MEDICAL SURGICAL NURSING DISCUSSION

ON

SHOCK

SUBMITTED TO BY MISS LIYA JOHN KAUR LECTURER NURSING 2ND YEAR

SUBMITTED NAVPREET M.Sc.

MEDICAL SURGICAL NURSING DATE: 13-02-2013

SHOCK
INTRODUTION: Shock is a serious, life-threatening medical emergency and one of the most common causes of death for critically ill people. The process of blood entering the tissues is called perfusion, so when perfusion is not occurring properly this is called a hypoperfusional. DEFINITION: Shock is a clinical syndrome characterized by a systematic imbalance between oxygen supply and demand. This imbalance results in a state of inadequate blood flow to body organs and tissue, causing life-threatening cellular dysfunctions. Shock is a syndrome characterized by decreased tissue perfusion and impaired cellular metabolism. This results in as imbalance between the supply of and demand for oxygen and nutrients. The exchange of oxygen and nutrients at the cellular level is associated to life. INCIDENCE: Both sexes are common Children and old age group more prone for shock 80% of mortality rate is caused by shock CLASSIFICATION OF SHOCK: In 1972 Hinshaw and Cox suggested the following classification which is still used today. It uses Four Types of Shock, 1. HYPOVOLEMIC SHOCK 2. CARDIOGENIC SHOCK 3. DISTRIBUTIVE SHOCK a. Septic Shock b. Anaphylactic Shock c. Neurogenic Shock 4. OBSTRUCTIVE SHOCK 5. ENDOCRINE SHOCK, (Recently a 5th form of shock has been introduced) 1. HYPOVOLEMIC SHOCK: This is the most common type of shock and based on insufficient circulating volume.

Its primary cause is loss of fluid from the circulation from either an internal or external source. An internal source may be haemorrhage. External causes may include extensive Bleeding, High Output Fistulae or Severe burns. 2. CARDIOGENIC SHOCK: This type of shock is caused by the failure of the heart to pump effectively. This can be due to damage to the heart muscle, most often from a large Myocardial infarction.

 Other causes of cardiogenic shock include Arrhythmias, Cardiomyopathy, Congestive heart failure (CHF), Contusio cordis or cardiac valve problems.

3. DISTRIBUTIVE SHOCK: As in hypovolaemic shock there is an insufficient intravascular volume of blood. This form of "relative" hypovolaemia is the result of dilation of blood vessels which diminishes Systemic vascular resistance. a) Septic shock: - This is caused by an overwhelming infection leading to vasodilation, such as by Gram negative bacteria i.e. Escherichia coli, Proteus species, Klebsiella pneumoniae which release an endotoxin which produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body. - Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as Grampositive bacterial toxins produce a similar syndrome. b) Anaphylactic shock: Caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the release of histamine which causes widespread vasodilation, leading to hypotension and increased capillary permeability. c) Neurogenic shock: Neurogenic shock is the rarest form of shock. It is caused by trauma to the spinal cord resulting in the sudden loss of autonomic and motor reflexes below the injury level. Without stimulation by sympathetic nervous system the vessel walls relax uncontrolled, resulting in a sudden decrease in peripheral vascular resistance, leading to vasodilation and hypotension. 4. OBSTRUCTIVE SHOCK: In this situation the flow of blood is obstructed which impedes circulation and can result in circulatory arrest. Several conditions result in this form of shock. o Cardiac tamponade in which blood in the pericardium prevents inflow of blood into the heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and hardens, is similar in presentation. o Tension Pneumothorax. Through increased intrathoracic pressure, blood flow to the heart is prevented (venous return). o Massive pulmonary embolism is the result of a thromboembolic incident in the blood vessels of the lungs and hinders the return of blood to the heart. o Aortic stenosis hinders circulation by obstructing the ventricular outflow tract. o 5. ENDOCRINE SHOCK: Based on endocrine disturbances. o Hypothyroidism, in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency. o Thyrotoxicosis may induce a reversible cardiomyopathy. o Acute adrenal insufficiency is frequently the result of discontinuing corticosteroid treatment without tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition. ETIOLOGY: Haemorrhage Burns Dehydration Myocardial Infraction

 Anaphylactic Shock Neurogenic Shock Septic Shock Vascular Insufficiency and Cardiac dysfunction Obstructive Condition Diarrhoea and Dysentery RISK FACTORS: Major Trauma History of previous myocardial damage Immosuppersive therapy STAGE OF SHOCK:

1. Early reversible and compensatory shock

Mean arterial pressure (MAP) drops 10 -15 mm Hg Decrease in circulating blood volume (25-35%) 1000ml Sympathetic nervous system stimulated; release of catecholamine Stages of Shock cont. To maintain blood pressure: increase in heart rate and contractility; increase in peripheral vasoconstriction Circulation maintained, but can only be sustained short time without harm to tissues Underlying cause of shock must be addressed and corrected or will progress to next stage.

