CASE

STUDIES ON
MAJOR
CONCEPTS
ACUTE BIOLOGIC CRISIS
 HEART FAILURE
By: ALCE
Case Scenario – Jeraldine Yates is a 70-year-old woman originally from Alabama. She lives alone and is able to manage herself independently. She
is active in her community and church. Mrs. Yates was admitted to the hospital two months ago with heart failure. Since her discharge, a visiting
nurse visits every other week to assess for symptoms of heart failure and see that Mrs. Yates is continuing to manage well on her own.

History of Present Illness – The visiting nurse stops in to see Mrs. Yates today. The nurse immediately notices that Mrs. Yates’s legs are very
swollen. Mrs. Yates states, “I noticed they were getting a bit bigger. They are achy, too.” The nurse asks Mrs. Yates if she has been weighing herself
daily to which Mrs. Yates replies, “I got on that scale the last time you were here, remember?” The nurse weighs Mrs. Yates and she has gained 10
pounds. Additional assessment findings indicate that Mrs. Yates gets short of breath when ambulating from one room to the other (approximately 20
feet) and must sit down to catch her breath. Her oxygen saturation is 95% on room air. Bibasilar crackles are heard when auscultating her lung
sounds. The nurse asks Mrs. Yates if she is currently or has in the past few days experienced any chest, arm, or jaw pain or become nauseous or
sweaty. Mrs. Yates states, “No, I didn’t have any of that. I would know another heart attack. I didn’t have one of those.” The nurse asks about any
back pain, stomach pain, confusion, dizziness, or a feeling that Mrs. Yates might faint. Mrs. Yates denies these symptoms stating, “No. None of that.
Just a little more tired than usual lately.” Her vital signs are temperature 97.6ºF (36.4ºC), blood pressure 140/70, pulse 93, and respirations 22. The
nurse reviews Mrs. Yates’s list of current medications. Mrs. Yates is taking aspirin, clopidogrel bisulfate, lisinopril, and carvedilol. The nurse calls the
health care provider who asks the nurse to draw blood for a complete blood count (CBC), basic metabolic panel (BMP), brain natriuretic peptide (B-
type natriuretic peptide assay or BNP), troponin, creatine kinase (CPK), creatine kinase-MB (CKMB), and albumin. The health care provider also
prescribes oral (PO) furosemide and asks the nurse to arrange an outpatient electrocardiogram (ECG, EKG), chest X-ray, and echocardiogram.
Pathophysiology

In heart failure, the heart may not provide tissues with adequate blood for metabolic needs, and cardiac-related elevation of pulmonary or systemic venous pressures may result in
organ congestion. This condition can result from abnormalities of systolic or diastolic function or, commonly, both. Although a primary abnormality can be a change in
cardiomyocyte function, there are also changes in collagen turnover of the extracellular matrix. Cardiac structural defects (eg, congenital defects, valvular disorders), rhythm
abnormalities (including persistently high heart rate), and high metabolic demands (eg, due to thyrotoxicosis) also can cause HF.

LV Failure

In heart failure that involves left ventricular dysfunction, CO decreases and pulmonary venous pressure increases. When pulmonary capillary pressure exceeds the oncotic
pressure of plasma proteins (about 24 mm Hg), fluid extravasates from the capillaries into the interstitial space and alveoli, reducing pulmonary compliance and increasing the work
of breathing. Lymphatic drainage increases but cannot compensate for the increase in pulmonary fluid. Marked fluid accumulation in alveoli (pulmonary edema) significantly alters
ventilation-perfusion (V/Q) relationships: Deoxygenated pulmonary arterial blood passes through poorly ventilated alveoli, decreasing systemic arterial oxygenation (PaO2) and
causing dyspnea. However, dyspnea may occur before V/Q abnormalities, probably because of elevated pulmonary venous pressure and increased work of breathing; the precise
mechanism is unclear.

In severe or chronic LV failure, pleural effusions characteristically develop, further aggravating dyspnea. Minute ventilation increases; thus, PaCO2 decreases and blood pH
increases (respiratory alkalosis). Marked interstitial edema of the small airways may interfere with ventilation, elevating PaCO2—a sign of impending respiratory failure.

