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36 Cards in this Set
- Front
- Back
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What is happening at the cellular level?
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Hemodynamic Principles
Circulatory system is composed of the heart, large blood vessels, and microcirculation (peripheral or capillary circulation) These 3 components work together to maintain adequate cardiac output and tissue perfusion Adequate blood flow depends on: 1. Competent vascular system that can maintain a good blood pressure 2. Red blood cells that have hemoglobin, appropriate amount of blood (preload) 3. A heart that is adequately pumping |
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Hemodynamics
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Cardiac output (HR x SV)
Heart rate (HR) Stroke Volume (SV) – volume/beat Preload – volume of blood available to be pumped Afterload – how much resistance the heart is beating against (diastolic pressure) or (systemic vascular resistance) Contractility – How strong each beat is Control of peripheral circulation – dilation/constriction |
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O2 Transport Principles
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All forms of shock involve impaired delivery of oxygen to the tissues.
Variables that influence O2 transport include: Oxygen delivered to the tissues Oxygen consumption by the tissues Oxygen extraction ratio - % of available O2 the cell is capable of taking in |
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O2 delivery depends on:
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Blood flow (cardiac output)
Amount of hemoglobin available to carry oxygen Percentage of arterial oxygen hemoglobin saturation |
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02 Delivery Wiggle Room
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The body normally provides 3-4 times more oxygen than needed for normal metabolism
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O2 Consumption
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Represents the body’s demand for Oxygen and is a reflection of the body’s metabolism
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Why is decreased O2 consumption common in all forms of shock
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Due to: reduction in blood flow (hypovolemic, cardiogenic, obstructive)
Or uneven distribution of blood (septic, anaphylactic, neurogenic) The magnitude of the O2 consumption deficit has been correlated with mortality rates. |
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O2 Extraction Ratio
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Extraction ratio (VO2/DO2)
Provides an estimate of the balance between tissue O2 demand (consumption – VO2) and O2 supply (delivery – DO2). Provides an indication of the ability of the tissues to extract and use the O2 delivered. |
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Stages of Shock
Initial & Nonprogressive |
1. Vasoconstriction occurs in response to a release of catecholamines or to poor venous return to the right ventricle
2. This results in a decrease in the rate of flow through the tissue capillaries |
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Stages of Shock
Progressive Shock |
Decrease capillary blood flow continues
Cells convert to anaerobic metabolism and lactic acid is produced (causes metabolic acidosis) Body tries to compensate by dilating capillaries Compensatory mechanisms eventually fail |
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Stages of Shock
Refractory/Irreversible Shock |
Refractory/Irreversible Shock
The continued decrease in circulation causes coagulation of stagnant, acid blood This causes the capillaries to become occluded The occluded capillaries causes perfusion to the cells to stop Cells that do not receive blood die DIC may result (disseminated intravascular coagulation) The decrease in microcirculation that occurs results in necrosis of vital organs which leads to multi system organ failure and death Even if cause of shock is reversed and MAP returns to normal, death is eminent |
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Types of Shock
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Hypovolemic – trauma, burns (loss of serum, plasma), diarrhea
Cardiogenic Distributive -Neurogenic – CNS disruption causes excessive dilation of vessels -Chemically Induced shock Anaphylactic Shock Septic Capillary Leak Obstructive – tumors, large clots, etc. |
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PA Catheter (Swan-Ganz)
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A balloon-tipped catheter introduced into the pulmonary artery to measure pressures and cardiac output/cardiac index
CVP (central venous pressure)- used to monitor blood volume and venous return to the heart PAP (pulmonary artery pressure) PAWP (pulmonary artery wedge pressure)- reflects pressures in the pulmonary capillary bed and left sided heart function |
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Hypovolemic Shock
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Caused by a loss of whole blood, plasma or interstitial fluids in such quantities that the body’s metabolic needs can no longer be met
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Causes of hypovolemic shock
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Loss of blood
Trauma GI bleeding Surgery Hemothorax Ruptured aortic aneurysm Burns Severe vomiting/diarrhea Diabetes insipidus Diuretic therapy Third spacing |
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Pathophysiology of Hypovolemic shock
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A decreased blood volume or plasma loss will cause a decrease in venous return (pre-load) which results in a decrease cardiac output.