2. Intermediate or progressive shock

Further drop in MAP (20%) Increase in fluid loss (1800 25400 ml) Vasoconstriction continues and leads to oxygen deficiency Body switches to anaerobic metabolism forming lactic acid as a waste product. Body increases heart rate and vasoconstriction. Heart and brain become hypoxic More severe effects on other tissues which become: ischemic and anoxic State of acidosis with hyperkalemia develops Needs rapid treatment

3. Refractory or irreversible shock

Tissues are anoxic, cellular death widespread Even with restoration of blood pressure and fluid volume there is too much damage to restore homeostasis of tissues Cellular death leads to tissue death; vital organs fail and death occurs PATHOPHYSIOLOGY: Whatever may be the initial cause of shock the patho physiological response is the same. Cell throught the body are deprived of oxygen, resulting in cell membrane damage. Histamine and kinins are released in response to the damage and cause released in response to the damage and cause vasodilation and increased capillary permeability. WBC leaks out of the capillaries and protein pars into extra cellular fluid. Edema results with in the cell and interstinal fluids volume increased the fluid breaks done. This results in decreased in the circulatory blood volume and consequent reduction in venous return in the amount, of the blood available for oxygenation and in cardiac output (Co). Metabolism continuous within the cell despite the lack of oxygen and lactic acid, produced as a result of cellular metabolism. The result is Metabolic Acidosis

HYPOVOLEMIC SHOCK: Hemorrhage or other fluid loss decreased intra vascular volume Decreased Cardiac Output Decreased Tissue Perfusion Compensatory Mechanism are Activated

Epinephrine and Nor Epinephrine

Renin-Angiotensin Aldosterone System relaxed ADH released

Stimulation

Increased Heart rate and Systemic Vascular Resistance

Intracellular fluid shift to Intravascular Space Increased Blood Volume Increased Cardiac Output Compensatory Mechanism Fails Decreased Cardiac Output Decreased Blood Pressure Decreased Perfusion of Vital Organ Multi System Organ Failure result

Sign and Symptoms: - Increased Heart Rate - Hypotension - Cold and Clammy Skin - Thirst Emergency Care: - Fluid Replacement

CARDIOGENIC SHOCK; Due to Myocardial Infarction, Cardiac Insufficiency Increased Hearts Pumping Ability Decreased Venous Return Increased carbon-dioxide Decreased Circulation / Circulated Blood Volume Decreased Inadequate Tissue Perfusion

Sign and Symptoms: - Increased Heart Rate - Hypotension - Cyanosis - Cold and Clammy Skin Emergency Management: - Initial drug therapy for Myocardial Infraction, - Replace Fluids, - Consider possible emergency coronary bypass surgery

ANAPHYLATIC SHOCK: Antigen re-Exposure Hypersensitive Antibody response Vasoactive mediator release

Massive Vasodilation Profound Hypovolaemia

Increased Capillary Permeability Vascular Collapse

Angio Edema Uriticaria Pulmonary Congestion Airway Obstruction Respiratory Arrest Cardiac Arrest

Sign and Symptoms: - Throat Edema - In congestion with Increasing breathing difficulty - Hypotension - Increased Heart Rate Emergency Care: - Manage ABC, - Administer (Adrenaline) Epinephrine, - Administer Diphenlydramine hydrochloride (Benadry)

SEPTIC SHOCK: Severe Localized Infection of Gram Negative Bacilli Bacterial Invasion of Blood stream (Septicaemia) Inflammatory Response Endotoxins are released into Circulation Immune system releases Histamine and many other Chemical Mediators

Massive Vasodilation

Increased Capillary Permeability Inadequate tissue Perfusion Compensatory mechanism are activated Decreased perfusion of Vital Organs