RV failure
 
In heart failure that involves right ventricular dysfunction, systemic venous pressure increases, causing fluid extravasation and consequent edema, primarily in dependent tissues
(feet and ankles of ambulatory patients) and abdominal viscera. The liver is most severely affected, but the stomach and intestine also become congested; fluid accumulation in the
peritoneal cavity (ascites) can occur. RV failure commonly causes moderate hepatic dysfunction, with usually modest increases in conjugated and unconjugated bilirubin, PT
(prothrombin time), and hepatic enzymes (particularly alkaline phosphatase and gamma-glutamyl transpeptidase [GGT]). The impaired liver breaks down less aldosterone, further
contributing to fluid accumulation. Chronic venous congestion in the viscera can cause anorexia, malabsorption of nutrients and drugs, protein-losing enteropathy (characterized by
diarrhea and marked hypoalbuminemia), chronic gastrointestinal blood loss, and rarely ischemic bowel infarction.
Concept Map

Risk
Risk Factors
Factors
••High
High blood
blood pressure
pressure
••Coronary
Coronary artery
artery disease
disease
••Heart
Heart attack
attack
••Diabetes
Diabetes
••Alcohol
Alcohol use
use

Types
Types of
of Heart
Heart Failure
Failure Signs
Signs and
and Symptoms
Symptoms

••Left-sided
Left-sided HF
HF ••Shortness
Shortness of of breath
breath (dyspnea)
(dyspnea) when
when
••Right-sided
Right-sided HF
HF you
you exert
exert yourself
yourself or
or when
when you
you lie
lie
••Systolic
Systolic HF
HF down
down
••Diastolic ••Fatigue
Fatigue and
and weakness
weakness
Diastolic HF
HF
••Swelling
Swelling (edema)
(edema) in in your
your legs,
legs, ankles
ankles
and
and feet
feet
••Rapid
Rapid or
or irregular
irregular heartbeat
heartbeat

Heart
Failure
 DIABETIC KETOACIDOSIS
By: ADUNA
A 15 year old woman presented to the hospital emergency department with a 5-day history of weakness, tactile fever, productive cough,
nausea, and vomiting. 
Chief complain: weakness, tactile fever, productive cough, nausea, and vomiting. 
Past: Patient has a history of obesity and diabetes. Patient stated that 2 years ago her diabetes had been managed with diet alone. In the
past year, glipizide and metformin were added because of poor glycemic control. No known allergies. Non smoker and non alcoholic.
Present: When her mother got home from work, 15 year old Roberta Cruz was found very lethargic and lying in vomit at his home. Her
heart was racing and he was breathing abnormally. Her mother called 911 when she could not get her to the car to transport her to urgent
care. When the paramedics arrived at the house, Roberta was complaining that she needed to go to the bathroom and repeatedly asking
for water. She was transported then to the ER.
Labs: On ER admission, Roberta’s VS were BP 85/53. HR 119, RR 32, T 39.1 and O2 96% on room air. She was drowsy, lethargic, and
slow to respond to questions. Her breathing was deep and labored with “fruity breath.” She had polydipsia and polyuria with abdominal
pain rated 5/10.
Pathophysiology

Insulin deficiency, increased insulin counter-regulatory hormones (cortisol, glucagon, growth hormone, and catecholamines)
and peripheral insulin resistance lead to hyperglycemia, dehydration, ketosis, and electrolyte imbalance which underlie the
pathophysiology of DKA. Hyperglycemia of DKA evolves through accelerated gluconeogenesis, glycogenolysis, and
decreased glucose utilization. Due to increased lipolysis and decreased lipogenesis, abundant free fatty acids are converted
to ketone bodies. Hyperglycemia-induced osmotic diuresis, if not accompanied by sufficient oral fluid intake, leads to
dehydration, hyperosmolarity, electrolyte loss, and subsequent decrease in glomerular filtration. With decline in renal
function, glycosuria diminishes and hyperglycemia/hyperosmolality worsens. (Reference: Diabetic Ketoacidosis:
Pathophysiology and Treatment, Laura Mumme, 2015)
Concept Map
 CONGESTIVE HEART DISEASE
By: BAYAUA
Case Scenario: Mr. SB, 60-year-old male is a retiree and was admitted to the hospital accompanied by his daughter. He is 100kg at a height
of 180cm so his calculated body mass index (BMI) was 30.9 indicating that he was overweight. When admitted, patient was complained of
shortness of breath for 2 weeks and was worsening on the day of admission. Besides, he also experienced orthopnea, fatigue, paroxysmal
nocturnal dyspnea and leg swelling up to his thigh. Mr. SB was admitted to the hospital for to the same problem last year.

