CS HG

Cotabato Medical Foundation College, Inc
Quezon Ave. Poblacion 8, Midsayap, Cotabato

Tel: 064-229-8207
CLINICAL
CASE ANALYSIS
WORKSHEET
Submitted by:
Julianne Richard P. Diaz BSN – 2A
Date Presented: April 29, 2023

Date Submitted: April 29, 2023
Semester SY: 2nd Semester, 22-23
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TABLE OF CONTENTS
Page
Cover Page
Introduction (Includes the Background and Rationale of the analysis) . . . . . . . . . . . .
Scenario (if presented in a virtual progressive scenario, write the summary) . . . . . . .
Phenomenon (Series of incidents leading to the occurrence
of the main (health) problem) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Concept Map (brief but concise graphical presentation of the phenomena) . . . . . . .
Learning Objectives (SMART; includes the main parts of the Clinical
Case Analysis Worksheet; Nursing Process – Approached) . . . . . . . . . . . . . .
Clinical Case Analysis Worksheet
Patient’s Personal Data
I. Family Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
II. Developmental Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
III. Chief Complaints . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
IV. Health History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
V. Complete Diagnosis of the case chosen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
a. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
b. Etiology …………………………………………………………………………………………...
c. Symptomatology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
d. Anatomy and Physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
e. Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
VI. Medical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
a. Laboratory Interpretation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
b. Drug Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
VII. Nursing Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
a. Nursing Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
b. Nursing Care Plan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
VIII. Evaluation and Implication of the case to: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
a. Nursing Practice (What might the case mean for other nurses?) . . . . . . . . . . . .
b. Nursing Education (What might the case contribute to education).. . . . . .
c. Nursing Theory (applicable nursing theory in the care of the case) . . . . . .
d. Nursing Research (any related issues that may need investigation) . . . . .
IX. Recommendations/Referrals/ Follow – ups . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
X. Journal Reading Related to the Case . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
XI. APPENDIX (Any relevant documentation as long as it will
not violate the Intellectual Property Rights) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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INTRODUCTION
Up to 80% off all pregnant women experience some nausea and vomiting during
their pregnancy (NVP). Hyperemesis Gravidarum (HG) is a condition of intractable
vomiting during pregnancy, leading to fluid, electrolyte and acid-base imbalance, nutrition
deficiency and weight loss often severe enough to require hospital admission. HG typically
occurs between the 4th and the 10th week of gestation, with resolution by 20 weeks of
gestation. While nausea and vomiting of pregnancy in general is estimated to occur in 50 to
90% of all pregnancies, hyperemesis gravidarum is estimated to occur in .5 to 2% of pregnant
women. Over 192,000 hospital visits and/or admissions occur in the US annually for HG and
approximately 4,000 Canadian women a year experience hyperemesis gravidarum. HG is the
second leading cause of hospitalization in early pregnancy and is more common in non-white
and Asian populations (National Organization for Rare Diseases, 2020) . No statistical data was
found in the occurrence of hyperemesis gravidarum in the Philippines.

The clinical presentation follows a 39-year-old woman who’ve had 5 previous
pregnancy and is currently on her 6 . All previous pregnancy was complicated by nausea and
th
vomiting but the current is probably the worst. She suffered a cardiac arrest which her family
happens to witness and urged them to call for help. Upon admision on ED, a CPR was
performed with 40 minutes downtime. Her hematology test reveals hypokalemia
(2.1mmol/L) and acidosis (pH 6.7, lactate 26mmol/L). A few hours had passed when she’s
already in the ICU, she happens to have another arrest specifically ventricular fibrillation
arrest. And her venous blood gas potassium level was 1.8 mmol/L. She miscarried due to
complications reqiuring D&C to remove RPOC. She remained an inpatient for 33 days.
Treatment program includes potassium infusion of 40mmol/hr adrenaline and noradrenaline
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infusion, 4 units of packed RBC, 4 units of albumin, commencement of IV Thiamine,
rehabilitation program for her acute encephalopathy and short-term dialysis for anuric renal
failure. After discharge she suffered from acute memory and concrete thinking problems.

This case analysis aims to analyze, discuss, and evaluate the clinical case occurring to
the patient. This case analysis will not be anything like our previous case study beecause we
will do this individually. Our perseverance and time management will surely be put to
test, and we need to work extra harder to achieve our goal to come out with this output and
pass it on time. Thus, primary goal of this case study is to reinforce the understanding and
engagement in figuring out the patient’s prognosis which can be a helpful tool for future
researchers.
SCENARIO
We present a case of a 39-year-old Pacific Islander woman who at 15+5 weeks
gestation was brought in by ambulance following an out-of-hospital cardiac arrest. The arrest
was witnessed by her family at home who contacted the ambulance service and commenced
cardiopulmonary resuscitation (CPR). She was resuscitated at the scene involving CPR with
approximately 40 minutes downtime, cold intubation, and multiple direct current
cardioversions for stabilisation. On arrival to the emergency department, she had fixed
dilated pupils and was found to be significantly acidotic (pH 6.7, lactate 26mmol/L) with
associated hypokalaemia of 2.1mmol/L (range 3.5-5.2mmol/L) (see Tables 1 and 2). Her
initial resuscitation and stabilisation involved a potassium infusion up to 40 mmol/hr and an
adrenaline and noradrenaline infusion, 4 units of packed red blood cells, and 4 units of
albumin. Following stabilisation and electrolyte repletion, she had a second 5-minute
ventricular fibrillation (VF) arrest 4 hours later in the ICU, where her potassium on her
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preceding venous blood gas was 1.8mmol/L. She was commenced on 300mg of IV Thiamine
daily from day one of her ICU admission. On day one of admission, the pregnancy was still
viable with an FHR of 150beats per minute detected. Unfortunately, on day two of her
admission, there was fetal demise and she spontaneously miscarried in the ICU and required
a dilatation and curettage for retained products of conception. Her inpatient stay was
complicated by multiorgan dysfunction including ischaemic hepatitis, mild encephalopathy
requiring rehabilitation, and anuric renal failure requiring short-term dialysis.
The patient’s pregnancy history was unremarkable preceding the out-of-hospital
cardiac arrest except for an early positive oral glucose tolerance test (OGTT) (in the absence
of evidence of type 2 diabetes mellitus with a normal HbA1C)
performed at 13 weeks’ gestation (see Table 3). On the day of her arrest her husband
did not notice any additional symptoms and her nausea and vomiting did not particularly
worsen, but she did manage to tolerate a small lunch meal prior to arresting. She had a
background history of 5 previous pregnancies to the same partner, complicated by some
nausea and vomiting in those pregnancies, with no definitive evidence of HG. In this
pregnancy, from an early gestation, the patient confirmed the presence of significant nausea
and vomiting, with emesis occurring after every meal on most days. She had limited oral
intake as a result and ensuing weight loss occured with approximately 10kg’s lost in total
(9% of total body weight).
The patient’s background medical history was otherwise unremarkable with no
symptoms or biochemical evidence of a disorder of potassium homeostasis preceding the
pregnancy. Specifically, she denied symptoms to suggest hypokalaemic periodic paralysis

