Digoxin is a cardiac glycoside which has positive inotropic

activity characterized by an increase in the force of

myocardial contraction. It also reduces the conductivity of
the heart through the atrioventricular (AV) node. Digoxin
also exerts direct action on vascular smooth muscle 

•FOR ADULT
•Loading dose, 0.75–1.25 mg PO or 0.125–0.25 mg IV.

•0.5–1 mg given as 50% of the dose initially and one

quarter of the initial dose in each of 2 subsequent doses at
6–12 hr intervals.

• Maintenance dose, 0.125–0.25 mg/day PO.

•INDICATIONS:

•Heart failure.
•Atrial fibrillation and atrial flutter (slows ventricular rate).
•Paroxysmal atrial tachycardia.

•Check dosage and preparation carefully.

•Avoid IM injections, which may be very painful.
•Follow diluting instructions carefully, and use
diluted solution promptly.
•Avoid giving with meals; this will delay absorption.
•Have emergency equipment ready; have K+
lidocaine, phenytoin, atropine, and cardiac monitor
readily available in case toxicity develops.
•WARNING: Monitor for therapeutic drug levels:
0.5–2 ng/mL.
•Monitor apical pulse for 1 full min before administering.
Withhold dose and notify health care professional if pulse rate is
<60 bpm in an adult, <70 bpm in a child, or <90 bpm in an
infant. Notify health care professional promptly of any
significant changes in rate, rhythm, or quality of pulse.
•Monitor BP periodically in patients receiving IV digoxin.
•Monitor ECG during IV administration and 6 hr after each
dose. Notify health care professional if bradycardia or new
arrhythmias occur.
•Observe IV site for redness or infiltration; extravasation can
lead to tissue irritation and sloughing.
•Monitor intake and output ratios and daily weights. Assess for
peripheral edema, and auscultate lungs for rales/crackles
throughout therapy.
•Before administering initial loading dose, determine whether
patient has taken any digoxin in the preceding 2–3 wk.
DIGOXIN TOXICITY
They commonly include lethargy, confusion and
gastrointestinal symptoms (anorexia, nausea, vomiting,
diarrhoea and abdominal pain)
Visual effects (blurred vision, colour disturbances)
Cardiac arrhythmias account for most deaths.
The primary treatment of digoxin toxicity is digoxin
immune fab, which is an antibody made up of anti-
digoxin immunoglobulin fragments. This antidote has
been shown to be highly effective in treating life-
threatening signs of digoxin toxicity such as hyperkalemia,
hemodynamic instability, and arrhythmias.
lithium carbonate

Treatment of manic episodes of manic-depressive illness; 

Nursing Considerations
• do not administer with NSAIDs
• monitor drug blood levels frequently
• may cause seizures, arrhythmias, fatigue, confusion,
nausea, anorexia, hypothyroidism, tremors
• Ace Inhibitors may increase serum levels
• instruct patient to maintain adequate fluid intake
• therapeutic level: 0.5-1.5 mEq/L
 Give with caution and daily monitoring of serum lithium
 

levels to patients with renal or CV disease, debilitation, or

dehydration or life-threatening psychiatric disorders.
· Give drug with food or milk or after meals.
        

· WARNING: Monitor clinical status closely, especially

        

during initial stages of therapy; monitor for therapeutic

serum levels of 0.6–1.2 mEq/L.
· Individuals vary in their reponse to this drug; some
        

patients may exhibit toxic signs at serum lithium levels

considered within the therapeutic range.
Ensure that patient maintains adequate intake of salt and
adequate intake of fluid (2,500–3,000 mL/day).
 
Symptoms of lithium toxicity include severe nausea and
vomiting, severe hand tremors, confusion, and vision
changes. If you experience these, you should seek
immediate medical attention to check your lithium levels.
Furosemide inhibits reabsorption of Na and chloride
mainly in the medullary portion of the ascending Loop of
Henle. Excretion of potassium and ammonia is also
increased while uric acid excretion is reduced.
Indications
•Oral, IV: Edema associated with CHF, cirrhosis, renal
disease
•IV: Acute pulmonary edema
•Oral: Hypertension

Contraindications
•Severe sodium and water depletion, hypersensitivity to
sulphonamides and furosemide, hypokalaemia,
hyponatraemia, precomatose states associated with liver
cirrhosis, anuria or renal failure. Addison’s disease.
•Potentially Fatal: Rarely, sudden death and cardiac arrest.
Hypokalaemia and magnesium depletion can cause
cardiac arrhythmias.

