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Critical Care > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Cardiac Output Calculation

A

Heart Rate x Stroke Volume

Normal Range: 4 - 6 L/min (at rest)

Measure of contractility

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2
Q

Preload

A

Volume entering ventricles allows stretch and enhances force of contraction

Fluid volume

Right Ventricle: Central Venous Pressure, Blood Pressure, Heart Rate

Left Ventricle: Pulmonary Artery Pressure

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3
Q

Contractility

A

Force of muscle contraction itself

Myocardial Strength

Cardiac Index, Cardiac Output

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4
Q

Afterload

A

Pressure LV needs to overcome to eject blood

Systemic vascular resistance, valve compliance, viscosity of blood, aortic compliance

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5
Q

Stroke Volume is composed of…

A

Preload

Contractility

Afterload

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6
Q

Flow is determined by…

A

Pressure

Resistance

Volume

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7
Q

Principle of Hemodynamic Assessment

A

Pressure does not always equal flow

HTN can be a result of atherosclerosis

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8
Q

Cardiac Output

A

Volume of blood ejected by left ventricle per minute

Normal is 4-8 liters/minute

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9
Q

Cardiac Index

A

Adjustment to cardiac output made for body size

Normal is 2.5-4 liters/minute/m2

CO/BSA

Measure of contractility

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10
Q

Stroke Volume

A

Volume ejected each beat

Normal is 60-120 ml/beat

SYSTOLIC BLOOD PRESSURE

Measure of contractility

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11
Q

Ejection Fraction

A

Percentage of blood ejected from the left ventricle

Normal is 55-60%

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12
Q

Right Ventricle Preload Indirect Assessment

A

Jugular Venous Distention

Hepatojugular Reflex

Peripheral edema

Weight gain

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13
Q

Left Ventricle Preload Indirect Assessment

A

Chest x-ray

BNP

Lung sounds

S3

Blood pressure

Urine output

Weight gain

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14
Q

Direct Right Ventricle Preload Assessment

A

Central Venous Pressure (right atrial pressure)

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15
Q

Direct Left Ventricle Preload Assessment

A

PA Diastolic

PCWP (left atrial pressure)

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16
Q

Left Ventricle Afterload Assesment

A

Diastolic BP

Pulse pressure

Systemic Vascular Resistance

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17
Q

Right Ventricle Afterload Assessment

A

Causes: hypoxemia, PEEP, pulmonary HTN

Direct Assessment: Pulmonary Vascular Resistance, PA Systolic

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18
Q

Blood Pressure Formula

A

Cardiac Output x Systemic Vascular Resistance

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19
Q

Low Blood Pressure

A

Due to low cardiac output

Heart rate slow/fast

Preload low/high

Contractility low

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20
Q

Low Systemic Vascular Resistance

A

Vasodilation

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21
Q

Pulse Pressure < 35 with Tachycardia

A

Early sign of inadequate blood volume

Blood pressure 88/64 = Pulse Pressure of 24 (constricted)

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22
Q

Pulse Pressure > 35 with Tachycardia

A

Early sign of vasodilatory state

BP 82/30 = Pulse Pressure of 52 (dilated)

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23
Q

Vasoconstriction

A

Increased vascular tone

Compensation for low stroke volume

Shock states

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24
Q

Vasodilation

A

Decreased vascular tone

Abnormal pathology

Anaphylaxis, altered neurological control

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25
Q

Systemic Vascular Resistance Formula

A

MAP – CVP/CO x 80

Normal: 900 - 1400 dyns/sec/mm

Afterload for the left ventricle

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26
Q

Pulmonary Vascular Resistance Formula

A

MPAP – PAOP/CO x 80

Normal: 100 - 250 dyns/sec/mm

Afterload for the right ventricle

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27
Q

Principles of Hemodynamic Monitoring

A

Don’t just look at the numbers, look at the client

Single readings are not as significant as trends of data

Use the patients own normal for a reference

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28
Q

Invasive Monitoring

A

Pressure line with transducer

Heparinized solution

Phlebostatic reference point (4th intercostal space, midaxillary line)

“Zeroing” the system

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29
Q

Arterial Pressures

A

First check Allen’s test

Sharp upstroke with systole

Dicrotic notch at diastole

Problems: infection, accidental blood loss, impaired circulation to extremity

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30
Q

Mean Arterial Pressure

A

[Systolic + (2x Diastolic)] / 3

Normal: 70 - 105 mmHg

Perfusion Pressure

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31
Q

“Invasive” Cardiac Output Measurements

A

Thermodilution boluses

Continuous thermodilution measurements

Esophageal doppler

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32
Q

“Noninvasive” Cardiac Output Measurements

A

Arterial waveform assessment

PiCCO2

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33
Q

Computation of Cardiac Index

A

Cardiac Output / Body Surface Area

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34
Q

Mixed Venous Oxygen Saturation (SvO2)

A

MEASUREMENT OF O2 SATURATION IN VENOUS BLOOD

INDICATOR OF O2 BALANCE

Factors: CO, Hgb, SaO2, tissue oxygen metabolism

NORMAL: 60-80%, usually 70-75%

If SvO2 decreases more than 10% for more than 3-5 minutes, troubleshoot factors

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35
Q

Steps for Investigating Clinically Significant Changes in SvO2

A
  1. Assess the patient
  2. Examine the oxygen supply to the patient
  3. Evaluate cardiac functioning (VS, CO, CI)
  4. Check patient’s most recent Hgb level
  5. Consider nursing activities (repositioning)
  6. Resolve the clinically significant change before resuming other nursing cares
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36
Q

Central Venous Pressure

A

Normal range: 2 - 5 mmHg, 3 - 8 cm water

Affects PRELOAD

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37
Q

PA Systolic

A

Normal range: 20 - 30 mmHg

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38
Q

PA Diastolic

A

Normal Range: 5 - 10 mmHg

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39
Q

PAP Mean (PAPm)

A

Normal Range: 10 - 15 mmHg

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40
Q

Pulmonary Artery Pressure (PAOP)

