SHOCK

Definition
Shock is defined as:
A physiologic state in which there is inadequate blood

flow to tissues and cells of the body Brunner & Suddarth, 2004 A condition in which systemic blood pressure is inadequate to deliver oxygen and nutrients to support vital organs and cellular functions Mikhail, 1999

Definition of Shock
A clinical state in which blood flow is inadequate for tissue requirements or oxygen utilization is impaired. There is either insufficient oxygen delivery, maldistribution of oxygen delivery or impaired utilization

SHOCK: AN OVERVIEW
SIGNIFICANCE OF SHOCK:
Shock affect all body systems. It may develop

rapidly or slowly, depending on the underlying cause. Nursing care of the patient in shock requires ongoing systemic assessment.

Types of Shock
Cardiogenic (intracardiac vs extracardiac) Hypovolemic Distributive
Septic neurogenic (spinal shock) anaphylactic

SHOCK: AN OVERVIEW
STAGES OF SHOCK
1. INITIAL STAGE 2. COMPENSATORY STAGE 3. PROGRESSIVE STAGE 4. IRREVERSIBLE STAGE

SHOCK: AN OVERVIEW
1.INITIAL STAGE
Cells deprived of O2 mitochondria cannot produce

ATP anaerobic respiration lactic acid builds up metabolic acidosis harmful to cells

Hypoxia occur due to hypo perfusion state

Cell membrane damage Anaerobic respiration

Build up of lactic and pyruvic acid

Metabolic acidosis

SHOCK: AN OVERVIEW
2. COMPENSATORY STAGE

This stage is characterised by the body employing the physiological mech, indusial, hormonal, neural, bio chemical in an attempt to reverse the condition Hyperventillation to correct acidosis baroreceptor reflexes sympathetic stimulation constrict arteriols in most parts of the body and venous reservoirs protection of coronary and cerebral blood flow - angiotensin-aldosteron, ADH vasoconstriction, water and salt retention by the kidneys absorption of fluid from ISF and GIT, increased thirst
In this compensatory stage of shock, the patients blood pressure remains within normal limits. This results from stimulation of the sympathetic nervous system. The patient displays signs of fight-or-flight response There is blood shunting

SHOCK: AN OVERVIEW
COMPENSATORY STAGE CLINICAL MANIFESTATIONS
Blood pressure

normal
Heart rate

>100 bpm
Respiratory status

>20 breaths/minute
Skin

cold and clammy

Urinary output (UO)

decreased
Mentation

confusion
Acid-base balance

Respiratory alkalosis

SHOCK: AN OVERVIEW
Compensatory stage
NURSING MANAGEMENT Monitoring tissue perfusion
Changes in LOC V/S UO Skin Lab values Hemodynamic status Administer IVF and meds

Reducing anxiety Promoting safety

SHOCK: AN OVERVIEW
2. PROGRESSIVE STAGE it should cause the crisis not been successfully

treat the shock will proceed to the progressive stage and the compensatory mechanism begins to fail
In the progressive stage of shock, the mechanisms

that regulate blood pressure can no longer compensate and the mean arterial pressure (MAP) falls below normal limits, with an average systolic blood pressure of less than 90 mm/Hg.

- circulatory system themselves begin to deteriorate,

without therapy shock becomes steadily worse until death - positive feedback mechanisms are developed and can cause vicious circle of progressively decreasing CO - Cardiac depression - coronary blood flow, contractility - Vasomotor failure - cerebral blood flow Release of toxins by ischemic tissues: histamine, serotonin, tissue enzymes Intestines hypoperfusion mucosal barrier disturbance endotoxin formation and absorption vasodilatation, cardiac depression Vasodilation in precapillary bed Generalised cellular deterioration: K+ , ATP, release of hydrolases first signs of multiorgan failure

SHOCK: AN OVERVIEW
PROGRESSIVE STAGE: PATHOPHYSIOLOGY
Although all organ system suffer from hypoperfusion

at this stage, two events perpetuate the shock syndrome:

(1)Cardiac dysfunction and; (2) Failure of the autoregulatory function of the microcirculation Even if the underlying cause of the shock is reversed, the breakdown of the circulatory system itself perpetuates the shock state, and a visual cycle ensues.