History Of Present Illness: Mr. SB had known case of heart failure since 3 years ago and he had also diagnosed with hypertension for 5
years. Before admitted to the hospital, patient was taking frusemide 40mg, aspirin 150mg, metoprolol 50mg, amlodipine 10mg, and
simvastatin 40mg for his hypertension and heart failure. Patient does not allergic to any medication and he does not take any traditional
medicines at home.

Family History: His family history revealed that his father had died of ischemic heart disease 4 years ago while his brother has hypertension.
2-3 cigarettes a day As for his social history, he smokes for 35 years and the calculated smoking pack years was 5 pack years. Besides, Mr.
SB also drinks occasional
PATHOPHYSIOLOGY

In the usual form of heart failure, the heart muscle has reduced contractility. This produces a reduction in cardiac output,
which then becomes inadequate to meet the peripheral demands of the body. The 4 primary determinants of left ventricular
(LV) performance are generally altered as follows: (1) There is an intrinsic decrease in muscle contractility. (2) Preload or
left atrial filling pressure is increased, resulting in pulmonary congestion and dyspnea. (3) Although systemic blood pressure
is often reduced, there is an increase in systemic vascular resistance (afterload), which can further reduce cardiac output.
(4) Heart rate is generally increased as part of a compensatory mechanism associated with an increase in sympathetic tone
and circulating catecholamines. In patients with coronary disease, there is often an imbalance between myocardial oxygen
supply and demand. An increase in heart size may be particularly deleterious by increasing wall tension because of the
Laplace relation and increasing myocardial oxygen consumption.
Concept Map

He is 100kg at Patient is 60 years

old
a height of patient was
180cm so his complained of
calculated body shortness of
mass index breath for 2
(BMI) was 30.9 Congestive Heart Disease
weeks and was
indicating that   worsening on the
he was day of admission
overweight
 
experienced
Mr. SB had known
orthopnea, fatigue,
he smokes for case of heart
paroxysmal
35 years and failure since 3 nocturnal dyspnea
the calculated years ago and he and leg swelling up
smoking pack had also to his thigh
years was 5 diagnosed with
pack years. hypertension for 5
Besides, Mr. SB years
also drinks His family history
occasional revealed that his
father had died of
ischemic heart
disease 4 years
ago
 TRAUMATIC BRAIN INJURY
By: BERNABEO

Case Scenario: A 65-year-old woman was getting groceries with her friend when she slipped on ice,
hit her head and lost consciousness. An ambulance was called, and she was rushed to the hospital.
The patient lost consciousness for one hour and remained in an altered state of consciousness for
24 hours. Diagnostic imaging confirmed right-sided focal subdural hematoma.

History of Present Illness:

The client slipped on ice, then hit her head and lost consciousness.
Pathophysiology

Traumatic brain injury usually results from a violent blow or jolt to the head or body. An object that goes through brain tissue,
such as a bullet or shattered piece of skull, also can cause traumatic brain injury. After brain injury, there are blood-brain
barrier breakdown and neurodegeneration in areas including the injured cortex, hippocampus, and a portion of the
diencephalon. Microglia, monocytes, macrophages, and neutrophils invade areas exhibiting blood-brain barrier damage,
which is also associated with extensive upregulation of neutrophil adhesion factors, including integrin receptors and
immunoglobulin superfamily members. This process is carried out through innate signaling pathways and, in the case of TBI,
through release of damage-associated molecular pattern molecules (DAMPs), better known as danger signals. This response
is an effort to restore normal homeostasis, but, if the extent of injury is too great, maladaptive immune responses can ensue.
This inflammatory response can persist for years and eventually contributes to neurodegeneration. However, the use of anti-
inflammatory medications shortly after TBI has not been shown to be an effective treatment, which suggests that inflammation
may play a beneficial role, particularly in the acute phase of TBI.
Concept Map:

SIGNS & SYMPTOMS RISK FACTORS

Confusion and
disorientation Adults - ages 60 Males in any age
Headache and older group
 
   

Dizziness Trouble speaking

coherently
 
Young adults,
Children, especially especially those
newborns to 4-year-old between ages 15 and
Nausea and Difficulty remembering 24
vomiting new information.