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and serial serum electrolyte testing revealed normal potassium levels before and after
pregnancy (see Table 1). Urine electrolyte testing was also unremarkable postpartum, with
no evidence of renal potassium wasting (see Table 4). Furthermore, she had no history to
suggest an arrhythmogenic disorder with no palpitations, presyncope, or syncope reported.
She had no significant family history of cardiomyopathy or sudden cardiac death and no
personal history of valvular heart disease or rheumatic fever. She denied symptoms to
suggest thyroid disease and pre-pregnancy had normal Thyroid Stimulating Hormone (TSH)
levels on serial testing, including a normal TSH level at 7-weeks gestation. She was not
hypertensive, and there was no evidence of primary hyperaldosteronism on testing. There
was no clinical evidence of cortisol excess, and screening 24- hour urinary free cortisol was
normal. She was not on any regular medications and had no known drug allergies.
The patient was thoroughly investigated for causes and contributors to her cardiac
arrest. Results of cardiac investigations included a normal coronary angiogram, normal left
ventricle ventriculogram, and a transoesophageal echocardiogram which demonstrated
preserved biventricular sys- tolic function and structurally normal valves with moderate
mitral regurgitation. She had a normal computed tomography pulmonary angiogram
(CTPA) with no evidence of pulmonary embolism. She had a largely normal CT head with a
10mm filling defect in her left transverse sinus but nil other acute pathology. She had a
normal baseline electrocardiogram (ECG) post-arrest with no evidence of long QT
syndrome.
Following stabilisation and correction of her potassium (see Table 1) and acute renal
failure, she was discharged home after a total 33-day admission. She transitioned well to
home where she is continuing to care for her children, the youngest of which is 3 years old.
She is independent with her activities of daily living and mobility and only suffered from
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mild short-term memory impairment and mild impairment in her concrete problem solving.
Importantly, her serum potassium level remains normal.
PHENOMENON

A 39-year-old Pacific Islander woman, Gravida 6, Para 5, Abortion 1, Living 5
History
➢Previous pregancies complicated with nausea aand vomiting
➢Positive Oral Glucose Tolerance Test (OGTT) @ 13-week gestation
Admission on Emergency Department

 Brought in by ambulance following an out-of-hospital cardiac arrest
 40 minutes of CPR
 Cold intubation
 Multiple direct current cardioversions
Labs
 Hypokalemic (2.1mmol/L)
 acidotic (pH 6.7, lactate of 26mmol/L)
Physical Examination
 Dilated pupils
Treatments
 Infused with potassium 40 mmol/L
 Infused with adrenaine and noradrenaline infusion
 Infused with 4 units of packed RBC
 4 units of albumin
Admitted to ICU
Treatment
 Commenced on 300mg of IV thiamine
 Electrolyte stabilisation and repletion
4 hours later
 5-minute Ventricular Fibrillation (VF) arrest
Labs
 Potassium venous blood gas level: 1.8mmol/L
Vital Sign
 FHT of 150 bpm
Day 2 in ICU

 Miscarried
 D&C of RPOC
During inpatient stay (3-32 days of admission)

 Ischemic hepatitis
 Mild encephalopathy
 Anuric renal failure
Cardiac Investigations (During inpatient stay)
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➢Head CT: 10mm filling defect in left transverse sinus.
Day 33 of admission
➢Potassium is stabilized
➢Correction of acute renal failure
Discharged (at day 34)

➢Mild short-term memory impairement.
➢Impairement in concrete problem solving.

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CONCEPT MAP
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Learning objectives
After completion and presentation of this clinical case study. The learners will acquire knowledge and skills in the
nursing care management of a 39-year-old woman with Hyperemesis Gravidarum. Specifically, the learners will:
1. discuss the phenomenon and concept map of the scenario;
2. obtain family background of the client;
3. define terms related to the care;
4. discuss the basic etiology and symptomatology of Hyperemesis Gravidarum;
5. review the physiology of Fluid and Electrolytes Homeostasis;
6. discuss the mechanism of Morning sickness during pregnancy;
7. trace the pathophysiology of Hyperemesis Gravidarum;
8. explain the laboratory test performed to the client and other basic laboratory test;
9. discuss the drugs administered to the client;
10. identify priority nursing diagnosis for the client;
11. formulate a relevant nursing management in terms of nursing diagnosis and nursing care plan ’
12. discuss the implication of this case in nursing practice, education and theory application;
13. enumerate the recommendation/referral/follow-ups; and
14. discuss journal of an evidence-based practice research related to Hyperemesis Gravidarum.
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CLINICAL CASE ANALYSIS WORKSHEET

CONCEPT
Concept: Care for High-Risk Pregnancy

PATIENT’S PERSONAL DATA:_
Name: N/A Age: 36 years old Sex: Female
Civil status: N/A Religion: N/A Address: Pacific Island
I. FAMILY BACKGROUND:
I. Family background
Occupation: N/A
Number of siblings/children: 5 children
Other relevant data: G-6 P-5 A-1 L-5
II. DEVELOPMENTAL DATA: Specify the Stage.

(Based on Havighurst’s and Erikson’s Life and Developmental Task/Psycho-Social).
According to Erikson, the developmental task of a middle adult is generativity versus
stagnation. Which takes place in the span of age 35-65 and is focused on generating new
experiences in order not to be stagnant in life. During this stage, middle-aged adults strive to
create or nurture things things that will outlast them, often by parenting children or fostering
positive changes that benefit others. Contributing to society and doing things to promote future
generations are important needs at the generativity vs stagnation stage of development.
In my case, The 36-year-old woman has had an illness affecting the heart which is one of the
most vital organ in the body which is a complication of her severe Hyperemesis Gravidarum.
Because of this problem she might have problem in doing her usual ADLs and maintaining her
generativity. Her cognitive function was also affected making it more challenging to maintain
generativity. However, I believe that with the treatment and rehabilitation she is capable of
getting back on track and generate new life experiences.
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Reference:
Cherry, K. (2022) Erikson’s Stages of Development Available at
https://www.verywellmind.com/generativity-versus-stagnation-2795734 Accessed at April 24, 2023
CHIEF COMPLAINTS:
Nausea & Vomiting
Short-term memory impairment
Impairment in concrete problem solving.
HEALTH HISTORY:
Past Illness/Surgery:
Patient’s previous pregnancies were complicated by severe nausea and vomiting but no definitive
evidence of HG
Present Illness:
The patient is diagnosed with Hypermesis Gravidarum with a complication of Cardiac Arrest.
III. COMPLETE DIAGNOSIS OF THE CASE CHOSEN

