NCM 118 Nursing Care of Clients w/ Life
Threatening Conditions, Acutely Ill, Multi-Organ
Problems, High Acuity & Emergency Situations,
Acute & Chronic
CARDIAC FAILURE
 Heart failure (HF), also known as congestive heart failure
(CHF), is a syndrome, a group of signs and symptoms,
caused by an impairment of the heart's blood pumping
function.
 The shortness of breath may occur with exertion or while
lying down, and may wake people up during the night.
 The severity of the heart failure is mainly decided based
on ejection fraction and also measured by the severity of
symptoms.
- Ejection fraction (EF) is a measurement, expressed as a
percentage, of how much blood the left ventricle pumps out
with each contraction.
- An ejection fraction of 60% means that 60% of the total
amount of blood in the left ventricle is pushed out with each
heartbeat.
- A normal heart’s ejection fraction is between 55 and 70%
- An EF from 41 to 49% might be considered too low.
- It does not always indicate that a person is developing heart
failure, but it could indicate damage, perhaps from a previous
heart attack.
- An ejection fraction measurement under 40% might be
evidence of heart failure or cardiomyopathy.
- In severe cases, EF can be even lower than 40%
SIGNS & SYMPTOMS
- Shortness of breath,
- Excessive fatigue
- Leg swelling
- Chest pain, including angina, is not usually caused by heart
failure, but may occur if the heart failure was caused by a
heart attack.
- Other conditions that may have symptoms similar to heart
failure include obesity, kidney failure, liver disease, anemia,
and thyroid disease.
Common Causes of Heart Failure
• Coronary artery disease
• Heart attack
• High blood pressure
• Atrial fibrillation
• Valvular heart disease
• Excessive alcohol consumption
• Infection
• Cardiomyopathy
 These cause heart failure by altering the structure or the
function of the heart or in some cases both.
DIFF. TYPES OF HEART FAILURE
 RIGHT-SIDED VENTRICULAR HEART
FAILURE - which affects the right heart,
 LEFT-SIDED VENTRICULAR HEART
FAILURE - which affects the left heart
- Left-sided heart failure may be present with a reduced
ejection fraction or with a preserved ejection fraction.
 BIVENTRICULAR HEART FAILURE - which affects
both sides of the heart
NOTE: Heart failure is NOT THE SAME as cardiac
arrest, in which blood flow stops completely due to the
failure of the heart to pump
DIAGNOSTICS
- Based on symptoms & physical findings
- Echocardiography
- Blood tests, and a chest x-ray may be useful to determine the
underlying cause
TREATMENT
NOTE: Treatment depends on severity and case4
 For people with chronic, stable, mild heart failure:
- Treatment usually consists of lifestyle changes, such as
cessation of smoking, physical exercise, and dietary
changes, as well as medications.
 In HF due to left-ventricular dysfunction:
- Angiotensin-converting-enzyme (ACE) inhibitors
- Angiotensin receptor blockers
- Angiotensin receptor-neprilysin inhibitors, along with beta
blockers
- Mineralocorticoid receptor antagonists
- SGLT2 inhibitors are recommended (Serum/ Glucose
Cotransporter 2)
- Diuretics may also be prescribed to prevent fluid retention
and the resulting shortness of breath.
TREATMENT OF CONGESTIVE HEART FAILURE
Remember U N L O A D F A S T
U – pright Position
N – itrates
L – asix
O – xygen
A – CE inhibitors
D – igoxin
F – luids (should be decrease)
A – fterload (should be decrease)
S – odium restriction
T – est (Dig Level, ABGs, Potassium Level)
 Depending on the case, an implanted device such as
pacemaker or implantable cardiac defibrillator may
sometimes be recommended.
 In some moderate/more severe cases:
- cardiac resynchronization therapy (CRT) or cardiac
contractility modulation
 In severe disease that persists despite all the measures:
- cardiac assist device ventricular assist device or heart
transplantation
 Some people with HF develop abnormal heart beats or
arrhythmias.
 Some arrhythmias may reduce how well the heart’s lower
chambers (ventricles) function.
 Cardiac Resynchronization Therapy (CRT), also known
as biventricular pacing, may be needed. In this procedure, a
special pacemaker is used to make the ventricles contact at
the same time. This helps the lower heart chambers pump
and relax together.
ACUTE MYOCARDIAL INFARCTION
A myocardial infarction
(MI), commonly known as a
heart attack, occurs when
blood flow decreases or stops
in the coronary artery of the
heart, causing damage to the
heart muscle.
 Myocardial infarction (MI) refers to tissue death
(infarction) of the heart muscle (myocardium) caused by
ischemia, the lack of oxygen delivery to myocardial tissue.
 It is a type of acute coronary syndrome, which describes a
sudden or short-term change in symptoms related to blood
flow to the heart.
 Unlike the other type of acute coronary syndrome, unstable
angina, a myocardial infarction occurs when there is cell
death, which can be estimated by measuring by a blood test
for biomarkers (the cardiac protein troponin).
 When there is evidence of an MI, it may be classified as an
ST elevation myocardial infarction (STEMI) or Non-ST
elevation myocardial infarction (NSTEMI) based on the
results of an ECG.
SIGNS & SYMPTOMS
- The most common symptom is chest pain or discomfort
which may travel into the shoulder, arm, back, neck or jaw.
- Often it occurs in the center or left side of the chest and
lasts for more than a few minutes.
- LEVINE’S SIGN is a clenched fist held over the chest to
describe ischemic chest pain.
- It is named for SAMUEL A. LEVINE (1891-1966) an
influential American cardiologist, who first observed that
many patients with chest pain made this same sign to
describe their symptoms
3 AREAS OF DAMAGE AFTER A MYOCARDIAL
INFARCTION
 Area of Infarction
– Oxygen deprived
- Damage irreversible
- Causes “Q” wave on EKG
 Area of Injury
- Tissue is viable as long as circulation remains
adequate
- Increasing oxygen may save this area from necrosis
- Causes S-T segment
- Elevation on EKG
 Area of Ischemia – viability may not be damaged as
long as MI doesn’t extend and collateral circulation is
able to compensate, that causes depressed ST segment
PROGRESSION OF AN ACUTE MYOCARDIAL
INFARCTION
An acute MI is a continuum that extends from the normal state
to a full infarction:
 ISCHEMIA – lack of oxygen to the cardiac tissue,
represented by ST segment depression, T wave
inversion, or both
 INJURY – Arterial occlusion with ischemia,
represented by ST segment elevation
 INFARCTION – death of tissue, represented by a
pathological Q wave
Clinical Tip: After the acute MI has
ended, the ST segment returns to
base-line, and the T-wave becomes
upright, but the Q wave remains
abnormal because of scar formation.

