SHOCK

BACKGROUND TO SHOCK SHOCK is a condition in which the cardiovascular system fails to perfuse tissues adequately. An impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissues PHYSIOLOGY OF PERFUSION Body cells require a constant supply of oxygen and nutrients and elimination of carbon dioxide and waste products Inadequate tissue perfusion can result in: generalized cellular hypoxia (starvation) widespread impairment of cellular metabolism tissue damage organ failure death PATHOPHYSIOLOGY OF SHOCK THREE COMPONENTS A. Pump (heart) B. Fluid volume (blood) C. Container (blood vessels) (Any derangement of any of these components can affect perfusion) A. THE PUMP The heart The pump of the circulatory system Receives blood from venous system Pumps it to the lungs to receive oxygen Pumps it to the peripheral tissues Stroke volume is the amount of blood pumped by the heart in one contraction (ave. 100ml/min) STROKE VOLUME is affected by: PRELOAD is defined as the amount of blood delivered to the heart during diastole. CONTRACTILE FORCE is defined as the force generated by the heart during each contraction. AFTERLOAD is defined as resistance against which the heart must pump. o When the resistance is overcome, blood can be ejected o Determined by the degree of arterial peripheral vasoconstriction o Vasoconstriction = increased resistance = increased afterload = decreased stroke volume

CARDIAC OUTPUT -defined as the amount of blood pumped by the heart in one by rhythmic ventricular contraction.

BLOOD PRESSURE -defined as the pressure of blood against the arterial walls. Systolic Pressure is the maximum pressure of blood exerted against the artery walls when the heart contracts (N 100-140 mmHg) Diastolic Pressure is the force of blood exerted against the artery walls during the hearts relaxation phase (N 60-90mmHg) B. THE FLUID Blood is the fluid of the cardiovascular system that transports oxygen, carbon dioxide, nutrients, hormones, metabolic waste products, and heat. The blood contains RBC which have protein called Hemoglobin. Oxygen molecules attach themselves to the hemoglobin so that they may be carried throughout the body. In the lungs deoxygenated blood travels through the capillaries surrounding the alveoli. Through the process of diffusion, oxygen which is at a higher concentration in the alveoli, crosses the alveolicapillary membrane into the blood where there is a lesser concentration of oxygen. At the same time, carbon dioxide which is at a higher concentration in the blood, crosses the capillaryalveoli membrane into the alveoli, where it is removed during exhalation. The oxygen molecules bind to the hemoglobin and is transported throughout the body. The blood enters capillaries within the tissue where again through diffusion oxygen is exchanged from the blood to the tissue, and carbon dioxide form the tissue to the blood. The blood, now deoxygenated returns the lungs where the process repeats it self. C. THE CONTAINER Blood vessels Serve as container for the cardiovascular system A continuous, closed, pressurized pipeline that moves blood Includes arteries, arterioles, capillaries, venules, and veins Under control of the autonomic nervous system, they regulate blood flow to different areas of the body by adjusting their size and rerouting blood flow through microcirculation

MICROCIRCULATION Responsive to local tissue needs Capillary beds can adjust size to supply undernourished tissue and bypass tissue with no immediate need Pre-capillary sphincters and post capillary sphincters open and close to feed or bypass tissues TISSUE PERFUSION Tissue perfusion dependent on circulatory system and oxygenation by respiratory system Inadequate tissue perfusion caused by Inadequate pump Inadequate preload Inadequate cardiac contractile strength Excessive afterload Inadequate heart rate Inadequate fluid volume Hypovolemia Inadequate container Excessive dilation without change in fluid volume Excessive systemic vascular resistance PHYSIOLOGICAL RESPONSE TO SHOCK 1. Systemic response Progressive vasoconstriction Increased blood flow to major organs Increased cardiac output Increased respiratory rate and volume Decreased urine output Decreased gastric activity PATHOPHYSIOLOGY IN SYSTEMIC LEVEL In the kidneys, the detection of low blood pressure stimulates the Renin-AngiotensinAldosterone system. The enzyme renin is released by the kidneys. Renin acts on a plasma protein called angiotensin, which is converted into angiotensin I. Angiotensin I is converted into angiotensin II in the lungs by angiotensin converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor which increases peripheral vascular resistants which increases blood pressure. Angiotensin II also stimulates the sympathetic response, and stimulates the pituitary glands secretion of antidiuretic hormone (ADH) which causes the kidneys to retain electrolytes and fluid. The hormone Aldosterone which is secreted by the adrenal cortex also stimulates the kidneys to reabsorb sodium potassium and water, increases the intravascular volume. As the blood pressure slowly decreases, so does the intravascular osmotic pressure, which causes fluid to shift from the interstitial space and the intracellular space, into the intravascular space to increase the circulating volume.

