Week 9

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heart disease factors

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1

heart disease factors

smoking, infections, alcohol, genetic predisposition, unhealthy food, obesity, sedentary lifestyle, age, stress

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2

PQRST characteristics of pain

palliative/provocative factors, quality, radiation/region, severity, temporal factors

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3

acute coronary syndrome

general term used for varying degree of blockage in a coronary artery

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4

varying degrees of ACS

unstable angina, NSTEMI, STEMI, MI, sudden cardiac death

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5

chronic stable angina

primarily caused by CAD/atherosclerosis, which results in a long-term but relatively stable level of obstruction in one or more coronary arteries; often triggered by increase in activity, emotional excitement, large meals, or cold exposure

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6

vasospastic angina (prinzmetal’s/variant)

ischemia-induced myocardial chest pain caused by spasms of the coronary arteries

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7

unstable angina

medical emergency; results from severe CAD complicated by vasospasm, platelet aggregation, and coronary thrombi or embolism

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8

unstable angina symptoms

angina at rest, now-onset exertional angina, or intensification of existing angina

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9

non-ST elevation MI (NSTEMI)

blockage of blood flow is only partial, no damage to cardiac muscle (+symptoms, + troponins, -ECG changes)

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10

ST-elevation MI (STEMI)

blockage is complete, but hasn’t been long enough to cause myocardial wall damage (+symptoms, +troponins, +ECG changes in ST segment)

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11

myocardial infarction

blockage is complete, causing necrosis of the myocardium

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12

hemostasis

physiologic process by which bleeding is stopped

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13

stage 1 of coagulation

formation of a platelet plug

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14

formation of a platelet plug

platelets come in contact with collagen on the exposed surface of a damaged blood vessel & adhere to site of vessel injury. adhesion initiates platelet activation, which in turn leads to platelet aggregation

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15

anti-platelet example

aspirin (ASA)

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16

aspirin (ASA) mechanism

inhibits cyclooxyrgenase and prevents platelet aggregation

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17

aspirin (ASA) uses

ischemic stroke, TIA, USA, coronary stenting MI, MI prevention

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18

aspirin (ASA) routes

PO

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19

aspirin (ASA) side effects

bleeding, especially GI bleed, dizziness, drowsiness, headache, flushing, visual changes, tinnitus, hearing loss, seizures, reye syndrome (children)

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20

aspirin (ASA) nursing considerations

325 mg for MI/TIA/CVA, 81-160 mg for prevention; must be stopped 7-10 days before invasive procedures

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21

anti-platelet (ADP inhibitor) example

clopidogrel (Plavix)

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22

clopidogrel (Plavix) mechanism

alters platelet membrane so that it can no longer receive the signal to aggregate and form a clot

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23

clopidogrel (Plavix) uses

prevent stenosis of coronary stent, secondary prevention of MI and ischemic stroke

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24

clopidogrel (Plavix) routes

PO

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25

clopidogrel (Plavix) side effects

bleeding, less than ASA for GI bleeding

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clopidogrel (Plavix) nursing considerations

can be used in conjunction with ASA but increased risk for bleeding; cannot be used with another ADP receptor antagonist; must be stopped 7-10 days before any invasive procedure

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27

ACS chest pain symptoms

crushing, constricting, or radiating pain, often substernal, radiating pain can be felt in arms or jaw, can be confused with angina, lasts longer than angina and not relieved by nitroglycerin

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three groups who do not have typical ACS symptoms

women, diabetics, elderly

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ACS diagnosis

chest pain, EKG changes, biochemical markers (blood lab test)

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30

ACS EKG changes

conduction of electrical impulses through heart becomes altered in the region of injury; ST elevation

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31

ACS blood lab test

when myocardial cells undergo necrosis, they release intracellular proteins called cardiac troponins; if serum blood levels of troponin are detected, it’s a sign of cardiac injury, as they are normally undetectable

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32

immediate treatment of suspected MI

morphine IV, oxygen, nitroglycerin SL/IV, aspirin, beta blockers PO or IV (MONAB)

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33

purpose of morphine in management of ACS

relieves pain, improves hemodynamics, promotes venodilation, reduces cardiac preload & some afterload

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34

purpose of oxygen in management of ACS

can increase arterial oxygen saturation and thereby increase oxygen delivery to ischemic myocardium; goal is titrate to keep SpO2 between 95-99%

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35

purpose of nitroglycerin in management of ACS

can reduce preload and therefore oxygen demand, increases collateral blood flow in the ischemic region of the heart, controls HTN