ST Segment Elevation and Depression
 A normal ST segment represents early ventricular
repolarization.
 Displacement of the ST segment can be caused by the
following various conditions.
PRIMARY CAUSES OF ST SEGMENT ELEVATION
 ST segment elevation exceeding 1 mm in the limb leads
and 2 mm in the chest leads indicates an evolving acute
MI or an ST-elevation MI (STEMI)
 Pericarditis (means inflammation of the pericardium, a
sac-like structure with two thin layers of tissue that
surround the heart to hold it in place and help it work. A
small amount of fluid keeps the layers separate so there’s
less friction between them as the heart beats) ventricular
aneurysm
 Pulmonary embolism (means a sudden blockage in the
pulmonary arteries, the blood vessels that send blood to
your lungs) intracranial hemorrhage
PRIMARY CAUSES OF ST SEGMENT DEPRESSION
 Myocardial ischemia/non-ST elevation MI (NSTEMI)
is caused by a partial obstruction of an epicardial
coronary artery
 Intraventricular conduction defects left ventricular
hypertrophy
 Medication (e.g., digitalis)
ACUTE RENAL FAILURE/ACUTE KIDNEY FAILURE
 Acute kidney failure — also called acute renal failure or
acute kidney injury — develops rapidly, usually in less than
a few days.
 Acute kidney failure occurs when your kidneys suddenly
become unable to filter waste products from your blood.
 When your kidneys lose their filtering ability, dangerous
levels of wastes may accumulate, and your blood's
chemical makeup may get out of balance.
 Most common in people who are already hospitalized,
particularly in critically ill people who need intensive care.
 Acute kidney failure can be fatal and requires intensive
treatment. However, acute kidney failure may be
reversible.
 If you're otherwise in good health, you may recover normal
or nearly normal kidney function
 An abrupt (within hours) decrease in kidney function which
encompasses both injury (structural damage) and
impairment (loss of function)
 Syndrome rather than has a sole & distinct pathophysiology
Normal Kidney Function
- Removal of waste products including drugs
- Maintains body fluid balance
- Maintains electrolyte balance
- Promotes hormone balance
- Regulates blood pressure
- Aids in the production of RBC
- Produces urine
- Aids in the promotion of healthy bones
SYMPTOMS
 Decreased urine output, although occasionally urine
output remains normal
 Fluid retention, causing swelling in your legs, ankles or
feet
 Shortness of breath
 Fatigue
 Confusion
 Nausea
 Weakness
 Irregular heartbeat
 Chest pain or pressure
 Seizures or coma in severe cases
 Sometimes acute kidney failure causes no signs or
symptoms and is detected through lab tests done for
another reason.
Acute kidney failure can occur when:
- You have a condition that slows blood flow to your kidneys
- You experience direct damage to your kidneys
- Your kidneys' urine drainage tubes (ureters) become
blocked and wastes can't leave your body through your urine
Impaired blood flow to the kidneys
 Diseases and conditions that may slow blood flow to the
kidneys and lead to kidney injury include:
- Blood or fluid loss
- Blood pressure medications
- Heart attack
- Heart disease
- Infection
- Liver failure
- Use of aspirin, ibuprofen (Advil, Motrin IB, others),
naproxen sodium (Aleve, others) or related drugs
- Severe allergic reaction (anaphylaxis)
- Severe burns
- Severe dehydration
Damage to the kidney
 These diseases, conditions and agents may damage the
kidneys and lead to acute kidney failure:
- Blood clots in the veins and arteries in and around the
kidneys
- Cholesterol deposits that block blood flow in the kidneys
- Glomerulonephritis (gloe-mer-u-loe-nuh-FRY-tis),
inflammation of the tiny filters in the kidneys (glomeruli)
- Hemolytic uremic syndrome, a condition that results
from premature destruction of red blood cells
- Infection, such as with the virus that causes coronavirus
disease 2019 (COVID-19)
- Lupus, an immune system disorder causing
glomerulonephritis
- Medications, such as certain chemotherapy drugs,
antibiotics and dyes used during imaging tests
- Scleroderma, a group of rare diseases affecting the skin
and connective tissues
- Thrombotic thrombocytopenic purpura, a rare blood
disorder
- Toxins, such as alcohol, heavy metals and cocaine
- Muscle tissue breakdown (rhabdomyolysis) that leads
to kidney damage caused by toxins from muscle tissue
destruction
- Breakdown of tumor cells (tumor lysis syndrome),
which leads to the release of toxins that can cause kidney
injury
Urine blockage in the kidneys
 Diseases and conditions that block the passage of urine out
of the body (urinary obstructions) and can lead to acute
kidney injury include:
- Bladder cancer
 Kidney biopsy. During a kidney biopsy, your doctor uses a needle
to remove a small sample of kidney tissue for lab testing. The
biopsy needle is inserted through your skin and is often directed
using the guidance of an imaging device, such as ultrasound.

