Mahlla Cardiac Center

Most of cardiac care unit (C.C.U) drugs

All data obtained from American Heart
Association (AHA) & medscape.com website

Anticoagulants

Heparin: (1 amp. 5000 I.U)

2

Heparin inhibits the conversion of prothrombin to thrombin and prevents

aggregation of platelets.
-Loading dose: 80u/kg (May be equal 1 amp.).
-Maintenance dose: 18 u/kg/hr Max dose: 1000 u/hr (May be equal 20cm/hr. (
-5 amps. Diluted on 500cc D5W or NS 0.9% and adjust dose according to that.
-Normal PTT = 30 40 seconds.
-Titrate drip to keep the PTT 1 to 2 times the pretreatment level.
-Follow up by PTT every 8hr (therapeutic dose = PTT: 50 - 70).
-If PTT blow 50 increase dose by 5u/hr.
-If PTT above 70 decrease dose by 5u/hr.
-When we reach therapeutic dose redo PTT after 24hr.
-In case of overdose, use Protamine Sulfate (1mg of protamine sulfate neutralizes
100 units of heparin given in i.v in slow rate not exceed 50mg over 10 min. to
avoid allergic reaction).
-Side effect of heparin: Thrombocytopenia.
--------------------------------------------------------------

Fondaparinux (Arixtra): (1 amp. 2.5, 5, 7.5, 10mg)

-In acute coronary syndrome (A.C.S) 2.5mg once daily.
-DVT/PE, Treatment < 50 kg: 5 mg SC qDay - 50-100 kg: 7.5 mg SC qDay >100 kg: 10 mg SC qDay.
-DVT/PE, Prevention >50 kg: 2.5 mg SC qDay.
-Used s.c or i.v 6-8hr after surgery & not make thrombocytopenia.
-Contraindication:
-renal impairment (CrCl <30 mL/min).
- Hypersensitivity.
- Body weight <50 kg for surgery.
- Active major bleeding, bacterial endocarditis,
thrombocytopenia with antiplatelet antibody in presence of fondaparinux.
-------------------------------------------------------

Enoxaparin

(Clexane):
(1 amp. 20mg/0.2mL, 40mg/0.4ml, 60mg/0.6ml & 80mg/0.8ml)
1-Deep Vein Thrombosis (Prophylaxis) Prevent the occurrence of pulmonary
embolism in patients at risk for thromboembolic complications who are
undergoing abdominal surgery or hip or knee replacement surgery, as well as in
medical patients with severely restricted mobility during acute illness.
.Abdominal surgery: 40 mg SC qDay; initiate 2 hours preoperatively.
.Knee or hip replacement surgery: 30 mg SC q12hr; initiate therapy 12-24 hours
postoperatively For hip replacement surgery, may consider administering 40 mg
SC qDay, initiated 12 hours preoperatively and continued for 3 weeks.
.Medical patients with restricted mobility: 40 mg SC qDay.
-Dosing considerations:
Abdominal surgery: Duration of administration is 7-10 days; up to 12 days has
been administered in clinical trials or until risk of DVT has diminished.
Knee or hip replacement surgery: Duration of administration is 7-10 days; up to
14 days has been administered in clinical trials or until risk of DVT has
diminished.
Medical patients with restricted mobility: Duration of administration is 6-11
days; up to 14 days has been administered in clinical trials.
2-Unstable Angina, Non-Q-Wave MI & DVT (Treatment) 1mg/kg/ SC q12hr
3-Acute STEMI
< 75 years loading dose: 30 mg IV bolus once plus 1 mg/kg SC once; not to
exceed 100 mg cumulative loading dose & Maintenance: 1 mg/kg SC q12hr.
> 75 years No IV bolus dose: 0.75 mg/kg SC q12hr Not to exceed 75 mg/dose for
first 2 doses only, followed by 0.75 mg/kg for remaining doses.
4-With PCI
if the last enoxaparin was given < 8 hr before balloon inflation, no additional
dosing is needed if the last enoxaparin was given > 8 hr before balloon inflation,
an IV bolus of 0.3 mg/kg should be administered.

-Administration:
Low body weight (< 45 kg for women or < 57 kg for men): Increased exposure
has been observed with prophylactic (non-weight adjusted) dosage; carefully
monitor for sign/symptoms of bleeding
Administer deep SC alternating right and left anterior and posterior abdominal
walls into skin fold held between thumb and forefinger
Use of tuberculin syringe (or equivalent) is recommended to assure appropriate
measurement of dose
For IV administration, may administer in IV line with 0.9% NaCl or D5W
-In case of renal impairment:
Severe (CrCl <30 mL/min): Dosage reductions required
Prophylaxis in abdominal surgery: 30 mg SC qDay
Prophylaxis in hip or knee replacement surgery: 30 mg SC qDay
Prophylaxis in medical patients with restricted mobility: 30 mg SC qDay
DVT treatment (inpatient or outpatient): 1 mg/kg SC qDay
Non-Q-wave myocardial infarction: 1 mg/kg SC qDay
Treatment of acute STEMI (<75 years): 30 mg IV single bolus plus 1 mg/kg SC,
THEN 1 mg/kg SC qDay
Treatment of acute STEMI (age 75 years or older): No initial bolus; maintenance
of 1 mg/kg SC qDay.
--------------------------------------------------------------

Antiplatlet

Type of antiplatelets
6

1-Irreverssible cyclooxygenase enzyme inhibitor-aspirin

--------------------------------------------------------------------inhibit formation of TX A2 w' is VC and cause platelat aggergation
2-ADP inhibitors
-----------------clopidogrel
prasugrel
ticlopidine
ticagrelor
3-Phosphodiesterase inhibitors
-----------------------------------cilostazole
4-Glycoprotein IIb / IIIa inhibitors--block receptors on platelets for
fibrinogen and von willbrand factor
---------------------------------------tirofiban (aggrestate)
eptifibatide (integriline)
abciximab (reopro)
5-Thromboxan inhibitors
----------------------------Thromboxan synthase inhibitor
thromboxan receptor antagonist
terutroban
6-PG2 analouge
------------------Used in hemodialysis & cardiopulmonary bypass.
7-Adenosine reuptake inhibitors
-------------------------------------Dipyridamole

Tirofiban (Aggrastat): (vial 125mg in 50cc)

7

This low-molecular-weight nonpeptide compound has a longer plasma half-life of

1.8 hours and a shorter biologic half-life of seconds as a result of reversible low
affinity binding kinetics to the IIb/IIIa receptor. Renal elimination of tirofiban
requires dosing adjustment in patients with renal insufficiency, and tirofiban has
no interaction with the vitronectin or MAC-1 receptors.
-Dilute on normal saline.
Acute Coronary Syndrome
Indicated in combination with heparin, is indicated for the treatment of acute
coronary syndrome, including patients who are to be managed medically and
those undergoing PTCA or atherectomy
0.4 mcg/kg/min IV for 30 minutes, THEN 0.1 mcg/kg/min IV for 48-108 hours.
Continue infusion through angiography and for 12-24 hr after angioplasty.
Percutaneous Cardiovascular Intervention
Loading dose: 25 mcg/kg IV over 3 min at time of PCI.
Maintenance dose: 0.15 mcg/kg/min IV for up to 18-24 hours.
-Renal Impairment: CrCl <30 mL/min: 50% of normal dose rate.
-Contraindications:
Hypersensitivity, history of thrombocytopenia w/ tirofiban
Active/history of internal bleeding (within last 30 d), intracranial hemorrhage or
neoplasm
History of stroke within last 30 d or any history of hemorrhagic stroke
AV malformation or aneurysm, aortic dissection, severe HTN, acute pericarditis

Current use of another parenteral glycoprotein IIb/IIIa inhibitor

- Cautions: Plts <150 K/cu.mm, hemorrhagic retinopathy, chronic
HD.
--------------------------------------------------------------

Eptifibatide (Integrilin):
Eptifibatide is a peptide that competitively and specifically
inhibits the GP IIb/IIIa receptor, resulting in a long plasma halflife (150 minutes) and short biologic half-life (2.5 hours). Like
tirofiban, eptifibatide undergoes renal clearance, requiring
appropriate dosing adjustments in patients with renal
insufficiency. Eptifibatide, like tirofiban, does not bind to MAC-1
receptors and has no clinically relevant affinity for the vitronectin
receptor.
-Acute Coronary Syndromes
180mcg/kg IV bolus over 1-2 min, THEN 2mcg/kg/min IV for up
to 72hr.
-Percutaneous Coronary Intervention
180 mcg/kg IV, THEN Continuous infusion 2 mcg/kg/min with
another 180 mcg/kg IV bolus 10 minutes after 1st one Continue
infusion for at least 12 hours.
-Renal Impairment: (CrCl < 50 mL/min)
ACS: 180 mcg/kg IV, THEN continuous infusion 1 mcg/kg/min
PCI: 180 mcg/kg IV, THEN continuous infusion 1 mcg/kg/min with
another 180 mcg/kg IV bolus 10 minutes after 1st one
Hemodialysis: Safety and using during hemodialysis not established
-Contraindications:
Hypersensitivity.
History of internal bleeding, intracranial hemorrhage or neoplasm, CVA,
thrombocytopenia.
AV malformation or aneurysm, aortic dissection, severe HTN, acute pericarditis.
Other parenteral glycoprotein IIb/IIIa inhibitors.
-Cautions:
Bleeding at the site of arterial sheath placement is the most common
complication.