   

Changes in
Ringing in the emotions or sleep
ears patterns

 
 HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS)
By: COCUSA
Mr. Pare a 65-year-old Male that lives alone presents to the emergency department stating that he doesn’t feel good. When questioned about
his symptoms he states that he “had the flu two weeks ago and just hasn’t gotten over it”. He is having difficulty remembering the questions
asked by the triage nurse and keeps asking the nurse to repeat the question. He states that he feels dizzy when he walks and that has been a
problem since he has had to go to the bathroom frequently to urinate and to the kitchen to get a drink since he has been very thirsty. His urine
has been a dark color for the past two days. He states he has no history of any medical problems. The triage nurse places Mr. Pare in a bed.
An IV is started with difficulty, blood is drawn for lab work and he is placed on a cardiac monitor. VS BP 90/60 HR 148 RR 22 SpO2 97% Pain
level 1-2 abdominal discomfort. The following labs are obtained.
BUN 35 mg/dL
Creat 1.5 mg/dL
Na 160 mEq/L
K 6.5 mEq/L
Cl 100 mmol/L
Glucose 856 mg/dl
Serum Acetone 0 mg/dL
Serum osmolality 420 mOsm/kg
Pathophysiology

The basic underlying mechanism of HHS is a relative reduction in effective circulating insulin with a concomitant rise in
counterregulatory hormones. Unlike patients with DKA, most patients with HHS do not develop significant ketoacidosis. Insulin
remains available in amounts sufficient to inhibit lipolysis and ketogenesis but insufficient to prevent hyperglycemia.
Hyperosmolarity itself may also decrease lipolysis, limiting the amount of free fatty acids available for ketogenesis
Under normal circumstances, all of the glucose filtered by the kidneys is reabsorbed. When blood glucose levels reach
approximately 180 mg/dL, proximal tubular transport of glucose from the tubular lumen into the renal interstitium becomes
saturated, and further glucose reabsorption is no longer possible. The glucose that remains in the renal tubules continues to
travel, passing into the distal nephron and, eventually, the urine, carrying water and electrolytes with it. Osmotic diuresis results,
causing a decrease in total body water. Diuresis also leads to loss of electrolytes, such as sodium and potassium. Glucose
concentration increases due to loss of circulating volume. In an insulinopenic state, hyperglycemia is exacerbated by continued
gluconeogenesis and inability to clear glucose. Due to loss of circulating water volume, patients with HHS can have up to 9L of
water deficit because of hyperosmolarity and diuresis.
The hyperosmolarity of the plasma triggers the release of antidiuretic hormone to ameliorate renal water loss by reabsorbing
water through collecting ducts in the kidney. Hyperosmolarity stimulates thirst, a defense mechanism that may prove
disadvantageous in patients who are dependent on others for care, such as the institutionalized elderly. In the presence of HHS,
if the renal water loss is not compensated for by oral water intake, dehydration leads to hypovolemia
Concept Map HYPEROSMOLAR
HYPERGLYCEMIC STATE (HHS)

Signs and Symptoms

include:
 
Risk Factors
 Blood sugar level
of 600 milligrams  Having type 2
per deciliter diabetes
(mg/dL) or 33.3  Age older than 65
millimoles per liter  Have another chronic
(mmol/L) or health condition
higher  Have an infection
 Excessive thirst  Take certain
 Dry mouth medication
 Increased
Complication
urination
 Warm, dry skin  Seizures
 Fever  Heart attack
 Drowsiness,  Stroke
confusion  Coma
 Hallucinations
 Vision loss Prevention
 Convulsions
 Coma  Monitor your blood sugar
 Know the symptoms of
high blood sugar
 Follow your diabetes
management plan
 CHRONIC KIDNEY DISEASE
By: DELA CRUZ