- Blood clots in the urinary tract Treating complications until your kidneys recover
- Cervical cancer
Your doctor will also work to prevent complications and allow
- Colon cancer
your kidneys time to heal. Treatments that help prevent
- Enlarged prostate
complications include:
- Kidney stones
- Nerve damage involving the nerves that control the  Treatments to balance the amount of fluids in your blood.
bladder - If your acute kidney failure is caused by a lack of fluids in
- Prostate cancer your blood, your doctor may recommend intravenous (IV)
fluids.
RISK FACTORS - In other cases, acute kidney failure may cause you to have
 Acute kidney failure almost always occurs in connection with
too much fluid, leading to swelling in your arms and legs. In
another medical condition or event. Conditions that can increase
these cases, your doctor may recommend medications
your risk of acute kidney failure include:
- Being hospitalized, especially for a serious condition that (diuretics) to cause your body to expel extra fluids
requires intensive care
 Medications to control blood potassium.
- Advanced age
- Blockages in the blood vessels in your arms or legs - If your kidneys aren't properly filtering potassium from
(peripheral artery disease) your blood, your doctor may prescribe calcium, glucose or
- Diabetes sodium polystyrene sulfonate (Kionex) to prevent the
- High blood pressure accumulation of high levels of potassium in your blood.
- Heart failure - Too much potassium in the blood can cause dangerous
- Kidney diseases irregular heartbeats (arrhythmias) and muscle weakness.
- Liver diseases
- Certain cancers and their treatments  Medications to restore blood calcium levels.
- If the levels of calcium in your blood drop too low, your
COMPLICATIONS doctor may recommend an infusion of calcium.
Potential complications of acute kidney failure include:
 Fluid buildup. Acute kidney failure may lead to a  Dialysis to remove toxins from your blood.
buildup of fluid in your lungs, which can cause shortness - If toxins build up in your blood, you may need temporary
of breath. hemodialysis — often referred to simply as dialysis — to
 Chest pain. If the lining that covers your heart help remove toxins and excess fluids from your body while
(pericardium) becomes inflamed, you may experience your kidneys heal.
chest pain. - Dialysis may also help remove excess potassium from your
 Muscle weakness. When your body's fluids and body. During dialysis, a machine pumps blood out of your
electrolytes — your body’s blood chemistry — are out of body through an artificial kidney (dialyzer) that filters out
balance, muscle weakness can result. waste. The blood is then returned to your body.
 Permanent kidney damage. Occasionally, acute kidney
CAUSES OF ACUTE RENAL FAILURE:
failure causes permanent loss of kidney function, or end-
 Pre-Renal
stage renal disease. People with end-stage renal disease
– low/decrease blood volume
require either permanent dialysis — a mechanical
- low/decrease blood pressure
filtration process used to remove toxins and wastes from
- heart failure
the body — or a kidney transplant to survive.
- liver cirrhosis
 Death. Acute kidney failure can lead to loss of kidney
- renal artery stenosis
function and, ultimately, death.
- renal vein thrombosis
TESTS & PROCEDURES
If your signs and symptoms suggest that you have acute kidney
failure, your doctor may recommend certain tests and procedures
to verify your diagnosis. These may include:
 Urine output measurements. Measuring how much you
urinate in 24 hours may help your doctor determines the
cause of your kidney failure.
 Urine tests. Analyzing a sample of your urine (urinalysis)
may reveal abnormalities that suggest kidney failure.
 Blood tests. A sample of your blood may reveal rapidly
rising levels of urea and
 Creatinine — two substances used to measure kidney
function.
 Imaging tests. Imaging tests such as ultrasound and
computerized tomography may be used to help your doctor STAGES OF CHRONIC KIDNEY DISEASE
see your kidneys.  Stage 1 – kidney damage with NML or increased GFR
 Removing a sample of kidney tissue for testing. In some - GFR ≥ 90
situations, your doctor may recommend a kidney biopsy to remove a - DX/RX of underlying condition and comorbidities
small sample of kidney tissue for lab testing. Your doctor inserts a  Stage 2 – consider as mild
needle through your skin and into your kidney to remove the - GFR 60 to 89
sample. - estimate the rate of progression
 Stage 3 – consider as moderate
- GFR 30 to 59
- evaluate and treat complications
 Stage 4 – consider as severe
- GFR 15 to 29
- prepare for renal replacement therapy
 Stage 5 – led to kidney failure
- GFR < 15 or dialysis
- dialysis or transplantation if uremic
STROKE
 A stroke is when blood flow to a part of your brain is
stopped either by a blockage or a rupture of a blood vessel.
 It is a medical emergency in which the blood supply to any
portion of the brain is interrupted or reduced
 Cerebrovascular accident is the medical term for a stroke.
 Alternative Names:
- CVA- Cerebrovascular Accident
- Cerebral Infarction
- Cerebral Hemorrhage
- Brain Attack

