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Shock and Hemorrhage

By Sai Choo


Preload: the end diastolic stretch on the heart before it contracts.

Afterload: the forces that impede the flow of the heart out of the heart. The heart contracts against the peripheral resistance, the compliance of the aorta and the mass and viscosity of the blood

Determinants of Cardiac Output






Stroke Volume X Heart Rate Cardiac Output: 5L/m


Failure of the circulatory system to maintain adequate perfusion of vital organs (Black & Hawks, 2009, p. 2154)

Classifications of Shock

Hypovolemic Cardiogenic Circulatory or distributive

Hypovolemic Shock
Causes: loss of intravascular fluid volume (most common type)
- blood loss (15-25% or about 500 to 1500 ml) from trauma and surgery - Loss of plasma proteins from burns - dehydration from prolonged diarrhea and vomiting

Due to decrease in Oxygen carrying blood cells

Cardiogenic Shock

Results primarily from an inability of the heart muscle to pump adequately or from mechanical obstruction of blood flow to or from the heart. Causes - Myocardial infarction - Obstructive conditions: Large pulmonary emboli, tension pneumothorax and pericardial tamponade (blood in the pericardial sac) - cardiac valve insufficiency from trauma or disease

e.g. Impaired heart muscle function due to M I

Due to insufficient amount of blood pump through the aorta

Circulatory Shock
- Also called distributive Shock - This shock is due to changes in blood vessel tone that increase the size of vascular space without an increase in the circulating blood volume. - Causes: (see coursepack for details) - Anaphylactic shock (acute allergic reaction) - Neurogenic Shock: interference with nervous system control of blood vessels (spinal cord injury, Spinal anesthesia) - Septic Shock (most common gram negative infection)

Neurogenic shock

Stages of Shock and manifestations

Non progressive Stage Progressive Stage Irreversible Stage

NON-Progressive State of Shock

Non Progressive Stage: manifestations

Decreased circulating blood volume Fluids shift into intravascular space from tissue Stimulation of SNS Activation of RAA system Blood shunted to vital organs (Brain and Heart)

BP within normal to low normal range Decrease in pulse pressure Tachycardia (weak and thready) Tachypnea Skin pale and clammy Hypoactive bowel sounds Decreased urine output Restless and anxious

Progressive Stage

Begins when compensatory mechanism fails. Anaerobic metabolism and lactic acidosis occur Increasing acidosis and increasing PaCo2 cause the microcirculation to dilate. Decreased venous return and decreased cardiac output

Progressive Stage

Decompensation Hypoperfusion of Heart, brain, kidneys, liver, GI tract

Increased respirations Pulmonary edema Decreased cardiac output, dysrhythmias Confusion Acute renal failure Increased liver enzymes Paralytic ileus, ulcers, GI bleed DIC Widespread clotting and bleeding

Anaphylactic Shock: Manifestations

Massive vasodilation may cause complaints of Headache Severe anxiety, dizziness, disorientation and loss of consciousness (due to cerebral hypoxia) Lump in the throat due to laryngeal edema and is followed by hoarseness, coughing, dyspnea and other signs of respiratory distress Pruritus (itchiness) and urticaria (hives)

Neurogenic Shock: manifestations

Due to inability in vasoconstriction Bradycardia and hypotension Skin is dry to touch due to inability to sweat Below the level of injury, the skin temperature takes on the same temperature as the room

Septic Shock: manifestations

Sepsis is diagnosed when two or more of the following are present - Temperature greater than 38o C or below 36o C - Heart rate greater than 90/min - RR greater than 20 per min - WBC greater than 12,000 cells/ml or 4000 cells/ml (normal is 5,000 to 10,000 cells/ml)

Septic Shock (Contd)

In the early stages, warm dry, flushed skin is apparent due to compensatory increase However, in the later stages, when decompensation occurs, the skin can become pale, cold, clammy and mottled

Irreversible Stage

If the cycle of inadequate tissue perfusion is not interrupted. Cellular ischemia and necrosis lead to organ failure and death Recovery is unlikely

Diagnostic Studies

No Single Study to determine the cause History and thorough physical examination ECG CBC, electrolytes, blood culture X rays Arterial blood gases (to determine AcidBase balance)

Diagnostic Studies

Pulse oximetry Hemodynamic monitoring (measurement of central venous pressure and pulmonary arterial pressure)

Collaborative Care

Interventions to control or eliminate the cause of decreased perfusion Ensure patent airway Optimize oxygen delivery Crystalloids, colloids and blood replacement Indwelling Foley Catheter Frequent monitoring of VS

Collaborative Care

Treat underlying infections Administer medications to elevate BP Treat allergic reactions Treat underlying trauma

* Black, J. & Hawks, J. (2009). Medical-surgical Nursing: Clinical management for
positive outcomes (8th ed.). St. Louis: MO: Elsevier. pp. 2154-2168 Braun, C. & Anderson, C. (2007). Pathophysiology: Functional alterations in human health. Philadelphia: PA: Lippincotts Williams &Wilkins. *Hannon, R. A., Pooler, C. & Porth, C. M. (2010). Porth pathophysiology: Concepts of altered health states (First Canadian Ed.). Philadelphia, PA: Lippincotts Williams &Wilkins . pp. 598-605 Lewis, S. Heitkemper, M. & Dirksen, S. (2006) Medical-surgical nursing in Canada: Assessment and management of clinical problems (1st Canadian edition). Toronto, ON: Elsevier Canada. McCance, K. & Huether, S. (2006). Pathophysiology: The biologic basis for disease in adults and children (5th edition). St. Louis, MO: Mosby Elsevier.
* Required Readings