The decreased CO results in: 1. inadequate cellular perfusion 2. susceptibility to infection and hemorrhage 3. organ damage The decreased CO also results in inadequate cellular perfusion which leads to an increased susceptibility to infection and hemorrhage which results in organ damage |
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S/S of Hypovolemic shock
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Skin- least reliable indicator
Cool, pale skin due to vasconstriction Decrease capillary refill time seen in nail beds Clammy, moist skin due to release of epinephrine and norepinephrine Thirst- thirst mechanism is activated due to increase serum osmolality Urine output falls due to vasoconstriction and decreased GFR. ADH is released to retain fluid Level of Consciousness- will improve initially then decrease Tachycardia- a very early sign. CO=HR X SV. In hypovolemic shock the SV decreases therefore the HR increases to maintain the CO Increased RR and Depth of resp- occurs in an attempt to improve blood oxygenation levels & blow off CO2 and compensate for impending acidosis and right heart filling volume BP- initially may increase but then drops as compensatory mechanisms fail. Also see a decreased pulse pressure Hematocrit- not a good indicator of shock (If volume replaced by NS or LR it may then drop Hemodynamic parameters- -CVP low -PCWP low |
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Interventions for Hypovolemic shock
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Interventions for Hypovolemic shock
1. Stop the cause of the loss 2. Replace whatever was lost 3. Airway and oxygenate Blood pressure going up, HR going back down and urine output going back up shows that they are starting to get enough fluid replacement and perfusion Fluid replacement Administer enough to correct problems, i.e. improve BP, UO Fluid selection for Hypovolemic shock Crystalloid solutions (RL – has buffers that can prevent metabolic acidosis by binding to the lactic acid , NS) Provides intravascular expansion May or may not be all that is needed Do not use D5W because it’s not isotonic, will go into interstitial spaces Albumin Is an effective volume expander Not usually used in shock because it may cause or exacerbate ARDS Hespan (hetastarch) Plasma volume expander No danger of hepatitis Cheaper than blood products Doesn’t replace Hbg Plasma- (FFP) Give if fluid loss is due to plasma loss, ie. Burns Also given for clotting disorders Blood Major blood losses should be replaced with blood products, ie. Whole blood, packed red blood cells, etc. |
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Interventions for Hypovolemic Shock
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Cardiovascular support
Improve left ventricular function by administering inotropic agents Examples- Dopamine, Dobutamine, Inocor, Norepinephrine, Digoxin Observe for signs of cardiac failure or pulmonary edema Improve preload by administering fluids or vasoconstrictors (after volume replaced) Examples- Dopamine, Norepinephrine (Levophed), Neo-synephrine, Epinephrine Dopamine (Intropin) Titrated in mcg/kg/min Renal perfusion 0.5-2mg/kg/min Inotropic (increase cardiac output)- 2-10mcg/kg/min Vasoconstriction- > 10mcg/kg/min Not given above > 20mcg/kg/min- severe vasoconstriction **Dose determines effect Restore blood volume first Maintain vascular tone Keep patient warm Elevate lower ext. – No longer using T-berg Interventions for Hypovolemic Shock Correct acid-base balance Monitor for fluid overload Meet nutritional needs Provide emotional support |
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Cardiogenic shock – A Review
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Caused whenever the heart’s pumping ability becomes impaired resulting in a decrease cardiac output
Causes of Cardiogenic shock Any condition that causes dysfunction of the left ventricle, the right ventricle or both due to ischemia, structural problems or dysrhythmias |
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Pathophysiology of Cardiogenic Shock
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When there is ischemic damage to the myocardium a downward spiral begins with altered myocardial metabolism
That leads to impaired myocardial contractility Which leads to diminished stroke volume Which leads to diminished CO/CI Which leads to decreased coronary artery perfusion pressure Which leads to increased myocardial hypoxia Which leads to more ischemia And the cycle begins again. |
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S/S of Cardiogenic Shock
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Decreased BP
Decreased CO/CI Increased PCWP (wedge pressure) due to decrease in the function of the left ventricle Absent or poor peripheral pulses Cool, clammy skin Decreased UO Change in LOC |
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Interventions for Cardiogenic Shock
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Oxygenation
Increased CO Correct any dysrhythmias Correct any hypovolemia Medications such as Dobutamine (not dopamine because it increases the O2 demand of the heart which is already not getting enough O2) Decrease left ventricular workload Vasodilators to decrease afterload Example- NTG, Nitroprusside Monitor PCWP Correct hypovolemia Intra-aortic balloon pump |
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Distributive Shock
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Neural Induced
Chemically Induced Sepsis Anaphylaxis Capillary Leak |
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Neurogenic Shock
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Occurs due to massive vasodilation as a result of loss of the sympathetic tone
Causes of Neurogenic Shock Spinal Cord injury Spinal anesthesia Drugs such as ganglionic blocking agents or barbiturates Brain damage (medulla)- rare Treatment of Neurogenic Shock Vasoconstricting Drugs Dopamine (Inotropin) >10mcg/kg/min Norepinephrine (Levophed) |
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Anaphylactic Shock
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Sudden life-threatening hypersensitivity reaction to an antigen.
