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488 > Class 2 CV > Flashcards

Class 2 CV Flashcards

1
Q

Coagulation modifiers

A

-Anticoagulants
-Antiplatelets

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2
Q

Coagulation modifiers: General overview

A

-Anticoagulants, antiplatelet & thrombolytic drugs
-Hemorheological drugs→ alter platelet function (don’t block)
-Antifibrinolytic drugs→ promote coagulation and manage conditions with excessive bleeding

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3
Q

Anticoagulant drugs and functions (SCDHg)

A

-Heparin & glycosaminoglycans; inhibit clotting factors IIa (thrombin) and Xa
-Direct thrombin (IIa) inhibitors
-Selective factor Xa inhibitor
-Coumadins; inhibit vitamin K clotting factors II, VII, IX & X

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4
Q

Heparin drugs

A

-“parins”

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5
Q

Coumadin drugs

A

Warfarin Na+

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6
Q

Glycosaminoglycan drugs

A

Danaparoid Na+

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7
Q

Direct thrombin inhibitor drugs (BDHA)

A

-Human antithrombin III
-Argatroban
-Bivalirudin
-Dabigatran etexilate mesylate

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8
Q

Selective factor Xa inhibitor drugs (FAR)

A

-Fondaparinux
-“abans”

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9
Q

Antiplatelet drugs (MGAP)

A

-P2Y12 inhibitors
-Aggregation inhibitors/vasodilators
-Glycoprotein IIb/IIIa inhibitors
-Miscellaneous

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10
Q

Aggregation inhibitors/vasodilators

A

Treprostinil

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11
Q

P2Y12 inhibitors

A

-“grel”

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12
Q

Glycoprotein IIb/IIIa inhibitors (TEA)

A

-Abciximab
-“fib”: Eptifibatide,Tirofiban

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13
Q

Miscellaneous antiplatelet drugs

A

-Anagrelide hydrochloride
-Dipyridamole

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14
Q

Coagulation modifiers

A

-Lyse clots
-Thrombolytics
-Promote clot formation
-Antifibrinolytics
-Reversal drugs

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15
Q

Thrombolytic functions

A

-Dissolve thrombi
-Activate plasminogen
-“plase”

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16
Q

Antifibronolytics

A

-Prevent lysis of fibrin
-Reduce blood viscosity

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17
Q

Prevent lysis of fibrin

A

-Systemic hemostats
-Tranexamic acid, aprotinin

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18
Q

Reduce blood viscosity (HP)

A

-Hemorheological
-Pentoxifyline

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19
Q

Reversal drugs

A

-Heparin Na+ antagonist; protamine sulphate
-Warfarin Na+ antagonist; vitamin K

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20
Q

Anticoagulants: General overview

A

-Prevent formation of a clot
-Remember, they cannot lyse any clot that has already been formed (as in the case of a stroke or pulmonary embolism)

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21
Q

Common anticoagulants

A

-“parins”, “abans”
-Warfarin (Coumadin)
-Argatroban, Bivalirudin, Dabigatran
-Fondaparinux

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22
Q

Low molecular weight heparin (LMWH); enoxaparin, dalteparin, tinzaparin: Indications for use

A

-AMI, UA, stroke
-Immobility, DVT, PE
-Indwelling devices such as heart valves
-Pre-op to prevent pooling of blood

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23
Q

Warfarin, rivaroxaban, or apixaban indications for use

A

Atrial fibrillation

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24
Q

Dabigatran indications for use

A

Prevention of strokes and thrombosis in patients with nonvalvular atrial fibrillation

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25
Q

Argatroban indications for use

A

Treatment of active or risk for HIT and PCI operation

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26
Q

About heparin (half-life, onset, peak, duration)

A

-1-2 hour half-life
-Onset:
-SC: 20-60 minutes
-IV: Immediate
-Peak
-SC: 2-4 hours
-Duration: Dose-dependent

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27
Q

Heparin (Hepalean, Heparin LEO, Hep LOK)

A

-Prevents
-“heparin” refers to “unfractionated heparin”
-Q6H measurement of PTT until anticoagulant effect is reached

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28
Q

Heparin (Hepalean, Heparin LEO, Hep LOK): SC & IV therapy indications for use

A

-S.C., dosing used post-op or with decreased mobility
-I.V. therapy: DVT, PE, AMI, A fib

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29
Q

Heparin (Hepalean, Heparin LEO, Hep LOK) toxicity symptoms

A

-hematuria, melena, petechiae, ecchymoses, and gum or mucous membrane bleeding

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30
Q

Heparin induced thrombocytopenia (HIT)

A

-Thrombocytopenia- low platelet count
-Allergic reaction mediated by the production of IgG antibodies
-Immune complexes bind to platelets, resulting in platelet activation and thrombin generation

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31
Q

Heparin induced thrombocytopenia (HIT) types of increased

A

-HIT I→ gradual reduction in platelets (heparin is usually continued)
-HIT II→ >50% acute drop in platelet level

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32
Q

Treatment of heparin induced thrombocytopenia (HIT)

A

thrombin inhibitors bivalirudin and argatroban

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33
Q

Nursing considerations of heparin induced thrombocytopenia (HIT)

A

-Thrombosis in the presence of HIT can be fatal

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34
Q

Low molecular weight heparin (LMWH) (form, function, why its better than heparin)

