Critical care: Exam III

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2015, Spring Semester Block 4 (222NUR)
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1

Pacemaker cells & automaticity

  • Electrical signals generated by pacemaker cells
  • Cells can generate stimulus w/out outside stimulation- it called automaticity
2

Cardiac Cycle: Composed of 2 activities

  1. Electrical (caused by automaticity)
  2. Mechanical (muscular) known as a contraction
3

Mechanical (muscular) activity is known as a ________

Contraction

4

A perfect electrical signal doesn't always mean there is a ______.

pulse

5

Cardiac cycle: Two phases of electrical activity:

Depolarization= active

Repolarization= resting

6

Cardiac cycle: Two mechanical responses

Systole

Diastole

7

The heart gets it blood during ________ the rest of the body gets it from _______.

diastolic / systolic

8

Cardiac Cycle:

Depolarization =

systole = contraction

9

Cardiac Cycle:

Repolarization =

diastole = resting or filling phase

10

Cardiac Cycle:

Electrical activity precedes_____ ______

mechanical activity

11

Cardiac Cycle:

Electrical + mechanical =

cardiac contraction

12

Cardiac action potential:

Cardiac muscle cells generate an electrical current =

cardiac action potential

13

Cardiac action potential:

  • Cardiac muscle cells generate an electrical current = cardiac action potential
  • Sinoatrial node (SA node)
  • Exchange of electrolytes
  • Depolarization
  • Repolarization begins
14

Cardiac action potential:

Depolarization:

  • Na outside cell; K inside the cell
  • Change cell permeability
  • Na enters cells; K leaves cells
  • Ca slowly enter cells
  • ATP (adenosine phosphate) needed to move electrolytes back to resting state
15

Depolarization:

Na+ is _____ the cell

outside

16

Depolarization:

K+ is ________ the cell.

inside

17

Depolarization:

Ca+ ____ _____ the cell

slowly enters

18

Depolarization:

_____ _________ needed to move electrolytes back to resting state

ATP (adenosine phosphate)

19

Muscular Contraction:

  • Depolarization leads to contraction
  • Repolarization leads to resting & fill of ventricles from atria
  • ECG is evidence of electrical activity, not contraction!
20

Cardiac Conduction Pathway

  • SA node
    Intraatrial & intermodal pathways to AV node
  • AV node
  • Bundle of His
  • Left & right bundle branches; fascicles
  • Purkinje fibers
21

Cardiac Conduction Pathway

SA node

  • Depolarization begins- atria fills
  • Atrial contraction or atrial kick
22

Cardiac Conduction Pathway

AV node

  • Delays impulse to ventricles; allows for filling
  • Back-up pacemaker- hopeful to get if sinus node goes out.
23

You lose atrial kick when in __ ___.

A. Fib

24

Inherent Rates:

SA node=

60-100 beats/min

25

Inherent Rates:

AV node =

40-60 beats/min

26

Inherent Rates:

Ventricles (Purkinje fibers) =

15 to 40 beats/min

27

12 lead ECG:

Impulses toward electrode

* Positive QRS complex

28

12 lead ECG:

Impulses away from electrode

* Negative QRS complex

29

Cardiac Monitoring:

Continuous monitoring via

three-lead or five-lead systems- not a 12 lead EKG

30

Cardiac Monitoring:

  • Record & interpret 6-second strip every 4hrs
  • Monitor ST segment
  • Monitor dysrhythmias
  • Daily 12-lead ECG for cardiac patients- this is not always true...
31

ECG graph paper: Uses

  1. Used to standardize tracings
  2. Vertical boxes measure voltage/amplitude
  3. Horizontal boxes measure time
32

Graph paper: Big box is how many seconds?

0.2

33

Graph paper: Small box equals how many seconds?

0.4

34

P Wave

Atrial depolarization

  • Normally indicates firing of the sinoatrial node
  • Not to exceed 3 boxes high
35

QRX Complex

-Ventricular depolarization

  • Q wave first negative deflection after P wave
  • R wave first positive deflection after P wave
  • S wave negative waveform after R wave

-Not everyone has a traditional QRS- doesn't mean anything is wrong.

36

Pathological Q waves:

  • 0.04 seconds in width
  • More than one fourth of the R-wave amplitude
  • Indication of a MI
37

PR interval

  • Atrial depolarization/delay in AV node
  • Beginning of P wave to beginning of QRS complex
  • 0.12 to 0.20 seconds
  • Shorter interval= impulse from AV junction
  • Longer interval = 1st° AV block
38

Which should be between 0.12 to 0.20 seconds?