SHOCK: AN OVERVIEW
PROGRESSIVE STAGE: ASSESSMENT AND DIAGNOSTIC FINDINGS
As shock progresses, organs systems decompensate RESPIRATORY EFFECTS Rapid and shallow respirations Crackles Decreased O levels and increased CO levels Alveolar collapse Pulmonary edema Interstitial inflammation and fibrosis ARDS

SHOCK: AN OVERVIEW
PROGRESSIVE STAGE: ASSESSMENT AND

DIAGNOSTIC FINDINGS contd..

CARDIOVASCULAR EFFECTS Dysrhythmias and ischemia Rapid heart rate Chest pain Rise in cardiac enzyme levels Further impairment of the hearts pumping capacity

SHOCK: AN OVERVIEW
PROGRESSIVE STAGE: ASSESSMENT AND

DIAGNOSTIC FINDINGS contd..

NEUROLOGIC EFFECTS Confusion Subtle change in behaviour Lethargy Sluggish pupillary reactions

SHOCK: AN OVERVIEW
PROGRESSIVE STAGE: ASSESSMENT AND

DIAGNOSTIC FINDINGS contd..

RENAL EFFECTS Acute Renal Failure (ARF)
Increase in BUN Increase in serum creatinine Fluid and electrolyte shifts Acid-base imbalances Decrease in urinary output

SHOCK: AN OVERVIEW
PROGRESSIVE STAGE: ASSESSMENT AND

DIAGNOSTIC FINDINGS contd..

HEPATIC EFFECTS Increased liver enzymes Decreased metabolic and phagocytic actions Elevated bilirubin levels

SHOCK: AN OVERVIEW
PROGRESSIVE STAGE: ASSESSMENT AND

DIAGNOSTIC FINDINGS contd..

GASTROINTESTINAL EFFECTS Gastric stress ulcers Bloody diarrhea Increased risk of bleeding and infection

SHOCK: AN OVERVIEW
PROGRESSIVE STAGE: ASSESSMENT AND

DIAGNOSTIC FINDINGS contd..

HEMATOLOGIC EFFECTS Disseminated intravascular coagulation (DIC) Bruises Bleeding Prolonged coagulation times

SHOCK: AN OVERVIEW
PROGRESSIVE STAGE: MEDICAL

MANAGEMENT
Depends on the kind of shock and its underlying

cause IV fluids and medications Early enteral nutritional support and use of drugs to prevent GI ulcers and bleeding

SHOCK: AN OVERVIEW
PROGRESSIVE STAGE: NURSING MANAGEMENT
Patient in the progressive stage are often cared for in the ICU.

Proper documentation Preventing complications

Monitoring Maintaining aseptic technique Positioning and repositioning Preventing pulmonary and integumentary complications

Promoting rest and comfort

Efforts are made to minimize cardiac workload by reducing patients physical activity and fear or anxiety. Protection from excessive warmth or cold

Supporting family members

The nurse should make sure that the family is comfortably situated and kept informed about the patients status.