Case Scenario
A 50-year-old male patient presents to his primary care provider with a chief complaint of loss of appetite and
generalized weakness & fatigue for the past month.
History of Past Illness
- Type II diabetes mellitus (DM) for 15 years and not on regular medication
- NPDR (Non-Proliferative Diabetic Retinopathy)
Family History
Father suffered with DM & HTN
History of Present Illness
History of fever at nighttime in the past 15 days.
Pathophysiology

Chronic renal failure is caused by a progressive decline in all kidney functions, ending with terminal kidney damage. During
this time, there is modulation and adaptation in the still-functional glomeruli, which keeps the kidneys functioning normally
for as long as possible. The remaining glomeruli, therefore, experience a rise in pressure through hyperfiltration. The
release of various cytokines and growth factors leads to hypertrophy and hyperplasia. At the same time, the function of the
glomeruli suffers due to the excessive demands on them, leading to increased permeability and proteinuria. Increased
protein concentrations in the proximal tube system are direct nephrotoxins and can further impair kidney function.
 Risk Factors
Signs and Symptoms
cigarette
Periorbital edema smoking 

Pedal edema obesity

Concept Map nausea

high
cholesterol
fatigue
Diabetes type 1
and 2
shortness of breath

vomiting, especially atherosclerosis

in the morning and
after eating CKD
cirrhosis and liver
abnormally dark failure cirrhosis
or light skin and liver failure

numbness in your
kidney cancer
hands and feet

brittle hair and bladder cancer

nails

muscle twitching
kidney stones
and cramps

easy bruising systemic lupus

and bleeding erythematosus 
Excessive thirst
 ABDOMINALAORTIC ANEURYSM
By: MUNGCAL

Case Scenario: A 79-year-old man presented to the Emergency Department reporting the acute onset of low back
pain radiating to the left side of his chest. The pain started earlier the same day, had become progressively worse,
and was not relieved by changes in position. The patient denied hematuria, dysuria, constipation, diarrhea, or any
recent trauma.
History of Present Illness: His medical history was remarkable for known cardiovascular disease, including coronary
artery disease with previous myocardial infarction and 4-vessel coronary artery bypass graft; a 31 pack-year history of
tobacco use; paroxysmal atrial fibrillation treated with warfarin anticoagulation; and hypertension. Other comorbidities
included stage 3 chronic renal insufficiency and hyperlipidemia. He had no known history of aortic aneurysm.
Pathophysiology
 
 Genetic Factors
 Abdominal Aorta: thick wall with low elastin content, high wall
tension, few vasa vasorum
 Atherosclerosis
 Damage to media: ischemic damage to medial VSMC, SMC
release pro-angiogenic factors
 Medial Neovascularization: Hyperpermeable vessels allow
establishment of chemotactic gradients for EC gradient,
chemotactic gradient also allows recruitment of inflammatory cells,
degradation of CM in media allowas EC migration.
 Inflammatory infiltration:production of proteases, production of
cytotoxic mediators
 Degradation of elastin and collagen
 Decrease SMC density
 Abdominal Aortic Aneurysm: wall thinning and focal dilatation
 Concept Map

SIGNS AND
RISK
DEFINITION
SYMPTOM
FACTORS
S
An abdominal aortic aneurysm is an enlarged
Deep, constant pain in
area in the lower part of the major vessel that your abdomen or on the Tobacco use.
side of your abdomen
supplies blood to the body (aorta). The aorta Age.
Being male.
runs from your heart through the center of your Back pain

chest and abdomen. The aorta is the largest

blood vessel in the body, so a ruptured Being white.
abdominal aortic aneurysm can cause life- A pulse near your
bellybutton
Family history.
Other aneurysms.
threatening bleeding. Depending on the size of
the aneurysm and how fast it's growing,
treatment varies from watchful waiting to
emergency surgery.
 ACUTE MYOCARDIAL INFARCTION
By: OMLANG