a. Definition (at least 2 Definition with Bibliography)
Hyperemesis Gravidarum
 an abnormal condition of pregnancy characterized by protracted vomiting, weight
loss, and fluid and electrolyte imbalance. If the condition is severe and intractable,
brain damage, liver and kidney failure, and death may result.
Reference: Mosby,S.L (2021). Mosby’s Dictionary of Medicine, Nursing & Health Professions
 Hyperemesis gravidarum (sometimes called pernicious or persistent vomiting) is
nausea and vomiting of pregnancy prolonged past week 16 of pregnancy or that is so
severe that dehydration, ketonuria, and significant weight loss occur within the first
12 weeks of pregnancy. It occurs at an incidence of 2% in pregnant women.
Reference: Flagg, J., & Pilliteri, A. (2018). Maternal & Child Health Nursing: Care of the childbearing
& Childrearing Family.
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Etiology
List all the basic etiology Actual etiology on Rationale

the patient
Unknown / The etiology of hyperemesis gravidarum is largely unknown, but several theories exist (see
pathophysiology). There are, however, risk factors associated with the development of
hyperemesis during pregnancy. (Jennings, L.K, 2022)
Human Chorionic Gonadotropin (theory) / Levels of hCG have been implicated. hCG levels peak during the first trimester,
corresponding to the typical onset of hyperemesis symptoms. Some studies show a
correlation between higher hCG concentrations and Hyperemesis. However, this data has
not been consistent. (Jennings, L.K 2022)
Estrogen (theory) / Estrogen is also thought to contribute to nausea and vomiting in pregnancy. Estradiol levels
increase early in pregnancy and decrease later, mirroring the typical course of nausea and
vomiting in pregnancy. Additionally, nausea and vomiting are the known side effects of
estrogen-containing medications. As the level of estrogen increases, so does the incidence of
vomiting. (Jennings, L.K, 2022).
Progesterone (theory) / Studies have examined a possible correlation between progesterone and onset of hyperemesis
gravidarum due to a hypothesis that progesterone alone, or in combination with estrogen,
may cause gastric dysrhythmias by decreasing gastric smooth muscles contractility. Although
research has shown that progesterone levels peak during the first trimester of pregnancy, no
association with hyperemesis gravidarum has been established. (Grube, et al 2021)
Helicobacter Pylori H. pylori is known to be a factor in gastrointestinal diseases. Pregnant women are thought to
have a predisposition for H. pylori because elevated hCG causes a shift in pH, decreased
gastrointestinal motility, and the altered cell mediated immune system. (Evidenced-based
Obstetrics & Gynecology, 2019).
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Risk Factors
List all the possible Risk Factors Actual risk factor present on the client Rationale
History of HG in previous pregnancy / Multiple studies shown that women who develops
HG has experienced severe vomiting in previous
pregnancy.(Gabra, A., 2018)
Age Most studies agreed that hyperemesis gravidarum is
more common among young, aged mothers.
Moreover, young age of pregnant women also
carries a risk of prolonged duration of the disease
more than 27 gestational weeks (Gabra A., 2018)
Smoking was found that women who vomit in pregnancy are less
likely to be smoker and this relation is considered
preexisting and it is not a response to either the
pregnancy or the vomiting]. It may be explained as
smoking pregnant women also have lower levels of
estrogen and there is a relationship between high
estrogen level and HG.
Multiple Pregnancy In multiple pregnancies, it was found that the incidence

of HG is higher in male-male twins and male-female
twins, all female twins have lower incidence which was
unexpected because of higher maternal estrogen levels.
Genetics An increased risk of hyperemesis gravidarum has been

demonstrated among women with family members who
also experienced hyperemesis gravidarum.Two
genes, GDF15 and IGFBP7, have been potentially linked
to the development of hyperemesis gravidarum.
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Molar Pregnancy  Abnormal tissue growth in the uterus,

called a molar pregnancy, which is
serious and requires treatment;
increased HCG with molar pregnancies
leads to increased risk of hyperemesis
gravidarum
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c. Symptomatology
List all the basic symptomatology Actual Rationale
symptomatology
Weight Loss (<5% of weight) / Continuous excessive vomiting causing loss of nutrients and eventually weight
loss.
Excessive Nausea and Vomiting / It is believed that this severe nausea is caused by a rise in hormone levels; however, the
absolute cause is still unknown. (Maternal & Child Health Nursing, 2018).
Weakness / Acute muscle weakness occurs in conjunction with low nutrients and electrolytes
levels.
Low blood pressure Extreme vomiting causes loss of the cell's extracellular fluids. This reduces the
red blood cell’s volume which will lead to hypotension.
Tachycardia
Tachycardia happens as the heart tries to compensate on the decreased blood
flow to other body parts. Tachycardia is just a compensatory mechanism of
hypotension.
Dehydration
Result of excessive fluid loss in vomiting.
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Anatomy and Physiology (Organ or System Involved)

Fluid and Electrolytes Homeostasis
1 The baroreceptors in the carotid sinuses and aortic arch detect reduced blood pressure, which signals
the hypothalamic thirst center.
2 Simultaneously, the juxtaglomerular apparatus detects low blood pressure, which activates the renin-
angiotensin system to produce angiotensin II. Angiotensin II stimulates the hypothalamic thirst center.
3 Osmoreceptors in the hypothalamus shrink when blood osmolality goes up, triggering action potentials
that stimulate thirst.
4 The combination of these inputs activates thirst and promotes water consumption.
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Sodium and Potassium homeostasis.

 Many cells have a
Na+/K+ ATP pump
that moves K+ into
the cell and pumps
Na+ out of the cell.
 movement of water
is determined by
changes in the
concentration of
solutes in the
extracellular and
intracellular fluids.
 For example, as
dehydration
develops, the
concentration of
solutes in the extracellular fluid increases, allowing water to move by osmosis
out of the cell and into the extracellular fluid. If dehydration is severe, the cells
can shrink and will function abnormally.
 Na is for water retention and K is for muscular contraction and excitability.
 Increased K = depolarization / Decreased K =hyperpolarization promoting
resting membrane potential.
 Aldosterone = Increases Na reabsorption and K excretion (in the urine)
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Mechanism of Action: Morning sickness during pregnancy
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 After Fertilization, Zygote migrates over the next 3 to 4 days toward the body of
uterus.
 Formation of blastocyst which contains both embryoblast (becomes the fetus) and
trophoblast (becomes the placenta)
 As early as 11th or 12th day after fertilization, minute resembling probing fingers -
chorionic villi (sincytiotrophoblast) appears.
 Syncitiotrophoblast secrete hCG to maintain corpus luteum function. At the same
time, it produces estrogen and progesterone.
 Corpus luteum continues to secrete estrogen and progesterone to maintain
endometrial lining.
 HCG level peak at 9 weeks. outer layer of trophoblast starts to create estrogen and
progesterone.
 Once the trophoblast iscapable of making estrogen and progesterone independently,
corpus luteum is no longer needed and thus explains the reduction of hCG levels.
 Morning sickness peaks at 9 weeks proportionate to the peak of hCG level.
 HCG is observed to decrease gastric emptying.
 Progesterone has synonymous effect. It is studied to decrease gastric motility.
 Occurrence of morning sickness is proportionate to the rise of hCG and progesterone
levels. Though there’s no definitive study confirming the etiology of morning
sickness, this is the generally accepted explanation as to why it happens.
Legend: Present: Text
Etiology-
Disease process-
S/S-
Dx.
Management
Leads to
Continuation A
Prognosis P
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Pathophysiology
Predisposing Factor: Precipitating Factor:
History of HG in previous Smoking