Multiple Organ Failure Sign and Symptoms: - Hot, Dry, Flushed skin, - Hypotension, - Increased Heart Rate, Emergency Care: - Locate the source of infection and trust with broad spectrum antibiotic, - Replace fluids,

NEUROGENIC SHOCK: Spinal Cord Injury, Spinal Anaesthesia centre Depression

Increased Sympathetic Tone

Arterial and Venous dilation

Arterial/ Venous Blood pooling

Hypotension

Bradycardia

Warm, Dry, Flushed skin

Decreased Perfusion of vital organs

Multisystem Organ Failure Sign and Symptoms: - Slowed heart rate, - Hypotension, Emergency Care: - Replace fluids, - Administer drugs to increase blood pressure and heart rate.

SIGN AND SYMPTOMS: HYPOVOLEMIC SHOCK: Anxiety, restlessness, altered mental state due to decreased cerebral perfusion and subsequent hypoxia. Hypotension due to decrease in circulatory volume. A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia. Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction.

Rapid and shallow respirations due to sympathetic nervous system stimulation and acidosis. Hypothermia due to decreased perfusion and evaporation of sweat. Thirst and dry mouth, due to fluid depletion. Fatigue due to inadequate oxygenation. Cold and mottled skin (cutis marmorata), especially extremities, due to insufficient perfusion of the skin. Distracted look in the eyes or staring into space, often with pupils dilated. CARDIOGENIC SHOCK: o Distended jugular veins due to increased jugular venous pressure. o Absent pulse due to tachyarrhythmia. o OBSTRUCTIVE SHOCK: o Distended jugular veins due to increased jugular venous pressure. o Pulsus paradoxus in case of tamponade, SEPTIC SHOCK: o Pyrexia and fever, or hyperthermia, due to overwhelming bacterial infection. o Vasodilation and increased cardiac output, NEUROGENIC SHOCK: o Skin is warm and dry. ANAPHYLACTIC SHOCK: o Skin eruptions and large welts. o Localised edema, especially around the face. o Weak and rapid pulse. o Breathlessness and cough due to narrowing of airways and swelling of the throat

DIAGNOSTIC STUDIES: History Collection, Physical Examination, Blood haemoglobin and hematocrit: change in haemoglobin and hematocrit concentration usually occur in hypovolemic shock. Arterial blood gas (ABG): to determine oxygen and carbon-dioxide levels and pH. The effects of shock and of the bodys compensatory mechanisms causes a decrease in pH (indication acidosis), a decrease in partial pressure of the oxygen (PaO2) and in total oxygen saturation, and an increase in the partial pressure of carbon-dioxide (PaCO2). HISTORY COLLECTION: - Obtaining the patients medical and surgical history of recent, (Upper respiratory tract infection, Surgery, Chest pain,) PHYSICAL EXAMINATION: - OBSERVATION: - Is done to identify the colour, type, of the skin to detect presence of cyanosis, cold and clammy skin, - PALPATION: - This is done to identify the flat neck veins etc.

DIAGNOSTIC STUDIES: o Laboratory Abnormalities in shock: S.No: Laboratory Studies Findings 1) Blood: A) Red blood cell count, Hematocrit, Hemoglobin, - Normal

Significance Of Finding - Remains within normal limits in shock because of relative hypovolemia and pump failure and in haemorrhagic shock before fluid restoration, - Decreased in hemorrhagic shock after fluid resuscitation which when fluids other than blood are used,

- Decreased

- Increased

- Increased in non haemorrhagic shock due to actual hypovolemic because of fluid lost does not contain erthocytes,

- Acute DIC can develop within hours to develop within hours to days after an initial assault on the body.(Eg: Shock) B) DIC Screen - Fibrin split Products(FSP) - Increased

- Fibrinogen Level - Decreased - Platelet Count - Decreased - Prolonged -Thrombin Time - Increased - D-Dimer - Increased - Creatine Kinase - Increased - Increases in MI, -Increase in trauma, MI in response to cellular changes ans / or hypoxia.