TYPES OF STROKE

ISCHEMIC (87%) HEMORRHAGIC

- Partial or Total Occlusion (13%)
- Raptured/ Bursting of
weakened blood
vessels
1. THROMBOSIS 1.
 Small Vessels INTRACEREBRAL
- Lacunar strokes: (central (10%)
portion, brain stem, pons and - Uncontrolled
basal ganglia) hypertension
 Large Vessels - AVM
- Carotid, vertebral, and basilar - Trauma
arteries - Bleeding
- Angiopathies
- Drug abuse
2. EMBOLISM 2. SUB-
- CHF and MI ARACHNOID (3%)
- Endocarditis - Hypertension
- Genetic
- Anticoagulant
- Aneurysm
3. GLOBAL LOSS OF BLOOD
FLOW
- Hemorrhagic shock
- Cardiac Arrest
- Septicemia
- Narcotic Overdose

ACT FAST
 GOLDEN HOUR (60 MINUTES)
- 60 mins after the onset of stroke symptoms, treatment
should be initiated to increase better outcome.
 TISSUE PLASMINOGEN ACTIVATOR
- Must be given within 3 hours or some eligible patients, up
to 4.5 hours after the onset of stroke,

CLINICAL MANIFESTATIONS
1. SUDDEN NUMBNESS OR WEAKNESS: FACE,
ARMS & LEGS
2. SUDDEN TROUBLE SPEAKING OR
UNDERSTANDING OTHERS- POORLY
ARTICULATED SPEECH

3. SUDDEN TROUBLE SEEING IN ONE OR BOTH

EYES- DAMAGE OF POST. CEREBRAL ARTERY
 4. SUDDEN DIZZINESS OR LOSS OF BALANCE OR
COORDINATION- CEREBELLAR BLOOD SUPPLY
5. SUDDEN SEVERE HEADACHE

NEUROLOGICAL DEFICITS

 MOTOR
- Hemiparesis: weakness or the inability to move on one
side of the body
- Hemiplegia: paralysis of the muscles of the lower face,
arm, and leg on one side of the body
- Ataxia: poor balance and coordination
- Dysphagia: slurred speech, drooling, facial paralysis,
running out of breath when speaking

 VISUAL
- Diplopia: double vision; auses people to see two of the
INCREASED INTRACRANIAL PRESSURE
same image—whether horizontal, vertical or diagonal—
instead of one  Intracranial pressure (ICP) is the pressure exerted by fluids
- Homonymous hemianopia: a field loss deficit in the such as cerebrospinal fluid (CSF) inside the skull and on
same halves of the visual field of each eye the brain tissue.
 ICP is measured in millimeters of mercury (mmHg) and at
 VERBAL rest, is normally 7–15 mmHg for a supine adult.
- Aphasia: person has trouble speaking or understanding  The body has various mechanisms by which it keeps the ICP
other people speaking stable, with CSF pressures varying by about 1 mmHg in
normal adults through shifts in production and absorption of
 COGNITIVE CSF.
- Poor abstraction  The most definitive way of measuring the intracranial
- Amnesia pressure is with transducers placed within the brain.
 To decrease ICP:
OUTCOME MANAGEMENT - catheter can be surgically inserted into one of the
 Maintain cerebral oxygenation brain's lateral ventricles and can be used to drain CSF
 Mechanical ventilation (cerebrospinal fluid)
- Optimum oxygen  This type of drain is known as an external ventricular
- Airway patency drain (EVD). This is rarely required outside brain injury and
 Maintain neck alignment brain surgery settings.
 HOB @ 30-45%  In situations when only small amounts of CSF are to be
- Below 30 % = cerebral edema drained to reduce ICP's (e.g. in IIH), drainage of CSF via
- Above 45% = arterial insufficieny lumbar puncture can be used as a treatment.
 Decreased cerebral inflammation
- Dexamethasone MONRO-KELLIE HYPOTHESIS
S/E  The Monro–Kellie hypothesis is named
- Hyperglycemia after Edinburgh doctors Alexander al Monro and George
- Hypernatremia Kellie.
- Delayed wound healing  The pressure–volume relationship between ICP, volume of
- Mannitol CSF, blood, and brain tissue, and cerebral perfusion
S/E pressure (CPP) is known as the Monro–Kellie doctrine or
- Dehydration hypothesis.
- Electrolyte imbalance  The Monro–Kellie hypothesis states that the cranial
ISCHEMIC STROKE PATHOPHYSIOLOGY compartment is inelastic and that the volume inside the
cranium is fixed. The cranium and its constituents (blood,
CSF, and brain tissue) create a state of volume equilibrium,
such that any increase in volume of one of the cranial
constituents must be compensated by a decrease in volume of
another.