pregnancy
Age
Multiple pregnancy
Genetics
Hormonal
Changes in
Pregnancy
Progesterone hCG Estrogen
Decreased GI Relaxation of lower

motility. Peaks at 9 weeks esophageal sphincter
S/S: gestation S/S:
Increased Htc Frequent Sunken eyeball
Stasis of bolus in
the stomach episodes of
Decreased Plasma Poor skin turgor
reflux
Weak pulse pressure Dry oral mucosa
Easy fatigabilty Vomiting Decreased urine
output
Capillary refill of <3sec
Dehydration Diagnostic:
blood test (liver function
test)
Diagnostic: Decreased ECF
blood test Decreased Hepatic
Hepatic Ischemia
Hypokalemia Low Blood Volume & Perfusion
Increased blood viscosity
S/S: S/S:
Weakness Low urine production

Hypotension
Fatigue Mental Confusion
Activation of RAAS system
Muscle cramps Fatigue
Arrhythmia Weakness
Secretion of Aldosterone
Management: Management:
IV or PO supplements of Hepatic Reperfusion

Potassium
Increased Sodium
Diagnostic:
Retention & Potassium UTZ, FHT monitoring
Excretion Decreased
Placental Miscarriage
Perfusion S/S:
Management: Vaginal Bleeding
Abdominal cramping
D&C, Psychological
A
Support Back ache 12
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A
Anuric
Renal
Decreased Blood flow to Failure
the Renal Artery
Hyperpolarization
Diagnostic:
Renal Function Tests
Lowers Cardiac Threshold
S/S:
Decreased
Rash or itching
Cerebrovascular Prolonging Cardiac Resting Phase
Diagnostic: Supply Flank pain in the
Head CT,EEG
back or side
Encepalopathy Brain Tissue Prolonged Ventricular Shortness of breath

Ischemia depolarization and repolarization
S/S:
Diagnostic:
Difficulty learning and Ventricular Fibrillation Arrest ECG
retaining information
Impaired Memory Ventricular

Filling defect
P Arrhythmia
Receptive aphasia S/S:

Disturbance in selective
Chest Pain
attention
Management: Dizziness/Lightheadedness
If Treated: If not treated, will
Nutritinal supplements, lead to death within Shortness of Breath
50-60% survival rate
anticonvulsants minutes
after dischage.
Management:
Common post-arrest
complications include Cardioversion, Potassium
neurologic Replacement
dysfunction, brain
injury, disorders of
consciousness,
neurocognitive
deficits, changes in
quality of life, as well
as physical and
psychological
wellbeing.
Early and intensive

management of post
arrest patients should
be focused on
hemodynamic stability
and neurologic
recovery.
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MEDICAL MANAGEMENT
Laboratory Management
Basic Diagnostic Purpose Result Of the Patient Clinical Significance Nursing Management
Procedure required
with Normal Values
CT scan (Brain) To visualize and 10 mm filling defect on To assess level of brain Before
assess the brain to left transverse sinus involvement following a
assist in diagnosing cardiac arrest and the  Obtain a history of the patient’s
tumor, bleeding, degree of brain tissue complaints or clinical symptoms.
infarct, infection, ischemia.  Metformin drug should be
structural changes, discontinued on the day of the test
and edema. Also and continue to be withheld for 48
valuable in evaluation hr after the test.
of medical, radiation,  Review the procedure with the
and surgical patient. Address concerns about
interventions. pain and explain that there may be
moments of discomfort and some
pain experienced during the test.
 Inform the patient the procedure is
usually performed in a radiology
suite by an HCP specializing in
this procedure, with support staff,
and takes approximately 15 to 30
min.
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During the test
 Ensure the patient has complied

with medication restrictions and
pretesting preparations.
 Observe standard precautions and
follow the general guidelines.
 Ensure the patient has removed
dentures and all external metallic
objects from the area to be
examined prior to the procedure.
 Instruct the patient to cooperate
fully and to follow directions.
Instruct the patient to remain still
throughout the procedure because
movement produces unreliable
results.
After the test
 Inform the patient that a report of
the results will be made available
to the requesting HCP who will
discuss the results with the patient.
 Monitor vital signs and
neurological status every 15 min
for 1 hr, then every 2 hr for 4 hr,
and then as ordered by the
Physician. Monitor temperature
every 4 hr for 24 hr. Monitor
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intake and output at least every 8

hr. Compare with baseline values.
Protocols may vary among
facilities.
 If contrast was used, observe for
delayed allergic reactions, such as
rash, tachycardia, hypertension,
palpitations, nausea, or vomiting.
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Before the Test

Venous Blood Gas: 26mmol/L To rule out the cause of  Inform the patient this test can
To assess for lactic
Lactic Acid the patients’s acidosis and assist with assessing organ
acid acidosis related degree of tissue hypo-
< 2.1 mmol/L function.
to poor organ perfusion.  Instruct the patient to fast and to
perfusion and liver
restrict fluids overnight. Instruct
failure. May also be
the patient not to ingest alcohol for
used to differentiate
12 hr before the test. Protocols
between lactic acid
may vary among facilities.
acidosis and
 Explain that there may be some
ketoacidosis by
discomfort during the
evaluating blood
venipuncture.
glucose levels.
During the Test
Direct the patient to breathe
normally and to avoid unnecessary
movement.
 label the appropriate specimen
container with the corresponding
patient demo- graphics, initials of
the person collect- ing the
specimen, date, and time of
collection.
 Instruct the patient not to clench
and unclench fist immediately
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before or during specimen

