WEEK 13: NEUROLOGIC EMERGENCIES - is the initial damage to the brain that results from the traumatic

1. Traumatic Brain Injury event.

TBI - is physical injury to brain tissue that temporarily or
- may include contusions, lacerations, and torn blood vessels
permanently impairs brain function.
from impact, acceleration/deceleration, or foreign object
penetration
Leading Cause of Traumatic Brain Injury
1. Falls – usually young children and older adults 2. Secondary injury
2. Blunt Force trauma
3. Vehicular-related collisions - may occur hours or even days after the initial injury and is due
 65% are the result of car accidents. primarily to brain swelling or ongoing bleeding
 15-20% are the result of motorcycle accidents.
 10% are from bicycle accidents.
4. Assaults
 including child abuse
 Violence – gunshot wound
5. Others:
 Sports injuries – soccer, boxing, football or any extreme
sports

Pathophysiology of TBI

Assessment for Traumatic Brain Injury

 The Glasgow Coma Scale (GCS) - which is determined when
the person first arrives at the hospital.
 Loss of consciousness (LOC)
 Post-Traumatic Amnesia (PTA) - which is a state of confusion
and memory loss right after a TBI.
- PTA occurs because there is an impairment in attention and
concentration.

Classification according to Location

1. Focal brain injury – usually due to contact and causing scalp
injury, it might present as skull fracture, contusions and or
intracranial hemorrhage.

Signs and symptoms of Mild TBI

- Loss of consciousness for a few seconds to a few minutes
- Memory or concentration problems
- Headaches
- Dizziness or loss of balance
- Nausea or vomiting
- Difficulty sleeping

Signs & symptoms of Moderate to Severe TBI

- Loss of consciousness from several minutes to hours
- Slurred speech
- Inability to awaken from sleep
- Weakness or numbness in fingers and toes
- Loss of coordination
- Persistent headache or headache that worsens

Classification according to Occurrence

1. Primary injury
2. Diffuse brain Injury - The patient may lie motionless, v/s are subnormal, cool, pale
- usually due to skin and the picture is somewhat similar to shock.
acceleration and
concussion resulting in A concussions are specific to injuries that affect the brain and may
diffuse axonal injury and not involve visible bruises or any apparent structural damage.
brain swelling. The tearing - This is a temporary loss of neurologic function which involves
of the nerve tissue period of unconsciousness lasting from a few seconds to a few
disrupts the brain’sregular minutes.
communication metabolic
processes. - Concussion effects varied depending on its location and
Types of TBI severity.
1. Closed Brain injury – without - If the brain tissue in the frontal lobe is affected, the patient may
the skull being broken or exhibit bizarre irrational behavior.
penetrated and the brain has not - Temporal lobe involvement can produce temporary amnesia
been exposed. or disorientation.
Ex: rapid movement of the head 4. INTRACRANIAL HEMORRHAGE/HEMATOMAS
backward and forward causes Is the most serious brain injuries, most common cause of death
the brain to move inside the skull and clinical deterioration after TBI
and slam against its inner bone
A hematoma (collections of blood) may be;
a) epidural (above the dura)
b) subdural (below the dura)
c) intracerebral (within the brain)
- Major symptoms are frequently delayed until the hematoma is
large enough to cause distortion of the brain and increased
ICP.
5. EPIDURAL HEMATOMA
- Extradural Hematoma or Hemorrhage
- After a head injury, blood may collect in the epidural
(extradural) space between the skull and the dura.
- This can result from a skull fracture that causes a rupture or
2. Open brain injury – open or penetrating head injury laceration of the middle meningeal artery, the artery that runs
- a TBI can be focal or diffuse, meaning damage maybe between the dura and the skull inferior to a thin portion of
isolated to one specific area of the brain in focal injuries temporal bone.
or widespread in the case of diffuse injuries. - Hemorrhage from this artery causes rapid pressure on the
brain.
6. SUBDURAL HEMATOMA
- It is a collection of blood between the dura and the brain, a
space normally occupied by a thin cushion of fluid.
- The most common cause of subdural hematoma is trauma, but
it may also occur from coagulopathies or rupture of an
aneurysm.
- A subdural hematoma may be acute, subacute, or chronic,
depending on the size of the involved vessel and the amount
of bleeding present.

