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46 Cards in this Set
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What is the first stage of shock and what happens in each of these:
BP? HR? RR? Skin? Output? Mentation? Acid-base balance? |
Compensatory.
BP = Normal Heart Rate > 100 Respiratory >20 PaCO2 <32 Skin=cold, clammy (because the body shunts blood from organs to the heart,lungs and brain) Urinary output=decreased (in response to the release of aldosterone and ADH) Mentation=confused (due to alkalotic state) Respiratory alkalosis |
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What are the clinical manifestations of the Compensatory stage?
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Despite a normal BP, there is inadequate organ perfusion, causing anaerobic metabolism and a build up of lactic acid, producing metabolic acidosis. This increases the respiratory rate. This rapid rate facilitates removal of excess carbon dioxide but raises the blood ph and causes a compensatory respiratory alkalosis.
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What is the medical management of the Compensatory stage of shock?
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treat underlying cause. fluid replacement and medicine therapy must be initiated to maintain an adequate BP and reestablish and maintain adequate tissue perfusion.
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What is the nursing management of compensatory stage of shock in regards to tissue perfusion?
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in this stage, serum sodium and blood glucose levels are elevated in response to the release of aldosterone and catecholamines. VS are key indicators of hemodynamic status and BP is an indirect measure of tissue hypoxia. REPORT a systolic BP lower than 90 or a drop in systolic by 40 mm HG from baseline. Check pulse pressure.
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What is a normal pulse pressure?
How do you get the pulse pressure? |
30 to 40
Systolic BP - Diastolic BP |
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What is an earlier indicator of shock than a drop in BP?
What happens if we let the BP fall by not catching on to the signs of shock early? |
Narrowing or decreased pulse pressure.
Damage has already been occuring at the cellular and tissue levels. |
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What is the second stage of shock and what happens in each of these:
BP? HR? RR? Skin? Output? Mentation? Acid-base balance? |
Progressive Stage.
Systolic <80-90 (requires fluids resuscitation to support blood pressure HR >150 RR Rapid, shallow respirations; crackles PaCO2 >45 Skin: Mottled, petechiae Urinary Output: 0.5 ml/kg/h Mentation: Lethargy METABOLIC ACIDOSIS |
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What happens in the progressive stage of shock?
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the mechanisms that regulate BP no longer comensate, and MAP falls below normal. Systolic <90 (clinically hypotensive) or decrease in systolic of 40 from baseline
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What's the pathophysiology of the progressive stage of shock?
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First, the overworked heart becomes dysfunctional, the boyd's inability to meet increased oxygen requirements produces ischemia. This leads to failure of the cardiac pump. Second, increased capillary premeability, with areas of arteriolar and venous constriction furthur compromising cellular perfusion. At this stage, the prognosis worsens. The relaxation of precapillary sphincters causes fluid to leak from the capillaries, creating interstitial edema and return of less fluid to the heart. The body increases O consumption to meet the increased metabolic needs of the underperfused tissues and cells.
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What are the respiratory effects of the progressive stage?
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Subsequent decompensation of the lungs increases the likelihood that mechanical ventilation will be needed. Decreased pulmonary blood flow causes arterial oxygen levels to decrease and co2 levels increase. The hypoperfused alveoli stop producing surfactant and subsequently collapse. Pulmonary edema occurs. and ARDS
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What are the cardiovascular effects of the progressive stage?
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a lack of adequate blood supply leads to dysrhythmias and ischemia. HR sometimes exceeds 150 bpm. chest pain and possible MI
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What are the neurologic effects of the progressive stage?
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changes in metnal status occur with decreased cerebral perfusion and hypoxia
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What are the renal effects of the progressive stage?
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When MAP drops below 70, kidneys can't be maintained, output drops to below 30 ml/hr
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What are the hepatic effects of the progressive stage?
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less able to metabolize meds and waste products like ammonia and lactic acid. pt will be jaundiced
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What are the GI effects of the progressive stage?
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gi ischemia causes stress ulcers in the stomach, putting them at risk fo GI bleeding. in the smal intestine, the mucosa can become necrotic and slough off, causing bloody diarrhea.
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What are the hematologic effects of the progressive stage?
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DIC can occur.
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Nursing considerations for pt in progressive stage of shock.
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Reduce the incidence of ventilator associated pneumonias. freq oral care, aseptic suctioning, turning, elevating HOB to at least 30 degrees. promote rest. avoid temp extremes which can increase the metabolic rate and oxygen consumption and thus cardiac workload. Pt should not be warmed too quickly, and never use warming blankets bc they can cause vasodilation and drop in BP
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What's the third stage of shock called?
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Irreversible (refractory)
BP requires mechanical or pharmalogic support. HR erratic or asystole RR intubation/ventilation/ O2 skin jaundice output anuric, require dialysis mentation unconscious acid-base balance Profound Acidosis |
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What happens during the the irreversible stage of shock?
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Organ damage is so severe that the pt doesn't respond to treatment and can't survive.
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Management in all types of shock and in all phases include these 4 things always:
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support of the respiratory system (O2/ mech ventilation)
fluid replacement to restore intravascular volume vasoactive meds to improve cardiac function nutritional support to address the metabolic requirements |
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What are crystalloids?
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electrolyte solutions that move freely between intravascular and interstitial spaces, given to shock pt's to improve cardiac and tissue oxygenation
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What are colloids?