collection.
 Remove the needle and apply
direct pressure with dry gauze to
stop bleeding.
After test
to the requesting HCP, who will
 Instruct the patient to resume
usual diet and fluids, as directed
by the HCP.
 Promptly transport the specimen
to the laboratory for processing
and analysis.
 Observe/assess venipuncture site
for bleeding or hematoma forma-
tion and secure gauze with
adhesive bandage.
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Before Test:
Blood Test: Potassium  Inform the patient this test can
To evaluate fluid and
Level assist in evaluating electrolyte
electrolyte balance 2.1mmol/L To assess patient’s
3.5-5.2mmol/L balance.
related to potassium potassium level and its
correlation to  Inform the patient that specimen
levels toward
development of arrest. collection takes approximately 5
diagnosing disorders
min.
such as acidosis,
renal failure,  Address concerns about pain and
dehydration, and explain that there may be some
monitor the discomfort during the
effectiveness of venipuncture.
therapeutic During Test
interventions.
 Instruct the patient not to clench
and unclench the fist immediately
before or during specimen
collection.
 Remove the needle and apply
direct pressure with dry gauze to
stop bleeding. Observe/assess
venipuncture site for bleeding or
hematoma formation and secure
gauze with adhesive bandage.
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After Test
to the requesting HCP, who will
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Before Test
Venous Blood Gas:  Obtain a list of the patient’s
To assess
pCO2 current medications, including
oxygenation and acid To assess tissue perfusion
35-45mmHg by measuring venous anticoagulants, aspirin and other
base balance. 102mmHg
carbon level. salicylates, herbs, nutritional
supplements, and nutraceuticals.
 Record the patient’s temperature.
 Review the procedure with the
patient and advise rest for 30 min
before specimen collection.
 Note that there are no food, fluid,
or medication restrictions unless
by medical direction.
During Test
movement.
 Apply a pressure dressing over the
puncture site. Samples should be
mixed by gently rolling the
syringe to ensure proper mixing of
the heparin with the sample.
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After Test
 Apply pressure to the puncture site
for at least 5 min in the
unanticoagu- lated patient and for
at least 15 min in the case of a
patient receiving anti- coagulant
therapy.
 Observe/assess puncture site for
bleeding or hematoma formation.
Apply pressure bandage.
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Before Test
Venous. Blood Gas: To assess fluctuations in  Obtain a list of the patient’s
To assess or monitor
Bicarbonate: HCO3 blood pH level caused by current medications, including
an electrolyte vomiting.
22-28mmol/L anticoagulants, aspirin and other
imbalance or acid-
salicylates, herbs, nutritional
base balance.
12mmol/L supplements, and nutraceuticals.
 Record the patient’s temperature.
 Review the procedure with the
patient and advise rest for 30 min
before specimen collection.
 Explain to the patient that an
arterial puncture may be painful.
 Note that there are no food, fluid,
or medication restrictions unless
by medical direction.
During Test
movement.
 Apply a pressure dressing over the
puncture site. Samples should be
mixed by gently rolling the
syringe to ensure proper mixing of
the heparin with the sample, which
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prevents the formation of small

clots leading to rejection of the
sample.
After Test
 Apply pressure to the puncture site
for at least 5 min in the
unanticoagu- lated patient and for
at least 15 min in the case of a
patient receiving anti- coagulant
therapy.
 Observe/assess puncture site for
bleeding or hematoma formation.
Apply pressure bandage.
Before Test:
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Computed  Inform the patient this procedure

Tomography Examines your blood can assist with assessment of lung
Emboli in pulmonary
Pulmonary Angiogram vessels in your lungs function and check for disease.
vessels is often one of the
(CTPA) to see if there is causes of cardiac arrest.  Note any recent procedures that
blood clot in your CTPA was ordered to see can interfere with test results,
Should not show blood lung blood vessels. including examinations using
if pulmonary embolism
clots or embolism in No evidence of could be the cause of her iodine-based contrast medium or
the lungs. pulmonary embolism. Cardiac Arrest. barium. Ensure that barium studies
were performed more than 4 days
before angiography.
 Obtain a list of the patient’s
current medications, including
anticoagulants, aspirin and other
salicylates, herbs, nutritional
supplements, and nutraceuticals,
especially those known to affect
coagulation.
 Inform the patient that a burning
and flushing sensation may be felt
throughout the body during
injection of the contrast medium.
After injection of the contrast
medium, the patient may
experience an urge to cough,
flushing, nausea, or a salty or
metallic taste.
 Instruct the patient to fast and
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restrict fluids for 2 to 4 hr prior to

the procedure. Protocols may vary
among facilities.
During Test:
 Place the patient in the supine
position on an examination table.
Cleanse the selected area, and
cover with a sterile drape.
 Instruct the patient to inhale
deeply and hold his or her breath
while the images are taken, and
then to exhale after the images are
taken.
After Test:
 Monitor the patient for
complications related to the
procedure (e.g., allergic reaction,
anaphylaxis, bronchospasm).
 Instruct the patient to resume
usual diet, fluids, medications, or
activity, as directed by the HCP.
Renal function should be assessed
before metformin is resumed.
 Monitor vital signs and
neurological status every 15 min
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for 1 hr, then every 2 hr for 4 hr,

and as ordered. Take the tem-
perature every 4 hr for 24 hr.
Monitor intake and output at least
every 8 hr.
 Instruct the patient to immediately
report symptoms such as fast heart
rate, difficulty breathing, skin
rash, itching, chest pain, persistent
right shoulder pain, or abdominal
pain. Immediately report
symptoms to the appropriate HCP.
Before Test
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Electrocardiogram  Inform the patient this procedure

(ECG) To evaluate the can assist in assessing cardiac
QT interval in men is electrical impulses (heart) function.
≤0.44 seconds and in generated by the Patient who experienced  Obtain a history of the patient’s
women is ≤0.45 to 0.46 heart during ventricular fibrillation cardiovascular system, symptoms,
No evidence on long
seconds. the cardiac cycle to arrest are prone to and results of previously
QT syndrome
assist with diagnosis developing post-arrest
Shows 60-100 bpm performed laboratory tests and
age, infection, or syndrome such as QT.
(ave.82) diagnostic and surgical
Prolongation.
enlargement. procedures.
 Inform the patient that it may be
necessary to remove hair from the
site before the procedure.
 Address concerns about pain
related to the procedure and
explain that there should be no
discomfort related to the
procedure.
 Inform the patient that the
procedure is performed by an HCP
and takes approximately 15 min.
 Ensure the patient has removed all
external metallic objects from the
E area to be examined prior to the
procedure.
 Instruct the patient to void prior to
the procedure and to change into
the gown, robe, and foot coverings
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provided.
During Test:
Instruct the patient to remain still
throughout the procedure because
movement produces unreliable
results.
 Prepare the skin surface with
alcohol and remove excess hair.
Use clippers to remove hair from
the site, if appropriate. Dry skin
sites.
 Apply the electrodes in the proper
position.
 If the patient has any chest
discomfort or pain during the
procedure, mark the ECG strip
indicating that occurrence.
After Test:
 When the procedure is complete,
remove the electrodes and clean
the skin where the electrode was
applied.
 Evaluate the results in relation to
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previously performed ECGs.