A

Normal Range: 5 - 12 mmHg

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41
Q

Contractility

A

Ability to contract

Cardiac glycosides increase effectiveness

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42
Q

Excitability/Irritability

A

Ability to respond to an impulse

Stimulated by isoproterenol, epinephrine

Depressed by lidocaine, procainamide, quinidine

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43
Q

Conductivity

A

Allowance of transmission of impulse

Slow/delay through AV node (Digoxin)

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44
Q

Automaticity

A

Ability to create an impulse

Atropine and epinephrine increase impulse

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45
Q

Refractoriness

A

Inability to respond to another impulse

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46
Q

Indications for Antidysrhythmic Medications

A

Ventricular rate rapid with cardiac output reduced

Minor dysrhythmias threatening to develop into major (PVCs)

Major dysrhythmias have developed which may become fatal

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47
Q

Objectives for Antidysrhythmic Medications

A

To restore normal sinus rhythm

Abolish abnormal rhythm

Prevent reoccurrence of dysrhythmia

Control ventricular rate

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48
Q

Nursing Implications for Antidysrhythmic Medicaitons

A

Know toxic vs. therapeutic serum levels

Administer at even intervals to maintain blood levels

Check apical HR for a full minute (hold if < 60 or > 120)

Check blood pressure (hold if < 100 systolic or 30mmHg drop in previous reading)

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49
Q

Vaughan Williams Classification of Antidysrhythmic Medications

A

Based on the medications’ effects on the CELL ACTION POTENTIAL

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50
Q

Class I Antidysrhythmic Drugs

A

Sodium channel blockers in fast action potentials

Slows impulse conduction in atria and ventricles

Delays repolarization

(Quinidine, Procainamide, Lidocaine, Phenytoin)

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51
Q

Quinidine Use

A

Long-term suppression of atrial and ventricular dysrhythmias

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52
Q

Adverse Effects of Quinidine

A

Diarrhea

Cinchonism

Cardiotoxicity

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53
Q

Signs of Quinidine Toxicity

A

Widening of QRS

Prolonged QT interval

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54
Q

Drug Interactions for Quinidine

A

Doubles digoxin levels (risk for digoxin toxicity)

Administer slow IVP

Monitor serum levels

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55
Q

Procainamide Use

A

Long term suppression of atrial and ventricular dysrhythmias

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56
Q

Adverse Effects of Procainamide

A

Hypotension

SLE syndrome (70%)

Blood dyscrasias

GI symptoms

Cardiotoxicity

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57
Q

Signs of Procainamide Toxicity

A

Widened QRS

PROLONGED QT INTERVAL

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58
Q

Administration of Procainamide

A

Bolus 20 mg/min slow IVP

Maximum dose 600mg

Infusion 2-6 mg/min

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59
Q

Actions of Lidocaine

A

Slows conduction

Reduces automaticity

Accelerates repolarization

Used for ventricular dysrhythmias

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60
Q

Adverse Effects of Lidocaine

A

Drowsiness

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61
Q

Lidocaine Toxicity

A

Early signs: confusion, agitation

Late signs: seizures

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62
Q

Administration of Lidocaine

A

NEVER with epinephrine

50-100 mg IV bolus

1-4 mg/min IV drip

Short half life

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63
Q

Class II Antidysrhythmic Drugs

A

BETA ADRENERGIC BLOCKERS

Slows SA node automaticity, conduction through AV node, decreases myocardial contractility

CARVEDILOL AND METOPROLOL

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64
Q

Propranolol Actions

A

Nonselective alpha-blocker

Decreased SA node automaticity

Decreased AV conduction

Decreased myocardial contractility

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65
Q

Uses for Propranolol

A

SVT

Recurrent VT, VFib

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66
Q

Adverse Effects of Propranolol

A

Hypotension

AV block

Heart failure

Sinus arrest

Bronchospasms

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67
Q

Administration of Propranolol

A

1-3 mg/5 min slow IVP

Watch cardiac monitor during administration

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68
Q

Class III Antidysrhythmics

A

Potassium channel blockers

Delay depolarization and refractoriness of fast potentials

Anti-fibrillatory action

Amiodarone

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69
Q

Uses of Amiodarone

A

Ventricular and supraventricular tachydysrhythmias

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70
Q

Action of Amiodarone

A

Delays repolarization

Prolonged serum half-life

Do not give with bradycardia because this drug slows down the heart rate

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71
Q

Adverse Effects of Amiodarone

A

Hypotension

Bradycardias

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72
Q

Signs of Amiodarone Toxicity

A

Pulmonary toxicity

Paradoxical dysrhythmias

SA and AV blocks

Photophobia and blindness

Blue-gray skin

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73
Q

Administration of Amiodarone

A

150 mg IV infusion over 10 minutes

Enhances digoxin levels

Monitor liver enzymes, serum level, pulmonary status, and ocular funduses

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74
Q

Class IV Antidysrhythmics

A

Calcium channel blockers

Reduced SA node automaticity, delayed AV conduction, reduced myocardial contractility

Verapamil, diltiazem, nicardipine

Calcium channel blockers relax the smooth muscle

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75
Q

Verapamil Uses

A

Paraoxysmal SVT (SVTs that occur out of nowhere and then disappear; not sustained)

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76
Q

Actions of Verapamil

A

Reduced SA automaticity

Delayed AV conduction

Reduced myocardial contractility

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77
Q

Adverse Effects of Verapamil

A

Hypotension

Constipation

Bradycardias

Headache

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78
Q

Administration of Verapamil

A

3-10 mg slow IVP over 5 minutes

Monitor cardiac rhythm for response

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79
Q

Diltiazem Uses

A

Slow ventricular rate of SVTs

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80
Q

Contraindication of Diltiazem

A

CHF or heart failure

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81
Q

Adverse Effects of Diltiazem

A

AV blocks

Heart failure

Headache

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82
Q

Administration of Diltiazem

A

.25 mg/kg slow IVP

IV infusion 5-15 mg/hour

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83
Q

Uses of Digoxin

A

SVT

Heart failure

Slows AV node conduction, increased vagal stimulation, increased myocardial contractility