Management of Brain Injuries

2. BRAIN INJURY
The most important consideration in any head injury
- Even seemingly minor injury can cause significant brain
damage due to obstructed blood flow and decreased tissue
perfusion.
- The brain cannot store oxygen and glucose to any significant
degree.
- The cerebral cells need an uninterrupted blood supply to obtain
nutrients irreversible brain damage and cell death occur when
the blood supply is interrupted for even a few minutes.
3. CEREBRAL CONTUSION
Contusion is any injury that causes blood to collect under the skin.
- Is a more severe injury in which the brain is bruised, with
possible surface hemorrhage. \
- The patient is unconscious for more than a few seconds or
minutes.
- Clinical signs and symptoms depend on the size of the
contusion and the amount of associated cerebral edema.
- Often there is involuntary evacuation of the bowels and the
bladder.
- Assessment and diagnosis of the extent of injury are
accomplished by the initial physical and neurologic
examinations.
- CT Scan, MRI and Positron emission tomography (PET scan)
- Any individual with a head injury is presumed to have a cervical
spine injury until proven otherwise.
- From the scene of the injury, the patient is transported on a
board with the head and neck maintained in alignment with the
axis of the body.
- A cervical collar should be applied and maintained until
cervical spine x-rays have been obtained
Treatment of Increased Intracranial Pressure
- As the damaged brain swells with edema, a rise in ICP occurs
and requires aggressive treatment.
- Initial management is based on the principle of preventing
secondary injury and maintaining adequate cerebral
oxygenation.
- ICP; if increased - elevate the head of the bed, and maintaining
normal blood volume.
- Devices to monitor ICP or drain CSF can be inserted during
surgery or at the bedside using aseptic technique.
- The patient is cared for in the ICU, where expert nursing care
and medical treatment are readily available.
Surgical Management: Assessment /Monitoring:
- Surgery is required for evacuation of blood clots, debridement Vital Signs
and elevation of depressed fractures of the skull, and suture of - BP – target SBP > 100mmHg
severe scalp lacerations. - CVP – (8-10cm H20)
- ICP – target is (< 20mmHg)
Medications:
Intake and Output monitoring
- Diuretics – given IV to reduce intracranial pressure. - Use of Indwelling catheters
- Anti-seizure drugs – given during first week to avoid any
additional brain damage might caused by seizure. Respiratory care:
- Coma-inducing drugs – sometimes use this drugs to put - Target ABG values
people into temporary comas because comatose brain needs - PaO2 > 60mmHg
less oxygen to function. - PaCO2 35 – 45mmHg
- pH 7.35 – 7.45
Nursing Management
- Suctioning
Goal of Nursing Care:
- Use of PEEP
- Maintain normal physiologic parameters
- Aspiration precautions
- Prevent secondary brain injury
- Provide emotional and psychological support to patient and Hemodynamic/Fluid Management
families - Avoid Hypotension
- maximize recovery and rehabilitative outcomes - Use of Isotonic fluids
- Use of Vasoactive drugs
Assessment /Monitoring:
- Osmotherapy
- History - Use of Mannitol
- Mechanism of injury - Use of hypertonic Saline
- Pre-existing Medical condition - Monitoring of volume status
- Medications - Maintain electrolyte Balance

Physical Exam Maintain normothermia and Analgesia

- Reflexes - Temperature – 35 to 37℃
- Sponge bath
- Signs of fracture
- Cooling blanket
- Cold saline solution
Level of consciousness
- Anti-pyretic medications
- Analgesic to avoid increase ICP
-Kept at minimum requirement to allow neurologic exam

Positioning and Nutrition:

- Elevate heat of bed at 30 ͦ
- Head and neck in neutral alignment
- Ensure ET tube ties, cervical collar do not compress the neck
- Enteral feeding should be initiated within 72hrs of injury or as
prescribed
- Full caloric requirement must be given
Pupils size and reactivity - Maintain normal blood glucose level