Characterized by massive vasodilation and increased capillary permeability which can actually cause hypovolemia to a certain extent from swelling and hives |
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Anaphylaxis- Pathophysiology
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Mediated by immunoglobin E (IgE) antibody
IgE produced after first exposure to antigen and binds to mast cells and basophils Subsequent exposures- stimulate mast cell degranulation and release of chemical mediators Chemical mediators cause vasodilation, capillary permeability, bronchoconstriction, increased coronary permeability Shock from profound vasodilation and low cardiac output Death can result from severe hypoxemia secondary to bronchoconstriction or from cardiovascular collapse |
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Anaphylaxis- S/S
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Earliest
Feelings of anxiety and uneasiness Flushing Diaphoresis Sneezing Weakness Quickly followed by: Nausea Dizziness Itching Sometimes edema Quickly followed by: Severe hypotension and increased capillary permeability |
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Complications of Shock (all types)
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Anaerobic metabolism occurs due to poor tissue perfusion.
This leads to a decrease in the amount of oxygen delivered to the cells resulting in anaerobic metabolism and eventually to metabolic acidosis Glucose metabolism- patient may become hyperglycemic to meet increased demands of energy Fluid shifts- Water moves into the cells taking sodium with it. This movement of water further decreases the circulating blood volume and leads to cellular edema and disruption of metabolic activity |
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Complications of Shock (all types)
Brain- |
The decrease in blood flow to the brain leads to cerebral hypoxia which can lead to either seizures or cerebral infarction.
Assess patient for anxiety, restlessness, changes in LOC, lethargy, stupor, coma, and seizures |
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Complications of Shock (all types)
-kidneys |
The vasoconstriction compromises the blood flow to the kidney leading to acute tubular necrosis
Assess the patient for oliguria, elevated BUN and creatinine |
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Complications of Shock (all types)
-myocardium |
the decrease in CO leads to decreased coronary perfusion
which leads to myocardial failure which leads to altered cell membrane potential which leads to an increased incidence of dysrhythmias. The dysrhythmias can further decrease cardiac output. |
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Complications of Shock (all types)
-Peripheral circulation |
Initially there is a vasoconstrictive response in an attempt to increase circulating blood volume.
Fluid moves from the interstitial space to the intravascular space to restore volume. Eventually the compensatory mechanisms fail and the body attempts to maintain blood flow to the heart and the brain at the expense of the other organs (shunting) |
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Complications of Shock (all types)
-GI system |
When the blood vessels vasoconstrict the bowel is affected more than any other system with blood being shunted away from the bowel.
This leads to mucosal ischemia which may lead to stress ulcers, bowel infarction, ileus. Assess patient for septic shock and listen to bowel sounds |
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Complications of Shock (all types)
-hepatic system |
the decreased blood flow to the liver leads to hepatic hypoxia
which may lead to infection, metabolic acidosis, bleeding problems (DIC), decreased ability of the liver to get rid of toxins or to clear certain medications |
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Complications of Shock (all types)
-ARDS (Acute Respiratory Distress Syndrome |
Decrease blood flow to the lungs leads to a decrease in the amount of surfactant that is produced which leads to a collapse of the alveoli.
Increased capillary permeability- fluid leaks from capillaries into lung causing pulmonary edema |