Slows the contraction of the heart muscles and makes the beats more effective

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84
Q

Adverse Effects of Digoxin

A

Prolonged PR interval

AV blocks

Nausea, vomiting, cramping

Visual disturbances (halos, based on hyperkalemia)

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85
Q

Signs of Digoxin Toxicity

A

Premature beats (PACs, PVCs)

AV blocks, prolonged PR interval

Nausea, vomiting, diarrhea

Halos seen around lights

Hyperkalemia

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86
Q

Administration of Digoxin

A

Loading dose: 1-1.5 mg slow IVP

May repeat bolus every 6-8 hours

MONITOR SERUM LEVELS

NOTE TIME OF CARDIOVERSION

MONITOR POTASSIUM

MANY DRUG INTERACTIONS

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87
Q

Adenosine Use

A

Paroxysmal SVT

WPW syndrome

Decreases SA automaticity

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88
Q

Adverse Effects of Adenosine

A

Sinus bradycardia

Bronchospasms

Hypotension

Facial flushing

Transient adverse effects, flatline for 3-6 seconds

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89
Q

Administration of Adenosine

A

6 mg rapid IVP with 10 mL flush –> next dose is 12 mg

No longer a priority drug in ACLS

Monitor cardiac rhythm

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90
Q

Uses of Ibutilide

A

Recent onset (< 90 days) of atrial fibrillation atrial flutter

Prolongs action protential

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91
Q

Adverse Effects of Ibutilide

A

Sustained ventricular tachycardia, PVCs

Prolonged QT interval

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92
Q

Administration of Ibutilide

A

1 mg/50 cc over 10 minutes IV infusion

0.01 mg/kg over 10 minutes

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93
Q

Antidysrhythmic-Antidysrhythmic Drug Interactions

A

Mechanism: Additive

Result: Pro-arrhythmic, may cause dysrhythmias

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94
Q

Antidysrhythmic-Anticoagulant Drug Interactions

A

Mechanism: Anticoagulants displaced from protein binding sites

Result: More pronounced anticoagulant effects

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95
Q

Antidysrhythmic-Phenytoin Drug Interactions

A

Mechanism: Phenytoin displaced from protein binding sites

Result: More pronounced Phenytoin effects

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96
Q

Antidysrhythmic-Sulfonylurea Drug Interactions

A

Mechanism: Sulfonylurea displaced from protein binding sites

Result: More pronounced sulfonylurea effects

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97
Q

Critical Thromboembolic States

A

CVA

MI

PE

DVT

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98
Q

Intrinsic Pathway Clotting Cascade

A

Activated by Factor XII

Blood comes in contact with foreign substance or damage endothelium in blood vessels

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99
Q

Extrinsic Pathway Clotting Cascade

A

Activated by Factor VII

Blood is exposed to substances released in response to tissue damage

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100
Q

Indications for Coumadin

A

PE, DVT treatment/prophylaxis

CVA prophylaxis in atrial fibrillation or valve replacement

Takes 8-14 days to reach full effect

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101
Q

Contraindications for Coumadin

A

Pregnancy

Recent or active hemorrhage

Recent surgery/trauma

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102
Q

Properties of Coumadin

A

Vitamin K antagonist

Effectiveness monitored by INR (target is 2-3)

Binds extensively to plasma proteins (lots of interactions)

Reversal: Vitamin K, Fresh Frozen Plasma

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103
Q

Dabigatran (Pradaxa)

A

Direct thrombin inhibitor (new alternative to Coumadin)

Fixed, more predictable dosing, minimal monitoring

History of compliance is necessary

Vitamin K not used for reversal–only FFP

Used for CVA prevention in AFib

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104
Q

Aspirin

A

Inhibits platelet aggregation

Inhibits COX enzyme

81 mg x4 in acute MI

Active stroke/MI prophylaxis

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105
Q

Clopidogrel (Plavix)

A

Irreversibly inhibits ADP, a promoter of platelet binding

600mg in AMI

Plavix plus aspirin given before coronary intervention and continued for a year

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106
Q

Integriln

A

Reversibly binds to GPIIb/IIIa platelet receptors and inhibits platelet aggregation

Bolus of 180 mcg/kg, then 2 mcg/kg/min infusion prior to and after PTCA

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107
Q

Reopro

A

Inhibits BP IIb/IIa platelet receptors and inhibits platelet aggregation

0.25 mg/kg bolus, then 10 mcg/min until PCI, and after

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108
Q

Heparin

A

Alters antithrombin III, stopping the clotting cascade

Prevents further thrombi in thrombotic events (DVT, PE, MI)

Weight-based protocols–bolus, then continuous drip

PTT monitored every 6 hours

Reversed with protamine sulfate

Contraindications: pregnancy, bleeding, epidural

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109
Q

Heparin Induced Thrombocytopenia

A

Occurs in up to 5% of clients receiving heparin therapy

Body forms antibodies to heparin-complexes, then attracts platelets

Vessel occlusion more likely than bleeding

Must discontinue heparin and use lepirudin

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110
Q

Symptoms of Heparin Induced Thrombocytopenia

A

MI: dyspnea, chest pain

CVA: headache, impaired speech

Peripheral: pain, pallor, mottling, decreased motor function

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111
Q

Fibrinolytics

A

“Clot busters” used only in emergencies (PE, AMI, CVA)

Reopens affected arteries

Very risky, extensive criteria for administration

112
Q

Administration of Fibrinolytics

A

CT prior to administration to rule out hemorrhage

TPA, streptokinase, retavase

Frequent neuro monitoring, vitals

No arterial sticks

113
Q

Contraindications of Fibrinolytics

A

Post CPR, recent surgery, recent trauma, BP greater than 180

Fall/injury precautions

CPR post administration usually fatal

114
Q

Alpha Adrenergic Receptors

A

Located in vessels of skin, kidney, intestines

When stimulated, peripheral vasoconstriction of arteries occurs

115
Q

Beta 1 Adrenergic Receptors

A

Located in cardiac tissue

When stimulated, heart rate increases, cardiac conduction and contractility increases