A

-Enoxaparin, dalteparin, tinzaparin
-Synthetic SC injection
-Greater affinity for factor Xa
-Higher bioavailability and longer half-life than unfractionated Heparin
-More predictable anticoagulant response than heparin
-Frequent lab monitoring not required
-Patients can be “bridged” with Coumadin therapy (warfarin)

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35
Q

Low molecular weight heparin reversal

A

Protamine, same as heparin reversal

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36
Q

About Warfarin (Coumadin) (half-life, onset, peak, duration, form, use, monitoring)

A

-Half-life: 0.5-3 days
-Onset: 12-24 hours
-Peak: 3-4 days
-Duration: 2-5 days
-PO, long-term anticoagulation
-Monitor PTT/INR
-A ‘normal’ INR is 1, for someone receiving Coumadin a therapeutic INR is usually 2-3 OR 2.5-3.5 for a mechanical valve

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37
Q

Warfarin (Coumadin) antidote (when to discontinue, how it works & how long to resynthisize, drug reversal, resistance time)

A

-Discontinued if INR is high
-Coumadin inactivates the vitamin K-dependent clotting factors which are synthesized in the liver; discontinuing therapy may take 36-42hrs before it can be resynthesized
-10-15 mg vitamin K IV can reverse anticoagulation effects within 6 hrs; risk of anaphylaxis
-Fresh Frozen Plasma to reverse the anticoagulation effects during an acute bleed
-Redraw INR
-After administration of vitamin K, warfarin resistance will occur for up to 7 days

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38
Q

Dibagatran: Thromboprophylaxis after elective hip or knee replacement

A

-150-220mg daily
-14 days for knees and 30 days for hips

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39
Q

Dabigatran dosing: Non-valvular atrial fibrillation

A

-110 or 150mg BID
-CR Cl>30mL/min

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40
Q

Rivaroxaban: Thromboprophylaxis after elective hip or knee replacement

A

-10mg daily
-14 days for knees, 30 days for hips

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41
Q

Rivaroxaban dosing: Non-valvular atrial fibrillation

A

-15 or 20mg daily
-CR Cl 30-49mL/min

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42
Q

Rivaroxaban dosing: Venous thromboembolism

A

-15mg BID for 21 days then 20mg daily

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43
Q

Anticoagulant contraindications

A

-Thrombocytopenia
-Pregnancy
-LMWHs cannot be administered to patients with indwelling epidural catheter; epidural hematomas

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44
Q

Anticoagulant adverse events

A

-Bleeding, no IM injections, be cognizant of surgery
-Use of aspirin or other drugs that impair platelet function
-N/V, abdominal cramps, thrombocytopenia
-Warfarin (Coumadin); bleeding, lethargy, muscle pain, necrosis, and “purple toes” syndrome

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45
Q

Warfarin: Drug to drug interactions: Acetaminophen, amiodarone, bumetanide

A

-Displacement from inactive protein-binding sites
-Increased anticoagulant effect

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46
Q

Warfarin: Drug to drug interactions: Furosemide, ASA/NSAIDs, broad spectrum anitbiotics

A

-Decreased platelet activity

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47
Q

Warfarin: Drug to drug interactions: Barbiturates, carbamazepine, rifampin, phenytoin

A

-Enzyme induction
-Decreased anticoagulant effect

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48
Q

Warfarin: Drug to drug interactions: Amiodarone, cimetidine, ciprofloxacin, erythromycin, ketoconazole, metronidazole, omeprazole, sulfonamides, macrolides

A

-Enzyme inhibition
-Increased anticoagulant effect

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49
Q

Warfarin: Drug to drug interactions: HMG-CoA reductase inhibitors (statins), cholestyramine, sucralfate

A

-Impaired warfarin, Na+ absorption
-Decreased anticoagulant effect

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50
Q

Warfarin: Drug to drug interactions: Natural Health Products: dong quai, garlic, ginkgo biloba

A

-Increased INR
-Increased bleeding risk

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51
Q

Warfarin drug to food interactions: St. John’s Wort, ginseng (alone & in cold-FX)

A

-Decreases INR
-Increased risk for clotting

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52
Q

Heparin Na+ drug to drug interactions: Aspirin & other NSAIDs

A

-Decreased platelet activity
-Increased bleeding risk

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53
Q

Heparin Na+ drug to drug interactions: Oral anticoagulants & thrombolytics

A

-Additive
-Increased anticoagulant effect

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54
Q

Antiplatelet drug to drug interactions: Aspirin & other NSAIDs

A

-Decreased platelet activity
-Increased bleeding risk

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55
Q

Antiplatelet drug to drug interactions: Warfarin, heparin Na+. thrombolytics, rifampin

A

-Additive
-Increased bleeding risk

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56
Q

Antiplatelet drug to drug interactions: Natural health products; garlic, ginkgo, kava

A

-Increased effects
-Increased bleeding risk

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57
Q

Antipatelet drug to food interactions

A

-Foods high in vitamin K increase risk of clotting

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58
Q

Anticoagulant nursing considerations

A

-Will administration increase or decrease bleeding or clotting, what conditions do I need to monitor for in this patient post administration, are there any procedures that warrant holding the medication
-Monitor labs daily when on anticoagulants; know what is important to follow for trends and why INR vs PTT
-Understand what bridging patient therapy means for management of conditions
-Monitor for treatment outcomes

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59
Q

Anticoagulant patient teaching

A

-Regular lab testing
-Avoid foods high in vitamin K
-Consume with 1 cup of water

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60
Q

Antiplatelet therapy: General overview

A

-Prevent clot formation by inhibiting platelet aggregation at the site of injury
-Each drug has unique mechanism of action properties