SHOCK: AN OVERVIEW
PROGRESSIVE STAGE: SUMMARY OF CLINICAL FINDINGS Blood pressure
Systolic <80-90 mmHg >150 bpm

Heart rate

Respiratory status Skin

Rapid, shallow respirations; crackles Mottled, petechiae 0.5 mL/kg/hr Lethargy

Urinary output Mentation

Acid-base balance
Metabolic acidosis

SHOCK: AN OVERVIEW
3. IRREVERSIBLE STAGE / REFRACTORY

STAGE
Represents the point along the shock continuum

at which organ damage is so severe that the patient does not respond to treatment and cannot survive Blood pressure remains low despite treatment Presence of an overwhelming metabolic acidosis Multiple organ dysfunction has occured and death is imminent

- despite therapy circulatory system continues

to deteriorate and death ensues marked hypoxic tissue damage - endothelial dysfunction adhesive molecules, neutrophils, macrophages inflammation

progressive acidosis - microcirculation failure plasma proteins leak to interstitium advanced disseminated intravascular coagulation

SHOCK: AN OVERVIEW
IRREVERSIBLE STAGE: SUMMARY OF CLINICAL FINDINGS Blood pressure
Requires mechanical or pharmacological support Erratic or asystole

Heart rate

Respiratory status Skin

Requires intubation

Urinary output Mentation

Anuric, requires dialysis Unconscious

Jaundice

Acid-base balance
Profound acidosis

SHOCK: AN OVERVIEW
IRREVERSIBLE STAGE: MEDICAL

MANAGEMENT
Usually the same as for the progressive stage
Experimental strategies may also be employed Antibiotic agents

EXTRACARDIAC HYPOVOLEMIC
Obstruction

CARDIOGENIC

DISTRIBUTIVE

Fluid loss, hemorrhage

e.g., Pericardial tamponade

Myocardial injury or necrosis

Decreased systemic vascular resistance

Reduced filling Reduced preload Low cardiac output

Reduced systolic performance Myocardiac dysfunction

Decreased arterial pressure

High or normal cardiac output

Shock Maldistribution of blood flow in microcirculation

Multiple organ system failure

DIFFERENT TYPES OF SHOCK

CARDIOGENIC SHOCK
CARDIOGENIC SHOCK
Occurs when the hearts ability to contract and

pump blood is impaired and the supply of oxygen is inadequate Causes:

Coronary
Myocardial Infarction

MI (most common) Aortic dissection PE Cardiac tamponade Ruptured viscus Hemorrhage Sepsis Cardiomyopathy (restrictive or dilated), myocarditis Medication overdose (beta/calcium-channel blockers) Cardiotoxic drugs (doxorubicin) Electrolyte abnormalities (calcium, phosphate) Valvular abnormalities (mitral/aortic stenosis) Papillary muscle or ventricular free wall rupture

Risk Factors for Developing CS

Older age Multivessel CAD Anterior MI location STEMI or LBBB HTN DM Prior MI

Prior CHF
33

Cardiogenic Shock, intracardiac

Myocardial Injury or Obstruction to Flow
Arrhythmias valvular lesions AMI Severe CHF

VSD
Hypertrophic Cardiomyopathy

Cardiogenic Shock, extracardiac (Obstructive)

Pulmonary Embolism Cardiac Tamponade Tension Pneumothorax Presentation will be according to underlying

disease process.

CARDIOGENIC SHOCK
CLINICAL MANIFESTATIONS

Angina pain Dysrhythmias Hemodynamic stability Rapid thready pulse JVD Pulmonary Edema oliguria Restless Hypotension Increase cvp Dependent edema Skin- pale, cyanotic, cold & moist

Differential Diagnoses (limited)

MI

Tension PTX
Aortic dissection PE

Cardiac tamponade
Ruptured viscus Valvular abnormalities (mitral/aortic stenosis)

37

Diagnosis
ECG ECHO Chest X-Ray Cardiac enzymes

 MEDICAL MANAGEMENT
Goals: 1. Limit further myocardial damage and preserve the healthy myocardium 2. Improve the cardiac function

CARDIOGENIC SHOCK
MEDICAL MANAGEMENT
Correction of underlying causes Coronary cardiogenic shock: thrombolytic therapy, angioplasty, CABG Non coronary: cardiac valve replacement, or correction of a dysrhythmia Initiation of first-line treatment Supplying supplemental O Controlling chest pain Providing selected fluid support Administering vasoactive medications Dobutamine, dopamine, Controlling heart rate with medication or by implantation of a transthoracic or intravenous pacemaker Implementing mechanical cardiac support