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36

purpose of aspirin in management of ACS

suppresses platelet aggregation for immediate antithrombotic effect, should be chewed (4 baby ASA=325 mg)

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37

purpose of beta blockers in management of ACS

reduce cardiac pain, infarct size, short-term and long-term mortality (by reducing HR and contractility, they reduce oxygen demand)

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38

three families of pharmacological antianginal agents

  1. organic nitrates

  2. rapid-acting (NTG SL) during ACS

  3. long-acting/XL (Isosorbide) after ACS when it is then called CAD

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39

short-acting nitrates example

nitroglycerin (NTG)

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40

long-acting nitrates example

isosorbide mononitrate (Imdur)

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41

nitrates mechanism

vasodilation in veins and arteries but potent vasodilator in coronary arteries=decrease in preload

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42

nitrates routes

SL, PO, IV drip, paste, transdermal

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43

nitrates side effects

excessive effects of drug=decrease in BP, headache

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44

nitrates nursing interventions

monitor BP closely=may need to put HOB flat and/or bolus with isotonic IV solution

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45

nitrates patient education

-sit down before taking NTG

-get up & change positions slowly

-teach patients about symptoms of hypotension & advise them to sit or lie down if these occur

-cannot have within 24-48 hours of ED medications

-avoid saunas & hot tubs

-NTG x3, 5 min apart, between 1 & 2 if CP is present=call 911

-if pt has chronic stable angina, precipitate CP & take NTG SL prior to event

-do not eat or drink until 5-10 min after SL dose

-potency is felt by a burning or stinging under the tongue

-take acetaminophen for headache (no ASA or NSAIDs)

-keep NTG in brownish lightproof bottle, keep with at all times

-NTG SL pills only good 3-6 months (some say 6-12)

-sprays last 1-2 years

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46

symptoms of hypotension

lightheadedness, dizziness

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47

ED medications

sildenafil (Viagra), tadalafil (Cialis)

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48

nitrates IV infusion/drips

-standard orders with parameters to adjust/titrate the rate up or down based on specific criteria; must be on a pump

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49

interventions specific to IV NTG infusion

-glass bottle, must be vented

-evaluation/adjustment criteria: BP and CP

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50

restoring perfusion

cardiac catheterization with percutaneous intervention, drug therapy (thrombolytic agents)

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51

percutaneous coronary intervention

usually balloon angioplasty coupled with placement of a drug-eluting stent to reopen an occluded coronary artery; success rate higher than with fibrinolytic therapy

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52

thrombolytic agents

-promote lysis of fibrin, causing dissolution of thrombi

-given to remove thrombi that have already formed

-used acutely and only for severe thrombolytic disease: ACS, PE, ischemic stroke

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53

alteplase (tPA) use

used for ACS (STEMI, MI), ischemic stroke, massive PEs

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54

alteplase (tPA) route

IV

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55

alteplase (tPA) side effects

major bleeding

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56

alteplase (tPA) contraindications

any previous or current bleeding risk

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57

alteplase (tPA) antidote

aminocarpmroic acid (Amicar)

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58

contraindications to fibrinolytic drugs

prior intracranial hemorrhage, known structural cerebrovascular lesion, ischemic stroke within the past 3 months, known intracranial neoplasm, active internal bleeding, suspected aortic dissection, severe uncontrolled hypertension

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59

guideline for CAD & ACS prevention regimen upon discharge

ASA, NTG PRN for CP, BB prevents another episode, PRN clopidogrel dual therapy for one year if stent placement, PRN cholesterol-lowering medications for lipid management (usually statins), PRN HTN or HF management with ACEI or ARB or ARB with thiazide, PRN stool softeners

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60

clot

insoluble solid elements of blood that have chemicaly separated from the liquid component of the blood

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61

embolus

a blood clot that has been dislodged from the wall of a blood vessel and is traveling throughout the bloodstream

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62

deep vein thrombosis

the formation of a thrombus in one of the deep veins of the body

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63

ischemia

damaged cells/tissue as the result of inadequate oxygen supply

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64

stage 2 of coagulation

production of fibrin that reinforces the platelet plug; produced by two convergent pathways: contact activation pathway and tissue factor pathway

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65

arterial thrombosis

starts with adhesion of platelets to the arterial wall due to damage or rupture by an atherosclerotic plaque. aggregation continues until occlusion of the artery can occur. blood flow stops, coagulation cascade is initiated and the plug is reinforced with fibrin

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66

venous thrombosis

develops at sites where blood flow is slow. stagnation of blood initiates the coagulation cascade. fibrin is produced, which enmeshes red blood cells and platelets to form the thrombus; has a long tail that can break off to produce an embolus. the emboli can traverse the vascular system and become lodged at other sites