116
Q

Beta 2 Adrenergic Receptors

A

Located in vascular and bronchial smooth muscle tissue

When stimulated, vasodilation and peripheral arteries and bronchodilator occurs

117
Q

Sympathomimetic Agents

A

Stimulate adrenergic receptors, stimulated cardiovascular effects

Effects vary on the receptor stimulated and the dose delivered

Catecholamines

118
Q

Naturally Occurring Catecholamines

A

Dopamine

Epinephrine

Norepinephrine

119
Q

Synthetic Catecholamines

A

Dobutamine

Phenylephrine

Isoproterenol

Cause extensive tissue damage if extravasation occurs

Requires transdermal/subcutaneous injections of PHENTOLAMINE

120
Q

Dopamine

A

Stimulates alpha and beta receptors, as well as dopamine receptors

Low doses: dopamine receptors stimulated, renal and mesenteric perfusion increases, urine output increases

Moderate doses: heart contractility increases, CO increases, HR increases

High doses: vasoconstriction

121
Q

Epinephrine

A

Stimulates both alpha and beta receptors

Lower doses: effects beta receptors, increasing HR, contractility, and vasodilation

Higher doses: alpha receptor stimulation is predominate, resulting in vasoconstriction (increased afterload)

Increases workload of the heart (not good in MI)

122
Q

Norepinephrine

A

Similar to epinephrine, but does not stimulate beta-2, so no vasodilation

Lower doses stimulate beta-1, increasing contractility

Higher doses create vasoconstriction

Preferable vasoconstrictor in MI, tachycardia

123
Q

Vasopressin

A

Antidiuretic hormone

Stimulates vascular smooth muscle

Adjunct to norepinephrine infusion in septic shock

124
Q

Dobutamine

A

Predominantly Beta-1 effects (increases CO by increasing contractility)

Also stimulates Beta-2, resulting in mild vasodilation

Not used for HTN

Useful in heart failure, post-op heart surgery to increase CO without vasoconstriction

125
Q

Phenylephrine

A

Blocks histamine, stimulates only alpha receptors, causing vasoconstriction and increasing SVR

Decreases HR–useful in tachycardia, used often in euro events to increase blood pressure and cerebral perfusion

126
Q

Milrinone

A

Phosphodiesterase inhibitor

Inotrope and vasodilator–increased contractility plus decreased afterload

Can cause hypotension

Useful in heart failure and post-open heart surgery

127
Q

Vasodilators

A

Arterial or venous

Decreases preload, afterload, or both

Increases CO and decreases workload of the heart

128
Q

ACE Inhibitors

A

Vasodilation occurs by stopping Renin-Angiotensin-Aldosterone System

Used in heart failure to decrease SVR and PAOP (LV preload and afterload)

129
Q

Nitroglycerin

A

Both arterial and venous dilation, but more pronounced venous effect

Dilates coronary arteries

Used in angina

Decreases preload, relieving pulmonary congestion in heart failure

Side effects: hypotension, tachycardia, HEADACHE

130
Q

Nitroprusside

A

Potent arterial vasodilator (decreases afterload)

Works quickly and aggressively, short half-life

Contains thiocyanate to prevent toxicity

Nipride can increase blood pressure if high afterload is causing decreased CO, and causes hypotension

131
Q

Nicardipine

A

Calcium channel blocker

Arterial vasodilator, no effect on preload

Used for hypertensive emergencies only

132
Q

Beta-Blockers

A

Decrease HR and BP by dilating arteries and veins

Decrease the workload of the heart

133
Q

Unstable Angina

A

Character of Pain: New onset or change in pattern or pain

Enzymes: Normal

EKG Changes: Normal or ST depression

134
Q

NON-STEMI

A

Character of Pain: Can develop at rest

Enzymes: Elevated

EKG Changes: Normal or may have ST depression

135
Q

STEMI

A

Character of Pain: Can develop at rest

Enzymes: Elevated

EKG Changes: ST elevation

136
Q

Chronic Stable Angina

A

Episodic pain lasting 5-15 minutes

Precipitating factor present

Relieved by rest or nitroglycerin

137
Q

Unstable Angina

A

New onset angina

Chronic stable angina that increases in frequency, duration, or severity

Occurs at rest without precipitation

Unrelieved by rest or nitroglycerin

138
Q

INFERIOR WALL INJURY

A

Right coronary artery

Right ventricle involvement, SA and AV node dysrhythmias

II, III, and AVF leads

139
Q

ANTERIOR WALL INJURY

A

Left anterior descending artery

Left ventricle pump failure, CHF, cardiogenic shock

140
Q

Normal Range for Creatine Kinase

A

55-170 IU/L

CK is released when any muscle is damaged

141
Q

Normal Range for CK-MB/CK

A

< 5% CK

142
Q

Normal Range for Troponin I and Troponin T

A

0 - 0.4 ng/mL

143
Q

Chest Pain Medications to Know

A

Aspirin

Heparin

Nitroglycerin

Beta Blockers (Metoprolol)

Clopidogrel

Glycoprotein IIb/IIIa Inhibitors

Fibrinolytics (Streptokinase, Alteplase, Retaplase, Tenectaplase)