Prevention of Complications:
- Seizure precaution and management
- Minimize noxious stimuli
- Prevent secondary Infections
- VAP/HAP
- Prevent pressure injuries
- Good skin care and pressure reduction
- DVT precautions
- ROM exercise
Muscle tone and Posturing Rehabilitation and Family Support:
- Physical Therapy
- Occupational therapy
- Speech therapy
- Cognitive therapy
- Social worker referral
- Religious and spiritual support
ACUTE ISCHEMIC STROKE
Etiology, Risk Factors, and Pathophysiology
- Stroke is the layman's term for a cerebrovascular accident.
- This refers to brain dysfunction that is caused by brain cell
damage and death as a result of inadequate blood flow to the
brain.
- Stroke - is a leading cause of death and disability world- Thrombosis
wide. - It is the most common
ISCHEMIC STROKE cause of ischemic stroke
- The blood clot formation are usually the cause of blockage in and is usually due to
blood vessel to the brain that causes ischemic stroke. atherosclerosis and the
formation of plaque within
- The affected part no longer receives enough blood or oxygen. an artery.
- Because the brain cannot store oxygen or glucose and - Thrombotic comes
therefore requires a constant flow of blood to supply these from thrombus, which is a
nutrients. blood clot
- That part of the brain without blood flow dies - A thrombus then forms at the site of the plaque and causes
- The blood supply to the brain can be altered through several brain tissue ischemia along the course of the affected vessel,
different processes: which results in infarct if not quickly reversed.
a) Embolism or thrombus formation accounts for - Edema often develops, further increasing ischemia by
approximately 85% of all ischemic strokes. compressing areas surrounding the infarct.
b) Hemorrhage
c) Compression or spasm of the vessels - Patients with a history of atherosclerosis or arteritis are at
highest risk for thrombotic strokes.
- Thrombotic strokes tend to develop during periods of sleep
- Edema occurs in the area of ischemic or infarcted or inactivity, or when blood flow is less brisk.
tissue and contributes to further neuronal cell
death.
- If ischemia is not reversed, neuronal cell death and
infarction of brain tissue occurs.
- The penumbra is an area of tissue that
surrounds the core ischemic area.
- The penumbra receives some blood
flow from adjacent vessels but
perfusion is marginal.
- If Cerebral Blood Flow is improved, the penumbra
may recover.

RISK FACTORS:
1. Hypertension
2. Cardiac disease
a. coronary artery disease
b. heart failure
c. atrial fibrillation EMBOLISM
d. endocarditis
- It refers to the occlusion of a cerebral vessel, most often by a
e. patent foramen ovale
blood clots, infectious particles, fat, air, or tumor fragments.
f. myocardial infarction
g. carotid artery disease - Embolism is often associated with heart disease that results
3. Diabetes in bacterial vegetations or blood clots that are easily detached
4. Increased age from the wall or valvesof the heart and then travel to the brain,
5. Male gender lodging in a cerebral vessel.
6. Prior stroke - Chronic atrial fibrillation, valvular disease, prosthetic valves,
7. Hypercoagulability cardiomyopathy, and atherosclerotic lesions of the proximal
a. cancer aorta are common causes of embolism.
b. pregnancy - The fragmented substance easily lodges at the bifurcation of
c. high RBCs, the middle cerebral artery, breaking apart and traveling
d. sickle cell further into the cerebral vascular system.
8. Family history
9. Dyslipidemia - The onset of an embolic occlusion is rapid, with symptoms that
10. Race (African American) develop without warning.
11. Smoking
12. Obesity Clinical Presentation Symptoms of stroke
13. Physical inactivity - Common signs and symptoms include:
14. Alcohol or illicit drugs 1. weakness in an extremity or on one side of the body
15. Hormone therapy. 2. sensory changes
TRANSIENT ISCHEMIC ATTACK (TIA) 3. difficulty speaking or understanding speech
- This is an 4. facial droop
important warning 5. headache
sign for stroke. 6. visual changes.
- The patient - Clinical presentation of stroke varies based on the area of
develops stroke ischemia or infarction.
symptoms but may
resolve without Diagnostic Tests
tissue infarction. - The goal of initial diagnostic testing in acute stroke is to rule
- The out intracranial hemorrhage (ICH).
pathophysiology of stroke varies based on the precipitating o evidence of ischemia may not appear or may be very
event. subtle on standard CT scanning until 12 to 24 hours after
symptom onset.
- Thrombosis and embolism formation result in acute ischemic
stroke.