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67

antithrombotic drugs

  1. antiplatelets: inhibit platelet aggregation

  2. thrombolytics: promote lysis of fibrin, causing dissolution of thrombi

  3. anticoagulants: disrupt the coagulation cascade thereby suppressing the production of fibrin

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68

antithrombotics nursing considerations & pt ed

soft bristle toothbrushes, no contact sports, monitor for blood in urine/stool, no aspirin/NSAIDs, wear a med bracelet, blood in emesis looks like coffee grounds, use an electric razor, apply firm pressure, minimize physical manipulation of the patient, avoid subQ & IM injections, minimize invasive procedures, minimize concurrent use of antiplatelet drugs

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69

anticoagulants

drugs that reduce the formation of fibrin by inhibiting the synthesis of clotting factors or inhibiting the activity of clotting factors

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70

anticoagulant examples

warfarin, DOAC, heparin, LMWH

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71

warfarin (Coumadin)

a vitamin K antagonist, oldest oral anticoagulant

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72

warfarin (Coumadin) uses

prevent thrombosis, DVT, PE, AFib/flutter

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73

warfarin (Coumadin) routes

PO

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74

warfarin (Coumadin) nursing considerations

not to be given while pregnant, monitor serum blood levels of PT/INR (2-3), will needs to stop warfarin/monitor INR/give vitamin K if patient is to undergo any invasive procedure

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75

warfarin (Coumadin) antidote

vitamin K (given sub Q, PO, or IV)

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76

warfarin (Coumadin) side effects

bleeding/hemorrhage

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77

warfarin (Coumadin) drug interactions

antibiotics, heparin, ASA, acetaminophen

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78

warfarin (Coumadin) food interactions

anything with vitamin K (green leafy vegetables, prunes, mayonnaise, canola oil), alcohol

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79

warfarin (Coumadin) nursing implications

include education on monitoring, diets, and risks of injury

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80

advantage of warfarin (Coumadin)

it’s cheap

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81

DOAC examples

rivaroxaban (Xarelto), apixaban (Eliquis), dabigatran (Pradaxa)

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82

rivaroxaban (Xarelto) mechanism

direct factor Xa inhibitors; causes selective inhibition of factor Xa (activated factor X)

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83

apixaban (Eliquis) mechanism

direct factor Xa inhibitors; causes selective inhibition of factor Xa (activated factor X)

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84

dabigatran (Pradaxa) mechanism

direct inhibition of thrombin

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85

anticoagulant uses

stroke prevention with nonvalvular AFib/flutter, DVT/PE prophylaxis after THA and TKA

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86

anticoagulant route

PO

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87

anticoagulant nursing implications

hold medication for 24-48 hours before any invasive procedures, unsafe while pregnant, educate on signs of bleeding, assist pt to see insurance coverage, don’t give to pts undergoing spinal puncture/anesthesia

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88

anticoagulant side effects

bleeding (lower than warfarin), neurologic injury

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89

anticoagulant reversal agent

rivaraxaban (Xarelto) & apixaban (Eliquis)=andexanet alfa (AndexXa), dabigatran (Pradaxa)=Praxbind

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90

heparin (unfractionated)

work by activating antithrombin (a protein that inactivates two major clotting factors)

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91

heparin (unfractionated) uses

PE, DVT, MI, low dose post-op, during dialysis, CABGs

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92

IV heparin

given to maintain steady levels of heparin; initial dosing is a weight-based bolus followed by a weight-based infusion titrated to lab results

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93

subq heparin

low dose is given for prophylaxis against thromboembolism while hospitalized; 5000 units Q 8-12 hours for duration of hospitalization; doesn’t require aPTT monitoring

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94

heparin (unfractionated) nursing implications

serum blood levels must be monitored with aPTT levels when given IV, MM uses factor Xa for monitoring; CBC must be monitored for anemia and thrombocytopenia; hemorrhage can occur at any site and can be fatal; pt ed extremely important (avoid falls while hospitalized)

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95

heparin side effects

hemorrhage, heparin-induced thrombocytopenia

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96

heparin contraindications

thrombocytopenia, uncontrolled bleeding, hemophilia, dissecting AAA, PUD, hemorrhagic stroke

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97

heparin antidote

protamine sulfate

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98

heparin orders

heparin 5000 units IVP STAT, then follow standard heparin IV protocol with Xa monitoring

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99

LMWH examples

enoxaparin (Lovenox), dalteparin (Fragmin)

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100

LMWH mechanism

heparin preparations composed of molecules that are shorter than those found in heparin

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