Statins

144
Q

Risk Factors for Chest Pain

A

Family history

Smoking

Diabetes, lipid disorder, hypertension, PVD

Previos CVA or TIA

Severe obesity

145
Q

Ischemia

A

Outer region of infarcted myocardial area

Viable tissue

T wave inversion

146
Q

Injury

A

Middle layer of tissue, potentially viable

ST segment elevation

147
Q

Infarction

A

Area of necrosis

Pathological Q waves, lack of depolarization of affected area

Replaced by scar tissue

148
Q

How to Manage LDL

A

Eat fresh fruits and vegetables

Ingest 20-30 grams per day of fiber

Use unsaturated vegetable oils instead of butter, coconut oil, lard

Reduce or avoid coconut or chocolate

149
Q

Blood Pressure Guidelines

A

Check blood pressure daily at the same time

Lopressor (Metoprolol) doses should be taken 12 hours apart

Restrict sodium

Limit alcohol consumption

Progressive aerobic exercise

150
Q

Cardiac Catheterization Lab Guidelines

A

Going within 90 minutes, no fibrinolytics

Going between 90-180 minutes, half-dose of thrombolytics

Going later than 2 hours, full dose of thrombolytics

151
Q

Contraindications to Fibrinolytic Therapy

A

Systolic > 180, Diastolic >110

Closed head/facial trauma, recent trauma, active bleeding (except menses)

Pregnancy

Active peptic ulcer, serious systemic disease

152
Q

Signs for Reperfusion due to Effective Fibrinolytic Therapy

A

Relief of chest pain

Ventricular dysrhythmias

ST segments return to baseline

Increase in cardiac enzymes

153
Q

Fibrinolytic Associated with Allergic Reactions

A

Streptokinase

154
Q

ER Priorities for Chest Pain

A

VS and pulse oximetry

O2 therapy

ECG monitor

Chewable ASA 324 mg PO

STAT 12 lead ECH

Nitroglycerin SL 1st dose

STAT cardiac enzymes

2 peripheral IVs 18-20 G

155
Q

Cautions with Aspirin

A

Allergies

Gastric bleeding

Bronchospasms

156
Q

Alternative for Aspirin due to Allergies

A

Plavix

157
Q

Eptifibatide

A

Glycoprotein IIb-IIIa inhibitor

Keeps clots from forming on catheters

158
Q

Rationale for Metoprolol

A

Vasodilator

Decrease workload of the heart

Decrease myocardial oxygen demand

159
Q

Post-Cardiac Catheterization Complications Associated with PTCA

A

Bleeding from femoral insertion site

Peripheral ischemia

160
Q

Prior to removing femoral sheath, what nursing intervention will protect from occlusion of femoral artery?

A

Aspirate 5-10 cc of blood from sheath

161
Q

Length of Bedrest Following Removal of Femoral Sheath

A

Flat in bed for 6-8 hours

162
Q

Chest Pain Following Cardiac-Catheterization

A

Prep for cardiac surgery

Nitroglycerin intravenous drip

163
Q

HDL Cholesterol Sources

A

Omega-3 fats (fish oil)

Dark chocolate

Nuts

Berries

164
Q

Proper Lipitor Schedule

A

Take at bedtime to maximize the effects on the liver

165
Q

Acute Coronary Syndrome

A

Thrombotic episode

Risk of acute myocardial infarction

Diagnosis: unstable angina, NSTEMI, STEMI

166
Q

Electrical Interventions for Cardiac Conditions

A

Defibrillation

Cardioversion

Pacemakers

Implanted Cardioverter

Defibrillators

Radiofrequency Ablation

Cardiac Resynchronization Therapy

167
Q

Defibrillation

A

Delivery of electrical current

Unsynchronized countershock

Asynchronous countershock

Sufficient intensity to depolarize cells

Used for VTACH and VFIB

Opportunity for heart’s natural pacemaker to take control

168
Q

Asynchronous Countershock

A

Delivery of current no relationship to cardiac cycle

169
Q

Manual Defibrillation

A

Place paddles/pads on chest

Professional interprets rhythm

Controls delivery of shock

170
Q

Automated External Defibrillator

A

Place pads on chest

Computer interprets rhythm

Computer gives instructions to deliver shock

171
Q

Steps for Defibrillation

A

Turn on machine

Place paddles/hold paddles on chest

CHARGE machine

CLEAR the area, look 360 degrees

Press shock

Assess patient

CPR

172
Q

Cardioversion

A

Delivery of electric shock; scheduled or emergency procedure

Patient is lightly sedated; IV line, ET tray available

Synchronized: timed to avoid relative refractory period of cardiac cycle (T wave, peak to end)

Machine identifies and released shock in safe period

173
Q

Rhythm Necessary for Cardioversion

A

Rhythm needs to have clearly identifiable QRS complex

Narrow QRS tachycardia

AFib, Atrial Flutter

Monomorphic Ventricular Tachycardia

174
Q

Pacemakers

A

ELECTRONIC DEVICE THAT DELIVERS CONTROLLED ELECTRIC SIMULATION TO THE HEART THROUGH ELECTRODES IN ORER TO CONTROL HEART RATE

175
Q

Indications for Pacemaker

A

Decrease or absent cardiac output

Failure of heart to initiate or conduct an intrinsic electrical impulse at a rate adequate to maintain organ perfusion

Bradyarrhythmias, AV block, sick sinus syndrome, tachycardia

176
Q

Components of Pacemaker

A

Pacing pulse generator

Pacing lead systems (bipolar, unipolar)

177
Q

Temporary Pacemaker

A

External (transcutaneous)

Transvenous

Epicardial

178
Q

Permanent Pacemaker

A

Pacing mode: asynchronous, synchronous, rate modulated

179
Q

Asynchronous Pacemaker

A

Delivers a pacing stimulus at a FIXED rate, regardless of the occurrence of spontaneous myocardial depolarization

Occurs in non-sensing modes

180
Q

Synchronous Pacemaker

A

Delivers a pacing stimulus only when the heart’s intrinsic pacemaker fails to function at a predetermined rate

181
Q

Five-Letter Pacemaker Codes

A

Chambers paced

Chambers sensed

Response to sensing

Rate modulation

Multisite pacing

182
Q

Chamber of the Heart Paced

A

ATRIAL

VENTRICULAR

DUAL

AAT, VVI, DDD

183
Q

Complications of Pacemakers

A

Related to insertion, subcutaneous implantation of generator, displacement of catheter electrode