- Specialized MRI scan detect areas of ischemia before they are
apparent on CT.
- CT Angiogram - detects areas of vascular abnormalities.
Management of Acute Ischemic Stroke
- Stroke is a medical emergency and is treated with the same
urgency as acute myocardial infarction.
- The goals of treatment are to restore circulation to the brain
when possible, stop the ongoing ischemic process, and
prevent secondary complications.
Management principles include the following:
1. Evaluation of Conditions - that Mimic Acute Ischemic Stroke
- hypoglycemia may cause stroke-like symptoms and is easily
detected by using a bedside monitor to check blood glucose
- toxic or metabolic disorders
- migraines
- seizures
- mass lesions such as brain tumors or abscesses
- psychological disorders
2. Fibrinolytic Therapy
- must be administered to restore perfusion to the affected area
- IV administration of (rtPA) Recombinant tissue plasminogen
activator can be treated within 3 hours of the onset of
symptoms
- recommended dose for rtPA is 0.9 mg/kg, with 10% of the total
dose given as a bolus over 1 to 2 minutes followed by the
remainder of the dose as an infusion over 1 hour
- Vital signs and neurologic checks are done every 15 minutes
for the first 2 hours, then every 30 minutes for 6 hours, and then
hourly until 24 hours following initial treatment
3. Endovascular Treatment
4. Blood pressure management
5. Management of increase intracranial pressure
6. Glucose management
7. Preventing and treating secondary complications
8. Preventing recurrent stroke
TERMINOLOGIES
- Increased ICP – the pressure inside the skull increases; it is a
medical emergency when this occurs suddenly
- Autonomic dysreflexia - a life-threatening emergency in
spinal cord injury patients that causes a hypertensive
emergency; also called autonomic hyperreflexia
- Brain injury - an injury to the skull or brain that is severe
enough to interfere with normal functioning
- Brain injury, closed (blunt) - occurs when the head
accelerates and then rapidly decelerates or collides with
another object and brain tissue is damaged, but there is no
opening through the skull and dura
- Brain injury, open - occurs when an object penetrates the
skull, enters the brain, and damages the soft brain tissue in its
path (penetrating injury), or when blunt trauma to the head is
so severe that it opens the scalp, skull, and dura to expose the
brain
- Concussion - a temporary loss of neurologic function with no
apparent structural damage to the brain
- Contusion - bruising of the brain surface
- Transient ischemic attack – a warning sign of stroke
- Penumbra is an area of tissue that surrounds the core
ischemic area
- Thrombus is a formation of plaque within an artery
- Embolus refers to the occlusion of a cerebral vessel, most
often by a blood clot
WEEK 14: NEUROLOGIC EMERGENCIES
SPINAL CORD INJURY
- occurs when a force is exerted on the vertebral column,
resulting in damage to the spinal cord.
- Damage to any part of the spinal cord or nerves at the end of
the spinal canal often causes permanent changes in strength,
sensation and other body functions below the site of the injury.
SCIs can be separated into two
categories:
1. Primary injuries - are the
result of the initial insult or
trauma and are usually
permanent.
2. Secondary injuries - are
usually the result of a
contusion or tear injury, in
which the nerve fibers
begin to swell and
disintegrate.
 REVIEW: SPINAL VERTEBRAE INNERVATIONS

- traumatic blow to the spine causing fractures, dislocation,

crushing or compression of one or more of the vertebrae
- Penetrating gunshot or knife wound
- Diseases/Conditions: Arthritis, cancer, inflammation, infections
or disk degeneration of the spine

Severity Classification:
1. Complete – if all sensory and all motor functions are lost below
the spinal cord injury
2. Incomplete – if some motor or sensory functions below the
affected area are still present; there are varying degrees of
incomplete injury.
 IMPORTANT!