DIABETES
 Diabetes is a chronic (long-lasting) health condition that
affects how your body turns food into energy.
 Your body breaks down most of the food you eat into sugar
(glucose) and releases it into your bloodstream.
 When your blood sugar goes up, it signals your pancreas to
I release insulin.
 Insulin acts like a key to let the blood sugar into your body’s
HEMORRHAGIC STROKE PATHOPHYSIOLOGY
cells for use as energy.
 FASTING BS:
- Pre-diabetes = 100-125 mg/dL
- Diabetes = Equal or more than 126mg/ dL
 - SODIUM BICARBONATE IV IF pH LEVEL IS
BELOW 7.0 (100ML OF NaHCO3 in 400ml of NS
over 4 hours repeat as necessary to bring pH above 7.0
but monitor carefully
 INSULIN ( REGULAR ) BOLUS 6 UNITS STAT-
usually done in ED/ AE.
 INSULIN IV INFUSION TITRATED ACCORDING TO
PROTOCOL: 50 units regular insulin in 50ml NS= 1:1
concentration
 MONITOR BLOOD SUGAR LEVEL EVERY HOUR
FOR 12H THEN EVERY 2 HOURS FOLLOWING
24Hours
- IF BS FALL BELOW 12mmol/L change IV fluid to
D5% Water
 MONITOR POTASSIUM LEVEL AND CORRECT
ACCORDINGLY
KEY PLAYERS - >5.1- no need for replacement
• GLUCOSE - 4.1-5 give 20meq in each bottle of 500ml of the infused
• “Sugar” necessary to survive fluid
• It fuels the cell in our body but it cannot enter the - 3.1-4.0 40meq in each bottle of 500ml of the infused
cell without insulin. fluid
• PANCREAS  WOF CEREBRAL EDEMA and PULMONARY EDEMA
• Control center of insulin. (EXCESSIVE FLUD)
• Beta cells of the Islet of Langerhans  WOF RENAL FAILURE (INADEQUATE REPLACEMENT)
 MONITOR PRESENCE OF KETONES IN THE URINE
• INSULIN
• Acts to promote uptake of glucose to the cells and
TYPES OF DIABETES
tissues
• Promotes synthesis of glycogen to decrease blood • Type 1 – insulin dependent
sugar level • Type 2 – non-insulin dependent
• GLUCAGON • Gestational diabetes – diabetes while pregnant
• Helps with low blood sugar which causes the liver to
turn glycogen into glucose TYPE I DIABETES
• Primarily released by Alpha cell of the Islet of • It was known previously as insulin dependent diabetes
Langerhans (Juvenile onset diabetes).
• LIVER • Type 1 diabetes is thought to be caused by an
• Absorbs extra sugar when BS and insulin levels autoimmune reaction (the body attacks itself by
are high mistake).
• Sugar is absorbed in the form of glycogen and • This reaction stops the body from making insulin.
breaks it down during glycogenolysis making it • Approximately 5-10% of the people who have diabetes
as glucose releases when blood sugar is low have type 1
• GLYCOGEN • If you have type 1 diabetes, you’ll need to take insulin
every day to survive.
• Is a sugar stored in the liver
• Currently, no one knows how to prevent type 1
• Released when there is demand for sugar EG.
diabetes.
Hypoglycemia
TYPE II DIABETES MELLITUS
MANAGEMENT
• With type 2 diabetes, your body doesn’t use insulin well
 Aim is to decrease the blood sugar gradually and can’t keep blood sugar at normal levels.
- Sudden decrease in blood sugar can cause shifting of • About 90-95% of people with diabetes have type 2.
fluid, cerebral edema, increase ICP, alteration LOC, coma • Type 2 diabetes can be prevented or delayed with healthy
 Hydration lifestyle changes, such as:
- IVF NS REPLENISH VASCULAR SYSTEM - Losing weight.
- IF BP IS BELOW 80mmHg SYSTOLIC→ GIVE 2 UN - Eating healthy food.
ITS OF WHOLE BLOOD OR OTHER PLASMA - Being active.
EXPANDER ( Haesteril)
- IVF NS 1L for 30mins Non-modifiable Risk Modifiable Risk Factors
- Then 1L for 1H Factors for Type 2 DM for Type 2 DM
- Then 1L for 2 hours History of gestational Physical inactivity
- Then 1L for 4 hours diabetes
- Then 1L for 6 hours Race/Ethnicity High body fat or body
- Then 125mls/ hour over the following 24H weight
- 13.5 (5 liter) Age over 45 years High blood pressure
- 10.5 hour 125ml= 1.3L Family history of diabetes High cholesterol
= 6.3 liters/ 24hours
 CORRECT ACID BASE IMBALANCES

- ABG AND VBG

GESTATIONAL DIABETES - Causes: NO INSULIN - Causes: CELL NOT
PRESENT RECEPTIVE TO INSULIN
• Gestational diabetes develops in pregnant women who have
- Illness, infection, (Just enough present to
never had diabetes.
skipping meals prevent ketosis)
• If you have gestational diabetes, your baby could be at
higher risk for health problems. - Seen in young and newly - Seen in older adults with
• Gestational diabetes usually goes away after your baby is diagnosed infection/illness
born. - Main Problem: - Main Problem: Extreme
• However, it increases your risk for type 2 diabetes later in Hyperglycemia & hyperglycemia causing
life. Ketoacidosis dehydration due to
• Your baby is more likely to have obesity as a child or teen hyperosmolarity
and develop type 2 diabetes later in life.
- Treatment: - Treatment:
HYPEROSMOLOR HYPERGLYCEMIC NON-KETOTIC IVF Decrease blood sugar
SYNDROME (HHNS) Insulin Rehydration IV
Electrolyte replacement Insulin injection
- Life threatening condition of DM Type 2 Metabolic Acidosis TX
- Extreme hyperglycemia of BS level > 600 mg/dl - Kausmull’s breathing and - Most likely to see mental
- Hyperosmolarity: very concentrated blood acetone breath and status decreases due to
metabolic acidosis severe dehydration
- “Without breakdown of fat”
- “Heavy duty hyperglycemia & dehydration POISONING & ANTIDOTE
- Happens gradually with warning signs 3P’s and high blood  A poison is any chemical substance that is harmful or lethal
sugar levels
to living organisms.
 The term is used in a wide range of scientific fields and
industries, where it is often specifically defined.
Remember INSULIN: “Ready Set Inject Love”
 Poisoning could be accidental or deliberate, and if the
• RAPID: Onset- 15 MINUTES: cause can be identified there may be ways to neutralize the
Peak- 1 HOURS: effects or minimize the symptoms.
Duration- 3 HOURS
• “ 15 MINUTES FEELS LIKE AN HOUR DURING FOUR MAJOR ROUTE OF POISONING
3 RAPID RESPONSES” 1. Inhalation
• Eg. HUMALOG, NOVOLOG 2. Skin/ Eye Contact
3. Swallowing (Ingestion or Eating)
4. Injection (Skin Penetration)
• SHORT: Onset- 30 MINUTES:
Peak- 2HOURS:
SEVERE ACUTE RESPIRATORY SYNDROME (SARS)
Duration- 8 HOURS
 Severe acute respiratory syndrome (SARS) is a viral
• “ SHORT STAFFED NURSES WENT FROM 30
PATIENTS (2) TO 8 PATIENTS” respiratory disease caused by a SARS-associated
• Eg. REGULAR INSULIN, HUMULIN R, , coronavirus.
NOVOLIN R  It was first identified at the end of February 2003 during an