Pacer Malfunction: failure to pace, failure to sense, failure to capture

184
Q

Implanted Cardioverter Defibrillators

A

Used for tachycardias/fibrillations unresponsive to medication

Atrial and/or ventricular tachycardias

Used to terminate life-threatening ventricular dysrhythmias

185
Q

Functions of ICD

A

Monitors heart rate and rhythm, detects abnormal rhythm

Tiered therapy: 1) anti-tachycardia pacing, 2) cardio version, 3) defibrillation; if systole, ventricular pacing

Delivers 25 Joule shock up to 3 times in a row

186
Q

S-ICD

A

Subcutaneous Implantable Converter Defibrillator

Electrode placed just under the skin over sternum

Eliminates potentially serious short/long term risks with venous/cardiac electrode placement

187
Q

Patient Teaching for Pacemaker

A

Check pulse daily at the same time (report if less than set rate)

Restrict arm movement for 2 weeks after insertion

Avoid contact sports

Keep ID card of pacemaker

Avoid large magnetic fields (MRI, arc welders, electrical substations)

188
Q

Patient Teaching for ICD

A

Pre-insertion assessment of patient’s dysrhythmia

Acceptance of life extender

What to do if ICD shock occurs

Family education: CPR, unanticipated shock when in contact during shock

No driving, avoid strong magnetic fields

189
Q

Radiofrequency Ablation

A

Percutaneous catheter interventions

Electrophysiology study: cath lab, isolate foci, stimulate dysrhythmias, ZAP it

190
Q

Cardiac Resynchronization Therapy

A

Ventricular Conduction Delays

Atrial Pacing

Atrial Arrythmia Suppression

Anti Tachycardia pacing

191
Q

Ventricular Conduction Delays

A

Lack of synchrony between RV and LV, biventricular pacing (wires in each ventricle)

192
Q

Atrial Pacing

A

Three pacing leads RA, RV, and LV; optimize synchrony for CO

193
Q

Atrial Arryhthmia Suppression

A

Bi-atrial pacing RA and LA, pace at higher rate than intrinsic sinus rate, then decrease rate to allow SA node to control

194
Q

Goal of Pacemakers

A

To stimulate normal physiologic cardiac depolarization and conduction

195
Q

Nursing Management of Pacemakers

A

Assessing and preventing pacemaker malfunction, protecting against micro shock, surveillance for complications, and patient education

196
Q

Nursing Management of ICDs

A

Assessing for dysrhythmias, monitoring for complications, and patient education

197
Q

Treatments for Bradycardia

A

Give oxygen

Meds: Atropine, Epinephrine, Dopamine

Transcutaneous Pacing

198
Q

Treatments for Tachycardia

A

Remove the stimulus (anxiolytics, pain medications)

Beta blocker, calcium channel blocker

199
Q

Undersensing Pacemaker

A

Failure to sense

Pacemaker continues to fire regardless of what the heart is doing

200
Q

Oversensing Pacemaker

A

Pacemaker is hyper vigilant of heart rhythm and pays attention to all activity

Need to decrease sensitivity of the pacer; increase the millivolts

201
Q

Failure to Capture

A

Problem with the heart

Heart is not picking up the pacer influence; need to increase the milliamps on the pacemaker

202
Q

Hypovolemic Shock

A

Loss of intravascular fluid volume

Reduced preload

203
Q

Cardiogenic Shock

A

Pump-Contractility

204
Q

Distributive Shock

A

Afterload

Neurogenic, anaphylactic, septic

205
Q

Obstructive Shock

A 
Caused By:
PE 
Cardiac Tamponade
Constrictive Pericarditis
Tension Pneumothorax

Treatment: Fix the cause

206
Q

Shock

A

Acute, widespread process of impaired tissue perfusion

Imbalance between cellular oxygen supply and demand

Leads to cellular dysfunction and death

207
Q

Nursing Diagnoses for Shock

A

Ineffective tissue perfusion

Impaired cardiovascular function

208
Q

Stages of Shock

A

Compensatory

Progressive

Refractory

Progression through stages varies on patient’s prior condition, duration of initiating event, response to therapy, correction of the underlying causes

209
Q

Pathophysiology of Shock Syndrome

A

Initial: decreased CO leads to threatened tissue perfusion

Compensatory: homeostatic mechanisms attempt to maintain CO, BP, and perfusion; mediated by SNS

210
Q

Neural Response

A

SNS Compensatory Response

Increased HR, contractility, arterial and venous vasoconstriction, shunting of blood to vital organs

211
Q

Hormonal Response

A

SNS Compensatory Response

Activation of Renin response (Ang II –> vasoconstriction, release of aldosterone and ADH for sodium and fluid retention)

Stimulation of anterior pituitary to produce glucocorticoids

Stimulation of adrenal medulla to release epi and norepi

212
Q

Chemical Response

A

SNS Compensatory Response

Tissue perfusion switches from aerobic to anaerobic (increases lactic acid, acidemia)

Systemic release of inflammatory mediators (impairment of microcirculation, SIRS)

213
Q

Assessment of Compensatory Shock

A 
Increased HR and contractility
Vasoconstriction
Clammy skin
Fight/flight response
Anxiety/fear
Decreased urine output
Hypoactive bowel sounds
214
Q

Interventions for Compensatory Shock

A

Identify cause of shock

Continuous assessment

Begin fluid replacement

215
Q

Progressive Stage of Shock Syndrome

A

Compensatory mechanisms begin to fail

Switch from aerobic to anaerobic metabolism (increased lactic acid)

Increased vascular permeability, tissue edema, and decline in tissue perfusion

SIRS

Irreversible damage begins

216
Q

Assessment of Progressive Stage of Shock

A 
Decreased BP
Increased capillary permeability
Crackles in lungs
Heart rate > 140 bpm
Confusion, coma
Anuria
217
Q

Interventions for Progressive Stage of Shock

A 
Aggressive fluid replacement
Colloids
Continuous assessments and documentation
Vasoactive drugs
TPN
Family support
218
Q

Refractory Stage of Shock

A

Shock syndrome

UNRESPONSIVE TO AGGRESSIVE INTERVENTIONS

ALI, AKI, Multi Organ Dysfunction Syndrome (MODS)