- For suspected back or neck injury, DO NOT move the

injured person (permanent paralysis and other serious
complications may result).
- Keep the person still.
- Place heavy towels on both sides of the neck to prevent
from moving

Emergency signs and symptoms

1. Extreme back pain or pressure in neck, head or back
2. Weakness, incoordination or paralysis in any part of the body
3. Numbness, tingling or loss of sensation in the hands, fingers,
feet or toes
4. Loss of bladder or bowel control
5. Difficulty with balance and walking
6. Impaired breathing after injury
7. An oddly positioned or twisted neck or back
 4. Myoclonic - are brief shock-like jerks of a muscle or group of
muscles.
- They occur in a variety of epilepsy syndromes that have
different characteristics.
- During a myoclonic seizure, the person is usually awake and
able to think clearly.

Seizure
a sudden, abnormal, excessive discharge of electrical activity within
the brain that disrupts the brain’s usual system for nerve conduction

5. Idiopathic (unclassified seizures) - Epileptic seizures are

defined as transient signs due abnormal excessive or
synchronous neuronal activity in the brain, and epilepsy refers
to at least two unprovoked seizures more than 24 hours apart.
- The term idiopathic means a disease of unknown cause.

Diagnostics:
1. Electroencephalography (EEG) – definitive test to diagnose
seizure activity
2. SPECT scan – scan of choice for a diagnostic evaluation of
certain types of CNS disorders

Treatment:
1. Medication therapy – hallmark of seizure management
Classification of Seizure 2. Surgery – respective procedures or palliative corpus
1. Absence (petit mal) - An absence callosotomy
seizure causes an individual to 3. Seizure precautions
blank out or stare into space for a 4. Oxygen and suction equipment at bedside
few seconds. 5. Re-orient client upon waking
- Absence seizures are most
common in children and typically
don’t cause any long-term
problems.
PETIT MAL ^

2. Atonic - are a type of seizure that

causes sudden loss of muscle
strength.
- These seizures are also called
akinetic seizures drop attacks
or drop seizures.

3. Tonic-Clonic - means sustained rhythmical jerking.

- During a Clonic seizure, jerking of the body or parts of the body
are the main symptom. SEIZURES(MEDICATIONS):
- They can begin in one area (focal motor) or affect both sides of - Levetiracem (keppra)
the brain (generalized Clonic). - Clonazepam (klonopin)
- Clonic seizure movements cannot be stopped by restraining - Valpronic acid (depakene)
the person. - Phenytoin (dilatin)
- Ethosuxamide (zarontin)
- Carbamazepine (tegretol)

STATUS EPILEPTICUS
- potential complication of all types of seizures.
- This is a seizure that lasts longer than 5 minutes, or more
than 1 seizure within a 5-minute period, without returning to
normal level of consciousness between episodes.
- Hence, this is a medical emergency that may lead to
permanent brain damage or death.

Causes:
- Stroke
- Low blood glucose levels
Hypovolemic shock
- Too much alcohol, withdrawal symptoms
- the most common
Diagnostic: type of shock
• EEG - caused by an
• CT inadequate
• MRI circulating blood
• LP volume in the
intravascular bed.
Principle of Management: - results in a
- Goal: control seizure as quickly as possible, preventing decreased
recurrence, maintaining patient safety and identifying the venous return,
underlying cause. decrease preload
to the heart
Medications: leading to
1. Lorazepam (Ativan) – induces respiratory depression decreased
2. Flumazenil (Romazicon) – decrease respiratory depression cardiac output
3. Phenytoin via central venous line
4. Phenobarbital (Luminal) - causing hypotension that may results to inadequate tissue
perfusion, causing cellular hypoxia, organ failure, and death
Patient education on DOs
- Ease the person to the floor.
- Turn the person gently onto one side. This will help the person
breathe.
- Clear the area around the person of anything hard or sharp.
This can prevent injury.
- Put something soft and flat, like a folded jacket, under his or
her head.
- Remove eyeglasses.
- Loosen ties or anything around the neck that may make it hard
to breathe.
- Time the seizure.