Early sheath removal is encouraged while eptifibatide is being infused; prior to

removing the sheath, it is recommended that heparin be discontinued for 3-4 hr
and an aPTT of <45 seconds or ACT <150 seconds be achieved.
Thrombocytopenia: Discontinue if platelet levels <100,000 mm/cu.mm.
INTEGRILIN Dosing Charts by Weight
180 g/kg
Patient
2.0 g/kg/min
1.0 g/kg/min
Bolus
Weight
Infusion Volume
Infusion Volume
Volume
(from 2
(from 2
(from 0.75
(from 2
(from 0.75
(kg) (lb)
mg/mL mg/mL 100- mg/mL 100- mg/mL 100- mg/mL 100vial)
mL vial)
mL vial)
mL vial)
mL vial)
3741 8191 3.4 mL
2.0 mL/h
6.0 mL/h
1.0 mL/h
3.0 mL/h
92
4246
4.0 mL
2.5 mL/h
7.0 mL/h
1.3 mL/h
3.5 mL/h
102
103
4753
4.5 mL
3.0 mL/h
8.0 mL/h
1.5 mL/h
4.0 mL/h
117
118
5459
5.0 mL
3.5 mL/h
9.0 mL/h
1.8 mL/h
4.5 mL/h
130
131
6065
5.6 mL
3.8 mL/h
10.0 mL/h
1.9 mL/h
5.0 mL/h
143
144
6671
6.2 mL
4.0 mL/h
11.0 mL/h
2.0 mL/h
5.5 mL/h
157
158
7278
6.8 mL
4.5 mL/h
12.0 mL/h
2.3 mL/h
6.0 mL/h
172
173
7984
7.3 mL
5.0 mL/h
13.0 mL/h
2.5 mL/h
6.5 mL/h
185
186
8590
7.9 mL
5.3 mL/h
14.0 mL/h
2.7 mL/h
7.0 mL/h
198
199
9196
8.5 mL
5.6 mL/h
15.0 mL/h
2.8 mL/h
7.5 mL/h
212
97 213
9.0 mL
6.0 mL/h
16.0 mL/h
3.0 mL/h
8.0 mL/h
103 227
104 228
9.5 mL
6.4 mL/h
17.0 mL/h
3.2 mL/h
8.5 mL/h
109 240
110 241
10.2 mL
6.8 mL/h
18.0 mL/h
3.4 mL/h
9.0 mL/h
115 253
116 254
10.7 mL
7.0 mL/h
19.0 mL/h
3.5 mL/h
9.5 mL/h
121 267
>121 >267 11.3 mL
7.5 mL/h
20.0 mL/h
3.7 mL/h
10.0 mL/h
--------------------------------------------------------------

10

Thrombolytic Agents

Alteplase:
-Acute MI

11

Accelerated infusion (1-1/2 hours):

<67 kg: 15 mg IVP bolus over 1-2 minutes, THEN 0.75 mg/kg IV infusion over
30 minutes (not to exceed 50 mg); THEN 0.5 mg/kg IV over next 60 minutes (not
to exceed 35 mg).
67 kg (100 mg total dose infused over 1.5 hr) 15 mg IVP bolus over 1-2 minutes,
THEN 50 mg IV infusion over next 30 minutes, and THEN remaining 35 mg over
next 60 minutes.
3 hour infusion:
<65 kg: 1.25 mg/kg in 1st hour (including 0.045-0.075 mg/kg IVP in 1st 1-2
minutes), THEN 1.25 mg/kg/hr for 2 hr.
65 kg: (100 mg total dose infused over 3 hr) 60 mg in 1st hour (including 6-10
mg IVP in 1st 1-2 minutes), THEN 20 mg/hr for 2 hr.
-Pulmonary Embolism 100 mg IV infused over 2 hours Initiate/restart IV
heparin therapy near end or immediately following alteplase infusion when PTT
returns to <2 times normal.
-Arterial Thrombosis & Embolism 0.05-0.1 mg/kg/hr by transcatheter intraarterial infusion for1-8 hours or until lysis of thrombus.
-Central Venous Catheter Occlusion Cathflo Activase: 2 mg in 2 mL instilled
into occluded catheter Assess catheter function after 30 minutes of dwell time by
attempting to aspirate blood; if unable to aspirate after 120 minutes dwell time, a
2nd dose may be administered and the process repeated If catheter function
restored, aspirate 4-5 mL blood to remove Cathflo Activase and residual clot
Gently irrigate with 0.9% NaCl
-Acute Ischemic Stroke Treatment should only be initiated within 3 hours
after onset of stroke symptoms, Exclude intracranial hemorrhage by cranial
computerized tomography (CT) scan or other diagnostic imaging method
sensitive for the presence of hemorrhage 0.9 mg/kg IV infused over 1 hour,
administer 10% of total dose as initial bolus over 1 minute; not to exceed total
dose of 90 mg.
--------------------------------------------------------------

Streptokinase: (1 amp. 1, 5 million units)

-Premeditations before starting streptokinase: 2amp. Hydrocortisone, avil,
primpran & available saline.

12

-For Myocardial Infarction dilute on 100 cc normal saline to be consumed in

30-60 mins.
-For Pulmonary Embolism dilute on 500 cc normal saline to be consumed
250.000 IU over 1 hour 83ml/hr THEN 100.000 IU over 48 hours 33ml/hr.
-Absolute Contraindications:
1-Aortic dissection.
2-Rt. To Lt. Arm systolic BP difference <15 mmHg.
3-G.I.T bleeding (active ulcers).
4-Haemorrhagic cerebral stroke within 3 months.
5-Major surgery 2-4 weeks (laser eye surgery).
6-Recent major trauma within 2-4 weeks.
7-I.N.R < 2.
-Relative Contraindications:
1-C.P.R < 10 mins.
2-BP < 180/110.
3-Pregnant female
4-Pancreatitis.
-------------------------------------------------------

13

Vasopressor Drugs

Adrenaline: (1 amp. 1mg).

-Indications:

14

1-Cardiac arrest, VF, Pulseless VT, Asystole & PEA.

2-Symptomatic bradycardia used after atropine and alternative infusion to
dopamine.
3-Severe hypotension: can be used when pacing and atropine fail, when
hypotension accompanies bradycardia, or with phosphodiesterase enzyme
inhibitor.
4-Anaphylaxis, severe allergic reactions: combined with large fluid volume,
corticosteroids, antihistamines.
- Dosing Forms:
Cardiac Arrest
0.5-1 mg IV q3-5min PRN
High dose: 1-5 mg IVP
ETT: 2-2.5 mg q3-5min until IV/IO access established or spontaneous circulation
restored

Intracardiac: 0.1-1 mg into left ventricular chamber; administration should be

restricted only to well-trained personnel May follow initial dose with 1-4
mcg/min IV infusion (1:10,000 solution).
Asthma, Severe/Anaphylaxis
0.2-1 mg SC q5-15min (1:1000 solution), OR
0.1-0.25 mg IM or SC (1:10,000 solution) over 5-10 minutes, OR
0.1 mg IV at rate of 1-4 mcg/min over 5 minutes
Autoinjector: 0.3 mg (contents of 1 autoinjector) SC/IM once in anterolateral
aspect of the thigh; may repeat dose after 5-15 minutes if symptoms persist.
-Infusion dose: 0.03 0.3 mcg/kg/min --- Dilute on N.S or D5W.
-------------------------------------------------------

Noradrenaline (levophed): (1 amp. 4mg).

-Indication:
1-Severe cardiogenic shock and haemodynamically significant hypotension (SBP
15

> 70 mm Hg) with low total peripheral resistance.