A 29-year-old Caucasian male with history of acute lymphoblastic leukemia (ALL) treated with full body radiation,
marrow transplant and chemotherapy 12 years ago, presents to the ER with acute chest pain and SOB that began
3.5 hours prior to arrival, while delivering food. He then walked into the local CVS to check his blood pressure,
which was “150s/90s.” Although unable to describe the quality of the pain, he is writhing in pain on the stretcher and
rates it a 10/10. Nothing seems to be giving him any relief. He denies any similar past episodes. The patient is not
currently on any medications, denies a history of smoking or illicit drug use.
Family History: The patient’s father has a history of CAD in his 50s, and his mother’s health is unremarkable. The
patient has been in complete remission from ALL for 12 years; he has no other medical conditions. 
Pathophysiology

The area of infarct occurs in the distribution of the occluded vessel. Left main coronary artery occlusion generally results in a large anterolateral infarct,
whereas occlusion of the left anterior descending coronary artery causes necrosis limited to the anterior wall. There is often extension to the anterior
portion of the ventricular septum with proximal left coronary occlusions.
In hearts with a right coronary dominance (with the right artery supplying the posterior descending branch), a right coronary artery occlusion causes a
posterior (inferior) infarct. With a left coronary dominance (about 15% of the population), a proximal circumflex occlusion will infarct the posterior wall; in
the right dominant pattern, a proximal obtuse marginal thrombus will cause a lateral wall infarct only, and the distal circumflex is a small vessel.
The anatomic variation due to microscopic collateral circulation, which is not evident at autopsy, plays a large factor in the size of necrosis and
distribution. Unusual patterns of supply to the posterior wall, such as wraparound left anterior descending or posterior descending artery supplied by
the obtuse marginal artery, may also result in unexpected areas of infarct in relation to the occluded proximal segment.
A proximal occlusion at the level of an epicardial artery results in a typical distribution that starts at the subendocardium and progresses towards the
epicardium (the so-called wavefront phenomenon). Therefore, an area of necrosis or scarring is considered to have an "ischemic pattern" if it is largest
at the endocardium, with a wedge-shaped extension up to the epicardial surface.
Ischemic injury, however, may be located in the mid myocardium or even the subepicardium if the level of the coronary occlusion is distal within the
myocardium. Therefore, in cases of thromboemboli from epicardial thrombi (especially plaque erosions), there may be patchy infarction, often
associated with visible thrombi within the myocardial vessels, not centered in the endocardium but occurring anywhere in the myocardium, including
midepicardial and subepicardial locations.
Concept Map

• Age • Pressure, tightness, pain,

RISK FACTORS

SIGNS AND SYMPTOMS

Acute Myocardial Infarction
• Smoking or a squeezing or aching
• High Blood Pressure sensation in your chest or
• Obesity arms that may spread to
• High Blood Cholesterol your neck, jaw or back
or triglyceride levels • Nausea, indigestion,
• Diabetes heartburn or abdominal
• Metabolic Syndrome pain
• Family history of heart • Shortness of breath
attacks
• Lack of physical ctivity • Cold sweat
• Stress • Fatigue
• Illicit drug use • Lightheadedness or
sudden dizziness
 ACUTE PANCREATITIS
By: ONIA

Case Scenario: A 36 year old male came to emergency department with a chief complaint of upper abdominal pain associated
with 2 episodes of vomiting, yellowish urine discoloration and decreased urine output. Patient is a heavy drinker that consumes 2-
3 bottles of beer 3 times a weeks.

History of Present Illness:

3 days prior to admission, the client was working in a factory when he suddenly experienced abdominal pain with vomiting.

2 days prior to admission, signs and symptoms persisted associated with yellowish discoloration of the urine as well as
decreased urine output.

1 hour prior to admission, client decided to seek consult because of the persistence of the signs and symptoms.