Denote cardiac rhythm
abnormalities on the strip.
 Monitor vital signs and compare
with baseline values. Protocols
may vary among facilities.
Basic Labs:
Urinalysis for ketones
Liver MRI
CBC: Htc
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NURSING DIAGNOSES
1. Imbalanced Nutrition: Less than body requirements related to nutritional loss in prolonged
vomiting as evidenced by weight loss of 9% of total body weight.
2. Deficient Fluid Volume related to excessive fluid loss in vomiting as evidenced by decreased
pulse pressure.
3. Decreased Cardiac Output related to prolonged cardiac resting phase as evidenced by altered
heart rhythm and prolonged QT interval in ECG.
4. Risk for Constipation related to insufficient fluid intake.
5. Risk for shock related to decreased fluid volume.
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a. Nursing Care Plan (Develop 3 NCP from the 5 Nursing Diagnosis)
Date/Cues Needs Nursing Objective of Nursing Actions with Evaluation

Diagnosis Care Rationale
(@ least 5 nursing
interventions)
P Imbalanced Nutrition: Within 12 hours of Independent Goal Met:
Subjective: Less than body nursing intervention, the 1. Assessed general Within 12 hours of
H
requirements related to patient will demonstrate condition; monitor V/S nursing intervention the
 “She had limited Y nutritional loss in adequate nutrition as R: to obtain base line date patient’s lab results will
oral intake and prolonged vomiting as evidenced by 2. Assess current weight show :
S
can only manage evidenced by weight loss normalization of compared to usual weight RBS: 80-140 mg/dL
to tolerate small I of 9% of total body laboratory values and norms for age and Albumin: 3.5-5 g/dL
meals” as weight. indicating nutritional gender. Globulin: 2.0-3.5 g/dL
O
verbalized by the status (serum proteins, R: to identify deviations Na: 136-144 mmol/L
husband. L RBS and electrolytes). from the norm and to K: 3.7-5.1 mmol/L
 “Emesis occurs establish baseline Ca: 8.5-10.2 mg/dL
O
after ever meal on Rationale: parameters. Cl: 97-105 mmol/L
most days” as G Decreased oral intake 3. Observe for muscle Mg: 1.7-2.2 mg/dL
patient confirmed. together with nutritional wasting, loss of hair, Pho: 2.5-4.8 mg/dL.
I
 5 previous losses in persistent fissuring of nails, delayed
pregnancy C vomiting has caused a healing, and gum bleeding.
complicated by substantial amount of R: indicates protein-energy Goal partially Met:
A
nausea and weight loss and malnutrition and need for Within 12 hours of
vomiting. L miscarriage; factors replacement. nursing intervention, the
Objective: suggesting Imbalanced 4. Assess nutritional needs patient will show
Needs
 10 kg weight loss nutrition: less than body appropriate for age and elevation in lab results
(9% of total body requirements. condition. but did not reach the
weight) (Food) R: to provide nutrition that normal range.
 Hypokalemia is individualized and
(2.1mmol/L) optimum for dietary
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 Administration demands.
of 300 mg 5. Contract with client
Thiamine regarding commitment to Goal not met:
 Administration therapeutic program and
of 4 units meeting specific dietary Within 12 hours of
albumin. needs and goals. nursing intervention the
 Electrolyte R: Individual success is patient did not show any
stabilisation and enhanced when client changes in laboratory
repletion commits to a contract. studies and remained
6. Provide small, frequent, low.
and nutritionally dense
meals and supplemental
snacks, as appropriate.
R: Gastric dilation may
occur if re-feeding is too
rapid. Client may feel
bloated for weeks while
body adjusts to increased
food intake.
7. Make selective menu
available and allow client
to control choices as much
as possible.
R: Client who feels in
control of environment is
more likely to eat
preferred foods.
Auscultate and record
presence of bowel sounds
R: determine ability of
intestinal tract to handle
digestive process.
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Dependent
1. Administer IV form of
electrolytes as ordered.
R: replacement therapy for
lost electrolytes. IV route
for rapid drug action.
2. Administer appetite
stimulants as ordered.
R: to encourage oral
intake.
3.Administer vitamin and
mineral supplements as
ordered
R: Provides extra nutrition
and recovery.
4. Administer antiemetics
as ordered.
R: to decrease or eradicate
occurrence of emesis.
5. Monitor patient’s
response to drugs.
R: to make modifications
if unwanted outcomes are
observed.
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Collaborative:
1. Collaborative with
dietitians on planning
meals for the patient.
R: to set nutritional goal
that is highly
individualized for the
patient and her specific
dietary needs.
2. Administer parenteral
feeding if unresponsive to
oral feedings.
R: provides alternative
route for nutrition.
3. Collaborate with
medical technologist in lab
interpretation and follow-
up labs that may be
ordered to assess nutrition.
R: to obtain precise
information regarding
patient’s nutritional status.
Health Teaching
1. Educate patient and family
members the importance of
proper nutrition, hydration,
and diet modification.
R: Knowledge heightens
compliance with the
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treatment plan.
2. Ascertain client’s
understanding of individual
nutritional needs and
client’s ways of meeting
those needs.
R: to determine
informational needs of the
client.
3. Encourage adequate fluid
intake and explain benefits.
R: Sufficient hydration
promotes urinary output
and aid preventing
infection.
4. Encourage questions and
address concerns of
client/SO regarding the
treatment regimen.
R: to fill in knowledge gaps
of client/SO and promotes
participation.
5. Promote pleasant,
relaxing environment
eliminating unpleasant
odors or sights which may
have a negative effect on
appetite.
R: enhances food intake.
1.
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Nursing Care Plan (Develop 3 NCP from the 5 Nursing Diagnoses)

(@ least 5 nursing
interventions)
Subjective: P Deficient fluid volume Within 8 hours of INDEPENDENT: GOAL MET:
“She had limited oral nursing intervention the 1. Assess Vital signs Within 8 hours of nursing
H related to excessive fluid
intake” as verbalized by patient will demonstrate R: to establish baseline intervention, the patient
the husband. Y loss in vomiting as appropriate fluid balance, data. was able to excrete 30cc
as evidenced by urine 2.Assess skin turgor and of urine every hour.
S evidenced by changes in
output of 30cc/hr. mucous membrane
Objective: I hemoconcentration, dry R: indicators of adequate Goal partially Met:
Decreased pulse pressure. hydration. Within 8 hours of nursing
O mucous membrane, and
3.Control humidity and intervention, the patient
L decresed pulse pressure. ambient air temperature. was able to excrete 15-25
R: to prevent fluid loss cc of urine every hour.
O
R: Excessive fluid loss through sweating.
G 4. Place the water within Goal not met:
prior to prolonged patient’s reach. Within 8 hours of nursing
I
vomiting decreases the R: for easy access when intervention, the patient’s
C feeling thirsty. urine output is <15cc/hr.
amount of water 5. Instruct patient to drink
A
using the given cup and
absorbed by the RBC
L note how many cups were
thus, reducing the ECF consumed.
Needs
R: for Intake measurement
Fluid leading to decreased 6. Instruct patient to pee un
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blood volume. the given container and

secure not to spill.
Decreased pulse R: to measure output.
pressure and changes in
DEPENDENT:
hemoconcentration are 1. Administer D5w as
suggestive of decreased ordered
R: to provide hydration
blood volume following intravenously.
2. Administer anti-emetics
inadequate fluid intake. as ordered.
R: prevent fluid loss in
vomiting.
3. Review patient’s response
to drug and the need for
modifications if unwanted
outcomes are observed.
R: to discontinue drugs not
conducive to patient’s
recovery.
COLLABORATIVE:
1. Collaborate with
physician in installation of
catheter when difficulty in
urination is experienced.
R: To assist in urination and
accurate measurement of
output.
2. Collaborate with dietitian
in planning diet rich in water
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and prevent foods which

exacerbate dehydration.
R: to provide additional
hydration.
HEALTH TEACHING
1. Educate patient about the
need for hydration therapy.
R: to gain knowledge
regarding treatment
regimen.
2. Encourage foods with
high fluid composition such
as watermelon and jello
R: provides extra hydration
in solid form.
3. Give patient suggestion
on how many cups of water
she needs to take in 1 hour.
R: provides adequate
hydration.
4. Instruct patient not to take
foods that exacerbate
dehydration such as sugary
foods, caffeine, and alcohol.
R: prevents dehydration.
2.
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Nursing Care Plan (Develop 3 NCP from the 5 Nursing Diagnosis)

