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65 Cards in this Set
- Front
- Back
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what is shock? |
a condition in which vital tissues and organs are not receiving enough blood flow to fx properly; inadequate blood flow to meet the body's needs |
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what is the severity of shock? why? |
a medical emergency; failure to reverse the causes and symptoms may lead to irreversible organ damage and death |
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what are S+S of shock? skin, neurological, respiratory : |
-pale, cool, clammy = skin -restlessness, anxiety, lethargy, confusion = neurological -rapid breathing, shallow respiration = respiratory |
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what are the S+S of shock metabolism/renal, cardiovascular : |
-low temperature, thirst, acidosis, low urine output = metabolism -tachycardia, thready pulse, low cardiac output, low blood pressure = cardiovascular |
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what is anaphylactic shock? how does it happen? |
acute allergic reaction; severe reaction to an allergen (ie: penicillin, nuts, shellfish, or animal proteins) |
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what is cardiogenic shock? how does it happen? |
failure of the heart to pump sufficient blood to tissues; LHF, myocardial ischemia, MI, dsyrhythmias, PE, myocardial or pericardial infection |
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what is hypovolemic shock? how does it happen? |
loss of blood volume; hemorrhage, burns, excessive diuresis, severe vomiting or diarrhea |
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what is neurogenic shock? how does it happen? |
vasodilation due to over-stimulation of the PNS or under-stimulation of the SNS; trauma to the spinal cord or medulla, severe emotional stress or pain, or drugs that depress the CNS |
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what is septic shock? how does it happen? |
multiple organ dysfx as a result of pathogenic organisms in the blood; causes vasodilation and changes in permeability of capillaries; often a precursor to ARDS and DIC; -widespread inflammatory response to bacterial, fungal, or parasitic infection |
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what is the most severe anaphylactic shock? |
a type 1 allergic response |
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what is the most lethal form of shock (has a 70-90% mortality rate)? |
cardiogenic shock *the leading cause of death from MI |
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septic shock most commonly occurs in who? |
those with weakened immune defenses |
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what are the initial treatment priorities for shock? |
1. ABC's to sustain normal BP *oxygen is administered at 15L/min 2. connect to a cardiac monitor and apply a pulse oximeter 3. identify the underlying cause of shock, then start more specific treatment 4. monitor LOC, keep the pt quiet/calm and warm |
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what are the primary two pharmacotherapeutic goals for any type of shock? |
-to restore normal fluid volume and composition -to maintain adequate BP |
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pharmacotherapy during hypovolemic shock includes what types of fluid replacement agents? |
blood or blood products colloids crystalloids |
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what is massive blood loss? when would whole blood be indicated for the treatment of acute, massive blood loss? |
depletion of 30% or more of the total volume; when there is a need to replace plasma volume AND supply RBCs to increase the O2-carrying capacity |
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what are colloids? |
proteins or other large molecules that stay suspended in the blood for a long period because they are too large to easily cross membranes |
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how do colloids increase blood volume? |
they increase plasma oncotic pressure which helps to draw water molecules from the cells and tissues into the blood vessels |
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what are some examples of colloids? |
human blood products: serum albumin, plasma protein fraction, serum globulins. non-blood-products: dextran (40, 70, and high molecular weight), hetastarch (Hespan) |
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what are crystalloids? |
IV solutions that contain electrolytes in concentrations resembling those of plasma. |
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what are crystalloids used for? how do they differ from colloids? |
to replace fluids that have been lost and promote urine output; they can readily leave the blood and enter cells |
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what are examples of some common crystalloids? |
normal saline, Ringer's Lactate, PlasmaLyte, hypertonic saline (3%NaCl), D5W |
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S+S of anaphylaxis: |
preorbital edema (swelling around the eyes), urticaria (hives), wheezing and difficulty breathing (bronchospasms), rapid fall in BP |
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treatment of anaphylaxis: |
-O2 -antihistamine: prevent the release of histamine -bronchodilator: relieves SOB -corticosteroids: suppresses inflammation |
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Prototype drug: "epinephrine" aka Adrenalin pharmacologic class: mechanism of action: |
prototype drug: "epinephrine" aka Adrenalin Pharmacologic class: nonselective adrenergic agonist; vasopressor MOA: stimulation of alpha1s = rise in BP beta1s = rise in CO beta2s = opens airway (promotes bronchodilation) and relieves SOB |
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Prototype drug: "epinephrine" aka Adrenalin adverse effects: onset: |
Prototype drug: "epinephrine" aka Adrenalin AE: hypertension (BP rises from alpha1 receptor stimulation) and dysrhythmias onset: 3-5 mins |
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true or false: stinging/burning at the site of injection is an adverse effect |
true; however, this is a common occurrence |
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(sympathomimetic) vasoconstrictors, aka vasopressors: what do they do and when are they meant to be used? |
stabilize BP in pts with shock; "critical care meds" they are used only after fluid and electrolyte restoration has failed to raise BP (since they cause rapid and intense vasoconstriction which can have AEs and lead to potential organ damage) |
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Prototype drug: norepinephrine aka "Levophed" pharmacologic class: mechanism of action: |
Prototype drug: norepinephrine aka "Levophed" pharmacologic class: nonselective adrenergic agonist: vasopressor MOA: acts directly on alpha-adrenergic receptors to raise BP; beta1 stimulation = rise in CO |
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Prototype drug: norepinephrine aka "Levophed" adverse effects: onset: |
Prototype drug: norepinephrine aka "Levophed" adverse effects: hypertension, dysrhythmias, skin and soft tissue injury (if extravasation occurs) onset: 1-2 minutes |
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With a diagnosis of shock, what does the assessment (for the nursing process) include? |
health history baseline vitals changes in urine and output BUN and creatinine levels (lab) LOC and neurological changes knowledge of meds and diagnosis |