CARDIOGENIC SHOCK
MEDICAL MANAGEMENT: FIRST-LINE TREATMENTS

Pain control: MORPHINE Hemodynamic monitoring

Measures:
Pulmonary artery pressures Cardiac output Pulmonary and systemic resistance

Pharmacologic therapy
Dobutamine
Increases strength of myocardial contraction Decreases pulmonary and systemic resistance

Nitroglycerin
Venous dilator Arterial dilator

Dopamine
Low-dose Medium-dose High-dose

Other Vasoactive medications

CARDIOGENIC SHOCK
MEDICAL MANAGEMENT: FIRST-LINE

TREATMENTS contd..
Fluid therapy
Mechanical assistive devices Intra-aortic balloon counterpulasation Left and right ventricular assist devices

Pharmacologic Treatment of Cardiogenic Shock

SBP <70 mm Hg + shock
Norepinephrine

SBP 70-100 mm Hg + shock

Dopamine

SBP 70-100 mm Hg shock

Dobutamine

Refractory hypotension + shock

Amrinone or milrinone may improve cardiac

output
43

CARDIOGENIC SHOCK
NURSING MANAGEMENT
Preventing cardiogenic shock Monitoring hemodynamic status Administering medications and IV fluids Maintaining Intra-aortic balloon counter pulsation

Enhancing safety and comfort

Hypovolemic Shock
Definition: Reduction in intravascular volume leading to insufficient oxygen delivery to cells (mitochondria)

HYPOVOLEMIC SHOCK
1. HYPOVOLEMIC SHOCK
Characterized by a decrease in intravascular

volume Occurs when there is a reduction in intravascular volume of 15% to 25% Can be caused by:
External fluid losses Internal fluid losses

PATHOPHYSIOLOGY
Loss of blood decreased filling of the right heart( dec. in venous return) decrease of filling of the pulmonary vasculature decreases filling of the left atrium and ventricle left ventricular stroke volume decreases Drop in arterial pressure which leads to reduced perfusion to vital organs leading to multiple organ failure and finally death if untreated

Etiology
Reduced circulating blood volume with secondary decreased cardiac output
Acute hemorrhage

Vomiting/Diarrhea
Dehydration Burns Peritonitis/Pancreatitis Third spacing Diabetics diuretics

Etiology
Non haemorrhagic Vomitting,diarrhoea Bowel obstruction ,pancreatitis Burns Neglect ,environmental(dehydration) Haemorrhagic Gl bleed Trauma Massive haemoptysis Ectopic pregnancy ,PPH

Clinical manifestation
Hypotensive flat neck veins clear lungs cool, cyanotic extremities evidence of bleeding?
Anticoagulant use trauma, bruising

oliguria

Clinical features
Skin: cool, moist, pale skin Resp. rate: rate and depth

are increased

Heart rate: pulse is weak

and thready, MAP is decreased, pulse pressure is narrow then decreases

Blood pressure: increases Urine output: decreased Mentation: Loss of

consciousness, restlessness, agitation, mild confusion

HYPOVOLEMIC SHOCK
MEDICAL MANAGEMENT
Major goals

Restore intravascular volume Redistribute fluid volume Reverse the underlying cause Treatment of the underlying cause Haemorrhage Diarrhoea/vomiting Fluid and blood replacement Insert two large-gauge IV line Administration of isotonic crystalloids Administration of blood and blood products Redistribution of fluid Pharmacologic therapy Drugs used in cardiogenic shock Also depends on the cause of hypovolemia

Management : A,B,C,D
IMMEDIATE MANAGEMENT RESUSCITATION : EXTRACELLULAR FLUID REPLACEMENT :-maintenance of

circulation and B.P

maintenance of patent airway(A), and breathing(B) IMMEDIATE CONTROL OF BLEEDING QUICK ASSESSMENT EXTRACELLULAR FLUID REPLACEMENT :-maintenance of circulation and B.P DRUGS : (D)