•BLACK BOX WARNING: Profound diuresis with water and

electrolyte depletion can occur; careful medical
supervision is required.
•Administer with food or milk to prevent GI upset.
•Reduce dosage if given with other antihypertensives;
readjust dosage gradually as BP responds.
•Give early in the day so that increased urination will not
disturb sleep.
•Avoid IV use if oral use is at all possible.
•WARNING: Do not mix parenteral solution with highly
acidic solutions with pH below 3.5.
•Do not expose to light, may discolor tablets or solution;
do not use discolored drug or solutions.
•Discard diluted solution after 24 hr.
•Refrigerate oral solution.
•Measure and record weight to monitor fluid changes.
•Arrange to monitor serum electrolytes, hydration, liver
and renal function.
•Arrange for potassium-rich diet or supplemental
potassium as needed.
What is Sickle Cell Anemia?
A severe hemolytic anemia
Normally RBC’s are flexible
and round like a doughnut
without the hole. They move
easily through the blood vessels. In SCA, the
RBC’s become rigid and sticky and are shaped
like sickles or crescent moons. They get stuck in
small blood vessels and cause tissue damage
An inherited gene in people of African American,
and Indian descent.

What are the Genetics of Sickle Cell

Anemia?
Two people who carry the Sickle Cell Trait marry.
They have a:
25% chance of having an unaffected child with normal
hemoglobin
50% chance of having a child who is also a carrier
25% chance of having a child with Sickle Cell
Sickled cells are rapidly hemolyzed and have a
short lifespan (10-20 days)
Jaundice Fatigue
Enlarged bones Anemia
Tachycardia, cardiac murmurs, enlarged heart,
dysrhythmias, heart failure

How is Sickle Cell Anemia

Managed?
Supportive therapy
Oxygen
Alternative paint relief therapies
Vaccinations
Emotional support
Manage complications
Monitor and alleviate pain
Plan to find balance between activity and rest
Assess all body systems
Assess for dehydration/encourage fluids
Neurologic exam
Assess for s/s of infection
Healthy lifestyle
What is Hemophilia?
A genetic disorder causing hemorrhages into
various parts of the body.
The blood doesn’t clot normally because it lacks
sufficient blood – clotting proteins

Several types of Hemophilia, including-

1. Hemophilia A- most common, is caused by
insufficient clotting Factor VIII
2. Hemophilia B- the second most common, is
caused by insufficient clotting Factor IX
3. Hemophilia C- with mild symptoms, is caused
by insufficient clotting Factor XI
Clinical Manifestations of
Hemophilia?
Bleeding- superficial or deep
Joints, hematuria, GI bleeding, head,
mouth, neck, thorax, nose
Can cause nerve damage
Prolonged bleeding after circumcision
First episode usually < 2 years of age
Family history
Mild hemophilia may not be diagnosed until
adulthood
Blood test- clotting factor deficiency, PTT, factor
assays, DNA testing)
Nursing Interventions
helpful in Hemophilia?

Assist with restrictions

Teach inherited
Instruct how to administer
factor concentrate at home
Meds to avoid
Teach good dental hygiene
Care of minor wounds
Avoid nasal packing Good dental hygiene
Splints Healthy weight
Avoid injections Avoid blood thinners
Wear Medical ID Avoid NSAIDS
Written emergency plan Child protection
Closely monitor bleeding
Analgesics for pain
Avoid warm baths during bleeding
The total blood volume in an adult?
A. 3-4 liters     
B. 5-6 liters
C. 6-8 liters     
D. 7-9 liters
Answer: 5-6 Liters

The pH value of Human blood?

A. 6.35-6.55   
B. 7.25-7.35
C. 7.35-7.45   
D. 7.45-7.55
Answer: 7.35-7.45
 Plasma protein fibrinogen has an active role in?
A. Clotting of blood   
B. Protection
C. Lubrication       
D. Nutrition
Answer: Clotting of blood.

RBC produced in the?

A. Liver   
B. Spline
C. Heart
D. Bone Marrow  

 
D. Answer: Bone marrow
A decrease in RBC count is known as?
A. Erythremia   
B. Polycythemia
C. Anemia   
D. Leukemia
Answer: Anemia

An increase in RBC count is known as?

A. Erythremia  
B. Polycythemia
C. Anemia   
D. Leukemia
Answer: Polycythemia
A hereditary bleeding disease?
A. Coagulopathy   
B. Haemophilia
C. Purpura   
D. Thrombocytopenia
Answer: Haemophilia

A type of Anemia with sickle shaped RBC?

A. hemolytic anemia
B. Aplastic anemia
C. Vitamin deficiency anemia
D. Sickle cell anemia
Answer: Sickle cell anemia
 Blood group which is called Universal donor?
A. A   
B. AB
C. B   
D. O
Answer: O

 Blood group which is called Universal recipient?

A. A   
B. AB
C. B   
D. O
Answer: AB
carl, an elementary student, was rushed to the hospital due
to vomiting and a decreased level of consciousness. The
patient displays slow and deep (Kussmaul breathing), and
he is lethargic and irritable in response to stimulation. He
appears to be dehydrated—his eyes are sunken and mucous
membranes are dry—and he has a two-week history of
polydipsia, polyuria, and weight loss. Measurement of
arterial blood gas shows pH 7.0, PaO2 90 mm Hg, PaCO2
23 mm Hg, and HCO3 12 mmol/L; other results are Na+ 126
mmol/L, K+ 5 mmol/L, and Cl- 95 mmol/L. What is your
assessment?