2-Agent of last resort for management of IHD and shock.
- Dilute on NS, dont administer in same IV line as alkaline solution,
extravasations cause tissue necrosis, if this occur administer phentolamine 5 to 10
mg in 10 to 15 ml saline solution; infiltrate into area.
-Doses:
Cardiac Arrest Initial: 8-12 mcg/min IV infusion; titrate to effect
Maintenance: 2-4 mcg/min IV infusion.
Acute Hypotension Initial: 8-12 mcg/min IV infusion; titrate to effect
Maintenance: 2-4 mcg/min IV infusion.
Sepsis & Septic Shock 0.01-3 mcg/kg/min IV infusion.
-------------------------------------------------------

Dopamine: (1 amp. 200 mg)

Strong Beta-1, Alpha, & Dopaminergic Effects
Effects based upon dosing rate:
Dopaminergic effects: 0.5-2 mcg/kg/min
Beta effects: 2-10 mcg/kg/min
Alpha effects: > 10 mcg/kg/min.
-Indication:
1-Used for hypotension (SBP > 70 mm Hg) with signs and symptoms of shock.
2-Second-line drug for symptomatic bradycardia after atropine.
-Precautions:
1-Correct hypovolemia with volume replacement before initiating dopamine.
2-dont mix with sodium bicarbonate.
3-May cause tachyarrhythmia, excessive vasoconstriction.
4-Extravasations cause tissue necrosis, if this occurs administers phentolamine 5
16

to 10 mg in 10 to 15 ml saline solution; infiltrate into area.

-Dose 3 20 mcg/kg/min Titrate to response
Low dose: 3 - 5 mcg/kg/min IV may increase urine output and renal blood flow.
Medium dose: 5-10 mcg/kg/min IV may increase renal blood flow, cardiac
output, heart rate, and cardiac contractility.
High dose: 10-20 mcg/kg/min IV may increase blood pressure and stimulate
vasoconstriction.
-------------------------------------------------------

Dobutamine: (1 amp. 250 mg)

-Indication: consider for pump problems (CHF, Pulmonary congestion) with SBP
of 70-100 mm Hg and no signs of shock.
-Precautions/Contraindications:
1-Contraindication when suspected or known poison/drug-induced shock.
2-Avoid with SBP > 100 mm Hg and signs of shock.
3-May cause tachyarrhythmia, fluctuations in blood pressure, headache &
nausea.
4-Don't mix with sodium bicarbonate.
5-Dobutamine and any other +ve inotropic agent shouldn't be taken in patients
with Hypertrophic Cardiomyopathy (HCOM).
-Usual infusion rate: is 2 20 mcg/kg/min no more than 40 mcg/kg/min.
-------------------------------------------------------

Infusion rate equation

Dose Body Weight in kg 60 Amount of fluid dilute in
---------------------------------------------------------------------------------- =
Concentration of drug 1000

---- ml/hr

-Amount of fluid = you dilute on 100cc, 200cc more or less and so on.
-Concentration of drug = if you use 2 amp. Of dopamine the concentration now
is 400mg = num. of amp. Dose of amp.
-If you divided the result ---- ml/hr / 4 == drop / min.
-------------------------------------------------------

17

Antiarrhythmic Drugs

Digoxin (Lanoxin): (1amp. 0.1 - 0.25 mg/mL)

-Indication (may be of limited use):
1-To slow ventricular response in atrial fibrillation or atrial flutter.

18

2-Alternative drug for reentry SVT.

-Precautions:
1-Toxic effects are common and are frequently associated with serious
arrhythmias.
2-Avoid electrical cardio-version (DC) if patient is receiving digoxin unless
condition unless condition is life threatening; use lower dose (10 20 J).
-Heart Failure, Atrial Fibrillation
-Rapid digitalizing (loading-dose regimen)
-IV: 0.004 - 0.006 mg/kg (4 to 6 mcg/kg) initially over 5 minutes. Second and
third boluses of 0.002 to 0.003 mg/kg (2 to 3 mcg/kg) to follow at 4 to 8 hour
intervals (total loading doses 8 to 12 mcg/kg divided over 8 to 16 hours).
-PO: 0.5-0.75 mg once, then may cautiously give additional doses of 0.1250.375 mg q6-8hr until clinical evidence of adequate effect, up to 0.75-1.25 mg (for
70-kg patient).
-Maintenance: 0.125-0.5 mg/day IV/PO.
-Check digoxin levels no sooner than 4 hours after IV doses; no sooner than 6
hours after oral doses.
-Monitor HR & ECG.
-Maintenance dose is affected by body mass and renal function.
-Caution: amiodarone interaction. Reduce digoxin dose by 50% when used with
amiodarone.
-Dosing Modifications:
Adjust maintenance dose by estimating CrCl and measuring serum levels.
In heart failure, higher dosages have no additional benefit and may increase
toxicity; decreased renal clearance may lead to increased toxicity.
In geriatric patients, use lean body weight to calculate dose.
-------------------------------------------------------

Amiodarone: (1amp. 150mg)

Amiodarone is a complex drug effects on sodium, potassium and calcium
channels as well as - and -adrenergic blocking properties. Patient must be
hospitalized while the loading doses of amiodarone are administered.
-Indication:
19

1-VF / pulseless VT unresponsive to shock delivery, CPR, and avasopressor

First dose: 300mg IV/IO push. Second dose (if needed): 150 mg IV/IO q 5
-10min not to exceed 2.2 g/day.
2-Recurrent, hemodynamically unstable VT. Life-threatening arrhythmias
Maximum cumulative dose: 2.2 g IV/day may be administered as follows:
-Rapid infusion: 150 mg IV over first 10 minutes (15mg/min). May repeat rapid
infusion (150 mg IV) every 10 mins. As needed.
-Slow infusion: 360mg IV over 6 hours (1mg/min).
-Maintenance infusion: 540 mg IV over 18 hours (0.5mg/min)
-Dilute 6 amps. On 500cc D5W by infusion rate 33ml/hr for 6 hours then by
infusion rate 16ml/hr for 18 hours.
-PO doses Loading: 800-1600 mg PO qDay x1-3 weeks until response; for load
>1000 mg/day divided BID-TID (1x3 x7 1x2 x7 1x1).
Maintenance: 200-600 mg qDay.
-Precautions:
1-Rapid infusion and with multiple dosing, < 2.2 g/ day may lead to hypotension.
2-Dont admister with other drugs that prolong QT interval (eg, procainamide).
3-Terminal elimination is extremely long (half-life lasts up to 40 days).
4- Avoid during breast-feeding.
5- Proarrhythmic effect:
-Like other antiarrhythmics, can exacerbate the arrhythmia (eg, by making the
arrhythmia less well tolerated or more difficult to reverse).
-2-5% incidence & includes significant heart block or sinus bradycardia.
-Manage arrhythmias in proper clinical setting.
-Effects are prolonged when they occur because of long drug half-life.
6- Pulmonary Toxicity and Liver Injury.
-------------------------------------------------------

Verapamil (Isopten): (1 amp. 5mg)

Indication:
1-Alternative drug (after adenosine) to terminate reentry SVT with narrow QRS
complex and adequate blood pressure and preserved LV function.

20

2-May control ventricular response in patients with atrial fibrillation, flutter, or

multifocal atrial tachycardia.
Precaution:
1-Give only to patients with narrow-complex reentry SVT or known SVT
arrhythmias.
2-Don't use for wide-QRS tachycardia of uncertain origin, and avoid use for
Wolff-Parkinson-White syndrome (WPW) and atrial fibrillation, sick sinus
syndrome, or second- or third-degree AV block without pacemaker.
3-May decrease myocardial contractility and can produce peripheral
vasodilatation and hypotension. IV calcium may restore blood pressure in toxic
cases.
4-Concurrent IV administration with -blockers may produce severe
hypotension. Use with extreme caution in patient receiving oral -blockers.
IV administration:
1-First dose: 2.5 to 5 mg IV bolus over 2 minutes (over 3 minutes in older
patients).
2-Second dose: 5 to 10 mg, if needed, every 15 to 30 minutes. Maximum total
dose: 20 mg.
3-Alternative: (0.075-0.15 mg/kg) 5mg bolus every 15 minutes to total dose of
30 mg.
Dosing Modifications:
1-Renal impairment: Use with caution; monitor ECG; for Verelan PM,
manufacturer recommends 100 mg at bedtime initially; if CrCl <10 mL/min,
reduce dose by 25-50%.
2-Hepatic impairment: In cirrhosis, reduce dose by 20-50% of normal for oral
and IV administration.
-------------------------------------------------------

propranolol (Inderal): (1 amp. 1 mg)

propranolol is non-selective -blocker.
-Supraventricular Arrhythmia:
PO: 10-30 mg q6-8hr.