QRS interval

ST segment

PR interval

PR interval

39

Longer PR interval means-

1st° AV block

40

QRS interval

  • Ventricular depolarization
  • 0.06 to 0.10 seconds
  • Various configurations
  • Wide: slowed conduction
    • Bundle branch block (BBB)
    • Ventricular rhythm
41

What does a wide QRS interval mean?

Slowed conduction:

- Bundle Branch Block (BBB)

- Ventricular rhythm

42

QRS interval should be between

0.06-0.10 seconds

43

ST segment

Look for depression or elevation:

  • ST elevation= Myocardial injury
  • ST depression= reciprocal changes- digoxin, and ischemia
44

What is myocardial injury necrosis determined by?

The time that it is fixed

45

T Wave

Ventricular repolarization

  • Follows a QRS complex
  • Bigger than a P wave
  • No greater than 5 small boxes high
  • Inversion indicates ischemia to myocardium
46

What does T wave inversion indicate?

Ischemia to myocardium

47

How tall should the T wave be?

No greater than 5 small boxes high

48

QT interval:

-Beginning of QRS complex to end of T wave

-0.32 to 0.50 seconds

-Varies w/heart rate

49

Which interval varies with heart rate?

QT interval

50

The QT should be between how many seconds?

0.32-0.50

51

U wave:

  • Sometimes seen after T wave
  • Unknown origin
    • May be normal
    • May indicate hyopkalemia
52

What might the U wave indicate?

Hypokalemia

53

Where is the U wave seen?

After the T wave (sometimes)

54

Rhythmicity:

  • Regularity or pattern of heart beats
  • PP intervals (atrial)
    • Is regular when distance between PP intervals is equal
  • RR intervals (Ventricles)
    • Is regular when distance between RR intervals is equal
55

QRS equals

Ventricular

56

P wave equals

Atrial

57

Rhythmicity:

When are PP intervals (atrial) regular?

When the distance between PP intervals is equal

58

Rhythmicity:

When are the RR intervals (Ventricles) regular?

When the distance between RR intervals is equal

59

Calculating Heart Rate

-Irregular- count for a full minute

-Calculate atrial PP and Ventricular rates RR

60

Normal Sinus Rhythm

  • Regular rhythm
  • Rate 60-100 beats/min
  • Normal P wave in lead II
  • P wave before each QRS
  • Normal PR, QRS, and QT intervals
61

Which rhythm has the following:

60-100 beats/min

Normal P wave

P wave before each QRS

Normal PR, QRS, and QT intervals

Sinus rhythm

62

Sinus Tachycardia

  • Sinus rhythm w/a rate of 100-150 beats/min

*Normal P wave, P before each QRS & normal PR, QRS, QT intervals- sinus

63

Sinus Tachycardia: causes

Stimulants, exercise, fever & alterations

64

Sinus Tachycardia: Assess for

Symptoms of low cardiac output:

  1. Hypotension
  2. ↓ urine output
  3. Chest pain
  4. Confusion
  5. Edema
  6. Weakness & fatigue
  7. Rapid breathing-> abnormal ABGs
  8. ECG changes- abnormal hear rhythm

* These are just to name a few, there are plenty more

65

Sinus bradycardia

  • Sinus rhythm w/rate less than 60 beats/min
66

Sinus bradycardia: Causes

*Vagal, drugs, ischemia, ICP, and normal in athletes.

67

Sinus bradycardia: Produces

* Various hemodynamic responses

68

Do we treat sinus bradycardia?

NO, do not treat unless patient is symptomatic

69

A symptom of ↓ cardiac output that is an indication of ↓ coronary artery perfusion is:

  1. Cyanosis
  2. Chest pain
  3. Dyspnea
  4. Decreased urine output

2- Chest pain

70

What assessments indicate that the patient is not tolerating the low heart rate?

  • Syncope
  • Hypotension
  • ↓ urinary output

This is just to name a few :)

71

Why might prolonged tachycardia result in heart failure?

Tachy causes ↓ cardiac output

72

Sinus Arrhythmia

Sinus rhythm

Rate varies w/respirations

Rarely affects hemodynamic status

73

Sinus Arrhythmia

Rate varies w/respirations:

  • Inspire= increase
  • Expire= decrease
74

With sinus arrhythmia, the rate varies w/respirations. When the patient exhales the rate _____.

decreases

75

With sinus arrhythmia, when the patient inhales the what happens to the rate?