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61
Q

Antiplatelet common medications

A

-Acetylsalicylic acid (ASA/aspirin)
-Dipyridamole, pentoxyfylline
-“grels”
-GP IIb/IIIa Inhibitors

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62
Q

Aspirin MOA

A

-Used for antiplatelet & analgesic, anti-inflammatory and antipyretic properties
-Effects last lifespan of platelet which is 7 days
-Prevents the formation of thromboxane A2 from leading to dilation of blood vessels and platelet aggregation

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63
Q

Dipyridamole MOA

A

-Prevent release of substances that stimulate platelet aggregation

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64
Q

Clopidogrel MOA

A

-ADP inhibitors
-Inhibits platelet aggregation by altering the platelet membrane so that it doesn’t receive signals to form a clot

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65
Q

Pentoxifylline MOA

A

-Reduces blood viscosity by increasing flexibility of red blood cells and reduces the aggregation of platelets
-Inhibits ADP, serotonin, and platelet factor IV

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66
Q

GP IIb/IIIa inhibitors MOA

A

-Block receptor protein GP IIb/IIIa that occurs in the platelet wall membranes

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67
Q

Aspirin indications for use

A

-CAD
-First line of defense for acute coronary syndrome
-Chronic stable angina
-Post PCI, CABG, prosthetic valve insertion, TIA, & cardiac endarterectomy
-Patients with PAD, secondary prevention for venous thrombosis events
-Daily doses of 75 mg to 160 mg

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68
Q

Dipyridamole indications for use

A

-Used with warfarin to prevent postoperative thromboembolisms

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69
Q

Clopidogrel indications for use

A

-Post AMIs prevention of thrombosis, reducing thrombotic strokes

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70
Q

Pentoxifylline indications for use

A

-Peripheral vascular disease

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71
Q

GP IIb/IIIa inhibitors indications for use

A

-UA & AMI, angioplasty procedures (typically have arrhythmias after PCI)

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72
Q

Antiplatelet contraindications

A

-Thrombocytopenia, leukemia
-Traumatic injury, GI Bleed, recent stroke
-Vitamin K deficiency

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73
Q

Aspirin adverse events (CNS)

A

Drowsiness, dizziness, confusion, flushing

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74
Q

Aspirin adverse events (GI)

A

-N/V, bleeding, diarrhea

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75
Q

Aspirin adverse events (hemotalogical)

A

-Thrombocytopenia, leukopenia, neutropenia, hemolytic anemia, agranulocytosis, bleeding

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76
Q

Clopidogrel adverse events (CV)

A

-Chest pain, edema

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77
Q

Clopidogrel adverse events (CNS)

A

-Flu-like symptoms, fatigue, headache, dizziness

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78
Q

Clopidogrel adverse events (GI)

A

-Abdominal pain, diarrhea, nausea

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79
Q

Clopidogrel adverse events (miscellaneous)

A

Epistaxis, rash, pruritus

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80
Q

Ticagrelor adverse events (respiratory & miscellaneous)

A

Dyspnea (on initiation)
Elevated uric acid levels

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81
Q

GP IIb/IIIa inhibitors adverse events (CV)

A

-Bradycardia, hypotension, edema

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82
Q

GP IIb/IIIa inhibitor adverse events (CNS)

A

Dizziness

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83
Q

GP IIb/IIIa inhibitor adverse events (hematological)

A

-Bleeding, thrombocytopenia

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84
Q

Antiplatelet nursing considerations

A

-aBleeding
-Withhold drugs 5-7 days prior to surgical procedures
-Perform baseline CV assessment for medications and document pre-existing chest pain, edema, headache, dizziness, epistaxis or flu like symptoms

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85
Q

Aspirin contraindications

A

-Aspirin not to be used in young ppl or patients with with any bleeding disorder, vit K deficiency or with peptic ulcer disease

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86
Q

Antiplatelets + Pt teaching

A

-2-3 months for therapeutic effect
-Change position slowly d/t dizziness and orthostatic hypotension

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87
Q

Thrombolytics overview

A

-“Clot Busters”
-Streptokinase, tissue plasminogen activator [t-PA (alteplase and Tenecteplase (TNK)]

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88
Q

Thrombolytics indactions for use

A

-MI, arterial thrombosis, DVT, PE
-Occlusion of catheter or shunts
-Acute ischemic stroke

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89
Q

Thrombolytic adverse effects

A

-Internal, intracranial, and superficial bleeding
-N/V, hypotension, dysrhythmias

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90
Q

Thrombolytic interactions

A

-Increased bleeding tendency from use of anticoagulants, antiplatelet, or other drugs that affect platelet function

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91
Q

Anti-thrombolytics

A

-Tranexamic acid
-Aprotinin
-DDAVP

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92
Q

Thrombolytic nursing considerations

A

-Monitor IV sites, no IM injections
-Monitor bleeding from wounds or from the GI, GU, or respiratory tract
-Monitor for internal bleeding (decreased BP, restlessness, increased pulse)

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93
Q

Thrombolytic nursing considerations when monitoring labs (aspirin)

A

Monitor CBC (Hgb, hematocrit, platelet counts), PTT and INR

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94
Q

Nursing considerations when monitoring labs: Clopidogrel

A

-Monitor CBC (Hgb, hematocrit, platelet counts), PTT and INR
-Contact healthcare provider if platelet levels are less than 90 x 109 /L