Two Categories of Hypovolemic shock:

1. Absolute
hypovolemia -
occurs as a result
of fluid loss from
the intravascular
space.
Example:
hemorrhage,
gastrointestinal
loss such as from
Patient education on DON’Ts vomiting or
1. Do not hold the person down or try to stop his or her diarrhea, diabetes insipidus, diuresis, or fistula drainage.
movements.
2. Do not put anything in the person’s mouth. This can injure teeth
or the jaw. A person having a seizure cannot swallow his or her 2. Relative hypovolemia – occurs when the fluid volume moves
tongue. out from the vascular space into extravascular space due to
3. Do not try to give mouth-to-mouth breaths (like CPR). People vasodilation and an increase in vascular capacitance.
usually start breathing again on their own after a seizure. - also termed as third spacing
4. Do not offer the person water or food until he or she is fully Example:
alert….. - increased cutaneous vasodilation from heat stress, hypoxia,
WEEK 15: ASSESSMENT OF CRITICALLY ILL CLIENTS WITH intense physical exercise, or systemic vasodilation from sepsis,
SHOCK AND MODS Burn injuries, ascites
Shock
- can be defined as a condition in which widespread perfusion CARDIOGENIC SHOCK
to the cells are inadequate to deliver oxygen and nutrients to - is a kind of shock during which the heart does not adequately
support the vital organs and cellular functions. pump enough blood to the body’s tissues.
- common to all types of shock - Which may result to decrease in the delivery of oxygen to the
o Hypoperfusion of tissue organs causing failure to its function and eventually break
o Hypermetabolism down or cellular destruction and die.
o Activation of the inflammatory response - The most common cause of cardiogenic shock is heart attack.
The 4 Main types of Shock Patients at risk for developing cardiogenic shock
1. Hypovolemic shock
- Acute MI (STEMI)
2. Cardiogenic shock
3. Distributive shock - Atrial thrombus
4. Obstructive shock - Cardiac contusion
- Cardiac tamponade Neurogenic shock
- Cardiac tumor - It is a combination of both
primary and secondary
- Cardiomyopathy injuries that lead to loss of
- Cardiopulmonary arrest sympathetic tone and thus
- Dysrhythmias unopposed
parasympathetic response
- Endocarditis
driven by the vagus nerve.
- Myocarditis
- Consequently, patients
- Open heart surgery suffer from instability in
- Pheochromocytoma blood pressure, heart rate,
- Pneumothorax and temperature
regulation.
- Pulmonary embolus Septic Shock
- Septic shock - It is an inflammatory response.
- •Ventricular aneurysm - The septic process is initiated by the launch of immune
- Valvular dysfunction (mitral or aortic regurgitation, mitral mediators that are part of the inflammatory reaction.
stenosis) - Eventually the immune system is overwhelmed, and the
process actually harms the body.
Obstructive Shock
- Systemic inflammatory response syndrome (SIRS)
- is a condition that prevents blood and oxygen from getting into
the organs due to the obstruction in the great vessels or major - refers to a host’s response to a variety of clinical
blood vessels connected to the heart. - insults, both infectious and noninfectious, and is
Examples include: - part of the acute sepsis process
- A large blood clot in your pulmonary artery. - The patient in septic shock can exhibit skin lesions that are
- Fluid around the heart. most often located on the lower extremities.
- High pressures in the chest because of a lung injury such as a - These lesions can be associated with the development of
tension pneumothorax disseminated intravascular coagulation (DIC), which is another
- collapse of the lungs. complication of septic shock; the lesions can also be
associated with the causative bacteria.
Distributive Shock - Hyperglycemia can be the first indicator of sepsis in the
- Also called circulatory shock is a medical emergency where in patient with diabetes
the body can’t get enough blood to the heart, brain and - is a distributive shock characterized by tachycardia,
kidneys. hyperthermia or hypothermia, and hypotension caused by
- This happens because the blood vessels are extremely dilated decreased SVR.
(flaccid or relaxed), which brings down the blood pressure and - A decline in SVR is one of the first indications of shock.
unable to deliver enough blood to the organs. - The blood volume is adequate but misplaced.
- fluid is lost in the interstitial space.
- Renal involvement during sepsis can vary from a minor
proteinuria to acute tubular necrosis (ATN) in septic shock.