PHYSICAL EXAMINATION AND MONITORING

SEDATIVES CHRONOTROPIC AGENTS INOTROPIC AGENTS VASODILATORS VASOCONSTRICTORS BETA-BLOCKERS DIURETICS

Immediate Management : POSITION

Immediate control of bleeding

Compression

bandages/pressur e packs
Local haemostatic

agents
ElectroCautery Ligature of vessels

 Surgical management

vascular repair surgical haemostasis closure of bleeding ulcer

Quick examination
The patients clothing is cut away & the whole body is

visualized, palpated & examined for other injuries or bleeding sites. Assessment of blood loss :

Blood loss with fractures considered as :1,000 to 2,000 mL for pelvic fractures, 500 to 1,000 mL for femur fractures,

250 to 500 mL for tibia or humerus fractures,

125 to 250 mL for fractures of smaller bones.

A hematoma the size of an apple usually contains at least 500 mL of blood.

Neurological examination :
Glasgow coma scale

Fluid replacement
Crystalloids : Fluid replacement should be started with a

crystalloid
3 liters. Over a time of 45 min is sufficient or depends on the vital

signs(pulse, b.p, CVP,urine output)

In the mean time blood should be sent for cross matching

Colloids: (ex: albumin)

Will increase osmotic pressure, watch for pulmonary edema Remains in vascular space longer (several hrs)

How much Fluid?

1. 2. 3. 4. 5. 6. Calculate total blood volume Determine the % of blood loss Multiple total blood volume by the % loss Replacement by: Colloid fluids, 1.5 times the result in step 3. Crystalloid fluids, 4 times the result in step 3.

 Blood: 500 ml whole blood increases Hct 2-3%, 250ml Packed RBCs increases Hct 3-4%

Drugs (common in all types)

Sedatives : to reduce pain
Morphine : 10 mg IM Pethidine : 100 mg IM

Chronotropic agents : increases H.R

Adrenaline : 1-8 mcg/min

Ionotropic agents : inc. cardiac contractility

Dopamine : 3-10 mcg/min

Vasoconstrictors
Phenylephrine : 20 mcg/min

Central Venous Pressure

Normal value : 10-15 mm of Hg In hypovolemic shock, the blood volume is decreased, so is the CVP is also decreased. In cardiogenic shock there is no depletion of blood volume and the CVP remains normal.

Urine
Urine output is a good indication of severity of shock.

Urine output is affected quite early even in moderate shock. It is also a good index of adequacy of replacement therapy. Normal output : 60-70 ml/hr. In shock : <30 ml/hr

HYPOVOLEMIC SHOCK
NURSING MANAGEMENT
Primary focus: prevention of shock, if possible Otherwise, nursing interventions focus on assisting

with treatment targeted at treating its cause and restoring intravascular volume.
Administering blood and fluids safely
Obtain blood specimens Monitor for potential complications Hemodynamic monitoring, vital signs, ABG, Hgb&Hct, temp., physical assessment

Implementing other measures

O administration

CIRCULATORY/DISTRIBUTIVE SHOCK
CIRCULATORY SHOCK
Occurs when blood volume is abnormally displaced in

the vasculature for example, when blood volume pools in peripheral blood vessels. The displacement causes a relative hypovolemia Causes:
Loss of sympathetic tone Release of biochemical mediators by cells
Three types: 1. Septic shock 2. Neurogenic shock 3. Anaphylactic shock

Septic Shock

Definition
Shock:- When the cardiovascular system fails to deliver

enough oxygen and nutrients to meet cellular metabolic needs.

Sepsis:- Presence of bacteria in the blood stream. Septic Shock:- Begins with the development of

septicaemia usually from bacterial infections, but can be viral in origin. This is the most common type of Distributive Shock.