21

IV: 1-3 mg at 1 mg/min initially; repeat q2-5min to total of 5 mg. Once response
or maximum dose achieved, do not give additional dose for at least 4 hours.
-Contraindications:
1-Asthma, COPD.
2-Sinus bradycardia, 2/3 heart block.
3-Cardiogenic shock.
4-Hypersensitivity.
5-Overt heart failure.
6-Sick sinus syndrome without permanent pacemaker.
7-propranolol and other -blockers relatively contraindicated in cocaine-induced
ACS.
-Cautions:
1-May exacerbate ischemic heart disease after abrupt withdrawal
2-Hypersensitivity to catecholamines has been observed during withdrawal.
3-Exacerbation of angina and, in some cases, myocardial infarction occurrence
after abrupt discontinuance.
4-When discontinuing long-term administration of beta blockers (particularly
with ischemic heart disease), gradually reduce dose over 1-2 weeks and carefully
monitor.
5-If angina markedly worsens or acute coronary insufficiency develops, reinstate
beta-blocker administration promptly, at least temporarily (in addition to other
measures appropriate for unstable angina).
6-Warn patients against interruption or discontinuance of beta-blocker therapy
without physician advice.
7-Because coronary artery disease is common and may be unrecognized, slowly
discontinue beta-blocker therapy, even in patients treated only for hypertension.
8-Monitor cardiac and pulmonary status during administration.
-------------------------------------------------------

Propafenone (Ritmonorm):
-Antidysrhythmics class Ic
-Ventricular Arrhythmias:
IR: 150 mg PO q8hr; may increase to 225 mg q8hr after 3-4Days, and, if
required, 300 mg q8hr; do not exceed 900 mg/day.

22

ER: 225 mg PO q12hr initially; may increase dose q5Days to 325 mg PO q12hr
OR 425 mg PO q12hr if necessary.
-Paroxysmal Atrial Fibrillation:
<70 kg (IR): 450 mg PO qDay; may not exceed 450 mg/day.
70 kg (IR): 600 mg PO qDay; may not exceed 450 mg/day.
-Other Indications & Uses:
Life-threatening ventricular arrhythmias, paroxysmal AF/Atrial flutter, PSVT.
Off-label: AF/Flutter with Wolf-Parkinson-White syndrome.
-Dosing Considerations:
Hepatic impairment: Administer 20-30% of normal dose and monitor closely.
Reduce dose in patients with significant widening of the QRS complex or 2nd or
3rd degree AV block.
-IV dose 2 mg/kg within 20 minutes then 2 mg/min.
-Cardioversion by oral dose 600mg (4 tablets) once then 150 300 mg/day.
-Contraindications:
-Bradycardia, asthma/bronchospastic disorders, cardiogenic shock, electrolyte
imbalances, CHF, severe hypotension, sick sinus syndrome, AV block (unless
artificial pacemaker present for last two), myasthenia gravis.
-Known Brugada syndrome.
-Concomitant ritonavir therapy.
-------------------------------------------------------

Lidocaine (Xylocaine 2%):

(1 amp. 100 mg each 1ml 20mg)
-Indication:
1-Alternative to amiodarone in cardiac arrest from VF/VT.
2-Stable monomorphic VT with preserved ventricular function.
3-Stable polymorphic VT with normal baseline QT-interval and preserved
ventricular function when ischemia is treated and electrolyte balance is
corrected.
23

4-Can be used for stable polymorphic VT with baseline QT-interval prolongation

if torsades suspected.
-Precautions/Contraindication:
-Contraindication Prophylactic use in AMI is contraindicated.
AV nodal rhythm.
2/3 heart block.
Idioventricular rhythm.
-Precautions Reduce maintenance dose (not loading dose) in presence of
impaired liver function or LV dysfunction.
Discontinue infusion immediately if signs of toxicity develop.
-Dose:
1-Cardiac arrest from VF/VT:
-Initial dose 1 to 1.5 mg/kg IV/IO.
-For refractory VF may give additional 0.5 to 0.75 mg/kg IV push, repeat in
(510) minutes; maximum 3 doses or total of 3mg/kg.
2-Perfusing arrhythmia for stable VT, wide-complex tachycardia of uncertain
type, significant ectopy:
-Doses ranging from 0.5 to 0.75 mg /kg and up to 1 to 1.5 mg/kg (5-7ml) may
be used.
- Repeat 0.5 to 0.75 mg/kg (2.5-3ml) every 5 to 10 minutes; maximum total
doses3mg/kg.
3-Maintenance infusion 1 to 4 mg/min (30 50 mcg/kg/min).
-Dilute on 500cc normal saline each ml contains 2mg now adjust dose to that.
-------------------------------------------------------

Magnesium Sulfate (MgSO4):

(4 mEq/mL (50 %) Solution)
1-Hypomagnesemia:
- Mild: 1 g IM q6hr for 4 doses.
- Severe: 5 g IV over 3 hours.
-Maintenance: 30-60 mg/kg/day IV.
2-Torsades de Pointes:
24

-With pulse (ACLS): 1-2 g slow IV (diluted in 50-100 mL D5W) over 5-60
minutes, then 0.5-1 g/hr IV.
-Cardiac arrest (ACLS): 1-2 g slow IV (diluted in 10 mL D5W) over 5-20
minutes.
3-Toxemia of Pregnancy:
-Indicated to prevent seizures associated with pre-eclampsia, and for control of
seizures with eclampsia.
-4-5 g (diluted in 250 mL NS/D5W) IV in combination with either (a) up to 10 g
(10 mL of undiluted 50% solution) divided and administered IM into each
buttock or (b) after initial IV dose, 1-3 g/hr IV.
4-Preterm Labor:
-Used as a tocolytic to stop preterm labor.
-Loading dose: 4-6 g IV over 20 minutes; maintenance: 2-4 g/hr IV for 12-24
hours as tolerated after contractions cease.
-Do not exceed 5-7 days of continuous treatment; longer treatment duration may
lead to hypocalcemia in developing fetus resulting in neonates with skeletal
abnormalities related to osteopenia.
-Dosing Modifications Severe renal impairment: Do not exceed 20 g/48 hr.
-Contraindications
-Hypersensitivity.
-Myocardial damage, diabetic coma, heart block.
-Hypermagnesemia.
-Hypercalcemia.
-Administration during 2 hours preceding delivery for
mothers with toxemia of pregnancy.
-Cautions
1-Fetal skeletal demineralization, hypocalcemia, and hypermagnesemia
abnormalities reported with continuous long-term use (ie, longer than 5-7 days)
for off-label treatment of preterm labor in pregnant women; the effect on the
developing fetus may result in neonates with skeletal abnormalities.
2-In patients with renal impairment, ensure that renal excretory capacity is not
exceeded.
3-Use with caution in digitalized patients.
4-Use with extreme caution in patients with myasthenia gravis or other
neuromuscular disease.
5-Hypomagnesemia is usually associated with hypokalemia (potassium levels
must be normalized).
6-Monitor renal function, blood pressure, respiratory rate, and deep tendon
reflex when magnesium sulfate is administered parenterally.
------------------------------------------------------25

Atropine Sulfate:
1-Sinus Bradycardia (ACLS)
-0.5-1 mg or 0.04 mg/kg IV q5min, no more than 3 mg.
-ET: Some experts suggest 2-2.5x IV dose diluted in 5-10 mL sterile water for
injection/NS (sterile water for injection may facilitate absorption better than NS,
but may produce more negative effect on arterial oxygen pressure).
-Ineffective in hypothermic bradycardia.
2-Asystole/Pulseless Electrical Activity (ACLS) 1 mg IV q3-5min PRN if
asystole persist up to 0.04 mg/kg.
3-Anesthesia Premedication 0.4-0.6 mg IV/IM/SC 30-60 minutes before
anesthesia; repeat q4-6hr PRN.
4-Bronchospasm 0.025 mg/kg in 2.5 mL NS q6-8hr via nebulizer; no more
than 2.5 mg/dose.
5-Cholinesterase Inhibitors (Organophosphates, Carbamates)
-AtroPen: 2 mg/dose IM.
-Mild symptoms: 1 AtroPen.
-If severe symptoms develop (eg, strange or confused behavior, wheezing,
sialorrhea, muscle fasciculations, involuntary urination/defecation, convulsion,
unconsciousness) give 2 additional AtroPen injections in rapid succession 10.
minutes after initial dose.
-Initial severe symptoms: give 3 AtroPen doses in rapid succession.
-Contraindications Narrow-angle glaucoma, GI obstruction, severe ulcerative
colitis, toxic megacolon, bladder outlet obstruction, myasthenia gravis,
hemorrhage w/ cardiovascular instability, thyrotoxicosis.
-Cautions Hepatic/renal impairment, BPH, CHF, tachyarrhythmias, toxinmediated diarrhea, hyperthyroidism, Down syndrome, brain damage in children,
salivary secretion d/o, urinary retention, hiatal hernia, reflux esophagitis, PUD,
pregnancy (IV admin may produce tachycardia in fetus).
-------------------------------------------------------

26

Blood pressure Controlling Drugs

Nitroglycerin (Tridil): (1 amp. 50mg)

-Dilute 50mg on 500cc. D5W. Each 5mcg/min. =3ml/hr.
-Doses:
>

40 mcg/min venodilator effect.