Respirations increase both in rate and depth. This increases the amount of oxygen available, and attempts to eliminate the build up of toxins from the anaerobic metabolism. If there is blood loss due to hemorrhage, the damaged blood vessels constrict slowing the amount of blood flow and the clotting and coagulation cascade begins. If the conditions causing shock are too serious, or progress too rapidly, the body will be unable to keep up with the demands and move into a state of decompensation. SHOCK AT THE CELLULAR LEVEL During hypoperfusion, the cells become ischemic and switch from a Aerobic metabolism ( with oxygen ) to a Anaerobic metabolism ( without oxygen ). The primary energy source for the cell is glucose. In a Aerobic metabolism glucose is broken down ( Glycolysis ) which produces pyruvic acid which is further broken down into carbon dioxide, water, and energy (ATP). However during hypoperfusion the cell switches to an Anaerobic metabolism (without oxygen) where only the first stage of glycolysis is possible. This produces very little energy and with out oxygen pyruvic acid can not be broken down, and instead is converted into lactic acid which accumulates in the cell, lowering the cellular pH. The acidosis reduces the ability of hemoglobin to transport oxygen which compounds the problem. The lower intracellular pH causes the membranes of the lysosomes and other organelles to rupture releasing enzymes that damage the Sodium-Potassium pump which causes an influx of sodium and fluid, which causes cellular edema, which causes the cell to rupture releasing the lysosomal enzymes, lactic acid, hydrogen and other cellular contents into the interstitial and intravenous space causing further acidosis. PATHOPHYSIOLOGY IN CELLULAR LEVEL

Metabolism in normal conditions Metabolism is aerobic Cell energy comes from glucose broken down through glycosis into pyruvic acid Pyruvic acid further broken down in cycle into CO2, water and energy

Metabolism in poor perfusion states Metabolism is anaerobic Glucose breaks down into pyruvic acid, but not enough oxygen is present to enter into the Krebs cycle Pyruvic acid accumulates, degrades into lactic acid, which also accumulates along with other metabolic acids Cells die; tissues die; organs fail; organ systems fail; death ultimately ensues

STAGES OF SHOCK A. NON PROGRESSIVE STAGE During the initial stage of shock, CO2 is slightly decreased because of loss of actual or relative blood volume. During this stage the bodys compensatory mechanisms can maintain BP within the normal to low-normal range and can maintain tissue perfusion to the vital organs. During the compensatory phase, the systemic circulation and microcirculation work together. Both undergo major readjustment in which their activities are coordinated to preserve the entire system. Concept Map of Non Progressive Stage

B. PROGRESSIVE STAGE If the cause of the crisis is not successfully treated, shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries. Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing slugging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion. If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock.

Concept Map of Progressive Stage

C. IRREVERSIBLE STAGE Occurs if the cycle of inadequate tissue perfusion is not interrupted. The shock state becomes progressively more severe, even though the initial cause of the shock is not itself become more severe. Cellular ischemia and neurosis lead to organ failure and death. TYPES OF SHOCK HYPOVOLEMIC SHOCK Loss of circulating volume Empty tank leads to decrease tissue perfusion thus to general shock response Etiology: 1. Internal or External fluid loss 2. Intracellular and extracellular compartments I.