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95
Q

Nursing considerations when monitoring labs: GP IIb/IIIa inhibitor

A

-Monitor PTT levels

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96
Q

Nursing considerations when monitoring labs: Thrombolytics

A

Monitor CBC (Hgb, hematocrit, platelet counts), PTT and INR, fibrinogen levels

97
Q

Antilipemic medications overview

A

-Reduce lipid levels
-Ezetimibe (Ezetrol)- cholesterol inhibitor
-PCSK9 Inhibitors Monoclonal Antibodies (Evolocumab and Airocumab); for abnormal accumulation of lipids
-For patients at risk of atherosclerotic CVD

98
Q

Classes of antilipemic medications

A

-HMG-CoA reductase inhibitors (statins)
-Bile acid sequestrants
-Vitamin B niacin (nicotinic acid)
-Fibric acid (fibrates)

99
Q

Antilipemic medications are prescribed for people with…

A

-Decreased cholesterol
-Increase HDL
-Decrease LDL

100
Q

Antilipemics: HMG-CoA reductase inhibitors

A

-Inhibit enzyme that catalyzes the rate-limiting step in the synthesis of cholesterol
-“statins”
-First line drug post AMI

101
Q

Antilipemics: HMG-CoA reductase inhibitors (statins): Contraindications

A

-Pregnant or breastfeeding
-Liver dysfunction or elevated transaminase levels
-Elevated liver enzymes

102
Q

Atorvastatin Ca+: Half-life, onset, peak, duration

A

-Half-life: 13-16 hours
-Onset: 1-2 hours
-Peak: 2 weeks
-Duration: Unknown

103
Q

Atorvastatin Ca+ (does what, administered when, approved for who, available in what)

A

-Lowers total cholesterol LDL and triglycerides, raises HDL
-Administered in the evening
-Only statin approved for use in children
-Available in combination with calcium channel blocker amlodipine (Caudet)

104
Q

Antilipemics: HMG-CoA reductase inhibitors (statins): Adverse effects

A

-Myopathy (muscle pain) which may progress to a serious condition known as rhabdomyolysis
-Rhabdomyolysis involves the breakdown of muscle protein leading to myoglobinuria
-Excretion of this abnormal urinary protein can lead to acute kidney failure
-Report muscle pain or discomfort

105
Q

Antilipemics: Ezetimibe (half-life, onset, peak, duration)

A

-Half-life: 22 hours
-Onset: Unknown
-Peak: 4-12 hours
-Duration: Unknown
-Only cholesterol absorption inhibitor

106
Q

Functions of ezetimibe

A

-Selectively inhibits absorption of cholesterol and related sterols in the small intestine
-Reduces total cholesterol, LDL-C, Apo B, and triglycerides
-HDL-C serum level increase
-These beneficial effects are enhanced when combined with a STATIN

107
Q

Contraindications of ezetimibe

A

-Active liver disease or unexplained elevations in liver enzymes

108
Q

Antilipemic lab nursing considerations

A

-Monitor liver function tests (bili, AST, ALT, Alk Phos, GGT) for toxicity, cholesterol lab test (TG, TC, HDL, LDL) for treatment outcomes, and creatinine, BUN, GFR for kidney dysfunction

109
Q

Antilipemic nursing considerations + CV adverse events/diabetes

A

-Monitor for CV events & diabetes (troponin, fasting blood glucose)

110
Q

Antilipemic nursing considerations + HMG-CoA reducase inhibitors adverse events

A

-Monitor for rhabdomyolysis (muscle soreness, changes in urine color, fever, malaise, & N/V). If rhabdomyolysis is suspected, CK levels will be drawn

111
Q

Antilipemic nursing considerations (adverse events)

A

-GI upset
-Increased liver enzymes
-Hepatomegaly
-Myalgias

112
Q

Acute HF management goals

A

-Improve ventricular function, gas exchange, oxygenation & CO
-Decrease preload, afterload & intravascular volume

113
Q

Clinical presentations of HF (respiratory)

A

-Dyspnea, decreased SpO2
-Crackles/wheezing

114
Q

Clinical presentations of HF (CV)

A

-Low BP, weak pulse
-Edema, JVD, ascites
-Infarct, S3 gallop, tachycardia

115
Q

Clinical presentations of HF (neurological)

A

-Anxiety, confusion, fatigue, dilated pupils

116
Q

Clinical presentations of HF (integumentary)

A

-Cool, moist, pale, gray or cyanotic

117
Q

Clinical presentations of HF (GI/GU)

A

-N/V
-Enlarged spleen & liver
-Decreased urine output

118
Q

Pharmacological management goals in heart failure

A

-Improve ventricular function
-Decrease intravascular volume
-Decrease preload
-Decrease afterload
-Improve gas exchange and oxygenation
-Increase CO

119
Q

Drugs to increase CO in heart failure

A

-Loop diuretic→ Furosemide
-O2, nitro patch, ACE I
-Digoxin, beta blockers
-In critical care: Dobutamine and nitro infusions

120
Q

Investigations in HF

A

-Chest x-ray, ECG
-Echocardiogram to assess ejection fraction; transthoracic echocardiogram

121
Q

Labs to monitor in HF

A

-CBC
-Kidney function tests
-Electrolytes
-BUN
-Creatinine
-Glucose
-Hemoglobin
-Liver enzyme
-Lipid
-Thyroid function tests