40 - 200 mcg/min mixed vasodilator effect.
< 200 mcg/min arteriodilator effect.

-Free time of nitrates (6 - 8 hrs) need to avoid sensitization of receptors &

27

development of tolerance.
-Continues use for 2-3 day may lead to methaemogloblinemia.
-Contraindications:
1-Not used when SBP > 100 mmHg & DBP > 70 mmHg.
2-Not use with severe bradycardia (HR> 50 bpm) or severe tachycardia (HR <
100 bpm).
3-NOT use in inferior wall MI with right ventricle MI.
4-Recent use (last 24 hr) sildenafil (Viagra), tadalafil (Cialis), or vardenafil
(Levitra) or other phopsphodiesterase-5 inhibitor: potential for dangerous
hypotension.
5-Narrow angle glaucoma (controversial: may not be clinically significant).
6-Hypersensitivity.
7-Symptomatic hypotension, uncorrected hypovolemia, severe anemia,
constrictive pericarditis, pericardial tamponade, restrictive cardiomyopathy.
-------------------------------------------------------

Calculating the mean arterial pressure (MAP)

-MAP, or mean arterial pressure, is defined as the average pressure in a patients
arteries during one cardiac cycle. It is considered a better indicator of perfusion
to vital organs than systolic blood pressure (SBP).
-True MAP can only be determined by invasive monitoring and complex
calculations; however it can also be calculated using a formula of the SBP and
the diastolic blood pressure (DBP).
MAP = SBP + 2 (DBP)
---------------------3
-------------------------------------------------------

Sodium Nitroprusside (Niprid): (1amp. 50mg)

-indications:
1-Hypertensive crisis.
2-To reduce aftreload in HF and acute pulmonary edema.
3-To reduce aftreload in acute mitral or aortic valve regurgitation.
-Precautions:

28

1-May cause hypotension and cyanide toxicity.

2-May reverse hypoxic pulmonary vasoconstriction in patient with pulmonary
disease, exacerbating intrapulmonary shunting, results in hypoxemia.
3-Other side effect including headache, nausea, vomiting & abdominal cramps.
4-Contraindicated in patient who have recently taken phopsphodiesterase-5
inhibitor for erectile dysfunction (eg, sildenafil).
-Dose:
-Add 50 or 100 mg to 250ml D5W. Begin at 0.1 mcg/kg/min and titrate upward
every 3 - 5 mins. To desired effect (usually up to 5mcg/kg/min but higher doses
up to 10 mcg/kg/min may be needed. Action starts within 1 to 2 mins.
-Light sensitive; cover drug reservoir and tubing with opaque material.
-------------------------------------------------------

Fruosemide (Lasix): (1amp. 40 mg)

-Indication: 1-Adjuvant therapy of acute pulmonary edema.
2-Hypertensive emergencies.
-Precautions: Dehydration, hypovolemia, hypotension, hypokalemia, or other
electrolyte imbalance may occur.
-Dose: - 0.5 1 mg/kg given over 1 - 2 minutes.
- If no response double dose to 2 mg/kg, given slowly over 1 2 minutes.
- For new-onset pulmonary edema with hypovolemia: > 0.5 mg/kg.
-Infusion dose:
-Dilute 6 amps. (40mg) on 250cc normal saline by rate 10 ml/hr normal
diuresis OR by rate 40 ml/hr forced diuresis.
-Max dose 169 mg/hr.
-------------------------------------------------------

Glucagon: (1 vial 1mg)

-Indication: Adjuvant treatment of toxic effect of calcium channel blocker or
-blocker.
-Precautions: May cause vomiting, hyperglycemia.
-Dose: 30 60 mg IV over 3 5 minutes, followed by infusion of 3 5 mg/hr.
-------------------------------------------------------

29

Insulin:
-Bolus dose 0.1 u/kg.
-Infusion dose 0.1 u/kg/hr.
-------------------------------------------------------

Theophylline (Aminophylline):
-Bolus dose 2 - 5 mg/kg over 20 minutes to avoid velocity reaction.
-Infusion dose 0.3 0.6 mg/kg/hr.
-------------------------------------------------------

Drugs of Choice
-Paracetamol poisoning: acetylcysteine
Acute bronchial asthma: salbutamolSevere DIGITALIS toxicity: DIGIBINDAcute migraine: sumatriptanAtropine poisoning: physostigmineCyanide poisoning: amyl nitriteIron poisoning: desferrioxamineMRSA: vancomycinWarfarin overdose: vitamin-KAnaphylactic shock: Adrenaline-------------------------------------------------------

30

Arterial Blood Gases (A.B.G)

Arterial Blood Gases (A.B.G)

Normal values
PH = 7.35 - 7.45
H = 35 - 45 mmol/L
PCO2 = 35 - 45 mmHg in Arterial Blood
31

PO2 > 80 mmHg in Arterial Blood in room

air
HCO3 = 22 - 28 mmol/L
Na = 135 145 mmol/L
K = 3.5 5 mmol/L
Ca = 95 105 mmol/L
Lactate = 0.4 1.5 mmol/L
Hypoxia severity SaO2
% Mild 90 94
% Moderate 75 89
% Sever < 75
PH Power of Hydrogen... Changes in H concentration
PO2 partial Pressure of O2 Free UN bounded O2 NOT
Total O2 Most of O2 Is Carried on Hb
PaO2 partial Pressure of O2 in Arterial Blood
SO2 O2 Saturation in any Blood
SaO2 O2 Saturation in Arterial Blood seen on monitor by
Pulse Oximeter
-Important rules:
PaCO2 is controlled by Ventilation & the level of Ventilation is
adjusted to maintain PaCO2 within tight limits by Respiratory center
adjustment
HYPOXIC DRIVE
Chronic high PaCO2 leads to desensitization of receptors SO body
relies on PaO2 receptors & Decreased PaO2 level becomes the
principal Ventilator stimulus >>> Correction by O2 may depress
Ventilation & increase PaCO2 So O2 must be in controlled fashion
32

with ABG monitoring .

When Hb approaches maximal O2 saturation further increase in
PO2 doesn't significantly increase Blood O2 Content
Both Oxygenation & CO2 elimination depends on Alveolar
Ventilation SO Impaired Ventilation leads to DECREASE PaO2 &
INCREASE PaCO2
Ventilation Perfusion mismatch & shunting " COLLAPSE OR
CONSOLIDATION " leads to INCREASE CO2 elimination but not
INCREASE O2 as Hb is maximally saturated SO PaO2 & SaO2 is
decreased While PCO2 Doesn't increased
In Type 1 respiratory failure there is LOW PaO2 with NORMAL or
LOW PaCO2 WHILE In Type 2 respiratory failure there is HIGH
PaCO2
*************************************
-Why ABG?
To establish a diagnosis Respiratory failure & Met. Acidosis "
To assess severity of illness
to guide & monitor the treatment
Acid base balance
H is generated from breakdown of fats & sugars this produces CO2
which dissolves in blood to form H2CO3
H is removed by respiratory system which removes CO2 , Renal "
Metabolic " excretes H in urine & reabsorb HCO3
H2O + CO2 << -- >> H2CO3 << -- >> H + HCO3
Increased CO2 = Resp. Acidosis & Its decrease = Resp. Alkalosis
WHILE Increased HCO3 = Met. Alkalosis & Its decrease =Met.
Acidosis
*************************************

Metabolic Acidosis
Any process that lowers PH other than Increased Pa CO2
Accumulation of mat. Acids Excess Ingestion, Production or
33

" Reduced Renal Excretion - or excessive loss of HCO3

Hyperventilation is a dominant symptom in Met. Acidosis " Resp.
" compensation
Anion Gap ( Na + K ) ( Cl + Hco3 ) = 10 18 mmol/ L
Gap is made up of un measured anions " phosphate , sulphate & -ve
" charged Ptn
Rise > 18 mmol/ L = increased un measured anions " lactate &
" salicylates
Lactic acidosis when O2 supply is decreased anaerobic metabolites "
e.g. lactic acid " are increased
= Met. Acidosis with increased anion gap
.... lactic A. hypoxia, Shock, Sepsis & Infarction
.... Keto A. DKA, Starvation & Alcohol Excess
Renal failure.... Poisoning " Aspirin , Methanol
= With Normal Anion gap
Renal Tubular Acidosis, Diarrhea, Ammonium chloride ingestion &
Adrenal insufficiency
*************************************