Most common causes: 1. Hemmorhage (eg. trauma: blunt and penetrating) 2. Dehydration (Nausea & vomiting, diarrhea, massive diuresis, extensive burns) Pathophysiology of Hypovolemic Shock

Intra vascular volume

venous return (Preload, RAP)

ventricular filling (Preload, PAWP)

stroke volume (HR, Preload, & Afterload)

CO (Compensat ory mechanism

Inadequate tissue perfusion!!! !

Assessment & Management S/S vary depending on severity of fluid loss: 15%[750ml]- compensatory mechanism maintains CO 15-30% [750-1500ml- Hypoxemia, decreased BP & UOP 30-40% [1500-2000ml] -Impaired compensation & profound shock along with severe acidosis 40-50% - refactory stage: loss of volume= death Clinical Presentation Tachycardia and tachypnea Weak, thready pulses Hypotension Skin cool & clammy Mental status changes Decreased urine output: dark & concentrated Hypovolemic Shock: Hemodynamic Changes Correlate with volume loss Low CO Decreased RAP ( Preload) Decreased PAP, PAWP Increased SVR (Afterload)

Management of Hypovolemic Shock

Etiology Blood loss Clinical Situation Massive trauma Gastrointestinal bleeding Ruptured aortic aneurysm Surgery Erosion of vessel from lesion, tubes, an other devices DIC Intervention Stop bleeding with direct pressure, pressure dressing, tourniquet (as last resort) Reduced intra-abdominal or retroperitoneal bleeding by applying PASG or prepare for emergency surgery Administer LR solution or normal saline Transfuse with FWB, PRBC, FFP, platelets or other clotting factors, if significant improvement does not occur with crystalloid administration. Use non-blood plasma expanders (albumin, dextran or hetostarch) until blood is available. Conduct autotransfusion if appropriate Administer low-dose cardiotonics (dopamine, dobutamine) Administer LR solutions an normal saline Administer albumin, FFP, hetastarch, or dextran if cardiac output is still low Administer isotonic or hypotonic saline with electrolytes as needed to maintain normal circulating volume and electrolyte balance

Plasma Crystalloid loss Burns Accumulation of intraabdominal fluid Malnutrition Severe dermatitis DIC Dehydration (e.g. diabetic ketoacidosis, heat exhaustion) Protracted vomiting, diarrhea Nasogatric suction

II CARDIOGENIC SHOCK The impaired ability of the heart to pump blood Pump failure of the right or left ventricle Most common cause Myocardial Infarction o Occurs when > 40% of ventricular mass damage o Mortality rate of 80 % or > Etiology: 1. Mechanical: complications of MI: Papillary Muscle Rupture Ventricular aneurysm Ventricular septal rupture 2. Other causes: Cardiomyopathies tamponade tension pneumothorax arrhythmias valve disease Pathophysiology of Cardiogenic Shock

Cardiogenic Shock: Pathophysiology Impaired pumping ability of LV Inadequate systolic emptying Left ventricular filling pressures (preload) Left atrial pressures

Pulmonary capillary pressure

Pulmonary interstitial & intra alveolar edema
Clinical Presentation Similar catecholamine compensation changes in generalized shock & hypovolemic shock May not show typical tachycardic response if on Beta blockers, in heart block, or if bradycardic in response to nodal tissue ischemia Mean arterial pressure below 70 mmHg compromises coronary perfusion (MAP = SBP + (2) DBP/3) Abnormal heart sounds o Murmurs o Pathologic S3 (ventricular gallop) o Pathologic S4 (atrial gallop) Pericardial tamponade o muffled heart tones, elevated neck veins Tension pneumothorax o JVD, tracheal deviation, decreased or absent unilateral breath sounds, and chest hyperresonance on affected side Clinical Assessments Pulmonary & Peripheral Edema JVD CO Hypotension Tachypnea, Crackles PaO2 UOP LOC Hemodynamic changes: PCWP,PAP,RAP & SVR