• INTERMMEDIATE: Onset- 7 HOURS: outbreak that emerged in China and spread to 4 other
Peak- 8 HOURS: countries.
Duration- 16HOURS  WHO co-ordinated the international investigation with the
• “ NURSES PLAYS HEROes T0 7 TO 8 16 Y/O”
assistance of the Global Outbreak Alert and Response
• Eg. NPH,, HUMULIN N, NOVOLIN N
Network (GOARN) and worked closely with health
• LONG: Onset- 2 HOURS: authorities in affected countries to provide epidemiological,
Peak- NONE:
clinical and logistical support and to bring the outbreak
Duration- 24HOURS
• “The two long nursing shifts never peak but lasted under control.
24hours”  SARS is an airborne virus and can spread through small
• EG. Lantus
droplets of saliva in a similar way to the cold and influenza.
 It was the first severe and readily transmissible new disease
COMPARISON OF DKA & HHNS
to emerge in the21st century and showed a clear capacity to
DKA HHNS
spread along the routes of international air travel.
- Mainly seen in Type I - Mainly seen in Type II
 SARS can also be spread indirectly via surfaces that have
- PRESENT ketones & - NO ketones & acidosis
acidosis been touched by someone who is infected with the virus.
- Hyperglycemia > - Heavy Duty  Most patients identified with SARS were previously
300mg/dL Hyperglycemia >
healthy adults aged 25–70 years. A few suspected cases of
600mg/dL
SARS have been reported among children under 15 years.
- Variable osmolarity - High osmolarity
- Happens suddenly - Happens gradually
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) supraglottic structures of the larynx, namely the arytenoids,
- It is a serious lung condition that causes low blood oxygen the false vocal cords, the laryngeal ventricles, the
- In ARDS, fluid builds up inside the tiny air sacs of the lungs, aryepiglottic folds and the epiglottis
and surfactant breaks down
- Syndrome of respiratory failure
- Characterized by dyspnea, difficulty of breathing, cyanosis,
hypoxemia, bilateral white lung opacification
- Diffused alveolar destruction & damage

CAUSES
1. Direct Injury to the Lungs
Type I PNEUMOCYTES
 Cover 70% of the internal
surface of each alveoli
 Thin & squamous; ideal for
gas exchange
Type II PNEUMOCYTES
 The synthesizing cell of the
alveolar surfactant
- Maintains alveolar & airway
stability
- Reduces the surface tension;
where it prevents alveolar &
airway collapse

 Poor gas & cough reflex

 Ciliary function impairment - this abnormal function
impairs the ability of cilia to function in a coordinated
manner, impairing mucociliary clearance and causing
chronic upper and lower respiratory inflammation
 Loss of consciousness
 Seizures
 Acid reflux
 Head/neck injuries
 Impaired Swallowing
 Incorrect NGT placement
 Loss of muscle tone or coordination

2. Indirect Injury to the Lungs

Common Causes of Aspiration – individuals with chronically

impaired airway defense mechanisms
 Supraglottic Disease - a serious and potentially life-
threatening condition, characterized by inflammation of the
 II. Bilateral Lung Opacities – “white out” on imaging
 Chest X-ray
 CT Chest = glass appearance opacification
 Lung Ultrasound = Signs of consolidation
– thickening of pleura
– b-lines
 Echocardiogram = to rule out cause of pulmonary edema

III. Decrease P/F Ratio

PATHOPHYSIOLOGY

IV. Non-Cardiogenic Cause of Pulmonary Edema

TREATMENT
 MILD ARDS

BERLIN CRITERIA FOR ARDS

A – bnormal Chest X-ray
R – espiratory Failure
D – ecrease P:F ratio
S – eclude CHF or volume overload

DIAGNOSIS (Berlin Criteria)

I. Signs of Acute Respiratory Failure
Signs & symptoms developing less than 1 week of initial suspected
cause -> most common sepsis; occurs when your immune system
has a dangerous reaction to an infection
 Septic Work Up
- Blood Culture ± Sensitivity
- Sputum Culture ± Sensitivity
- Urine Culture & Analysis
- CT Abdomen/Chest; to determine & rule out other
sources of infection
- SWAB; nose, throat, hairline, axilla, groin, wound etc.
 LUNG PROTECTIVE VENTILATION PROTOCOL

 MODERATE – SEVERE ARDS (P/F Ratio <150)

BURNS

 Tissue damage caused by exposure to excessive heat.