Metabolic Alkalosis
Any process that increases PH other than decreased Pa CO2 "
Increased loss of Cl, K, & Na " e. g. Diuretics " or sustained Vomiting
which leads to H loss
Resp. compensation by increasing Pa CO2 is limited to avoid
Hypoxia
Loss of Cl, K, or Na leads to Retain Na& K by kidney at expense of H

34

= Met. Alkalosis
Vomiting, K depletion, diarrhea, Cushing's & Conn's Syndrome
*************************************
Res. Acidosis is increased Pa CO2 leads to hyperventilation occurs in
type 2 Resp. failure or in met. Alkalosis
Res. Alkalosis is decreased Pa CO2 caused by hyperventilation or in
Met. Acidosis
*************************************

PH Pco2

Hco3

Normal

Clinical Finding
Respiratory acidosis

Possible Causes

Pneumonia ,
Emphysema , Drug
overdose
Respiratory acidosis with Pneumonia ,
metabolic compensation Emphysema , Drug
overdose
Metabolic & Respiratory Cardiac arrest
acidosis

35

 Normal

Metabolic acidosis

D.M , Shock , Renal

Failure

Normal

Metabolic alkalosis

Iatrogenic ,
Hypokalemia ,
Vomiting , N.G
Suction , Diuresis ,
HCO3
Administration

Metabolic alkalosis with

respiratory compensation

Metabolic & respiratory

alkalosis

Normal

Respiratory alkalosis

36

Hypertension , Fever ,
Anxiety , Hypoxia ,
Hyperthyroidism ,
Bucking respirator

Hco3 deficit = (24 - Hco3) (body weight in kg 0.6)

-Correct the acidosis when ph > 7.1 in metabolic acidosis only.
-Do half correction first then redo ABG and give the rest of deficit if still there is
acidosis.
--------------------------------------------------------------

Cockcroft's equation for creatinine clearance (ml/min)

Men:

body weight in kg (140 - age in years)

-----------------------------------------------------72 serum creatinine in mg/dl

Women: multiply the product of the above equat by 0.85

--------------------------------------------------------------

37

Management of Different
Electrolyte Imbalance

38

A- Hyperkalemia
1- Common Causes of Hyperkalemia

Endogenous Causes
Chronic renal failure
Metabolic acidosis (eg, diabetic ketoacidosis)
Pseudohypoaldosteronism type II (also known as Gordons
syndrome; familial hyperkalemia and hypertension)
Chemotherapy causing tumor lysis
Muscle breakdown (rhabdomyolysis)
Renal tubular acidosis
Hemolysis
Hypoaldosteronism (Addisons disease, hyporeninemia)
Hyperkalemic periodic paralysis
Exogenous Causes
Medications: K+-sparing diuretics, ACE inhibitors,
nonsteroidal anti-inflammatory drugs, potassium
supplements, penicillin derivatives, succinylcholine, heparin
therapy (especially in patients with other risk factors), blockers
Blood administration (particularly with large transfusions of
older bank blood)
Diet (rarely the sole cause), salt substitutes
Manifestation:
1-signs and symptoms of hyperkalemia include weakness,
ascending paralysis, and respiratory failure.
2-A variety of electrocardiographic (ECG) changes
suggest hyperkalemia. Early findings include peaked T
waves (tenting).
3- As the serum potassium rises further, flattened P
waves, prolonged PR interval (first-degree heart block),
widened QRS complex, deepened S waves, and merging of
S and T waves can be seen.
4- If hyperkalemia is left untreated, a sine-wave pattern,
idioventricular rhythms, and asystolic cardiac arrest may
develop
39

Treatment of Hyperkalemia

Stop sources of exogenous potassium administration

(eg, consider supplements and maintenance IV fluids)
and evaluate drugs that can increase serum
potassium (eg, potassium-sparing diuretics,
angiotensin-converting enzyme [ACE] inhibitors,
nonsteroidal anti-inflammatory agents).

Additional treatment is based on the severity of the

hyperkalemia and its clinical consequences.

The following sequences list the treatments for

hyperkalemia in order of priority.

For mild elevation (5 to 6 mEq/L), remove potassium from the body

with

Diuretics: furosemide 40 to 80 mg IV

Resins: Kayexalate 15 to 30 g in 50 to 100 mL of 20% sorbitol

either orally or by retention enema

For moderate elevation (6 to 7 mEq/L), shift potassium intracellularly

with

Glucose plus insulin: mix 25 g (50 mL of D50) glucose and 10

U regular insulin and give IV over 15 to 30 minutes

Sodium bicarbonate: 50 mEq IV over 5 minutes (sodium

bicarbonate alone is less effective than glucose plus insulin or
nebulized albuterol, particularly for treatment of patients with
renal failure; it is best used in conjunction with these
medications)
Nebulized albuterol: 10 to 20 mg nebulized over 15 minutes
For severe elevation (>7 mEq/L with toxic ECG changes):
you need to shift potassium into the cells and eliminate potassium from
the body

40

Therapies that shift potassium will act rapidly but they are temporary; if
the serum potassium rebounds you may need to repeat those therapies.
In order of priority, treatment includes the following:

Shift potassium into cells:

Calcium chloride (10%): 500 to 1000 mg (5 to 10 mL)

IV over 2 to 5 minutes to reduce the effects of
potassium at the myocardial cell membrane (lowers risk
of ventricular fibrillation [VF])

Sodium bicarbonate: 50 mEq IV over 5 minutes (may

be less effective for patients with end-stage renal
disease)

Glucose plus insulin: mix 25 g (50 mL of D50) glucose

and 10 U regular insulin and give IV over 15 to 30
minutes

Nebulized albuterol: 10 to 20 mg nebulized over 15

minutes/57
Promote potassium excretion:
5. Diuresis: furosemide 40 to 80 mg IV
6. Kayexalate enema: 15 to 50 g plus sorbitol PO or per
rectum
7. Dialysis
--------------------------------------------------------------

41

B-Hypokalemia
Hypokalemia is defined as a serum potassium level <3.5
mEq/L.
The most common causes of low serum potassium
are:
1-gastrointestinal loss (diarrhea, laxatives)
2-Renal loss (hyperaldosteronism, severe hyperglycemia,
potassium-depleting diuretics, carbenicillin, sodium
penicillin, amphotericin B)
3- Intracellular shift (alkalosis or a rise in pH), and
malnutrition.
The major consequences of severe hypokalemia:
1-It result from its effects on nerves and muscles
(including the heart).
2-The myocardium is extremely sensitive to the effects of
hypokalemia, particularly if the patient has coronary
artery disease or is taking a digitalis derivative.
3-Symptoms of mild hypokalemia are weakness, fatigue,
paralysis, respiratory difficulty, constipation, paralytic
ileus, and leg cramps
4- More severe hypokalemia will alter cardiac tissue
excitability and conduction.
5- Hypokalemia can produce ECG changes such as U
waves, T-wave flattening, and arrhythmias (especially if
the patient is taking digoxin), particularly ventricular
arrhythmias.
6-Pulseless electrical activity or asystole may develop.
Treatment of Hypokalemia
1- IV administration of potassium is indicated when
arrhythmias are present or hypokalemia is severe
(potassium level of <2.5 mEq/L).
42

2-

IV K replacement

Serum K

20-40mEq

3-3.4

40-80mEq

Less3

When

indicated, the maximum amount of IV potassium replacement should be

10 to 20 mEq/h with continuous ECG monitoring during infusion
3-A more concentrated solution of potassium may be infused if a central
line is used, but the tip of the catheter used for the infusion should not
extend into the right atrium.

-Recheck serum K after 1 hour from the end of the infusion

4-If cardiac arrest from hypokalemia is imminent (ie, malignant
ventricular arrhythmias are present), rapid replacement of potassium is
required.
Give an initial infusion of 10 mEq IV over 5 minutes; repeat once if
needed
5-Patients with renal impairment should receive only 50% of dose.
6-Serum K will fall by 0.6mEq/L for every o.1 increase in PH and vice
virsa
7- Potassium deficit in mmol is calculated as given below:
Kdeficit (mmol) = (Knormal lower limit - Kmeasured) x kg body weight x
0.4
8- Daily potassium requirement is around 1 mmol/Kg body
weight.
9- 13.4 mmol of potassium found in 1 g KCl. (molecular
weight KCl = 39.1 + 35.5 = 74.6)
10-Now suppose we get a patient of 70kg with a serum
43

potassium level of 3.0 mmol/L and he is on nil by mouth,

we proceed this way.
- Deficit of potassium in mmol = (3.5 - 3.0) x 70 x 0.4 = 14
mmol
- Daily potassium requirement = 1 x 70 = 70 mmol
- Total requirement = 14+70 = 84 mmol = (84/13.4) = 6.3
g KCl
-1 mmol = 1 mEq
-1g KCl = 14 meq K, Cl
Therefore we can give the patient 1.0 g KCl in N/S solution
to run 4 hourly and reassess the serum potassium level
after 1 day.