Management of Cardiogenic Shock

Etiology Myocardial disease or injury Clinical Situation AMI Myocardial contusion cardiomyopathies Intervention Fluid-challenge with up to 300ml of normal saline solution or LR to rule out hypovolemia, unless heart failure or pulmonary edema is present Insert CVP or pulmonary artery catheter, monitor CO, PAP, and PCWP, administer IV fluids to maintain left ventricular filling pressure of 15-20 mmHg Administer inotropics (dopamine and dobutamine, Vasodilators (NA Nitroprusside, nitroglycerin, Ca-channel blockers, morphine), Diuretics(mannitol, furosemide),Cardiotonics (digitalis), Betablockers (propranolol), Glucocorticoteriods Intra-aortic balloon pump or external counterpulsation device if unresponsive to other therapies Same as MCD, if rapid response does not occur; prepare for cardiac surgery

Valvular disease or injury

Ruptures aortic curps Ruptured papillary muscle Ball thrombus

External pressure on the heart interferes with heart filling or emptying

Pericardial tamponade due to trauma, aneurysm, cardiac surgery, pericarditis Massive pulmonary embolus Tesion pneumothorax Ascites Hemoperitoneum Mechanical ventilation Tachydysrhymias Bradydysrhymias Pulseless electrical activity

Relieve tamponade with ECG-assisted pericardiocentesis; repair surgically if it reccurs Thromolytic (stryptokinase) or anticoagulant (haparin) therapy; surgery for removal of clot Relieve air accumulation with needle thoracostomy or chest tube insertion Relieve fluid accumulation with parasenthesis Reduce inspiratory pressure Treat dysrhythmias; be prepare to initaite CPR, cardiac pacing

Cardiac dysrrhymias

III DISTRIBUTIVE (VASOGENIC) SHOCK Inadequate perfusion of tissues through maldistribution of blood flow Intravascular volume is maldistributed because of alterations in blood vessels Cardiac pump & blood volume are normal but blood is not reaching the tissues Etiologies 1. Anaphylactic Shock 2. Neurogenic Shock 3. Septic Shock (Most Common) A. ANAPHYLACTIC SHOCK A type of distributive shock that results from widespread systemic allergic reaction to an antigen This hypersensitive reaction is LIFE THREATENING Pathophysiology Anaphylactic Shock Antigen exposure body stimulated to produce IgE antibodies specific to antigen (drugs, bites, contrast, blood, foods, vaccines) Reexposure to antigen (IgE binds to mast cells and basophils) Anaphylactic response a. Vasodilatation b. Increased vascular permeability c. Bronchoconstriction d. Increased mucus production e. Increased inflammatory mediators recruitment to sites of antigen interaction Clinical Presentation Anaphylactic Shock Almost immediate response to inciting antigen a. Cutaneous manifestations urticaria, erythema, pruritis, angioedema b. Respiratory compromise stridor, wheezing, bronchorrhea, resp. distress c. Circulatory collapse tachycardia, vasodilation, hypotension B. NEUROGENIC SHOCK A type of distributive shock that results from the loss or suppression of sympathetic tone Causes massive vasodilatation in the venous vasculature, venous return to heart, cardiac output.

Most common etiology: Spinal cord injury above T6 Pathophysiology of Neurogenic Shock
Distruption of sympathetic nervous system

Loss of sympathetic tone

Venous and arterial vasodilation

Decreased venous return

Decreased stroke volume

Decreased cardiac output

Decreased cellular oxygen supply

Impaired tissue perfusion

Impaired cellular metabolism

Assessment, Diagnosis and Management of Neurogenic Shock PATIENT ASSESSMENT a. Hypotension b. Bradycardia c. Hypothermia d. Warm, dry skin e. RAP f. PAWP g. CO h. Flaccid paralysis below level of the spinal lesion