219
Q

Interventions for Refractory Stage

A

Continue interventions

Be attentive to family needs

Continue to speak to the client

220
Q

MAP

A

SBP + 2(DBP) / 3

Average pressure in arteries during cardiac cycle

221
Q

CVP

A

Measured in right atrium

Right heart preload

222
Q

PAS

A

Pulmonary Artery Systolic pressure

PA pressure measured in the pulmonary artery

Right heart afterload

223
Q

PAD

A

Pulmonary Artery Diastolic pressure

Pa pressure is measured in the pulmonary artery

Non-occlusive measure of left heart preload

224
Q

PCWP/PAOP

A

Pulmonary Capillary Wedge Pressure/Pulmonary Artery Occlusive Pressure

Measured in pulmonary artery with balloon up

Left heart preload

225
Q

SVR

A

Force left ventricle must overcome

Left heart afterload

226
Q

PVR

A

Force right ventricle must overcome

Right heart afterload

227
Q

Assessment and Diagnosis of Shock Syndrome

A

Shock state

Clinical manifestations

Global indicators

Hyperlactemia

228
Q

Medical Management of Shock Syndrome

A 
TISSUE PERFUSION
PULMONARY GAS EXCHANGE
CO and hemoglobin levels
Fluid administration
Blood
Vasoconstrictor agents
Nutritional supplementation
Glucose control
229
Q

Nursing Management of Shock Syndrome

A

Patient status
Explaining procedures and routines
Supporting the family
Encouraging the expression of feelings
Facilitating problem solving and shared decision making
Individualizing visitation schedules
Involving the family in the patient’s care
Establishing contacts with necessary resources

230
Q

Causes of Hypovolemic Shock

A

Hemorrhage

Dehydration

Burns

3rd spacing

Diuresis (DI)

Excessive diarrhea

231
Q

Class I Hypovolemic Shock

A

15% of fluid volume (750mL)

232
Q

Class II Hypovolemic Shock

A

15-30% of fluid volume (750-1500mL)

233
Q

Class III Hypovolemic Shock

A

30-40% of fluid volume (1500-2000mL)

234
Q

Class IV Hypovolemic Shock

A

> 40% of fluid volume (>2000mL)

235
Q

Absolute Hypovolemia

A

Loss of fluid from intravascular space

236
Q

Relative Hypovolemia

A

Vasodilation produces increase in vascular capacity relative to circulating volume

237
Q

Interventions for Hypovolemic Shock

A

LARGE BORE IV ACCESS

FLUID REPLACEMENT WITH CRYSTALLOIDS (Lactated Ringers, NS)

Hetastarch or Dextran IV solutions

COLLOIDS (albumin)

MODIFIED TRENDELENBURG

MILITARY ANTI-SHOCK TROUSERS

RAPID IV FLUID INFUSER

238
Q

Noninvasive Hemodynamics

A

SVI (Stroke Volume Index)

Change of SVI with 250mL infusion over 3-5 minutes

If > 10% – fluid responder
If < 10% – non responder

Leg Raise Noninvasive Test = 250mL

239
Q

Cardiogenic Shock

A

PUMP FAILURE

LOSS OF CONTRACTILITY

MYOCARDIAL INFARCTION

CARDIOMYOPATHY

CARDIAC TAMPONADE

DYSRHYTHMIAS

240
Q

Interventions for Cardiogenic Shock

A

OXYGEN THERAPY

REDUCE CARDIAC WORKLOAD

MORPHINE SULFATE

HEMODYNAMIC MONITORING

VASODILATORS (NITROGLYCERIN, NITROPRUSSIDE)

DOBUTAMINE, DOPAMINE

ANTIDYSRHYTHMIC MEDS

INTRA-AORTIC BALLOON PUMP

WATCH FOR FLUID OVERLOAD

241
Q

Benefits of Intra-Aortic Balloon Pump

A

Decreased afterload

Increased coronary artery perfusion

242
Q

Contraindications for Intra-Aortic Balloon Pump

A

AORTIC VALVE INSUFFICIENCY

SEVERE PERIPHERAL VASCULAR OCCLUSIVE DISEASE

PAST AORTIC GRAFTS

AORTIC ANEURYSM

243
Q

IABP Timing

A

1: Use arterial or aortic waveform
2: Inflation after dicrotic notch (beginning of diastole)
3: Compare diastolic peak to systolic peak pressures
4: Deflation prior to systole (note end-diastolic pressure)
5: Compare systolic peaks between unassisted and assisted systolic peaks

244
Q

Monitoring IABP Therapy

A

WATCH URINE OUTPUT

CHECK LEFT RADIAL PULSE

CHECK PEDAL PULSES

MONITOR HR, MAP, PCWP

MONITOR EXTREMITIES FOR PULSES, COLOR, SENSATION

245
Q

Nursing Interventions for IABP

A

PREPARE FAMILY

ASSESS NEED FOR RESTRAINT

REVERSE TRENDELENBURG

MONITOR IABP MACHINE FUNCTION AND TIMING

ANTICOAGULATION THERAPY

WEANING

246
Q

Prognoses for IABP Therapy

A

WEANING AND RECOVERY

DETERIORATION AND DEATH

IABP DEPENDENCY AND HEART TRANSPLANT

247
Q

Ventricular Assist Devices

A

Designed to support or replace a failing natural heart with flow assistance

248
Q

Nursing Management of VADs

A

Monitor for hemodynamic changes and for complications

Complications include bleeding, infection, thromboembolism, and device failure

249
Q

Distributive Shock

A

NEUROGENIC (SPINAL CORD INJURY, SPINAL ANESTHESIA)