122
Q

Disorders of the heart wall

A

Acute pericarditis, pericardial effusion, cardiac tamponade

123
Q

Acute pericarditis diagnostic indicators

A

-12-lead ECG (ST elevation) & chest pain that is relieved by sitting forward

124
Q

Management of acute pericarditis

A

-NSAIDs (Ibuprofen 600 mg TID)
-ASA
-Corticosteroids
-Proton pump inhibitor to prevent GI bleed

125
Q

Pericardial effusion diagnostic tests

A

-Echocardiogram to identify presence of fluid
-CT chest or cardiac MRI

126
Q

Pericardial effusion medications

A

-NSAIDs
-ASA
-Corticosteroids
-PPI

127
Q

Pericardial effusion labs

A

-CRP
-Troponin
-WBCs if on corticosteroids

128
Q

Cardiac tamponade management

A

-Pericardiocentesis guided by ultrasound
-Post procedure monitor for infection and leaking of fluid from the site

129
Q

Cardaic tamponade medications

A

-NSAIDs
-ASA
-Corticosteroids
-PPI

130
Q

All disorders of the heart wall (pericarditis, pericardial effusions & cardiac tamponade) have what in common?

A

Medications

131
Q

DVT lab values

A

-CBC: Hemoglobin, hematocrit, platelets
-Coagulation: ACT, PTT, INR, D-dimer (to rule out PE)

132
Q

Invasive investigations for DVT

A

-CT
-Venography

133
Q

DVT interventions

A

-TED stockings
-Intermittent pneumatic compression device

134
Q

DVT management to prevent DVT (prophylaxis)

A

-Prophylaxis tx: Heparin or LMWH sc injections, “abans”, and dabigatran

135
Q

DVT management after diagnosis

A

-Heparin IV, thrombolytics
-Venous thrombectomy or insertion of a filter to prevent movement of the embolus
-Pain management

136
Q

DVT patient teaching

A

-Modify risk factors for developing another clot
-Explain S&S (sudden onset of dyspnea, tachypnea, and pleuritic chest pain)
-Create medication regime including dosages, actions, adverse effects, reason for routine blood tests, and symptoms to report
-Avoid activities with high risk for trauma
-If injury occurs, instruct patient and family to apply pressure to wound for 10-15 minutes
-Well-balanced diet→ calcium and vitamin E

137
Q

Modified risk factors for developing another clot

A

-Encourage mobility
-Compression stockings
-Smoking cessation
-Discontinue birth control or oral hormone replacement therapy
-Avoid stagnation

138
Q

Aortic aneurysm diagnostic studies

A

-Chest x-ray, EKG, Echocardiography, CT scan, MRI, and angiography

139
Q

Collaborative care for an aortic aneurysm

A

-Hydraton and all electrolyte, coagulation and hematocrit abnormalities corrected prior to surgery
-Surgery with goal of normal tissue perfusion, intact motor and sensory function, and no complications related to surgical repair
-ICU post op

140
Q

Endovascular abdnominal aortic aneurysm repair

A

-Most common complication from EVAR is endoleak; the seepage of blood back into the old aneurysm
-May require open surgical repair
-Discovered by inserting a catheter and using a transducer system

141
Q

Aortic aneurysm: Abdominal compartment syndrome

A

Patients may also develop intra-abdominal hypertension associated with abdominal compartment syndrome; reduces blood flow to the viscera

142
Q

Aortic aneurysm repair: Post operative care

A

-Monitor for abdominal compartment syndrome & BP for graft patency
-Infection
-CV&GI status

143
Q

Monitoring BP graft for patency

A

-Hypotension may lead to the graft clotting; IV fluids and blood products for adequate blood flow. Monitor urine output.
-Hypertensive periods may cause leaking or rupture suture lines; Furosemide or IV antihypertensive medications (nitroprusside, esmolol, and labetalol)

144
Q

Monitoring CV status post aortic aneurysm repair

A

-Monitor for AMI d/t decreased myocardial O2 supply or increased demands
-Monitor for cardiac dysrhythmias d/t electrolyte imbalances, hypoxemia, hypothermia, or MI
-ECG, ABG draws, pain control, IV antidysrhythmic and antihypertensive meds

145
Q

Monitoring for infection post aortic aneurysm repair

A

-Administer broad spectrum antibiotics cefazolin (Ancef)
-Monitor Labs and wound for signs of infection

146
Q

Monitoring GI status post aortic aneurysm repair

A

-Paralytic ileus may occur; nasogastric tube may be placed
-Monitor for pain (ischemic gut or bowel infarction due to low blood supply)

147
Q

Aortic aneurysm repair: Post operative care overview

A

-Close monitoring of neurological status
-Maintenance of peripheral & renal Perfusion

148
Q

Aortic aneurysm labs to monitor

A

-CBC
-Coagulation factors
-Electrolytes
-Kidney function tests
-Specialty labs
-ABG

149
Q

Aortic dissection nursing management

A

-HR, BP control & pain management
-Maintain MAP >65 mm Hg (diastolic pressure ~ 44 mm Hg (antihypertensives))
-Cardiac monitoring
-Monitor urine output, peripheral pulses & capillary refill

150
Q

Preoperative and postoperative care for an aortic dissection

A

-Maintain quiet, calm environment
-SF position (HF increases stroke volume)

151
Q

Discharge teaching following an aortic dissection

A

antihypertensive therapy for life, regular follow-up, emergency treatment if pain recurs

152
Q

Types of congenital heart disease

A

-Acyanotic
-Cyanotic

153
Q

Acyanotic shunting of blood

A

-Left to right

154
Q

Acyanotic cyanosis

A

Not usual (unless CHF)