C. SEPTIC SHOCK Systemic Inflammatory Response (SIRS) to INFECTION manifested by two or > of following: Temp > 38 or < 36 centigrade HR > 90 RR > 20 or PaCO2 < 32 WBC > 12,000/cu mm or > 10% Bands (immature wbc) Sepsis with: Hypotension (SBP < 90 or > 40 reduction from baseline) & Tissue perfusion abnormalities invasion of the body by microorganisms & failure of bodys defense mechanism. Risk Factors Associated with Septic Shock a. Age b. Malnutrition c. General debilitation d. Use of invasive catheters e. Traumatic wounds f. Drug Therapy Pathophysiology of Septic shock Initiated by gram-negative (most common) or gram positive bacteria, fungi, or viruses Cell walls of organisms contain Endotoxins Endotoxins release inflammatory mediators (systemic inflammatory response) causes... Vasodilation & increase capillary permeability leads to Shock due to alteration in peripheral circulation & massive dilation Pathophysiology of Septic Shock

Clinical Presentation Septic Shock Two phases: 1. Warm shock - early phase hyperdynamic response, VASODILATION 2. Cold shock - late phase hypodynamic response, DECOMPENSATED STATE Clinical Manifestations EARLY---HYPERDYNAMIC STATE---COMPENSATION a. Massive vasodilation b. Pink, warm, flushed skin c. Increased Heart Rate Full bounding pulse d. Tachypnea e. Decreased SVR* f. Increased CO & CI g. SVO2 will be abnormally high h. Crackles i. Clinical Manifestations L ATE--HYPODYNAMIC STATE--DECOMPENSATION a. Vasoconstriction b. Skin is pale & cool c. Significant tachycardia d. Decreased BP e. Change in LOC f. Increase SVR g. Decreased CO h. Decreased UOP i. Metabolic & respiratory acidosis with hypoxemia

Management of Distributive Shock

Etiology Anaphylactic shock Clinical Situation Allergy to food, medicines, dyes, insect bites, stings, or latex Intervention Prepare for surgery management of the airway further absorption of antigen (eg. Stop IVF, place tourniquet between injection or sting site and heart if feasible Epinephrine (1:100) 2 inhalations q 3hrs, or Epinephrine (1:1000) 0.2-0.5 q 5-15min given SQ Epinephrine (1:10,000) 0.5-1.0 q 5-15min given at a rate of 1mg/min IVF resuscitation with isotonic solution Diphenhydramine HCl or H1-receptor antagonist IV Theophilline IvVdrip for bronchospasm Steroid IV Vasopressors (norepinephrine, metaraminol bitartrate, high dosage dopamine) Gastric lavage for ingested antigen Ice pack to injection of sting site Meat tenderizer paste to sting site Identify origin o sepsis; culture all suspected sources Vigorous IVF resuscitation with normal saline Empirical antibiotic therapy until sensitivities are reported If suspected organism is gram-positive, vancomysin is used; if gram-negative, give expanded-spectrum penicillin or a cephalosporin and animoglycoside Administer cardiotonic agents (dopamine or dobutamine, noreepinephrine, isoproterenol, digitalis, calcium) Naloxone (narcotic antagonist) Prostaglandins Monoclonal antibodies Temperature control (both hyper and hypothermia are noted Heparin, clotting factors blood products if DIC develops Normal saline to restore volume Treat bradycardia with atropine Vasopressors (norepinephrine, metaraminol bitartrate, high dosage dopamine, and phenylephrine) may be given Place client in modified Trendelenburg position Place client in a head-down or recumbent position Give atropine if bradycardia an profound hypotention; eliminate pain

Septic shock Often gramnegative septicemia but also caused by other organisms in debilitated, immuno deficient, or chronically ill clients

Neurogenic (spinal) shock

Spinal anerthesia Spinal cord injury

Vasovagal reaction

Severe pain Severe emotional distress

URDANETA CITY UNIVERSITY SAN VICENTE WEST, URDANETA CITY, PANGASINAN GRADUATE STUDIES

By: May Judeniah S. Parayno, RN

Prof. Consuelo Reyes, M.D. Advanced Medical-Surgical Nursing