CIRCULATORY SHOCK: SEPTIC SHOCK

1. SEPTIC SHOCK
Most common type; caused by widespread

infection The greatest risk of sepsis occurs in patients with bacteraemia and pneumonia Risk factors in the increased incidence of septic shock:
Increased number of immunocompromised patients Increased incidence of invasive procedures Increased number of resistant microorganisms Increase in the older population

Septic Shock
Results due to a severe infections Usually a bacterial infection(gram-negative bacteria) Definitions: SIRS (Systemic inflammatory response syndrome Severe SIRS Sepsis Severe Sepsis Septic Shock

Septic Shock
Systemic inflammatory response syndrome (SIRS): The systemic inflammatory response to a wide variety of severe clinical insults manifests by 2 or more of the following conditions: Temperature greater than 38C or less than 36C Heart rate greater than 90 beats per minute (bpm) Respiratory rate greater than 20 breaths per minute or PaCO2 less than 32 mm Hg White blood cell count greater than 12,000/mL, less than 4000/mL, or 10% immature (band) forms

Septic Shock
Causes
1)Lower respiratory tract infections
>Streptococcus pneumonia >Klebsiella pneumonia >Staphylococcus aureus >Escherichia coli >Legionella species >Haemophilus species >Anaerobes >Gram-negative bacteria >Fungi

Septic Shock
2)Urinary tract infections
>E coli >Proteus species >Klebsiella species >Pseudomonas species >Enterobacter species >Serratia species

Septic Shock
3) GI tract infections
E coli Streptococcus faecalis Bacteroides fragilis Acinetobacter species Pseudomonas species Enterobacter species Salmonella species

Septic Shock
5) Invasive procedures Catheters Intravascular devices Prosthetic devices Hemodialysis and peritoneal dialysis catheters Endotracheal tube 6) Prior antibiotic treatment 7) Prolonged hospitalization 8) Childbirth, abortion 9) Other factors Malnutrition

Pathophysiology
MO invades body tissues immune response release of chemical mediators vasodilatation & micro thrombi formation obstruction of blood flow to tissue & organs hypoxia lactic acidosis

Dignosis
Vital signs

Narrow pulse pressure and tachycardia

Peripheral vasodilatation warm shock

Stroke volume and cardiac out put decrease

Altered mental status and oliguria

Work up

Lab Studies Imaging Studies

Lab studies
Serum chemistry Serum electrolyte Platelet WBC PT &APTT LFT Blood & urine culture

Gram staining

Imaging studies
CT X-RAY MRI

Diagnosis
To diagnose septic shock, the following two criteria must be met:
Evidence of infection, through a

In addition, two out of four of the following must be present also:

Heart rate > 90bpm. Body Temp < 36 or > 38C. Hyperventilation. White blood cell count

positive blood test.

Hypotension, despite adequate

fluid replacement.

<

4000 cells/ mm3 or >12000 cells/mm3.

Diagnostic Criteria
SIRS Requires 2 of the following: a. Temp >38.3 or <36.0 C b. Tachypnea (RR>20 ) c. Tachycardia (HR>90, in the absence of intrinsic heart disease) d. WBC > 10,000/mm3 Severe SIRS Must meet criteria for SIRS, plus 1 of the following: a. Altered mental status b. SBP<90mmHg or fall of >40mmHg from baseline c. Impaired gas exchange d. Lactic acidosis (pH<7.30 & lactate > 1.5 x upper limit of normal) e. Oliguria or renal failure (<0.5mL/kg/hr) f. Hyperbilirubinemia g. Coagulopathy (platelets < 80,000100,000/mm3, INR >2.0, PTT >1.5 x control, or elevated fibrin degredation products)

Management of Septic Shock

Early goal directed therapy Identification of source of infection Broad Spectrum Antibiotics IV fluids Vasopressors Steroids ?? Recombinant human activated protein C ( Xygris) Bicarbonate if pH < 7.1