(@ least 5 nursing
interventions)
Subjective: P Decreased Cardiac Within 8 hours of nursing DEPENDENT: Goal Met:
Output related to intervention, the patient 1. Administer Oxygen Within 8 hours of nursing
H prolonged cardiac resting will demonstrate supplementation as intervention, the patient
Objective: phase as evidenced by hemodynamic stability as ordered and regulate. demonstrated
 Hgb: 108 g/L Y altered heart rhythm and evidenced by: R: increase oxygen hemodynamic stability as
 40 minute CPR prolonged QT interval in BP: ≥ 100/70 mmHg available for cardiac evidenced by:
 Cardioversion S ECG. O2Sat: ≥ 95% function/tissue BP: ≥ 100/70 mmHg
 Fixed dilated Peripheral pulses: 60–100 perfusion. O2Sat: ≥ 95%
pupil I bpm 2. Administer BT as Peripheral pulses: 60–100
Rationale: Potassium is bpm.
 Infusion of ordered.
pRBC, 4 units O responsible for Goal partially Met:
R: aids in establishing
 Infusion of conduction of cardiac Within 8 hours of nursing
cardiac output.
albumin, 4 units L action potential and its intrvention, the patient
3. Infuse albumin as
 Miscarried resting membrane ordered demonstrated elevation in
 Ischemic hepatitis O potential. With R: Maintains osmotic BP, O2sat, and peripheral
 Anuric renal decreased potassium, pressure. pulses but still hasn’t
failure G your cardiac threshold 4. Assist in chest reached the normal range.
 Encephaopathy decreases as well radiograph, ECG, Goal not met:
I resulting to prolonged echocardiogram. Within 8 hours of nursing
conduction of action R: Provides information intervention, the patient’s
C potential and resting about heart’s status. BP, O2sat, and peripheral
potential. This decreases 5. Administer inotropic pulses did not
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your cardiac output. drugs as ordered. demonstrate changes and

Needs Evidence can be seen in R: to maintain systemic remained low.
Circulation patient’s ECG. perfusion and preserve
end-organ performance.
6. Provide IV fluids and
electrolytes.
R: minimize dehydration
and dysrhythmias.
7. Evaluate response to
drugs and make
modifications to drug of
choice when unwanted
outcomes are observed.
R: to make the
pharmacologic
management
individualized to the
client’s case.
INDEPENDENT:
1. Assess Vital Signs
R: establish baseline data
2. Place client on bed in a
position of comfort.
R: decreases oxygen
consumption and risk for
decompensation.
3. Monitor IV rate of
drugs closely. Use
infusion pump when
necessary.
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R: avoid overdose.
4. Avoid prolonged sitting
or supine position.
R: to maximize vascular
return.
COLLABORATIVE:
1. Review laboratory data
indicating heart function.
R: identify imbalances
and provides information
on what pharmacological
agents to be used.
2. Assist with
preparations for support
procedures such as
cardioversion and
intubation as ordered.
R: aids in maintaining
heart function.
HEALTH TEACHING:
1. Emphasize importance
of treatment regimen.
R: promotes compliance.
2. Promote rest and
relaxation.
R: reduces anxiety and
muscle tension.
3. Start gradually when
engaging in physical
activities.
R: for oxygen
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conservation.
4. Instruct patient to
report signs of muscle
cramps, headaches,
dizziness, or skin rashes.
R: requires immediate
action as this signifies
drug toxicity, or
electrolyte loss especially
potassium.
5.
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VII. EVALUATION AND IMPLICATION OF THE CASE TO:

Nursing Practice
Further evaluation of the case will help nurses assess what is normal in terms of
the frequency of vomiting . It will help nurses establish a parameter which will help
differentiate a normal frequency of vomiting from an alarming frequency of vomiting
which may necessitate for further interventions. From that, it will help nurses identify the
priorities of the patient and impose nursing actions predicated with those priorities.
Nursing Education
In the realm of nursing academe, the case will help learners on the etiology of the
disease. It will give them knowledge on what to look out for when this disease is
diagnosed. It will inform them about the deviations it will cause from the normal findings
of lab tests which will help them further understand the pathophysiology of the disease.
Nursing Theory
The nursing theory which perfectly applies on the case is Ida Jean Orlando’s
Deliberative Nursing Process. This theory stresses out the reciprocal relationship between
patient and nurse giving emphasis on the patients behavior and responses to the
interventions in order to come up to a positive outcome. This can be done with the use if
schematic nursing process consists of assessment, diagnosis, planning, implementation,
and evaluation. The nursing care is highly individualized and patient’s response is
considered before progressing into the treatment plan.
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VIII. RECOMMENDATION/REFERRALS/FOLLOW-UPS
TO THE CLIENT:
1. Cognitive stimulation therapy (CST) to encourage thinking, concentration,
and memory function.
2. Encourage rest and relaxation.
3. Recognize and foods that trigger nausea and vomiting.
4. Eating pattern should be modified into small but frequent meals.
5. Drink plenty fluids
6. Maintain Adequate Nutrition especially protein and carbohydrates.
7. Verbalize her response to the treatment plan to assess improvement.
TO THE FAMILY:
1. Health education is a priority. They need to be informed about the patient’s disease
process and how it affects her.
2. They also need to be informed about the treatment plan and monitor if the patient is
following the advice given by the doctor.
3. Exclude the patient temporarily from chores and there should be someone in the
family who will temporarily assume the patient’s family role.
4. Work hand in hand with the health care providers by reporting any unusualities
observed on the patient.
5. Provide support and positive reinforcements to the patient on her progress.
TO THE COMMUNITY:
1. Health care provider must be available with good equipment and facilities.
2. Provide education to the community about the causes, symptoms, and treatments of
hyperemesis gravidarum and when to get professional help to avoid complication.
3. The community should provide a clean and unpolluted environment to promote the
safety of its residents furthermore, it will help in the prevention of health
complications.
TO THE HEALTH CARE PROFESSIONALS:

1. Conduct physical examination and laboratory tests for further medication and
treatment.
2. Prepare nutritional menu that is appropriate to the patient for fast recovery.
3. Monitor patient’s response to treatment regimen and make appropriate modifications
to the treatment plan.
TO THE NURSES:
1. Encourage close monnitoring of the patient and document if vomiting still occurs.
2. Monitor intake and output to assess hydration and nutrition of the patient.
3. Assess overall general appearance to note cues necessary for further intervention.
4. Aside from these, nurses should also provide nonpharmacologic therapy such as
giving positive reinforcements and counseling to the patient to somehow give the
patient some form of relief.
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IX. JOURNAL READINGS RELATED TO THE CASE