N.B:

1) Never give potassium I.M or rapid I.V push

2) Never give more than 2 g KCl over 1 hour without any
continuous ECG monitor.
3) Do not just add the KCl solution to the hanging I.V fluid
bag. Fully invert it around 10 times to ensure proper
mixing.
4) 1 tab of Slow K gives around 8 mmol potassium.
5) Peripheral veins are damaged by a potassium
concentration greater than 30 mmol/L i.e. 1.1 g KCl/ 500
mL I.V infusion solution. For higher concentrations, central
lines are preferred.
6) The 0.4 in the equation above is there because
potassium is mainly an intracellular ion and intracellular
fluids make up 40% of our body weight.
7) As a first approximation, for every decrease in serum
potassium of 1 mEq/L, the potassium deficit is
approximately 200-400 mEq.

44

8) However, bear in mind that many factors in addition to

the total body potassium stores contribute to the serum
potassium concentration.
9) Therefore, this calculation could either overestimate or
underestimate the true potassium deficit.
10) A 20meq K replacement will raise the K by 0.25meq/L.
--------------------------------------------------------------

C-Hypernatremia
Hypernatremia is defined as a serum sodium concentration >145 to 150
mEq/L.
Causes
1- It may be caused by a primary gain in Na+ or excess loss of water.
2-Gains in sodium can result from hyperaldosteronism (excess
mineralocorticoid), Cushings syndrome (excess glucocorticoid), or
excessive hypertonic saline or sodium bicarbonate administration.
3-Loss of free water can result from gastrointestinal losses or renal
excretion (eg, osmotic diuresis or diabetes insipidus).
Manifestation
1-Hypernatremia may cause neurologic symptoms such as altered mental
status, weakness, irritability, focal neurologic deficits, and even coma or
seizures.
2-The severity of symptoms is determined by the speed and magnitude of
the change in serum sodium concentration.

Treatment of Hypernatremia
1-Treatment of hypernatremia includes reduction of ongoing water losses
(by treating the underlying cause) and correction of the water deficit

45

2- For stable, asymptomatic patients, replacement of fluid by mouth or

through a nasogastric tube is effective and safe.
3-In hypovolemic patients the extracellular fluid (ECF) volume is
typically restored with normal saline or a 5% dextrose in half-normal
saline solution to prevent a rapid fall in the serum sodium concentration.
4- Avoid D5W because it will reduce the serum sodium too rapidly
5- During rehydration, monitor serum sodium closely to ensure a gradual
fall (and prevent rapid fall) in serum sodium.
6-The quantity of water needed to correct hypernatremia can be
calculated by using the following equation:

7-Total body water is approximately 50% of lean body weight in men and
40% of lean body weight in women.
8-For example, if a 70-kg man had a serum Na+ level of 160 mEq/L, the
estimated free water deficit would be

9-Once the free water deficit is calculated, administer fluid to lower

serum sodium at a rate of 0.5 to 1 mEq/h with a decrease of no more than
approximately 12 mEq/L in the first 24 hours and the remainder over the
next 48 to 72 hours.
--------------------------------------------------------------

46

D-Hyponatremia
Hyponatremia is defined as a serum sodium concentration <130 to 135
mEq/L.
Causes:
It is caused by an excess of water relative to sodium.
Most cases of hyponatremia are caused by reduced renal excretion of
water with continued water intake or by loss of sodium in the urine.
Impairment of renal water excretion may be caused by

Use of thiazide diuretics

Renal failure

ECF depletion (eg, vomiting with continued water intake)

Syndrome of inappropriate antidiuretic hormone (SIADH)

secretion

Edematous states (eg, congestive heart failure, cirrhosis with

ascites)

Hypothyroidism

Adrenal insufficiency

Most cases of hyponatremia are associated with low serum osmolality

(so-called hypo-osmolar hyponatremia).
The one common exception to this is in uncontrolled diabetes, in which
hyperglycemia leads to a hyperosmolar state despite a serum sodium that
is below normal (hyperosmolar hyponatremia).
47

Manifestation:
1-Hyponatremia is usually asymptomatic unless it is acute or severe
(<120 mEq/L).
2- An abrupt fall in serum sodium produces a free water shift from the
vascular to the interstitial space that can cause cerebral edema.
3- In this case the patient may present with nausea, vomiting, headache,
irritability, lethargy, seizures, coma, or even death.

Treatment of Hyponatremia
1-Treatment of hyponatremia involves administration of sodium and
elimination of intravascular free water.
2-in stable normotensive patients,fluids should be restricted to 5001500mL water daily
3- If SIADH is present, the treatment is restriction of fluid intake to 50%
to 66% of estimated maintenance fluid requirement.
4-Correction of asymptomatic hyponatremia should be gradual: typically
increase the Na+ by 0.5 mEq/L per hour to a maximum change of about
12 mEq/L in the first 24 hours.
5- Rapid correction of hyponatremia can cause coma, which may be
associated with osmotic demyelination syndrome or central pontine
myelinolysis, lethal disorders thought to be caused by rapid fluid shifts
into and out of brain tissue.
6-If the patient develops neurologic compromise, administer 3% saline IV
immediately to correct (raise) the serum sodium at a rate of 1 mEq/L per
hour until neurologic symptoms are controlled.
7- Some experts recommend a faster rate of correction (ie, increase
concentration 2 to 4 mEq/L per hour) when seizures are present.
8-After neurologic symptoms are controlled; provide 3% saline IV to
correct (raise) the serum sodium at a rate of 0.5 mEq/L per hour.
9-To determine the amount of sodium (eg, 3% saline) required to correct
the deficit, calculate the total body sodium deficit. The following formula
may be used:

48

10-Na+ deficit=(desired [Na+]current [Na+])0.6*body wt (kg) (*use

0.6 for men and 0.5 for women).
11-Once the deficit is estimated, determine the volume of 3% saline (513
mEq/L Na+) necessary to correct the deficit (divide the deficit by 513
mEq/L).
12-Plan to increase the sodium by 1 mEq/L per hour over 4 hours (or
until neurologic symptoms improve); then increase the sodium by 0.5
mEq/L per hour.
13-To calculate this amount, use the amount you wish to correct the
sodium in an hour (eg, 0.5 mEq/L) and multiply by 0.6 (or 0.5 in women)
and then multiply by the body weight; that will calculate the amount of
sodium to administer that hour.
14- Check serum sodium frequently and monitor neurologic status.
15-In severe hyponatremia,Na less than 120mEq with CNS
changes,hypertonic saline should be given ,3% NS (513mEq/L) at 25100mL/h.Concomitant use of 20-40 mg furosemide will decrease the
incidence of central pontine myelinosis(CPM).
--------------------------------------------------------------

49

E-Hypermagnesemia
Hypermagnesemia is defined as a serum magnesium concentration >2.2
mEq/L (normal: 1.3 to 2.2 mEq/L).
Causes:
1-The most common cause of hypermagnesemia is renal failure.
2-Note that pre-eclampsia in pregnant women is treated with magnesium
administration, often titrated to maintain the serum magnesium near the
maximum normal concentration, without complications of
hypermagnesemia.
Manifestation:
1-Neurologic symptoms of hypermagnesemia are muscular weakness,
paralysis, ataxia, drowsiness, and confusion.
2-Moderate hypermagnesemia can produce vasodilation
3-Severe hypermagnesemia can produce hypotension.
4-Extremely high serum magnesium levels may produce a depressed
level of consciousness, bradycardia, cardiac arrhythmias, hypoventilation,
and cardiorespiratory arrest
Treatment of Hypermagnesemia
1-Hypermagnesemia is treated with administration of calcium, which
removes magnesium from serum.

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2-It is important to eliminate sources of ongoing magnesium intake.