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large-molecule IV solutions given to shock pt's to improve cardiac and tissue oxygenation
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Pt's in shock are given crystalloids, colloids and blood components...what are blood components?
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packed red blood cells, fresh frozen plasma, and platelets.
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What's the best IV fluid for a pt in shock?
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the one that's readily available!
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What are the IV crystalloids commonly used for resuscitation in hypovolemic shock?
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0.9% sodium chloride (NS)
and lactated ringers. Ringer's lactate is an electrolyte solution containing the lactate ion which converts to bicarbonate, which helps buffer the overall acidosis that occurs in shock. |
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What are the problems associated with insufficient fluid replacement?
What about excessive fluid replacement? |
insufficient: higher incidence of morbidity and mortality from lack of tissue perfusion.
Excessive: systemic and pulmonary edema which progresses to ARDS, abdominal compartment syndrome and MODS |
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During hypovolemic shock, hypertonic crystalloid solutions such as 3% sodium chloride is given. What do they do and what are some complications?
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these solutions eert a large osmotic force that pulls fluid from the intracellular space to the extra cellular space to achieve a fluid balance. this osmotic effect results in fewer fluids being administered to restore intravascular volume. Complications include excessive serum osmolality, which can cause rapid fluid shifts overwhelming the heart and hypernatremia.
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How do colloidal solutions work?
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They are similar to plasma proteins, so certain moldcules are too large to pass through capillary membranes. colloids expand intravascular volume by exerting oncotic pressure, thereby pulling fluid into the intravascular space. less volume is required than with crystalloids, although they have the same effect. they also have a longer duration.
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If colloids are used to treat hypoperfusion, what agent is usually prescribed?
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Albumin which is a plasma protein; this solution prepared from human plasma is heated during production to reduce its potential to transmit disease. Disadvantage is cost.
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Synthetic colloid preperations such as hetastarch and dextran may be given. When is dextran contraindicated?
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since it interferes with platelet aggregation, it is not indicated if hemorrhage is the cause of the hypovolemic shock or if the pt has a coagulation disorder.
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What are the most common and serious side effects of fluid replacement?
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cardiovascular overload and pulmonary edema (indicated by crackles)
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What is Abdominal Compartment Syndrom (ACS)?
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in ACS, fluid leaks into the intra-abdominal cavity, increasing pressure that is displaced onto surrounding vessels and organs. Venous return, preload, and c.o. are compromised. The pressure elevates the diaphragm, making it difficult to breathe effectively. dc output/ absent bowel sounds/ intolerance of tube feeding.
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What causes ACS?
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when large volumes of fluid are administered. also occurs after trauma, abdominal surgery, severe pancreatitis or sepsis.
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When are vasoactive medicines given?
What do they do? |
when fluid therapy alone can't maintain adequate MAP. these meds help increase the strength of myocardial contractility, regulate the heart rate, reduce myocardial resistance, and initiate vasoconstriction to maximize tissue perfusion.
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How frequently should VS be taken when vasoactive meds are given?
How are they administered? What can infiltration and extravasation cause with these meds? These meds maintain a MAP at what rate? This rate ensures adequate tissue perfusion. |
q15 min until stable.
through a central venous line tissue necrosis and sloughing (shedding) can occur. 65 mm Hg |
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What are some inotropic vasoactive medications?
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Dobutamine dopamine epinephrine and milrinone all improve contractility, increase stroke volume, and increase c.o. Disadvantage: increase O demand of the heart
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What are some vasodilator vasoactive medications?
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Nitroglycerin and Nitroprusside. These reduce preload and afterload, reduce O demand of the heart. Disadvantage: cause hypotension
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What are some vasoprressor vasoactive medications?
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norepinephrine, dopamine, phenylephrine, vasopressin
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How many calories may a shock pt require?
Why? |
about 3000 daily. The release of catecholamines early in the shock continuum causes depletion of glycogen stores in about 8 to 10 hours. Also skeletal muscle mass is broken down
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Hypovolemic shock
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(most common type) decreased intravascular (inside blood vessels) volume. occurs with a blood loss of 750-1500 ml
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What causes hypovolemic shock?
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traumatic blood loss, surgery, vomiting, diarrhea, diuresis, diabetes insipidus. or internally: severe dehydration, severe edema, peritonitis, burns, hemorrhage or ascites.
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What's the pathophysiology of hypovolemic shock?
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begins with decrease in intravascular volume. this results in decreased venous return of blood to the heart and subsequent decreased ventricular filling. decreased ventricular filling results in decreased stroke volume ( amount of blood ejected from the heart) and decreased c. o. when c.o. drops, bp falls, tissues aren't adequately perfused.
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What's the 3:1 rule?
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if hypovolemia is due to blood loss, 3 ml of crystalloid stolution for each milliliter of estimated blood loss.
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Which position is recommended for hypovolemic shock?
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Modified trendelenburg. Elevation of the legs 20 degrees promotes return of venous blood.
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What's Cardiogenic Shock?
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occurs when the heart's ability to contract and to pump blood is impaired and the supply of oxygen is inadequate for the heart and tissues.
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What's the difference between coronary and noncoronary cardiogenic shock?
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Coronary: more common, seen in pt's with acute MI resulting in damage
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