- Troponin

- Indicates impaired kidney function due to hypoperfusion as a result severs vasoconstritionan occurs secondary to

- Increased - BUN - Increased

catabolism of cell(Eg: Trauma,Infecton)

- Indicates impaired kidney function due to hypoperfusion a result of sever vasoconstriction is more sustitive indicator or renal function than BUN,

-Creatinine - Increased - Found in early shock because of release of live glycogen stores in response to symptoms nervous system stimulation and control, insulin will be developed. - Occurs because of depleted glycogen stores with hepatocellular dysfunction possible as shock progress, - Increased

- Glucose

- Found in early shock because of increased secretion of aldosterone causing renal retention of Sodium, - Decreased - May occur iatrogenic ally when excess hypotonic fluids is administered after fluid loss, - Serum Electrolyte Sodium - Increased - Results when cellular duration liberates intracellular potassium, also occurs in acute renal failure and the pressure of acidosis,

-Decreased - Found in early shock secondary to hypoventilation, - Potassium - Increased - Occurs late in shock when organic acid such as blood from anaerobic metabolism,

- Decreased

- Indicates acid production secondary to hypoxia,

- Arterial Blood gases - Respiratory alkalosis - Metabolic acidosis

- May organism grows in patient who are in septic Shock, - Usually increases once significant hypoperfusion and improvement at the cellular level have occurred by product of anaerobic metabolism,

- Base Deficit >-6 - Elevation indicates liver cell destruction in progressive stage of shock, -Blood Cultures - Increased - Occurs secondary to the action of ADH, - Occurs in renal failure,

- Liver Enzymes (AZT, AST, GST)

- Increased

-Urine Specific Gravity - Increased fixed at 1.010

 TREATMENT: o DRUG THERAPY o FLUID THERAPY IN SHOCK DRUG THERAPY: o Dobutamine (Dobutrex) o Nitroglycerin (Tridic) o Sodium Nitroprusside (Nipride) o Dopamine (Itropin) o Epinephrine (Adrenalin) o Non-Epinephrine (Levophed) o Phenylephrine (Neo-Synephrine)

FLUID THERAPY IN SHOCK: S.No: Fluid type 1) CRYSTALLOIDS ISOTONIC: - 0.9% Nacl - Lactate Ringers 2) BLOOD/BLOOD PRODUCTS: -Whole blood / packed red blood cells -Replace blood loss, increase oxygen caring Capacity, - All types of shock if haemoglobin is <12g/dl (120g/L) or if the - Same precaution as any patient does not response to administered, crystalloids, Mechanism of Action - Fluid primarily remains in the intravascular space, Increasing intravascular Volume, Type of Shock - Used for initial volume replacement in most types of shock, Nursing Implication - Monitor patient closely for circulatory overload LR should be used in patient with Liver failure.

3)

COLLOIDS: - Hetastarat (Hespan) - Made from starch and act as volume expander is at as effective as albumin can exert osmotic effect for up to 36 hours, - All types of shock, - May be 50% less costly than albumin use cautiously in patient with congestion heart failure, renal failure a bleeding disorder,

- Human serum albumin protein fraction (5% albumin is 500 ml NSS)

- All types of shock expect cardiogenic - Can increase plasma colloid osmotic pressure, Rapid volume expansion,

- Monitor for circulatory overload , - Mild side effect of chills, fever, and urticaria may develop

- DEXTRAN - DEXTRAN 40 - DEXTRAN 70 - Hyperosmotic glucose polymer has similar degree of volume expansion with dextran 40 and dextran 70, and longer duration of action with dextran70, - Limited use because of side effect including platelets, dilution - Increases risk bleeding clotting factor, important to monitor patient for aller

 NURSING DIAGNOSIS: Fluid volume deficit related to loss of circulatory volume, Decreased cardiac output related to decreased central venous pressure, Ineffective breathing pattern related to inadequate Oxygenation, -Impaired systemic tissue perfusion related to hypovolemic shock, Impaired skin integrity related to Oedema, Fear and anxiety related to severity of the disease Condition, Nutritional pattern less than body requirement related to anorexia nervosa. Sleep pattern disturbance related to hospitalization, Impaired sensory and Perceptual activities related to dilated pupils,