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coronary arteries: what do they do and where do they arise from? |
supply the myocardium with blood; arise within the aortic sinuses at the base of the aorta |
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what is myocardial ischemia? |
a condition where blood flow to the heart is reduced, depriving the cells of needed oxygen and nutrients |
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true or false: coronary arteries may be occluded 50% or more and cause no symptoms |
true; if the ischemia develops over a long period, the heart may compensate for the inadequate supplies and the pt may by asymptomatic-- ischemia occurs at 75% obstruction |
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what is the primary defining characteristic of coronary artery disease (CAD) |
the narrowing or occlusion of a coronary artery (which leads to myocardial ischemia) |
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the most common etiology of CAD is atherosclerosis. what is it? |
the presence of plaque (a fatty, fibrous material) within the walls of the coronary arteries, which narrows the lumen of the vessel |
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what is angina pectoris? why does it happen? |
reversible cardiac ischemia; acute chest pain caused by insufficient O2 to a portion of the myocardium (an imbalance between supply and demand) |
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true or false: angina can be relieved with rest |
true; with physical rest and/or stress reduction, the increased demands on the heart diminish, and the discomfort subsides within 5-10 minutes |
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how does classic angina present? |
usually described as substernal pain; constricting, squeezing, or suffocating in nature; pain may radiate |
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what is stable angina? |
when the episodes are fairly predictable as to the frequency, intensity, and duration and the pain associated with the angina is typically relieved by rest. |
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what is unstable angina? |
when episodes arise more frequently, become more intense, or occur during periods of rest |
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what is vasospastic or Prinzmetal's angina? |
when the decreased myocardial blood flow is caused by spasms of the coronary arteries in which there may or may not be atherosclerotic plaque |
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when does Prinzmetal's angina occur? |
most often during periods of rest, although it may occur unpredictably, and be unrelated to rest or activity. |
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what is silent angina? |
a form of the disease that occurs in the absence of chest pain; the pt remains asymptomatic and has a high risk for acute MI and sudden death |
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how can you tell if the pt with chest pain is having angina or MI? |
angina is relieved by rest and sublingual nitroglycerin |
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what nonpharmacological factors have been shown to reduce the incidence of CAD? |
limit alcohol consumption to small amounts; eliminate foods high in cholesterol or saturated fats; keep BP, blood glucose, blood cholesterol and other lipid indicators within normal ranges; no not use tobacco; limit salt/sodium intake; exercise regularly and maintain optimal weight |
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what are the pharmacological goals of therapy for anti-anginal meds? |
along with lifestyle modifications: decrease the # and severity of episodes; improve exercise tolerance and quality of life; delay CAD progression; prevent MI and sudden cardiac death; |
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list the primary 3 classes of anti-anginal meds: |
organic nitrates; beta-adrenergic antagonists; CCBs; |
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what is the drug of choice for terminating an acute angina episode? |
rapid-acting organic nitrates |
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what is the drug of choice for preventing angina pain? |
beta-adrenergic blockers |
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what are 2 types of procedures that must be done when the coronary arteries are significantly obstructed? |
Apercutaneous coronary intervention (PCI) which may include an atherectomy (removing the plaque), or an angioplasty (compressing the plaque against the vessel wall) with or without a stent. -coronary artery bypass graft (CABG) surgery (severe cases) |
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what is the main purpose of all anti-anginal medications? |
relieve pain by decreasing myocardial oxygen demands OR by increasing blood supply to the myocardium |
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what are the drugs of choice for terminating an acute angina episode? |
rapid-acting organic nitrates |
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what are the first-line drugs for preventing angina pain? |
beta-adrenergic blockers |
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when are CCBs used? |
when beta blockers are not tolerated well by the pt |
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these drugs, given PO or transdermal, are effective alternatives for prophylaxis: |
long-acting nitrates |
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what is the MOA of beta-adrenergic antagonists? |
-decrease the HR and myocardial contractility -reduce CO and workload |
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what is the MAO of CCBs? |
-dilate arteriole smooth muscle, reducing BP and decreasing cardiac workload *some also decrease the HR, reducing the workload on the heart, and dilate the coronary arteries |
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what is the MOA for organic nitrates? |
-dilate veins, reducing the amount of blood return to the heart -dilate the coronary arteries, bringing more blood to the myocardium (act directly on the smooth muscle; lower HR and BP) |
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Prototype drug: nitroglycerin (NTG) pharmacologic class: MOA: |
prototype drug: nitroglycerin pharm class: organic nitrate, vasodilator MOA: act directly on smooth muscle by dilating arterioles and coronary arteries and reduces venous pressure and venous return to the heart = relaxation (do not influence any nerve activity) |
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Prototype drug: nitroglycerin (NTG) adverse effects: onset: |
prototype drug: nitroglycerin (NTG) AE: hypotension, dizziness, light-headness, tachycardia, palpitations (mainly cardiovascular) -blurred vision, dry mouth, or severe headache could indicate OD onset: 1-3mins SL tabs; 40-60mins transdermal patch |
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organic nitrates: routes of administration |
-(short-acting) SL tabs, transmucosal spray, IV -(long-acting) Oral tablets, adhesive patches, transdermal paste |
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contraindications for NTG |
do not take with Viagra (combined effect may cause life-threatening hypotension) do not give to anyone with a head injury or cerebral hemorrhage (will increase intracranial pressure) |
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nitrate storage: (3) |
-store in a glass container (medication can actually absorb plastic) -only good for 6 months -store away from light (store in dark/covered bottle) |
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beta blockers |
2255 |