155
Q

Acyanotic surgery

A

-Usually done in one stage

156
Q

Acyanotic prognonsis

A

Very good/excellent

157
Q

Acyanotic types

A

-Ventricular septal defect
-Coarctation of the aorta

158
Q

Cyanotic shunting of blood

A

Right to left

159
Q

Cyanotic cyanosis

A

Always “blue babies”

160
Q

Cyanotic surgery

A

Usually done in several stages

161
Q

Cyanotic prognosis

A

Guarded

162
Q

Cyanotic types

A

-Tetralogy of Fallot
-Transposition of the great arteries (TGA)

163
Q

Congenital heart disease (acyanotic)

A

-Defects with increased pulmonary blood flow; ventricular septal defect (VSD)
-Obstructive defects; coarctation of the aorta

164
Q

Ventricular septal defect (VSD) surgical treatments

A

-Palliative- Pulmonary artery banding
-Complete repair: Small defects repaired with sutures. Large defects usually require that a knitted patch be sewn over the opening.
-Cardiopulmonary bypass is used for both procedures

165
Q

Nonsurgical treatment of ventricular septal defect (VSD)

A

Device closure during cardiac catheterization

166
Q

Obstructive defects: Coarctation of the aorta (surgical treatment)

A

-Resection of the coarctation portion with an end-to-end anastomosis of the aorta or enlargement of the constricted section using a graft of prosthetic material or a portion of the left subclavian artery
-Percutaneous balloon angioplasty techniques have proved to be effective in relieving residual postoperative coarctation gradients

167
Q

Obstructive defects: Coarctation of the aorta surgical treatment & post operative HTN management

A

-IV Na+ nitroprusside, esmolol, or milrinone followed by PO ACE I or beta blockers
-To prevent HTN, elective surgery for COA is advised within the first 2 years of life

168
Q

Nonsurgical treatment of coarctation of the aorta

A

-Balloon angioplasty is being performed as a primary intervention for COA in older infants and children
-In adolescents, stents may be placed in the aorta to maintain patency

169
Q

Congential heart disease: Cyanotic

A

-Defects with decreased pulmonary blood flow; tetralogy of fallot
-Mixed blood flow; transposition of great arteries (TGA)

170
Q

Defects with decreased pulmonary blood flow: Tetralogy of Fallot (surgical treatment)

A

-Palliative shunt- Provides blood flow to the pulmonary arteries from the left or right subclavian artery via a tube graft
-Complete repair- Closure of the VSD and resection of the infundibular stenosis, with placement of a pericardial patch to enlarge the right ventricular outflow tract. In some repairs the patch may extend across the pulmonary valve annulus (transannular patch), making the pulmonary valve incompetent
-Procedure requires a median sternotomy and the use of cardiopulmonary bypass

171
Q

Mixed defects: Transposition of the great arteries (TGA)

A

-Therapeutic management (to provide intracardiac mixing)- IV prostaglandin E1. During cardiac catheterization or under echocardiographic guidance, a balloon atrial septostomy
-Surgical treatment; an arterial switch procedure
-Rastelli procedure—This procedure is the operative choice in infants with TGA, VSD, and severe pulmonic stenosis (PS)

172
Q

Acquired heart disease

A

-Kawasaki disease
-Rheumatic fever

173
Q

Kawasaki disease treatment

A

-IV immunoglobulin; single large infusion of 2g/kg over 10-12 hours
-Steroids (prednisone)
-ASA; 80-100 mg/kg/day in divided doses every 6 hours to control then after fever, continued as an antiplatelet doses (3-5 mg/kg/day) until platelet count as returned back to normal (6-8 weeks)
-Clopidogrel, enoxaparin or Warfarin may be indicated for medium-size or giant coronary artery aneurysms

174
Q

Kawasaki disease: Nursing considerations

A

-Echo to monitor for coronary artery aneurysms
-Encourage fluids and nutrition. Administer fluids cautiously d/t usual finding of myocarditis
-Clear liquids and soft foods
-Assess child for HF
-Provide symptomatic relief
-Family support due to irritability of child (hallmark sign of Kawasaki disease)

175
Q

Kawasaki disease: Patient teaching

A

-Follow-up monitoring
-Irritability to persist up to 2 months after onset of symptoms
-Monitor for arthritis
-Defer live immunizations after as antibodies may not form
-CPR training, monitor for AMI and cardiac ischemia in child

176
Q

Rheumatic fever treatment

A

-Eradication of hemolytic streptococci
-Prevention of recurrences & mitral stenosis
-Symptom relief

177
Q

Pharmacological intervention of rheumatic fever

A

-Penicillin with erythromycin as a substitute
-Salicylates, naproxen, or prednisone; controls inflammatory response (especially in the joints), and reduces fever and discomfort

178
Q

Rheumatic fever patient teachings

A

-Chorea is transitory and all manifestations eventually form into a disease

179
Q

Rates of the conduction system

A

-SA node; 60-100 times/min
-AV junction; 40-60 times/min
-Purkinje fibers; 20-40 times/min

180
Q

Paroxysmal supraventricular tachycardia

A

-150-250 bpm and regular
-Abnormal P shape (may be hidden)
-Variable P-R interval

181
Q

Clinical significance of SVT

A

-In a prolonged episode with a HR >180 bpm may decrease cardiac output resulting in hypotension, dyspnea, and angina