A. Respiratory Acidosis, Uncompensated

B. Respiratory Acidosis, Partially Compensated
C. Metabolic Alkalosis, Uncompensated
D. Metabolic Acidosis, Partially, Compensated
Metabolic Acidosis, Partially, Compensated The student was
diagnosed with diabetes mellitus. The results show that he has
metabolic acidosis (low HCO3 -) with respiratory compensation
(low CO2).

Reference ranges for arterial blood gases

pH 7.35 – 7.45 10.6 – 13.3 kPa

PaO2 80 – 100* mmHg 4.7 – 6.0 kPa
PaCO2 35 – 45 mmHg
HCO3ˉ 22 – 26 mmol/L
Base excess –2 – +2 mmol/L
baby Angela was rushed to the Emergency Room following her
mother’s complaint that the infant has been irritable, difficult to
breastfeed, and has had diarrhea for the past 3 days. The infant’s
respiratory rate is elevated and the fontanels are sunken. The
Emergency Room physician orders ABGs after assessing the
ABCs. The results from the ABG results show pH 7.39, PaCO2
27 mmHg, and HCO3 19 mEq/L. What does this mean?

A. Respiratory Alkalosis, Fully Compensated

B. Metabolic Acidosis, Uncompensated
C. Metabolic Acidosis, Fully Compensated
D. Respiratory Acidosis, Uncompensated
Metabolic Acidosis, Fully Compensated Baby Angela has
metabolic acidosis due to decreased HCO3 and slightly acidic
pH. Her pH value is within the normal range which made the
result fully compensated.

The pH determines the presence of acidaemia or alkalaemia. If

the body has compensated for the disorder, the pH may be in the
normal range.

The base excess

The metabolic component of the acid–base balance is
reflected in the base excess. This is a calculated value
derived from blood pH and PaCO2. The base excess
increases in metabolic alkalosis and decreases (or becomes
more negative) in metabolic acidosis
Mr. Wales, who underwent post-abdominal surgery, has a
nasogastric tube. The nurse on duty notes that the nasogastric
tube (NGT) is draining a large amount (900 cc in 2 hours) of
coffee ground secretions. The client is not oriented to person,
place, or time. The nurse contacts the attending physician and
STAT ABGs are ordered. The results from the ABGs show pH
7.57, PaCO2 37 mmHg and HCO3 30 mEq/L. What is your
assessment?

A. Metabolic Acidosis, Uncompensated

B. Metabolic Alkalosis, Uncompensated
C. Respiratory Alkalosis, Uncompensated
D. Metabolic Alkalosis, Partially Compensated
 Metabolic Alkalosis, Uncompensated The postoperative
client's ABG results show that he has metabolic alkalosis
because of an increased pH and HCO3. It is uncompensated due
to the normal PaCO2 which is within 35 to 45 mmHg.
Metabolic imbalances Respiratory imbalances

Metabolic Metabolic Respiratory Respiratory alkalosis

acidosis alkalosis acidosis
pH ↓ ↑ ↓ ↑
PaC N N ↑ ↓
O2 (uncompensated) (uncompensated)
↓ (compensated) ↑ (compensated)

HCO ↓ ↑ N N (uncompensated)
3ˉ (uncompensated) ↓ (compensated)
↑ (compensated)

Base ↓ ↑ N/↑ N/↓

exces
s
Clini Kussmaul-type Paraesthesia, Acute: air Acute: hyperventilation, paresthesia, light-
cal breathing tetany, weakness hunger, headedness
featu (deeper, faster disorientation Chronic: hyperventilation, latent tetany
res respiration), Chronic:
shock, coma hypoventilation,
hypoxia,
cyanosis
Step 1
If the patient's pH is 7.35 or lower, an acidosis is present.
A pH of 7.45 or higher indicates that the patient has an
alkalosis.
Step 2
If the PCO2 drives the pH in the opposite direction, there is
a primary respiratory process (as PCO2 increases, pH
decreases, and vice versa). If the PCO2 and pH move in the
same direction, a metabolic process is occurring
The patient's pH is 7.16, PCO2 is 70 mm Hg, and PO2 is 80
mm Hg.
•Step 1: The pH is less than 7.35, so an acidosis is
present.
•Step 2: The values are moving in opposite directions, so it
is a respiratory process.
the patient's pH is 7.50, PCO2 is 50 mm Hg, and PO2 is 100
mm Hg.
•Step 1: Since the pH is greater than 7.45, an alkalosis is
present.
•Step 2: The pH and the PCO2 are moving in the same
direction, so this is a metabolic process
The patient's pH is 7.25, PCO2 is 25 mm Hg, and PO2 is 90
mm Hg.
•Step 1: The patient has a low pH, so an acidosis is
present.
•Step 2: The pH and PCO2 are both decreased. The
PCO2 has not driven the pH in the opposite direction, so
this process is a metabolic process.
The patient's pH is 7.50, the PCO2 is 20 mm Hg, and the
PO2 is 75 mm Hg.
•Step 1: The pH is greater than 7.45, so an alkalosis is
present.
•Step 2: The pH and PCO2 are moving in opposite
directions, so this is a respiratory process.