Family History: HPN on paternal side

Pathophysiology

CAUSES: Pancreatic Duct Obstruction (fat necrosis), Acinar Cell Injury

(d/t ischemia, viral infections mumps, drugs, direct trauma), Defective
intracellular transport of proenzymes within acinar cells, Excessive
alcohol intake> Interstitial edema> Impaired blood flow> activation of
enzymes intracellular or extracellular> Acinar cell injury> activated
enzymes causing lesions> Acute pancreatitis
Concept Map

ACUTE PANCREATITIS

SIGNS AND SYMPTOMS RISK FACTORS

- Upper abdominal pain. - Gallstones
- Abdominal pain that radiates to your - Alcohol Abuse
back. - Increased Triglycerides (>1000 mg/
- Abdominal pain that feels worse after dL
eating. - Autoimmune
- Fever. - Drug induced
- Rapid pulse. - Infections
- Nausea. - Trauma
- Vomiting. - Idiopathic
TREATED WITH:
- Tenderness when touching the
abdomen. - NPO and IV fluid hydration
- Jaundice - Analgesics for pain
  - Low fat diet
- If gallstone of origin, cholecystectomy may
be performed
- Treat metabolic complications
(hyperglycemia and hypocalcemia)
 HYPOVOLEMIC SHOCK
By: PANOPIO
You are dispatched to transport a 12 year old with abdominal injuries case with abdominal injuries caused by flipping over bicycle handlebars. Mother reports this happened
about four hours ago. There was no loss of consciousness and the child was wearing a helmet. Patient appears in obvious discomfort, and he says he has worsening
abdominal pain. There are no indications of spinal injury

Vital signs of the patient are the following:

HR: 130/min

BP: 110/50 mm Hg

RR: 30/min

Spo2: 92% on room air

Temperature: 37.5 C

Weight: 46kg

Age: 12 years

History of Present Illness: Parents arrive with their 12 year old with abdominal injuries case with abdominal injuries caused by flipping over bicycle handlebars. Mother reports
this happened about four hours ago. There was no loss of consciousness and the child was wearing a helmet. Patient appears in obvious discomfort, and he says he has
worsening abdominal pain. Spinal injuries has been ruled out.

Family history: Mother has hypertension and is taking hypertensive medications.

Pathophysiology

Hypovolemic shock results from depletion of intravascular volume, whether by extracellular fluid loss or
blood loss. The body compensates with increased sympathetic tone resulting in increased heart rate,
increased cardiac contractility, and peripheral vasoconstriction. The first changes in vital signs seen in
hypovolemic shock include an increase in diastolic blood pressure with narrowed pulse pressure ). As
volume status continues to decrease, systolic blood pressure drops. As a result, oxygen delivery to vital
organs is unable to meet oxygen demand. Cells switch from aerobic metabolism to anaerobic
metabolism, resulting in lactic acidosis. As sympathetic drive increases, blood flow is diverted from other
organs to preserve blood flow to the heart and brain. This propagates tissue ischemia and worsens lactic
acidosis. If not corrected, there will be worsening hemodynamic compromise and, eventually, death.
 H
By: PERENA
 SEPTIC SHOCK
By: SANTOS
CASE SCENARIO A 39-year-old man felt unwell overnight with swelling and pain in his scrotum and penis. In the morning he felt
breathless and had blood-stained fluid oozing from his penis. He called 999 and the ambulance crew took him to accident and
emergency. The patient admitted that he had not attended earlier because he was frightened and because he was sole guardian
of his teenage son, who had to come with him.
The patient was cared for in a cubicle in A&E. As a general practice trainee my first contact with him was when a concerned
nursing assistant showed me his ECG, which revealed a sinus tachycardia with a rate of 140bpm.
Observations showed a respiratory rate of 39 per minute with BP 120/75, oxygen saturations of 97% in air and tympanic
temperature of 37.9C. Capillary blood glucose was 13.4mmol/l with no history of diabetes.
The patient’s arterial blood gas showed a marked compensated alkalosis with a lactate 3.9mmol/l. Venous blood results showed a
CRP of 535 mg/l, urea of 11 mmol/l and creatinine 200 µmol/l.
HISTORY OF PRSENT ILLNESS The patient had no significant medical or sexual history, regular medications or allergies, and his
last sexual contact was over two years ago.
 MAP 10-15mmHg from
baseline
Map 10mmHg from baseline
Renin ADH
Effectice compensation MAP 20mmHg from
O2 vital organs Vasoconstriction baseline

Heart rate Pulse rate Tissue / Organ

hypoxia
Hear rate
Urine (oliguria)
pH Weak rapid pulse

Restless pH
Excessive cell/organ damage
Sensory neural
Apprehensive
Multi system organ failure changes

pH