Shock

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 OVERVIEW1.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 kidneysabsorption of fluid from ISF and GIT, increased thirst

In this compensatory stage of shock, the patient’s 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 O₂ levels and increased CO₂ levels▪ Alveolar collapse▪ Pulmonary edema▪ Interstitial inflammation and fibrosis▪ ARDS

SHOCK: AN OVERVIEW

PROGRESSIVE STAGE: ASSESSMENT AND DIAGNOSTIC FINDINGS cont’d.. CARDIOVASCULAR EFFECTS

Dysrhythmias and ischemia Rapid heart rate Chest pain Rise in cardiac enzyme levels Further impairment of the heart’s pumping

capacity

SHOCK: AN OVERVIEW

PROGRESSIVE STAGE: ASSESSMENT AND DIAGNOSTIC FINDINGS cont’d.. NEUROLOGIC EFFECTS

Confusion Subtle change in behaviour Lethargy Sluggish pupillary reactions

SHOCK: AN OVERVIEW

PROGRESSIVE STAGE: ASSESSMENT AND DIAGNOSTIC FINDINGS cont’d.. 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 cont’d.. HEPATIC EFFECTS

Increased liver enzymes Decreased metabolic and phagocytic

actions Elevated bilirubin levels

SHOCK: AN OVERVIEW

PROGRESSIVE STAGE: ASSESSMENT AND DIAGNOSTIC FINDINGS cont’d.. GASTROINTESTINAL EFFECTS

Gastric stress ulcers Bloody diarrhea Increased risk of bleeding and infection

SHOCK: AN OVERVIEW

PROGRESSIVE STAGE: ASSESSMENT AND DIAGNOSTIC FINDINGS cont’d.. 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

patient’s 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 patient’s status.

SHOCK: AN OVERVIEW

PROGRESSIVE STAGE: SUMMARY OF CLINICAL FINDINGS Blood pressure

Systolic <80-90 mmHg Heart rate

>150 bpm Respiratory status

Rapid, shallow respirations; crackles Skin

Mottled, petechiae Urinary output

0.5 mL/kg/hr Mentation

Lethargy 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 Heart rate

Erratic or asystole Respiratory status

Requires intubation Skin

Jaundice Urinary output

Anuric, requires dialysis Mentation

Unconscious 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

HYPOVOLEMICEXTRACARDIAC Obstruction

CARDIOGENIC DISTRIBUTIVE

Fluid loss,hemorrhage

e.g., Pericardial tamponade

Myocardialinjury ornecrosis

Decreasedsystemicvascularresistance

Myocardiacdysfunction

Reducedsystolic performance

Reducedfilling

Low cardiacoutput

Reducedpreload

Decreased arterialpressure

Shock

Multiple organsystem failure

High or normalcardiac output

Maldistributionof blood flow inmicrocirculation

DIFFERENT TYPES OF SHOCK

CARDIOGENIC SHOCK

CARDIOGENIC SHOCK

CARDIOGENIC SHOCK Occurs when the heart’s 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

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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)

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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 O₂▪ 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 cont’d.. 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

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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

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

Blood pressure: increases then decreases

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)

SEDATIVES CHRONOTROPIC AGENTS INOTROPIC AGENTS VASODILATORS VASOCONSTRICTORS BETA-BLOCKERS DIURETICS

PHYSICAL EXAMINATION AND MONITORING

Immediate Management : POSITION

Immediate control of bleeding

Compression bandages/pressure 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. Calculate total blood volume2. Determine the % of blood loss3. Multiple total blood volume by the %

loss4. Replacement by:5. Colloid fluids, 1.5 times the result in

step 3.6. Crystalloid fluids, 4 times the result

in step 3.

Blood: – 500 ml whole blood increases Hct 2-

3%, 250ml Packed RBC’s 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

▪ O₂ administration

CIRCULATORY SHOCK

CIRCULATORY/DISTRIBUTIVE SHOCKCIRCULATORY 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 38°C or less than 36°C

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 Shock3) 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 tube6) Prior antibiotic treatment7) Prolonged hospitalization8) Childbirth, abortion9) 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 positive blood test.

Hypotension, despite adequate fluid replacement.

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

Heart rate > 90bpm. Body Temp < 36 or > 38˚C. Hyperventilation. White blood cell count < 4000 cells/ mm3 or

>12000 cells/mm3.

Diagnostic Criteria

SIRSRequires 2 of the following:

Severe SIRSMust meet criteria for SIRS, plus 1 of the

following:a. Temp >38.3° or <36.0° Cb. Tachypnea (RR>20 )c. Tachycardia (HR>90, in the

absence of intrinsic heart disease)

d. WBC > 10,000/mm3

a. Altered mental statusb. SBP<90mmHg or fall of >40mmHg from

baselinec. Impaired gas exchanged. Lactic acidosis (pH<7.30 & lactate > 1.5 x

upper limit of normal)e. Oliguria or renal failure (<0.5mL/kg/hr)f. Hyperbilirubinemiag. Coagulopathy (platelets < 80,000-100,000/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 syndr

ome 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

*Hemodynamic phenomenon- * Loss of vasomotor tone & Loss of sympathetic nervous system tone > impaired cellular metabolism

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 bradycardiaspinal 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

Decreased SVR

Reduction in vascular tone

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 Shock- Management

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 -pacemakermethylprednisolone -used only for blunt injury - high dose therapy for 23 hrs - must be started within 8 hrscontroversial –risk for infection ,GI bleed-monitor temp-provide supplementary o2- Alpha agonist to augment tone if perfusion still inadequatedopamine 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 Hypotentiono hives (urticaria)o Itcho 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 capillarypermeability

Peripheralvasodilation Constriction of

Smooth Muscle, BronchospasmLaryngospasm GI tract cramps

Fluid leaves Intravascular space

Oedema

Decreased SVR

Hypovolaemia

CO

tissue perfusion

Impaired cellular metabolism

Fig 4: Anaphylacticshock

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

• ABC’s• 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