(Should be an Evidence-Based Practice (EBP) Reading: Attach the
photocopy of your journal reading)
TITLE: Evidence-Based Obstetrics & Gynecology: Hyperemesis Gravidarum.
Summary
The article mainly talks about the possible treatments for hyperemesis gravidarum. A lot of
these proposed treatment is not backed by Randomized Controlled Trials (RCT) or still hasn't
been tested thoroughly in most cases but they are backed by evidence of some patient who
achieved improvement in their health.
In the nonpharmacologic treatment, the first proposal was modifications in dietary intake. It
was basically teaching the patient on how to deal with HG by the means of monitoring her
eating pattern. Next is with the use of herbals particularly the ginger. It's known mechanism
of action is to act as an antagonist on serotonergic receptors. Lastly in this portion is with the
use of acupuncture and hypnosis. A lot of researchers were skeptical in this idea so they
conducted a study and it shows that there's really no statistically significant difference
between this method and placebo so it remains as a theoretical benefit.
Moving on to pharmacologic treatments, there are multiple drugs proposed to treat HG. Most
of them are antihistamine, dopamine antagonist, serotonin antagonist, and phenothiazine. A
meta-analysis was conducted on the side effects of these drugs and it varies greatly. It ranges
from only causing drowsiness, to causing serious abnormalities to the fetus such as cleft
palate, skeletal & muscular abnormalities, cardiac malformations and etc.
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Reaction
The treatments proposed were divided whether they are pharmacologic or
nonpharmacologic treatment. Under the nonpharmacologic treatment is with the use of
hypnosis and acupuncture. This method was probably the least expected. It's hard to think
that these methods work for some clients experiencing HG. It also include diet therapy which
tackles about the use of nutrition in the management of HG. It was discovered that diet
mainly comprising of protein and carbohydrates can help aid in the condition. I believe that
nutrition therapy is the best in nonpharmacologic treatment.
On the other hand, pharmacologic treatments were mainly comprising of antiemetics but
there were a tremendous amount of drugs and each has it's own side effects. Antihistamines
are antiemetic drug which I think is the most operative and absolutely, the best treatment
overall for Hyperemesis Gravidarum. They show no teratogenicity among 200,000 tested
pregnant women and manifested great effects in combating morning sickness including
nausea and emesis. This drug has also the least damaging side effect which is only drowsiness
whereas other drug could potentially cause limb malformations and other abnormalities of
the fetus. Which leads me to the conclusion that it is the best treatment amongst the others.
In conclusion, Hyperemesis Gravidarum is a complex condition. There are only minimal

research conducted for this topic and it's etiology is still not stabilized. Nevertheless, there are
accessible treatments for this condition, it is still best recommended to consult a General
Practitioner or a professional health care provider.
57
Tel: 064-229-8207
References:
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58
Tel: 064-229-8207
59

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Cotabato Medical Foundation College, Inc

Quezon Ave. Poblacion 8, Midsayap, Cotabato

Date Presented: April 29, 2023

their pregnancy (NVP). Hyperemesis Gravidarum (HG) is a condition of intractable

gestation. While nausea and vomiting of pregnancy in general is estimated to occur in 50 to

90% of all pregnancies, hyperemesis gravidarum is estimated to occur in .5 to 2% of pregnant

approximately 4,000 Canadian women a year experience hyperemesis gravidarum. HG is the

found in the occurrence of hyperemesis gravidarum in the Philippines.

performed with 40 minutes downtime. Her hematology test reveals hypokalemia

complications reqiuring D&C to remove RPOC. She remained an inpatient for 33 days.

Treatment program includes potassium infusion of 40mmol/hr adrenaline and noradrenaline

infusion, 4 units of packed RBC, 4 units of albumin, commencement of IV Thiamine,

approximately 40 minutes downtime, cold intubation, and multiple direct current

initial resuscitation and stabilisation involved a potassium infusion up to 40 mmol/hr and an

complicated by multiorgan dysfunction including ischaemic hepatitis, mild encephalopathy

requiring rehabilitation, and anuric renal failure requiring short-term dialysis.

of evidence of type 2 diabetes mellitus with a normal HbA1C)

background history of 5 previous pregnancies to the same partner, complicated by some

(9% of total body weight).

The patient’s background medical history was otherwise unremarkable with no

symptoms or biochemical evidence of a disorder of potassium homeostasis preceding the

pregnancy. Specifically, she denied symptoms to suggest hypokalaemic periodic paralysis

suggest an arrhythmogenic disorder with no palpitations, presyncope, or syncope reported.

suggest thyroid disease and pre-pregnancy had normal Thyroid Stimulating Hormone (TSH)

hypertensive, and there was no evidence of primary hyperaldosteronism on testing. There

ventricle ventriculogram, and a transoesophageal echocar- diogram which demonstrated

normal baseline electro- cardiogram (ECG) post-arrest with no evidence of long QT

Importantly, her serum potassium level remains normal.

Admission on Emergency Department

Day 2 in ICU

During inpatient stay (3-32 days of admission)

➢Head CT: 10mm filling defect in left transverse sinus.

Discharged (at day 34)

1. discuss the phenomenon and concept map of the scenario;

2. obtain family background of the client;

3. define terms related to the care;

4. discuss the basic etiology and symptomatology of Hyperemesis Gravidarum;

5. review the physiology of Fluid and Electrolytes Homeostasis;

6. discuss the mechanism of Morning sickness during pregnancy;

7. trace the pathophysiology of Hyperemesis Gravidarum;

9. discuss the drugs administered to the client;

10. identify priority nursing diagnosis for the client;

13. enumerate the recommendation/referral/follow-ups; and

14. discuss journal of an evidence-based practice research related to Hyperemesis Gravidarum.

CLINICAL CASE ANALYSIS WORKSHEET

Concept: Care for High-Risk Pregnancy

II. DEVELOPMENTAL DATA: Specify the Stage.

According to Erikson, the developmental task of a middle adult is generativity versus

generations are important needs at the generativity vs stagnation stage of development.

getting back on track and generate new life experiences.

III. COMPLETE DIAGNOSIS OF THE CASE CHOSEN

 an abnormal condition of pregnancy characterized by protracted vomiting, weight

nausea and vomiting of pregnancy prolonged past week 16 of pregnancy or that is so

12 weeks of pregnancy. It occurs at an incidence of 2% in pregnant women.

List all the basic etiology Actual etiology on Rationale

Multiple Pregnancy In multiple pregnancies, it was found that the incidence

Genetics An increased risk of hyperemesis gravidarum has been

Molar Pregnancy  Abnormal tissue growth in the uterus,

Anatomy and Physiology (Organ or System Involved)

Sodium and Potassium homeostasis.

Mechanism of Action: Morning sickness during pregnancy

Legend: Present: Text

History of HG in previous Smoking