Cardiorespiratory support may be needed until magnesium levels are
reduced.
3-Administration of 10% solution of calcium chloride (5 to 10 mL [500 to
1000 mg] IV) will often correct lethal arrhythmias. This dose may be
repeated if needed.
4-Dialysis is the treatment of choice for severe hypermagnesemia.
5-If renal function is normal and cardiovascular function adequate, IV
saline diuresis (administration of IV normal saline and furosemide [1
mg/kg]) can be used to increase renal excretion of magnesium until
dialysis can be performed.
6- Diuresis can also increase calcium excretion; the development of
hypocalcemia will make signs and symptoms of hypermagnesemia worse.
--------------------------------------------------------------

F-Hypomagnesemia
Hypomagnesemia, defined as a serum magnesium concentration <1.3
mEq/L.
Causes:
1- Hypomagnesemia usually results from decreased absorption or
increased loss of magnesium from either the kidneys or intestines
(diarrhea).
2-Alterations in thyroid hormone function and certain medications (eg,
pentamidine, diuretics, alcohol) can also induce hypomagnesemia.
3-Hypomagnesemia interferes with the effects of parathyroid hormone,
resulting in hypocalcemia.
4- It may also cause hypokalemia.
Manifestation:
Symptoms of low serum magnesium are:
1- muscular tremors and fasciculations,
2-ocular nystagmus,
3- tetany,
4- altered mental state,
5- cardiac arrhythmias such as torsades de pointes (multifocal ventricular
tachycardia).

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6- Other possible symptoms are ataxia, vertigo, seizures, and dysphagia.

Treatment of Hypomagnesemia
1-For severe or symptomatic hypomagnesemia, give 1 to 2 g of IV
MgSO4 over 5 to 60 minutes.
2- For torsades de pointes with cardiac arrest, give 1 to 2 g of MgSO4 IV
push over 5 to 20 minutes.
3-If torsades de pointes is intermittent and not associated with arrest,
administer the magnesium over 5 to 60 minutes IV.
4-If seizures are present, give 2 g IV MgSO4 over 10 minutes.
5-Administration of calcium is usually appropriate because most patients
with hypomagnesemia are also hypocalcemic.
Another method for correction of Serum Mg
Iv Mg dose

Serum Mg level

Mg sulphate 2gm Iv in 100ml over 2 1.5-1.9

hours
Mg sulphate 4gm Iv in 250ml over 4 1.1-1.4
hours
Mg sulphate 6gm Iv in 250ml over 6 Less1.1
hours
-Fluids used for iv mixture: normal saline or glucose 5%
-serum Mg 2 hours after the end of infusion
-serum Mg in AM
--------------------------------------------------------------

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G-Hypercalcemia
Hypercalcemia is defined as a total serum calcium concentration >10.5
mEq/L (or an elevation in ionized calcium >4.8 mg/dL).
Causes:
1- Primary hyperparathyroidism and malignancy account for >90% of
reported cases.
2-In these and most forms of hypercalcemia, release of calcium from the
bones and intestines is increased, and renal clearance may be
compromised.
Manifestation:
1-Symptoms of hypercalcemia usually develop when the total serum
calcium concentration is 12 to 15 mg/dL.
2-Neurologic symptoms are depression, weakness, fatigue, and confusion
at lower levels.
3-At higher levels patients may experience hallucinations, disorientation,
hypotonicity, seizures, and coma.
4- Hypercalcemia interferes with renal concentration of urine; the diuresis
can cause dehydration.
5-Cardiovascular symptoms of hypercalcemia are variable:
I- Myocardial contractility may initially increase until the calcium level
reaches >15 mg/dL.
II- Above this level myocardial depression occurs.
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III-Automaticity is decreased and ventricular systole is shortened.

IV- Arrhythmias occur because the refractory period is shortened.
V-Hypercalcemia can worsen digitalis toxicity and may cause
hypertension.
VI-In addition, many patients with hypercalcemia develop hypokalemia.
Both of these conditions contribute to cardiac arrhythmias.
VII-The QT interval typically shortens when the serum calcium is >13
mg/dL, and the PR and QRS intervals are prolonged.
VIII- Atrioventricular block may develop and progress to complete heart
block and even cardiac arrest when the total serum calcium is >15 to 20
mg/dL.
6-Gastrointestinal symptoms of hypercalcemia include dysphagia,
constipation, peptic ulcers, and pancreatitis.
7-Effects on the kidney include diminished ability to concentrate urine;
diuresis, leading to loss of sodium, potassium, magnesium, and
phosphate; and a vicious cycle of calcium absorption in the intestines and
calcium release from the bones that worsens hypercalcemia
Treatment of Hypercalcemia
1-Total serum calcium is directly related to the serum albumin
concentration.
2-The total serum calcium will increase 0.8 mg/dL for every 1 g/dL rise
in serum albumin and will fall 0.8 mg/dL for every 1 g/dL fall in serum
albumin.
3-Treatment for hypercalcemia is required if the patient is symptomatic
(typically a total serum concentration of approximately >12 mg/dL) or if
the calcium level is >15 mg/dL
4- Immediate therapy is directed at restoring intravascular volume and
promoting calcium excretion in the urine.
5- In patients with adequate cardiovascular and renal function this is
accomplished with infusion of 0.9% saline at 300 to 500 mL/h (saline
diuresis) until any fluid deficit is replaced and diuresis occurs (urine
output 200 to 300 mL/h).
6- Once adequate rehydration has occurred, the saline infusion rate is
reduced to 100 to 200 mL/h.

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7- During this therapy, monitor and maintain potassium and magnesium

concentrations closely because the diuresis can reduce potassium and
magnesium concentrations.
8-Hemodialysis is the treatment of choice to rapidly decrease serum
calcium in patients with heart failure or renal insufficiency.
9-Chelating agents (eg, 50 mmol PO4 over 8 to 12 hours or EDTA 10 to
50 mg/kg over 4 hours) may be used for extreme conditions.
10-Use of furosemide (1 mg/kg IV) for treatment of hypercalcemia is
controversial. In the presence of heart failure, administration of
furosemide is required, but it can actually foster release of calcium from
bone, thus worsening hypercalcemia.
--------------------------------------------------------------

H-Hypocalcemia
Hypocalcemia is defined as a serum calcium concentration <8.5 mg/dL
(or ionized calcium <4.2 mg/dL).
Causes:
1-Hypocalcemia may develop with toxic shock syndrome,
2-with abnormalities in serum magnesium,
3-after thyroid surgery,
4-with fluoride poisoning, and
5-with tumor lysis syndrome (rapid cell turnover with resultant
hyperkalemia, hyperphosphatemia, and hypocalcemia).
Manifestation:
1-Symptoms of hypocalcemia usually occur when ionized levels fall to
<2.5 mg/dL.
2-Symptoms include paresthesias of the extremities and face, followed
by muscle cramps, carpopedal spasm, stridor, tetany, and seizures.
3-Hypocalcemic patients show hyperreflexia and positive Chvostek and
Trousseau signs.
4-Cardiac effects include decreased myocardial contractility and heart
failure.
5-Hypocalcemia can exacerbate digitalis toxicity.
Treatment of Hypocalcemia

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1-Treatment of hypocalcemia requires administration of calcium.

2- Treat acute, symptomatic hypocalcemia with 10% calcium gluconate,
93 to 186 mg of elemental calcium (10 to 20 mL) IV over 10 minutes.
3-Follow this with an IV infusion of 540 to 720 mg of elemental calcium
(58 to 77 mL of 10% calcium gluconate) in 500 to 1000 mL D5W at 0.5 to
2 mg/kg per hour (10 to 15 mg/kg).
4-Alternatively, administer 10% calcium chloride, giving 5 mL (136.5 mg
of elemental calcium) over 10 minutes, followed by 36.6 mL (1 g) over
the next 6 to 12 hours IV.
5-Measure serum calcium every 4 to 6 hours.
6-Aim to maintain the total serum calcium concentration at 7 to 9 mg/dL.
7- Correct abnormalities in magnesium, potassium, and pH
simultaneously.
8-Note that untreated hypomagnesemia will often make hypocalcemia
refractory to therapy.
9-Therefore, evaluate serum magnesium when hypocalcemia is present
and particularly if hypocalcemia is refractory to initial calcium therapy.
10-If the patient is asymptomatic,oral calcium gluconate 1-4 g/d divided
every 6 hours,with or without vitamin D(calcitrol,0.2mic wtwice daily).
Another method for correction of serum Ca
Iv calcium dose

Serum ionized ca

Ca gluconate 1gm in 100ml Iv over 30min

1-1.1

Ca gluconate 2gm in 100ml Iv over 60min

0.9-0.99

Ca gluconate 3gm in 100ml Iv over 60min

0.8-0.89

Ca gluconate 4gm in 100ml Iv over 120min

Less0.8

-Fluids used for IV mixture: normal saline or glucose 5%

56

-ionized Ca 2 hours after the end of infusion

-ionized Ca in AM
-------------------------------------------------------------

) (
-------------------------------------------------------------

57