It increases

76

Sinus arrest or Exit block (same thing)

  • Sinoatrial node fails to initiate impulse
  • Causes: vagal, heart disease, and drugs that slow heart rate
  • Heart rate can be normal to slow
  • Irregular rhythm
  • Can decrease cardiac output
77

What causes a sinus arrest or exit block?

Sinoatrial node fails to initiate impulse

78

What contributing factors can cause sinus arrest/exit block?

Vagal, heart disease, and drugs that slow heart rate

79

What is the HR like in sinus arrest/exit block?

Can be normal or slow

80

Atrial dysrhythmias

Increased automaticity in the atrium

Generally have P-wave changes

81

Atrial dysrhythmias: Causes due to psychosocial or medical mismanagement

  • Stress
  • Digitalis toxicity
  • Alcohol
82

Atrial dysrhythmias: Physiological causes

  1. Electrolyte imbalances
  2. Hypoxia
  3. Atrial injury
  4. Hypothermia
  5. Hyperthyroidism
  6. Pericarditis
83

Premature Atrial contractions

  • Early beats initiated by atrium
  • P waves and PR interval may vary
  • Noncompensatory pause
  • P wave may be found in T wave
84

Premature Atrial contractions: Strip presentation

* Narrow QRS

* Has a P wave

* Compensatory pause after a PAC

85

Nonconducted premature atrial contractions:

Pause noted on rhythm strip

Premature P wave

May alter cardiac output

86

Which contraction has a premature P wave & may alter cardiac output?

A nonconducted premature atrial contraction

87

Wandering atrial pacemaker

  • Varying configurations of P waves
  • At least 3 different P-wave shapes must be seen
  • Heart rate not >100
  • PR interval varies
  • Irregular rhythm
88

What causes 3 different P wave shapes, is irregular on a strip and has a heart rate equal to or less that 100 beats/min

Wandering atrial pacemaker

89

Multifocal atrial tachycardia

  • Almost identical to wandering atrial pacemaker
  • Heart rate exceeds 100 beats/min
  • Common in COPD patients
90

Which type of tachycardia exceeds 100 beats/min, common in COPD patients and is almost identical to Wandering atrial pacemaker?

Multifocal atrial tachycardia

91

Multifocal atrial tachycardia has abundant _ ___ & is ____than QRS

P waves/faster

92

Atrial flutter

  1. Ectopic foci in atria, heart disease
  2. Classic "sawtooth" pattern in leads II, III, and aVF
  3. Atrial rate fast & regular (250-350 beats/min) with AV block
  4. Degree of conduction varies; may be 1:3 or 1:4, etc
93

Atrial fibrillation

Erratic impulse formation in atria

No discemible P wave

Irregular ventricular rate

Aberrant (abnormal) ventricular conductions can occur

Results in loss of atrial kick

High risk for pulmonary or systemic emboli

94

Hemodynamic monitoring : Regulation of blood flow

  • Heart rate
  • Strength of contraction
  • Blood vessels diameter
  • Degree of turbulence
  • Pressure
95

Pressure = ______ x ____________

flow / resistance

96

Pressure

Force exerted on the liquid

* mm Hg

Flow: amount of fluid moved over time

* L/min or mL/min

Resistance: Opposition to flow

97

Cardiac output:

Volume of blood ejected from heart/min

98

Cardiac output = ____ x ____ ______

HR / Stroke volume (volume of blood ejected w/each beat)

* 4 to 8 L/min

99

Ejection fraction

Fraction of blood ejected w/each beat

* Normal 60% to 70%

100

Preload:

Degree of muscle fibers stretch before systole

* Volume of blood in ventricle prior to contraction (LVEDV/LVEDP)

101

Preload: Frank-Starling law

* Increased stretch = volume

* Stretch is within physiological limits

- Example= balloon

102

Afterload:

  • Pressure or resistance against flow
  • Related to lumen size & viscosity

- Example: Opening a door against wind

103

After load: Related to lumen size & viscosity

Systemic vascular resistance

- Force overcome by the left ventricle upon contraction

Pulmonary vascular resistance

- Force overcome by the right ventricle upon contraction

104

Contractility:

Force of ventricular contraction

How well the heart is pumping

105

Systemic Vascular Resistance (SVR):

  • Peripheral vascular resistance
  • Diameter of blood vessels

Arterial BP= CO x SVR

106

Cardiac output versus index

  • Index is better assessment; based on body size
  • CI= CO ÷ body surface area
  • Calculated on the computer after entering patient's height & weight.
107

Hemodynamic monitoring: Noninvasive modalities

  1. Noninvasive blood pressure
  2. Assessment of jugular venous pressure
  3. Assessment of serum lactate levels
108

Hemodynamic monitoring: Invasive modalities

  1. Arterial pressure monitoring
  2. Pulmonary artery pressure monitoring
  3. Right atrial pressure monitoring
109

Components of invasive hemodynamic monitoring

  • Invasive catheter
  • Noncompliant pressure tubing
  • Transducer & stopcocks
  • Flush system
  • Bedside monitor
110

Accuracy in hemodynamic monitoring: Level

Level = phlebostatic axis

* Fourth intercostal space, midaxillary line

* Approx. level of right atrium.