 NURSING PROCESS: S.No: 1) ASSESSMENT Subjective Data: -Fluid volume deficit related to loss of circulatory Volume Objective Data: - The client is suffering from sever haemorrhage - Administer blood transfusion, plasma to the client, - To maintain and improve circulatory volume, - Start immediately the IV infusion, - To improve and maintain fluid loss, - Assess the current fluid volume status, - To plan for necessary informations, - The client fluid - To avoid further loss of health fluid continuously, - To maintain fliud volume, volume will be Improved and Maintained. NURSING DIAGNOSI GOAL INTERVENTION RATIONAL EXPECTED OUTCOME

- Identify the causes of shock and stop the haemorrhage,

S.No: 2)

ASSESSMENT Subjective Data: -

NURSING DIAGNOSI

GOAL

INTERVENTION - Monitor vital, CVP, Pulmonary artery every 15 min to 1 hour,

RATIONAL - To monitor patient status and detect or excess,

EXPECTED OUTCOME

- Decreased cardiac output related to decreased central venous pressure Objective Data: - The patient is suffering from decreased blood volume in systemic circulation (CVP)

- To Improve And Maintain cardiac out put,

- The client Cardiac output will

- Administer crystalloids colloids and/ or blood ,

- To restore blood and fluid volume to maintain perfusion of vital Organs, - To evaluate patient response to treatment, - To prevent an increase in metabolism need for oxygen and Co2 is increased Production, - To monitor fluid balance status,

be improved and mentioned..

- Examine laboratory and X-Ray findings,

- Keep patient at normal body temperature, - Record accurately Input and Output Chart daily ,

S.No: 2)

ASSESSMENT Subjective Data: -

NURSING DIAGNOSI

GOAL

INTERVENTION - Assess the current breathing sounds, and other respiratory parameters, (Respiratory Rate) - Monitor the clients ABC and go for a investigation, - Administer comfortable position and device to client (Folwer Position) - Provide humidified oxygen to the client, - Monitor patient respiratory distress and place patient back on Ventilator,

RATIONAL - To monitor trends and effectiveness of intervention,

EXPECTED OUTCOME

- Ineffective breathing pattern related to Inadequate O2. Objective Data: - The patient is suffering from hypoxia, Cyanosis.

- To Improve And Maintain Breathing Pattern.

- The client Breathing pattern

- To check arterial oxygen saturation level in the blood, - To improve lung expansion to for good breathing, - To increase oxygen level in the blood, - To ensure adequate ventilation,

will be improved.

 HEALTH EDUCATION: o Given printed notes to the client and family members regarding shock its causes, stage and it types and sign and symptoms, o Taught all initial treatment measures to family members to avoid shock, o Asked the client not to worry about the disease condition, Because it may lead to stress that may still worsen the condition, o Advised the client to take good nutritious food to improve nutritious status, o Encouraged the client to take medication regulatory and come for regular checkups, CONCLUSION: o Shock is a serious,life threating medical condition where insufficient blood carries oxygen and nutrients around the body is reduced flow hinders the delivery of these components to tissue, Which stops functioning. Which results in coma and brain Death, If not treated at correct time.

BIBLIOGRAPHY
BOOK REFERENCE: LEWIS HEITKEMPER, Medical and Surgical Nursing, 6th Edition 2000, Published by Mosby, Page No: 1760, JOYCE AND BLACK, Medical and Surgical Nursing,7th Edition 2001, Published by Lippincott, Page No:2444-443 BRUNNER AND SUDDARTHS, Medical and Surgical Nursing,9th Edition, Published by Lippincott, Page No:274-276, MANDHAN NEIGHBOURS, Medical and Surgical Nursing,2nd Edition 1998,Published by Saderson Company, BRIAN DOLAN AND LYNDA HOLT, Accident and Emergency, 4th edition, Published by Bailliere Tindal, Page No:303, TORTORA.G.J, Principles of Anatomy and Physiology New Jerrsy willy Publication, Pricilla lemone & Karen burke Medical surgical nursing critical thinkinh in client care 4th edition. Published by Dorling Kindersely (India). Journal reference: o LEDINGHAM AND RAMSEY, Shock, British Journal of Anaesthesia Vol:58, Page No: 169-189, o IRWIN,R.S.RIPPE, Procedure and Techniques in Intensive care medicine, Lippincott publication, o KARL JASPER, Nursing Times , Subdural Haemorrhage, Mosby Publication, NET ABSTRACT: o http://en.wikipedia.org/wiki/Bleeding, o http://en.wikipedia.org/wiki/Shock