Treatments
Fluid resuscitation Vasopressors Antibiotics initially : empirical antibiotics later : specific antibiotics(based on appropriate culture and

sensitivity test) Empirical therapy Cephalothin (6 to 8 Gm/day I.V. in 4 to 6 divided doses), Gentamicin ( 5 mg/Kg./,day ), Clindamycin (particularly when infecting organism is Bacteroids) Nutritional therapy Enteral rather than parenteral route

 Respiratory Support Transfusions Recombinant Activated Protein C Corticosteroids Glycemic Control

CIRCULATORY SHOCK: SEPTIC SHOCK

SEPTIC SHOCK: NURSING MANAGEMENT

Use strict septic technique in all procedures Monitor for signs of infection Obtain appropriate specimens for C&S Address an elevated body temperature
Administer acetaminophen as prescribed Provide hypothermia blankets Monitor for shivering Provide comfort

Adminidtration of prescribed IV fluids and medications Monitor blood levels of medications, BUN, creatinine, WBC Monitor other values

Hemodynamic status I&O Nutritional status

Complication
Septic shock Acute respiratory distress syndrome Arrhythmias DIC Hepatic and renal failure Fetal and maternal death

Neurogenic shock

Definition
Definition:

hypotension as a result of the loss of sympathetic vascular tone below the level of spinal cord injury
phenomenon * Loss of vasomotor tone & Loss of sympathetic nervous system tone > impaired cellular metabolism

*Hemodynamic

Occurs
Within 30 min cord injury level T 5

or above; last up to 6 weeks; also due to effect some drugs that effect vasomotor center of medulla as opioids, benzodiazepines

 Spinal shock & neurogenic shock can in same

patient-BUT not same disorder

Mechanism: Loss of autonomic

innervation of the cardiovascular system (arterioles, venules, small veins, including the heart)

 -it occur after acute spinal shock

-sympathetic outflow is disrupted leaving unopposed vagal tone -result in hypotension and bradycardia spinal shock temporary loss of spinal reflex activity below a total spinal cord injury

Neurogenic Shock
Causes:
1. Spinal cord injury 2. Drugs

3. Regional anesthesia
4. Neurological disorders

Imbalance bet: sympathetic & parasympathetic stimulation

Massive vasodilation

Reduction in vascular tone

Decreased SVR

Inadequate CO, falling BP

Tissus perfusion of O2&nutri

Impared cellular metabolism

Fig 3: NEUROGENIC SHOCK

Clinical manifestation

- Hypotension (due to massive vasodilatation

- Bradycardia- due to unopposed parasympathetic stimulation - Poikilothermia; *Unable to regulate temperature- CVP decrease - skin- pale and cool -oliguria to anuria -Flaccid paralysis below level of spinal cord injury

Risk factors
Spinal cord injury Spinal anaesthesia Depressed action of medication

Neurogenic ShockManagement fluid replacement Resuscitation initiation of vasopressor drugs to counteract vasodilatation. Administer atropine if bradycardia occurs

management

-keep MAP at 85-90mm Hg for first 7 days -thought to minimize secondary cord injury -if crystalloid is insufficient use vasopressure -search for other cause of hypotension -for bradycardia -atropine -pacemaker methylprednisolone -used only for blunt injury - high dose therapy for 23 hrs - must be started within 8 hrs controversial risk for infection ,GI bleed -monitor temp -provide supplementary o2 - Alpha agonist to augment tone if perfusion still inadequate dopamine at alpha doses (> 10 mcg/kg per min) ephedrine (12.5-25 mg IV every 3-4 hour)

Nursing Management
Elevate bed atleast 30 degree when patient

receiving spinal or epidural anaesthesia Carefully immoblize the patient to prevent complication
Support cardiovascular and neurologic function

Apply elastic compression stockings Monitor for and prevent complications associated with immobilty