111

Accuracy in hemodynamic monitoring: Zero reference

  • Negate atmosphere pressure
  • Zeroing stopcock is leveled at phlebostatic axis & "zeroed"
112

Accuracy in hemodynamic monitoring: Dynamic response testing

Square wave test

113

Arterial pressure monitoring:

Invasive technique to monitor arterial blood pressure

114

Arterial pressure monitoring: Sites

  1. Radial artery

* Allen's test prior to insertion to verify collateral circulation in the extremity

* Issues related to predictability of Allen's test

2. Brachial artery

3. Femoral artery

115

Arterial pressure monitoring: Equipment

  • Pressurized flush solution w/transducer
  • Pressure at 300 mm Hg
  • Why does this need to by high?
  • A-line catheter (angiocath)
116

Arterial pressure monitoring: Major Complications

Thrombosis
* Clot if flush not used appropriately

Embolism

* Air entering system/clot dislodgment

Hemorrhage

* Loose connections/catheter dislodgement

Infection

117

RAP/CVP Monitoring

Right atrial pressure (RAP)- catheter in right atrium

* Proximal port of pulmonary artery catheter

Central venous pressure (CVP)- catheter in superior or inferior vena cava

* Triple lumen

Values are similar & terms interchanged

118

RAP/CVP

  • Direct measurement of pressure in right atrium
  • Right ventricular preload or right ventricular end diastolic pressure (RVEDP)
  • Normal value

- 2 to 6 mm Hg

- Recorded end exhalation as a mean value

119

Nursing implications RAP/CVP

  • Zero/ balance
  • Waveform analysis
  • Respiratory variation and PEEP
  • Patient position- Head of bed between 0 & 60°
  • Correlate values w/assessment
  • Monitor for complications
120

Complications of RAP /CVP

  1. Infection
  2. Pneumothorax or hemothorax
  3. Carotid puncture
  4. Heart perforation
  5. Dysrhythmias
121

Pulmonary artery catheter

Flow directed catheter

* Inserted via subclavian, internal jugular, or femoral vein

* Balloon tipped

* Multiple lumens

Variations

* SvO2 catheter

* Continuous cardiac output (CCO)

122

Insertion of PA catheter: Position

Proper position of patient

- Trendelenburg common

- Towel roll between shoulder blades

123

Insertion of PA catheter:

  • Inserted w/balloon deflated, selected inflation to "float" catheter into PA
  • Waveform changes as catheter progresses
  • Check for proper "wedging" for PAOP
  • Chest x-ray
124

Pulmonary artery catheter: Measurement capabilities

  • PA systolic
  • PA diastolic
  • PAOP/PCWP/PAWP

* Inflated balloon flows into wedge position in pulmonary capillary measuring pressure

  • Cardiac output/Index

- Thermodilution CO

- Proximal injectate port

125

Nursing implications: Measure pulmonary artery pressure

  • Pulmonary artery occlusive pressure (PAOP) reflects left ventricular end-diastolic pressure

- In many patients the PADP can be substituted for PAOP measurements if values are similar

- Record amount of air to inflate balloon- no more than 1.5 mL

126

Complications of PA catheters

  1. Infection
  2. Dysrhythmias
  3. Air embolus
  4. Thromboembolism
  5. PA rupture
  6. Pulmonary infarction
127

TdCO Method

Procedure:

  1. Inject solution within 4secs
  2. Increased accuracy at end expiration
  3. Check waveform
  4. Repeat at least three measurements
  5. Average values within 10% of each other
  6. Calculate CO and cardiac index (computer does this)
128

CCO Method

Continuous monitoring via specialized PAC

* Copper filament at distal catheter end

* Pulses of energy at intervals warms blood

Accurate w/head of bed up to 45°

129

Monitoring O2 delivery and consumption

  • Calculated values
  • Obtained via monitoring catheters

- SvO2- mixed venous oxygen saturation via specialized PAC

- ScvO2- central venous oxygen saturation via specialized central line

130

Monitoring O2 delivery and consumption: Normal values

  • SvO2- 60% to 75%= adequate balance between supply and demand
  • ScvO2- 65% to 85%= adequate balance between supply and demand
131