182
Q

SVT treatment

A

-Vagal maneuvers
-Adenosine
-Beta adrenergic & calcium channel blockers
-Amiodarone
-Defibrillation

183
Q

Atrial flutter

A

-Atrial: 250-350 bpm and regular
-Ventricular: >100 bpm and irregular
-Sawtooth P wave shape
-Variable P-R interval

184
Q

Clinical significance of atrial flutter

A

-Decrease cardiac output; HF
-Stroke

185
Q

Treatment of atrial flutter

A

-Calcium channel blockers, beta adrenergic blockers
-Defibrillation
-Amiodarone, propafenone, and ibutilide
-Radiofrequency ablation; catheter in the right atrium in between the IVC and tricuspid valve. Tissue is ablated and dysrhythmia is terminated

186
Q

Atrial fibrillation

A

-Atrial: 350-600 bpm and irregular
-Ventricular: >100 bpm and irregular
-Chaotic fibrillatory P wave
-P-R interval is absent

187
Q

Clinical significance of atrial fibrillation

A

-Decreased cardiac output because of loss of atrial kick
-Stroke

188
Q

Treatment of atrial fibrillation

A

-Calcium channel blockers and beta adrenergic blockers
-Amiodarone
-If clots are present defibrillation is contraindicated

189
Q

Junctional rhythms

A

-40-140 bpm and regular
-P wave inverted (may be hidden)
-P-R interval is variable

190
Q

Clinical significance of junctional rhythms

A

-Decreased cardiac output

191
Q

Treatment of junctional dysrhythmias

A

-Atropine
-Beta adrenergic blockers, calcium channel blockers and amiodarone

192
Q

First-degree AV heart block

A

-Regular rhythm
-Normal P wave
-P-R interval >0.20 seconds, constant

193
Q

Type I (mobitz type I, Wenckebach’s)

A

-Atrial: Regular
-Ventricular: Slower and irregular
-Normal P wave
-Progressively lengthened P-R interval
-Normal width with a pattern of one nonconducted QRS complex

194
Q

Clinical significance of type I (mobitz type I, Wenckebach’s)

A

-Usually results from myocardial ischemia or infarction
-May indicate AV conduction disturbance

195
Q

Treatment of type I (mobitz type I, Wenckebach’s)

A

-Atropine, temporary pacemaker

196
Q

Type II (Mobitz II)

A

-Atrial: Regular or irregular
-Ventricular: Slower and regular or irregular
-More P waves than QRS complex
-Normal or prolonged P-R interval
-Widened QRS, preceded by two or more P waves

197
Q

Type II (Mobitz II) clinical significance

A

-Decreased cardiac output
-Hypotension and myocardial ischemia

198
Q

Treatment of type II (Mobitz II)

A

-Temporary and then permanent pacemaker

199
Q

Third-degree AV heart block

A

-Ventricular rate 20-40 bpm
-Normal P wave with no connection to the QRS complex
-No P-R intervals related to the QRS; more P waves than QRS complexes
-Normal or widened QRS with no connection to P waves

200
Q

Third-degree AV heart block clinical significance

A

-Reduced cardiac output; ischemia, HF, shock
-Syncope

201
Q

Treatment of third-degree AV heart block

A

-Temporary and then permanent pacemaker
-Atropine, epinephrine, isoproterenol, and dopamine

202
Q

Premature ventricular contraction (PVC)

A

-6o-100 bpm and irregular
-No P wave
-No P-R interval
-Wide and distorted QRS complex

203
Q

Clinical significance of PVC

A

-May reduce cardiac output and cause angina and HF

204
Q

Ventricular tachycardia

A

-100-250 bpm and regular or irregular
-No P wave
-No P-R interval
-Wide and distorted QRS complex

205
Q

Clinical significance of ventricular tachycardia

A

-Decreased cardiac output
-Hypotension, pulmonary edema, decreased cerebral perfusion, cardiopulmonary arrest
-Ventricular fibrillation may develop

206
Q

Treatment of ventricular tachycardia

A

-Amiodarone
-Defibrillation
-Epinephrine

207
Q

Ventricular fibrillation

A

-Rhythm not measurable and irregular
-No P wave
-No P-R interval
-Immeasurable QRS complex

208
Q

Ventricular fibrillation clinical significance

A

-Unresponsiveness, pulselessness, apneic state

209
Q

Treatment of ventricular fibrillation

A

-CPR, defibrillation

210
Q

Sinus bradycardia

A

<60bpm

211
Q

Sinus bradycardia clinical significance

A

-Pale, cool skin
-Hypotension
-Weakness, angina, dizziness, syncope
-Confusion
-SOB

212
Q

Treatment of sinus bradycardia

A

-Atropine, pacemaker

213
Q

Sinus tachycardia clinical significance

A

-Depends on patients tolerance of increased HR
-Dizziness, dyspnea, and hypotension
-Angina or increased infarction size may occur if persistent

214
Q

Premature atrial contraction

A

-Irregular rhythm
-P wave is different than the one originating from the SA node
-PR interval may be shorter or longer but with normal length

215
Q

Premature atrial contraction clinical significance

A

-In people with heart disease, PACs may enhance automaticity of the atria or re-entry mechanism
-May initiate more serious dysrhythmias (SVT)