Patients at greatest risk for septic shock

Compensatory Mechanisms
- is a self-protective process to maintain the whole physiological
function of the body.
Three Types of Distributive Shock:
Septic shock - caused by a bacterial infection.
Anaphylactic shock - caused by an allergic reaction or asthma
attack.
Neurogenic shock - caused by a damage from a spinal cord or
injuries in the nervous system.

Anaphylactic Shock
- It is a rare but severe allergic reaction that can be deadly if
not treated right away.
- It's most often caused by an allergy to food, insect bites, or
certain medications.
- A shot of epinephrine is needed immediately
 - Confusion
Compost of a number of physiologic events:
A. Neural - Lethargy
- Pressoreceptors or baroreceptors – they sense the BP and Peripheral Effects:
relay the information to the brain so that the normal BP can be
maintained. - Skin causing cold clammy
B. Hormonal
Hepatic Effects:
- Catecholamines
- Impaired metabolism and phagocytic functions
- ACTH – regulates the BP, blood sugar, immune system in
- Increase Ammonia and Lactic Acid
- response to stress
- Gluconeogenesis and glycogenolysis are impaired
- RAAS – regulates blood volume, electrolyte balance and
systemic vascular resistance. - Infection
- Compensatory mechanisms include baroreceptor reflex, which - Liver enzyme are increased
causes an increased heart rate and vasomotor tone. - Jaundice
- The SNS is stimulated, which results in the release of
Gastrointestinal Effects and Manifestations:
epinephrine and norepinephrine, which causes systemic
vasoconstriction. - causing hypoactive bowel movement
- This release causes blood to be shunted to the vital organs - Stress Ulcers in Stomach – risk for bleeding
- bloody diarrhea
Kidney Effects:
- bacterial toxins translocation
- decrease renal blood flow and decrease in glomerular filtration
rate causing a decrease in urine output General Management and strategies in Shock
- initiation of the (RAAS) renin-angiotensin (I and II) and
aldosterone system which may results in vasoconstriction and
sodium and water retention.
- The retention of sodium and water is the body’s attempt to
compensate for the decrease in blood flow by increasing the
venous return to the heart and possibly increasing the patient’s
BP.
- Continued decrease in blood flow to the vital organs ultimately
causes tissue ischemia and acidosis from anaerobic
metabolism.
- Anaerobic metabolism leads to depletion of cellular ATP and
the failure of the sodium-potassium pump, which results in
further hemodynamic compromise and an inability to maintain
BP

Renal Effects and Manifestations:

- Decrease MAP – due to the GFR cannot
- maintained
- Identify the cause of shock
- ARF may develop
- Fluid replacement
- Increased in BUN, Creatinine level
- Medication therapy
- Loss of renal hormonal regulation for BP
- UO decreases to < 0.5 ml/kg/hr - Maintain adequate tissue perfusion

Fluid resuscitation
Cardiac effects:
- Administer in all types of shock
- increased in cardiac contractions
- Improve cardiac, tissue oxygenation
- increased in heart rate > 150bpm
- crystalloids
- increased in cardiac output
o an electrolyte solutions that move freely between
- dysrhythmias and ischemia intravascular and interstitial spaces
- chest pain or myocardial infarction - colloids
- increase in CK-MB and Troponin o large molecule IV solutions
- increase in BNP – B type Natriuretic Peptide - blood components
o PRBC, FFP, and platelets
Respiratory Effects: MEDICATION THERAPHY
- Tachypnea – one of the first signs that reflex reduced blood MEDICATION DESIRED ACTION IN SHOCK
flow and oxygen transport Inotropic Agents Improve contractility, increase
- crackles are heard over the lung fields • Dobutamine (Dobutrex) stroke volume, increase cardiac
• Dopamine output
- decreased in pulmonary blood flow causes arterial oxygen • Epinephrine (Adrenalin)
level to decrease and carbon dioxide increase. • Milrinone
- alveolar collapse Vasodilators Reduce preload and afterload.
- pulmonary edema • Nitroglycerine Reduce oxygen demand in the
- The patient may progress into acute respiratory distress • Nitroprusside heart
syndrome (ARDS) Vasopressor agents Increase blood pressure by
• Norepinephrine (Levophed) vasoconstriction
Neurologic Effects: • Dopamine
• Phenylephrine
- Mental Status • Vasopressin
- Subtle changes in behavior or agitation
Monitoring tissue perfusion - Heart Rate : tachycardia > 90 beats/minute
- Monitor level of consciousness, vital signs and urine - Respiratory Rate : tachypnea > 20 breaths/min
output, skin and laboratories (base deficits and lactic acid
levels) - White Blood Cells : leukocytosis > 12X109 /l or leucopenia <
4x 109 /l
- report vital signs Multiorgan Dysfunction Syndrome
- Pulse pressure 30-40mmHg • Multiorgan dysfunction syndrome (MODS) is the progressive
dysfunction of more than one organ in patients who are
Nutritional support critically ill or injured.
- more than 3000 calories • It is the leading cause of death in ICU.
- early in shock: depletion of glycogen stores in about 8 to Causes including, but not limited to:
10 hours • extensive burns
- parenteral nutrition • trauma
- enteral nutrition • cardiorespiratory failure
• multiple blood transfusions
- glutamine: fuel source for lymphocytes and macrophages
• systemic infection - most common
- antacids, H2 blockers (Famotidine, Ranitidine) -> stress
ulcers

