most useful tools are Insulin and Dialysis.

Be prepared for an extended code, and transport your patient to an appropriate Emergency Room.

Advise the ED you suspect this cardiac arrest is related to hyperkalemia.

Page 20: Hyperkalemia protocol presentation

Please review attached policy CLN 14-001.

Please complete quiz attached to this LearnEMS module.

Any questions can be directed to Clinical Services or Dr. Janikas.

Thank You.