216
Q

Antidysrhythmic drugs

A

-Class I: Na+ channel blockers; Decrease conduction velocity in the atria, ventricles and His-Purkinje system
-Class Ia (procainamide, quinidine); delays repolarization, Widened QRS and prolonged QT interval
-Class Ib (Lidocaine, mexiletine, and phenytoin); accelerates repolarization
-Class Ic (flecainide, propafenone); decrease impulse conduction, Pronounced prodysrhythmic actions, widened QRS, prolonged QT interval
-Class II: Beta adrenergic blockers; Delay repolarization increasing prolonged duration of actional potential and prolonged refractory period, Prolonged PR and QT intervals, widened QRS, bradycardia
-Class IV: Calcium channel blockers; Decrease automaticity of SA node, delay AV node conduction; reduce myocardial contractility, Bradycardia, prolonged PR interval, AV block
-Other antidysrhythmics; Decrease conduction through AV node; reduce automaticity of SA node, ECG effects: Prolonged PR interval, AV block

217
Q

Cardiomyopathy

A

-Group of diseases affecting the structural or functional ability of the myocardium
-Primary cardiomyopathy; etiology of disease is unknown (idiopathic)
-Secondary cardiomyopathy; etiology of disease is known and is secondary to another disease process

218
Q

Causes of secondary cardiomyopathy: Dilated

A

-Cardiotoxic agents
-Alcohol, cocaine, doxorubicin
-Genetic
-HTN
-Ischemia
-Metabolic disorders
-Muscular dystrophy
-Myocarditis
-Pregnancy
-Valve disease

219
Q

Causes of secondary cardiomyopathy: Hypertrophic

A

-Aortic stenosis
-Genetic
-HTN

220
Q

Causes of secondary cardiomyopathy: Restrictive

A

-Amyloidosis
-Endomyocardial fibrosis
-Neoplastic tumor
-Post-radiation therapy
-Sarcoidosis
-Ventricular thrombus

221
Q

Dilated cardiomyopathy manifestations

A

-Fatigue, weakness, palpitations, dyspnea
-Cardiomegaly
-Contractility decreases
-Valvular incompetence
-Dysrhythmias
-Decreased cardiac output

222
Q

Hypertrophic cardiomyopathy manifestations

A

-Exertional dyspnea, fatigue, angina, syncope, palpitations
-Cardiomegaly is mild to moderate
-Decreased or increased contractility
-Mitral valve incompetence
-Atrial and ventricular dysrhythmias
-Normal or decreased cardiac output
-Increased outflow tract obstruction

223
Q

Restrictive cardiomyopathy manifestations

A

-Dyspnea & fatigue
-Mild cardiomegaly
-Normal or decreased contractility
-Atrioventricular valve incompetence
-Atrial and ventricular dysrhythmias
-Normal or decreased cardiac output

224
Q

Cardiomyopathy diagnostic methods

A

-History & physical exam
-Electrocardiogram
-B-type natriuretic peptide (BNP)
-Chest radiograph
-Echocardiogram
-Nuclear imaging studies
-Cardiac catheterization
-Endocardial biopsy

225
Q

Cardiomyopathy collaborative therapy

A

-Nitrates (except in HCM)
-Beta adrenergic blockers
-Antidysrhythmics
-ACE inhibitors
-Diuretics
-Mineralocorticoid receptor antagonist
-Digitalis (except in HCM) (unless used to treat atrial fibrillation)
-Anticoagulants
-Sacubitril valsartan
-Ventricular assist device
-Cardiac cardioverter-defibrillator
-Cardiac transplant

226
Q

Dilated cardiomyopathy

A

-Causes heart failure in 25-40% of cases
-Characterized by a diffuse inflammation and rapid degeneration of myocardial fibers
-Causes contractile dysfunction, in contrast to HF the walls do not hypertrophy
-Often follows an infectious myocarditis

227
Q

Hypertrophic cardiomyopathy

A

-Asymmetrical left ventricular hypertrophy without ventricular dilation
-Septum between the two ventricles becomes enlarged and obstructs blood flow from the left ventricle
-Often seen in active, athletic individuals

228
Q

Characteristics of hypertrophic cardiomyopathy

A

-Ventricular hypertrophy
-Rapid forceful contraction of the left ventricle
-Impaired relaxation
-Obstruction of LVOT

229
Q

Goals of intervention for hypertrophic cardiomyopathy

A

Improve ventricular filling by reducing contractility and relieving LVOT obstruction

230
Q

Treatment of hypertrophic cardiomyopathy

A

-Beta adrenergic blockers and calcium channel blockers

231
Q

Restrictive cardiomyopathy

A

-Impairs diastolic filling and stretch
-No current treatment exists other than trying to improve diastolic filling

232
Q

Primary varicose veins

A

caused by congenital weakness of the veins and are more common in women and are idiopathic

233
Q

Secondary varicose veins

A

-Typically occurs from a previous VTE
-May occur in the esophagus, vulva, spermatic cords, and anorectal area and as abnormal arteriovenous connections

234
Q

Reticular veins

A

smaller varicose veins that appear flat, less tortuous, and bluish green

235
Q

Telangiectasias (spider veins)

A

very small visible vessels that appear bluish-back, purple, or red

236
Q

Etiology of varicose veins

A

-Increased venous pressure
-Multifactorial and idiopathic

237
Q

Sclerotherapy

A

Injection that obliterates varicose veins 5mm or larger in diameter

238
Q

Nursing management of varicose veins

A

-Avoid stasis, avoid constrictive clothing and walk daily, deep breathing, and compression stockings

239
Q

High intakes of vitamin A is associated with

A

osteoporosis, fracture, and metaphyseal irregularity

488 (16 decks)

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