Anaphylactic Shock

CIRCULATORY SHOCK: ANAPHYLACTIC SHOCK

ANAPHYLACTIC SHOCK:
A circulatory shock state resulting from a severe

allergic reaction producing an overwhelming systemic vasodilation and reactive hypovolemia There is widespread vasodilation and capillary permeability Can be prevented

 Anaphylaxis- rapid generalized

immunologically mediated events involving an antigen specific IgE mediated mechanism that occur after exposure to foreign substances in previously sensitized person - IgE mediated - Anaphylatoid reaction clinically indistinguishable from anaphylaxis ,do not require a sensitizing exposure - not IgE mediated

Anaphylactic Shock
Results from severe

allergic reaction Body responds to allergen by releasing histamine Histamine causes vessels to dilate and become leaky

Anaphylactic Shock

Anaphylactic Shock
Patients with anaphylaxis develop: o Hypotention
o hives (urticaria) o Itch o wheezing and difficulty

breathing (bronchospasm)
o angioedema

Antigen(allergen) meets antibody Body mounts an immune attack Release of chemicals such as Histamine, kinin, prostaglandin

Increased capillary permeability Fluid leaves Intravascular space

Peripheral vasodilation Decreased SVR Hypovolaemia

Constriction of Smooth Muscle, Bronchospasm Laryngospasm GI tract cramps

Oedema

CO
tissue perfusion

Fig 4: Anaphylactic shock

Impaired cellular metabolism

symptoms of anaphylaxis
First- Pruritus, flushing, urticaria appear Next- Throat fullness, anxiety, chest tightness,

shortness of breath and lightheadedness Finally- Altered mental status, respiratory distress and circulatory collapse Hypotension Pulmonary edema Warm skin Restless Anxious Abdominal cramp diarrhoea

management
ABCs
Angioedema and respiratory compromise require

immediate intubation Removing the causative antigen

IV, cardiac monitor, pulse oximetry IVFs, oxygen Epinephrine Second line
Corticosteriods H1 and H2 blockers

Anaphylactic Shock Management

1. basic and circulatory management. 2. Specific management. Includes immediate and late. Immediate Stop administering suspected agent and call for help Early intubation Client to be placed immediately in supine or Trendelenburg position with leg elevation to increase venous return. Start epinephrine IM. Repeat every 5-15 min. until improvement occurs in blood pressure. if need IV in severe cases.

 Replacement with crystalloids solution for rapid intravascular fluid volume expansion. Advanced life support measures if cardiac arrest occurs. Secondary (late)- Management IV epinephrine if hypotension persist. Atropine in cases with significant bradycardia IV salbutamol if brancho spasm persist. If need Anti histamines preferable Refer to critical care centers

 Epinephrine
0.3-0.5 mg IM Repeat every 5-10 min as needed Caution with patients taking beta blockers- can cause

severe hypertension due to unopposed alpha stimulation For CV collapse, 1 mg IV If refractory, start IV drip

 Corticosteroids
Methylprednisolone 125 mg IV Prednisone 60 mg PO

Antihistamines
H1 blocker- Diphenhydramine 25-50 mg IV H2 blocker- Ranitidine 50 mg IV

Bronchodilators
Albuterol nebulizer Atrovent nebulizer Magnesium sulfate 2 g IV over 20 minutes

Glucagon
For patients taking beta blockers and with

refractory hypotension 1 mg IV q5 minutes until hypotension resolves

CIRCULATORY SHOCK: ANAPHYLACTIC SHOCK

NURSING MANAGEMENT
Assess all patients for allergies

Observe patient for allergic reaction when

administering new medications Identify patients at risk for anaphylaxis in diagnostic testing sites Be adept with the clinical signs of anaphylaxis, CPR and other emergency measures Teaching the client and the family about preventing future anaphylacticc episodes and administering emergency medications to treat anaphylaxis