 A type of painful wound caused by thermal, electrical,
chemical or electromagnetic energy.
 Smoking & open flame are the leading causes of burn
injury for older client.
 Scalding is the leading cause of burn injury for children.
 Both infants and the older adults are at the greatest risk for
burn injury.

TYPES OF BURN BY ETIOLOGY

  Thermal Burns skin injuries caused by excessive heat, 1. CRITICAL BURN
typically from contact with hot surfaces, hot liquids, steam,  Partial thickness burn > 25-35% TSBA
or flame  Full thickness burn > 10% TSBA
 Chemical Burns damage to tissue on your body due to a  Burns complicated by:
harsh or corrosive substance - Respiratory distress
- tissue damage caused by strong acids, drain cleaners, - Fractures
paint thinner, gasoline and many other substances - Major soft tissue damage
 Electrical Burns a skin burn that happens when electricity - Cerebral contusion- increase ICP
comes in contact with your body - Spleen, kidney, liver damage
 Radiation Burns caused by UV-rays, X-rays or radiation - Bleeding
therapy to treat cancer  All electrical burns
 Ionizing Radiation a form of energy that acts by removing
electrons from atoms and molecules of materials that include 2. MODERATE BURNS
air, water, and living tissue.  Partial Thickness Burn > 15%, < 25- 30% TSBA
- Ex. nuclear energy, radiation energy  Full Thickness Burn > 2% < 10% TSBA provided
that face, feet, hands, neck and genitalia are NOT
CLASSIFICATION OF BURN INVOLVED.
I. According to TSBA (Total Surface of Burned Area) 3. MINOR BURNS
 Determine extent of damage  PTB < 15% TSBA
 Assessment guide  FTB < 2% TSBA
- Rule of Nine’s estimation of body surface area burned is  No need for hospitalization & IVF replacement/
based on assigning percentages to different body areas treatment on an OPD basis.
- Palmar Method this rule indicates that the patient's palm
(with the exclusion of the fingers and wrist) is
approximately 1% of the patient's body surface area

FIRST AID INTERVENTION

Goal: Stop the burning process.
 Smother the flames
 Do not run
 Lie horizontally
 Discourage standing
 Remove clothing provided not stock to skin
 Throw a rug, coat, blanket, towel over a client to shut
off O2 which supports burning.
 Remove metal objects such as rings, wigs (synthetic
material) → hot object continue the burning process.
 Immerse in cool water (stops the burning process &
eliminate pain). Or wrap in towels soaked in cool water.
 Avoid use of ice water
- It interferes with capillary perforation & viability of
injured area.
II. DEPTH OF INJURY - It will further increase the depth of burned area
 Layers of the skin damaged by heat - It may also precipitate cardiac arrythmias secondary to
1. EPIDERMIS – First Degree (Superficial) rapid decrease in body temperature (if applied to a
i. Stratum Corneum large surface areas)
ii. Stratum Lucidum
iii. Stratum Granulosum FLUID REPLACEMENT
iv. Stratum Spirosum  PARKLAND (BAXTER) FORMULA this formula is
v. Stratum Germinativum used for burns that encompass more than 20% of the total
body surface area or 10% of the body surface in children or
2. DERMIS – Second Degree (Deep) the elderly, that are either deep partial thickness (i.e.,
i. Hair root & shaft second-degree burns) or full thickness (i.e., third-degree
ii. Oil gland burns)
iii. Sweat gland - Plain Crystalloids
3. FATTY LAYER/FASCIA MUSCLE – Third Degree - Plain LR 4mL/kg/ 1% TSBA
Example: 50% TSBA / 60 kg
4. DEEP MUSCLES/BONES – Fourth Degree = 12,000 cc (12L) in 1st 24 hours

III. Location of Burns
i. Head, neck, & face – Smoke inhalation, respiratory
obstruction and cosmetic problem
ii. Ears – Decrease blood supply; increase for infection
iii. Hands & feet – Abundant blood & supply; contracture
deformities
iv. Joints – Deformities and decrease ROM
v. Genitalia – Urethral structure; decrease sensitivity
vi. Chest – Restriction of breathing
CLASSIFICATION OF BURN ACCORDING TO
SEVERITY
 BROOKE FORMULA
- 0.5 ml/ kg/ 1% TSBA (COLLOIDS) eg. Albumin,
dextrans plasma protein fraction.
- 1.5 ml/ kg/ 1% TSBA (CRYSTALLOID eg NSS, LR) +
2000 cc of D5W
Example:
0.5 ml/ 60kg/ 50% TSBA= 1500 cc colloids
1.5 ml/ 60kg/ 50% TSBA= 4500ml + 2000cc D5W
NOTE: The modified Brooke formula is 2mls x body surface
areas burned (BSAB) x weight. While, the Parkland formula is
4mls x body surface areas burned (BSAB) x weight.
 NURSING CARE OF BURN
1. Potential or Actual
- Ineffective airway clearance r/t smoke inhalation.
- Impaired breathing pattern
- Gas exchange impaired
Goal: Maintain adequate airway & ventilation
 Assess for S/S of airway obstruction r/t smoke inhalation.
 History of burns of face, neck, head.
 Soot in nasal passageway & septum.
 Singed nasal hair
 History of burns in an enclosed area
 Hoarseness, stridor, stertorous respiration.
 Hx of burns in an upright position.
- S/S of CO2 poisoning
- History of burn in enclosed space
- Cherry pink skin with s/s of hypoxia
- S/S of pulmonary edema.
 Suction oropharyngeal airway PRN.
 Anticipate insertion of tracheal intubation.
 O2 inhalation/ NC 6- 7LPM humidify
 Assisted ventilation if s/s of respiratory insufficiency:
pO2 < 50, pCO2 > 50
 Assist in insertion of central line before pulmonary edema sets
in.
b. Apply antibacterials (Flammazine, Mebo
ointment)
c. Sterile sheets
d. Use bed cradles to protect from bed clothes.
e. Use circo-electric bed or stryker frame
B. Semi open - cleanse, debride and used a thin layer of
dressing.
C. Closed - use of sterile gauze after application of anti-
microbials.
BURN WOUND GRAFT
Goal: Close burn wound to prevent infection & fluid loss &
restore appearance and function.
Types: Temporary & Permanent
Kinds:
 Homograft- Allograft
- An allograft (termed homograft in older texts) is tissue
transplanted between unrelated individuals of the same
species
- Genetically disseminated members of same species.
- For temporary covering of the extensive burns until
patient own skin is available for grafting.
- Performed early- 2 to 3 days post burn.
- Rejection is expected 2-3 weeks post graft.
- Sources: Cadaver amniotic membrane.