Managing Hypovolemic Shock

Treatment of the underlying cause
• Fluid resuscitation or blood replacement
• Restore intravascular volume
• Administer fluids that will remain in the intravascular
compartment to avoid fluid shifts from intravascular to
intracellular

Blood transfusions
• Basis of BT
• Lack of response to fluid resuscitation
• Volume of blood lost
• Need for hemoglobin
• Correct coagulopathy
Patients at greatest risk for developing MODS
Managing Hypovolemic Shock • Patients with systemic infection (particularly, a gram-negative
• Fluid Replacement – first choice in emergency cases sepsis)
• Monitor closely for cardiovascular overload • Extensive burns
• Signs of difficulty in breathing • End-organ failure
• Signs of Pulmonary edema • Pancreatitis
• Vital Signs monitoring • Hypovolemia
• Watch out for Jugular vein distention • Cardiogenic shock
• Report in any changes and abnormalities in BP, HR, Rhythm, • Human immunodeficiency virus (HIV)
RR, lung sounds CVP and MAP. • Aspiration
• Parameters: • Multiple blood transfusions
- Hemodynamic pressure monitoring • Trauma
- vital signs Nursing intervention:
- ABG analysis prevention and treatment of infection:
- Lactate or Lactic acid levels 1. aggressive infefction control and strategies
2. inititate broad spectrum and antibiotics therapy
- Hgb & Hct 3. early aggressive surgery to remove necrotic tissue
- Intake and Output 4. aggressive pulmonary management
5. strict aseptic techniques
Managing Cardiogenic shock
GOAL: Prognosis
- limit further myocardial damage • Mortality is high with MODS
• Potential for recovery depends on:
- preserve the health myocardium
o the severity of illness or injury
o improve cardiac function
o underlying organ reserve
o increasing cardiac contractility
o the speed of instituting effective treatment
o decreasing ventricular afterload
o the adequacy of treatment
- treat the underlying cause o and the number and severity of subsequent injuries and
- Preserving the patient energy complications.
- Relief the angina • If treatment is unsuccessful, death usually occurs between 21
and
- Oxygen supplementation • 28 days after the initial insult.
Managing Anaphylactic shock Terminologies
Epinephrine (SUBCUTANEOUSLY) - Distributive shock – this is also called circulatory shock, the primary
- 0.2 TO 0.5 of a 1:1000 solution cause of decreasing BP is massive vasodilation of blood into the
peripheral vessels. Anaphylactic, Septic and Neurogenic shock are
- may be repeated every 10-15 minutes
distributive shock
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)
- MODS – Multiorgan dysfunction syndrome
- SIRS is the body’s response to an infectious or noninfectious
- Shock – inadequate tissue perfusion
insult affecting the whole body
- Systemic Inflammatory Response Syndrome (SIRS) – is the body’s
response to an infectious or noninfectious insult affecting the whole
Criteria of SIRS: at least two of the following:
body
- Temperature : hyperthermia > 38 C or hypothermia < 36.0 C