ANAPHYLACTIC

SEPTIC

ADRENAL CRISIS

250
Q

Assessment of Neurogenic Shock

A

Loss of sympathetic tone

Dry, warm skin

Bradycardia, confusion

Risk of thrombophlebitis

Poikilothermic

251
Q

Interventions for Neurogenic Shock

A

Spinal cord immobilization

Glucose if hypoglycemic

IV fluid therapy

Vasoactive drips

Elastic stockings, elevate legs, pneumatic stockings

Anticoagulation therapy

252
Q

Characteristics of Anaphylactic Shock

A

RAPID ONSET

PRESENCE OF ALLERGEN

HISTAMINE AND BRADYKININS

BRONCHO/LARYNGEAL SPASMS

INCREASED CAPILLARY PERMEABILITY

TACHYCARDIA

HYPOTENSION

253
Q

Prevention of Anaphylactic Shock

A

Assess allergy history

Watch closely after first doses of new drugs

254
Q

Interventions for Anaphylactic Shock

A

Ensure airway (ET tube, tracheostomy)

100% O2

Epinephrine IVP or DRIP

Antihistamine (diphenhydramine)

Steroids

Glucagon or Ipratroprium if patient takes beta-blockers

255
Q

Sepsis

A

Life-threatening organ dysfunction due to a dysregulated host response to infection

256
Q

Septic Shock

A

Subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities substantially increase mortality

Persisting hypotension requiring vasopressors to maintain MAN > 65 and serum lactate > 2 mmol

257
Q

Sepsis-Induced Hypotension

A

BP < 90 mmHg Systolic

Or reduction of > 40 mmHg from baseline

258
Q

Multiple Organ Dysfunction Syndrome

A

Homeostasis cannot be maintained without intervention

259
Q

Intrinsic Factors Associated with Septic Shock

A

Extreme of age

Coexisting conditions (malignancies, burns, AIDS, diabetes, substance abuse)

Malnutrition

260
Q

Extrinsic Factors Associated with Septic Shock

A

Invasive devices

Drug therapy

Fluid therapy

Surgery and trauma

Immunosuppressive therapy

261
Q

End Result of All Shock

A

Ineffective tissue perfusion and impaired cellular metabolism

262
Q

Sequential Organ Failure Assessment

A

Respiration: PaO2/FiO2 ratio

Coag: Platelets

Liver: Bilirubin

CV: BP, MAP, need for vasopressors

CNS: GCS

Renal: Cr, UO

263
Q

qSOFA

A

SBP < 100 mmHg

RR > 22/min

Mental Status: GCS < 15

Positive score if two or more indicators present

264
Q

Septic Shock Pathophysiology

A

Inflammatory response (mediators released; tumor necrosis factor, interleukin, chemokines, prostaglandins, platelet activating factor)

Sepsis results in systemic inflammatory response with excessive coagulation in microvasculature

Tissue oxygenation becomes critical

265
Q

Pro-Inflammatory Responses

A

Initial response or result to infection

Prostaglandin, leukotriene, production/release

Coagulation cascade

Complement cascate

Implications of persistent pro-inflammatory state (thrombi, DIC, ALI)

266
Q

Anti-Inflammatory Response

A

Compensatory attempt to regulate the pro-inflammatory response

Period of immunosuppression

Implications of persistent anti-inflammatory state (nosocomial infection, death)

267
Q

2016 Sepsis Guidelines for Hemodynamics

A

Target MAP: > 65

Fluid resuscitation with > 30 mL/kg of crystalloids within first 3 hours

Target: normalize lactate

Echocardiography

Use dynamic over static measures to predict fluid responsiveness

268
Q

2016 Sepsis Guidelines for Infection

A

Start with broad spectrum antibiotics

Recommend AGAINST sustained antimicrobial prophylaxis with inflammatory states with noninfectious origins

Procalcitonin levels used to stop unneeded antimicrobial therapy

269
Q

2016 Sepsis Guidelines for Ventilation

A

Patients with ALI/ARDS should be prone

DO NOT use HFJV

NMBA < 48 hours

Use of lower TV with ALI

270
Q

2016 Sepsis Guidelines for Metabolism

A

Early full enteral nutrition

Only test gastric residual volume in patients at high risk for aspiration or feeding intolerance

Suggest use of post pyloric feeding tubes for patients at high risk for aspiration

271
Q

Summary of Shock

A

Patients with MAP < 60 are considered to be in shock

Management focuses on supporting oxygen delivery

Prevention of shock is a primary responsibility of nurses

272
Q

Summary of Hypovolemic Shock

A

Results from loss of intravascular volume

Decreased CO/CI, CVP, PAOP, and Increased SVR

Manage by identifying and stopping source of fluid loss and administering fluid

Minimize fluid loss, assess therapy response, provide support, prevent complications

273
Q

Summary of Cardiogenic Shock

A

Results from impaired ability of heart to pump

Decreased CO/CI, Increased PAOP, CVP, and SVR

Manage by identifying etiologic factors of pump failure and administering drugs to enhance CO

Limit myocardial oxygen demand, enhance myocardial oxygen supply, maintain tissue perfusion, monitor for complications

274
Q

Summary of Anaphylactic Shock

A

Results from an immunologic antibody-antigen activation

Decreased CO/CI, right arterial pressure/PAOP, and SVR

Remove offending antigen, reduce effects of biochemical mediators, promote tissue perfusion

Administer epinephrine, facilitate ventilation, volume replacement

275
Q

Summary of Neurogenic Shock

A

Results from loss of sympathetic tone due to interrupted impulse transmission or blockage of sympathetic outflow

Decreased CO/CI, RAP/PAOP, SVR, HR

Prevent cardiovascular instability and promote tissue perfusion

Treat hypovolemia, maintain perfusion, maintain normothermia, monitor for and treat dysrhythmias

276
Q

Summary of Septic Shock

A

Results from initiation of SIRS due to microorganisms entering body

Decreased CO/CI, RAP, PAOP, SVR, and increased HR

Early identification of sepsis, administer fluids, give medications, provide nutrition

277
Q

Summary of MODS

A

Results from progressive physiologic failure of two or more separate organ systems

Fluid resuscitation and hemodynamic support, prevention and treatment of infection, maintenance of tissue oxygenation, nutritional and metabolic support

Critical Care (3 decks)

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