2. Alteration in comfort pain  Heterograft- Xenograft

Goal: Relief of pain - A xenograft (termed heterograft in older texts) is tissue
 Assess pain transplanted between individuals of different species
 Administer narcotic analgesics as ordered (Morphine - Graft from synthetic skin
SO4). - Sources: Pig skin synthetic graft
 Monitor VS frequently esp. RR including depth,
pattern of respiration  Isograft
- An organ transplanted from a donor who is genetically
3. Fluid volume deficit; Alteration in CO identical to the recipient (ie, identical twins)
Goal: Maintain adequate fluid balance. - Graft between identical or histo-compatible androgens
 Assess S/S of hypovolemia
 VS→ Hyponatremia  Autograft
 CVP, PCWP, CO→ Note significant changes. - The transplant that comprises individual's own organ,
 UO→ SG tissue, or cells, transferred from one part of the body to
 I&O, Wt., Hct→ Evaluates the effectiveness of fluid another.
replacement. - Graft of the same person
 Monitor urea, BUN, crea: Nitrogenous waste
LIFE MAINTAINING INTERVENTION FOR ACUTE
 Assist in IVF replacement.
BIOLOGIC CRISIS: Airway Management
4. Alteration in nutrition: < body requirement 1. CPR/ Basic Life Support
Goal: Maintain adequate nutrition.  The BLS Course focuses on preparing students to
 NPO for 1st 48 hours until GIT peristalsis return. perform CPR skills.
 Monitor for signs of paralytic ileus.  CPR is a lifesaving procedure for a victim who has
 Moist oral mucosa→ thirst signs of cardiac arrest:
 Frequent oral hygiene - Unresponsive
 Feed via NGT if cannot tolerate by mouth. - No normal breathing
 High protein, high caloric diet - No Pulse
 Dressing to be done before mealtime.
 Components of CPR are CHEST COMPRESSIONS
and BREATHS.
5. Potential/ Actual for infection
 High quality CPR improves a victim’s chance for
Goal: Prevent and control of infection
SURVIVAL.
 Reverse Isolation (Isolation tent, + air pressure unit, air
circulation system)→ Pushed the used air & keep
HIGH QUALITY CPR
constant flow of fresh air into the room.
 Start compression within 10 seconds of recognition of
cardiac arrest.
 Proper handwashing/ hand hygiene
 Push hard, push fast: Compression at the rate of 100- 120/
 Wound skin precaution.
min with a depth of:
 Diagnose early
- At least 5 cm for adults
 Massive doses of antibiotics
- At least one third the depth of the chest, about 5 cm- for
children
CARE OF BURN WOUND
- At least one third the depth of the chest, about 4 cm- for
1. Use sterile technique
infants
2. Clean with sterile NSS or distilled H2O.
3. Debridement of detached epithelium.  Allow complete chest recoil after each compression.
4. Use Methods:  Minimize interruptions in compression- less 10 seconds.
A. Open method- used in burns of face, neck, trunk,  Give effective breaths that make the chest rise.
limbs, back & perineum.  Avoid excessive ventilation.
a. Clean eschar (dead tissues)
CHEST COMPRESSION DEPTH
 Chest compression is more often too shallow than too deep.
 However, research suggests that compression depth greater
than 6 cm in adults may cause injuries.
 (Optimal to target you compression depth from 5 to 6 cm).

PERSONAL PROTECTIVE EQUIPMENT

- PPE IS EQUIPMENT WORN TO HELP PROTECT THE
RESCUER FROM HEALTH OR SAFETY RISK.
 Medical gloves
 Eye protection
 Full body coverage
 High- visibility clothing
 Safety footwear
 Safety helmets

CHAIN OF SURVIVAL
 The term Chain of Survival provides a useful metaphor
for the element of ECC system of care concept.
 Cardiac arrest can happen anywhere- on the street, at
home or in the hospital emergency department, ICU or
inpatient bed.

 The system of care is different depending on whether

the patient has an arrest inside or outside the hospital.
 The 2 distinct COS which reflect the setting as well as
the availability of rescuer and resources:
- IHCA- In- hospital cardiac arrest
 Surveillance, prevention and treatment of
prearrest conditions
 Immediate recognition of cardiac arrest and
activation of emergency response system.
 Early CPR with an emphasis on chest
compressions
 Rapid defibrillation
 Multidisciplinary post- cardiac arrest care.

- OHCA- Out- of- hospital cardiac arrest.

In-Hospital Cardiac Arrest

Out-of-Hospital Arrest