Monitoring O2 delivery and consumption: High values

High values= tissues not able to use oxygen

132

Monitoring O2 delivery and consumption: Low values

Low values= oxygen demand exceeds delivery

133

Trends in hemodynamic monitoring

- Esophageal Doppler

* Thin silicone probe placed in the distal esophagus

* Evaluates descending aortic blood flow

- Pulse contour cardiac output

134

Effects of respiratory variation

  1. Right atrial pressure variation
  2. Systolic pressure variation
  3. Arterial pulse pressure variation
  4. Stroke volume variation
135

Heart murmur

  • Caused by a turbulence of blood flow through the valves
  • Rumbling, blowing, harsh, or musical in sound
  • Identify location, sound, loudness, and intensity & whether other heart sounds are heard.
136

Coronary artery disease (CAD)

* Progressive narrowing of coronary arteries by atherosclerosis

- Coronary heart disease

- Atherosclerotic heart disease

137

Pathophysiology of CAD

  1. Injury to epithelial cells in intima

* Platelet aggregation

* Migration of monocytes

* Lipoproteins enter intima

2. Fatter streak

- Monocytes develop into macrophages

- Lipid-rich "foam cells" develop

3. Atheroma

4. Damage to intima- liberates platelet-derived growth factor

5. Proliferation of smooth muscle cells

6. Fibrous cap forms

* From connective tissue & low-density lipoprotein (LDL)

7. Fibrous cap often ruptures

- Thrombus

- Clotting cascade initiated

8. Adhesion: platelets bind to receptors

9. Activation: platelets change shape & activate receptors

- Release: thromboxane A2 & serotonin

- Activate glycoprotein IIb/IIa receptors

10. Aggregation: platelets clump together

138

Drugs administered to stop the platelet aggregation process

  1. Aspirin
  2. Glycoprotein IIb/IIIa inhibitors
  3. Heparin
  4. enoxaparin (Lovenox)
  5. Warfarin- coumadin
139

Risk factors for CAD:

- Age:

* Men > 45

* Women > 55

- Family history

- Cholesterol

* High LDL

* Low levels of HDL

- Smoking

- Hypertension

- Inactivity

- Overweight

* Diabetes

140

CAD History

  • Risk factors
  • Prior hospitalizations
  • Shortness of breath, chest pain
  • Medications

- Erectile dysfunction meds if considering nitroglycerin

  • Psychosocial history

- Include stressors

141

CAD diagnostic studies

  1. 12 lead ECG
  2. Holter monitor
  3. Exercise tolerance test (stress test)
  4. Chest x-ray
  5. Echocardiography
  6. Transesophageal echocardiography
  7. Diagnostic heart scans
  8. Single photon emission computed tomography
  9. Magnetic resonance imaging
  10. Electrophysiology study
142

CAD diagnostic studies: Stress test

AKA- Exercise tolerance test

  • Exercise to increase demand on heart
  • Stressed via drugs if patient cannot tolerate exercise (e.g., adenosine)
  • Monitoring vital signs, ECG

*Tries to induce symptoms of patients complaints*

143

CAD diagnostic studies: Echocardiography

Ultrasound to visualize cardiac structures

144

CAD diagnostic studies: Diagnostic heart scans

  1. Technetium-99m stannous pyrophosphate
  2. Thallium-201
  3. Multigated blood pool study
145

Cardiac catheterization & arteriography:

Catheter (Right or Left)

- Heart pressures (similar to PA catheter)

- Cardiac output

Arteriography

- Visualize blood vessels

146

Post catheterization care

  • Bed rest; head of bed no higher than 30°
  • Monitor bleeding; newer collagen agents for hemostasis may be used
  • Monitor pulses
  • Antiplatelet drugs after the procedure (usually after interventions such as PCI)
  • May be discharged in 6 to 8hrs; depends on diagnosis & procedures done in catheterization laboratory.
147

Laboratory tests

  1. CBC- Hemoglobin & Hematocrit (H&H)
  2. Potassium
  3. Magnesium
  4. Calcium
  5. Sodium

* Want labs to be w/in normal ranges, if not must fix!

148

Cardiac enzymes

* CK (total)

2 to 6hrs; peak 18 to 36hrs

* CK-MB (cardiac specific)

4 to 8hrs; peak 18 to 24hrs

* Troponin I and T

As early as 1hr after injury

* Myoglobin

30 to 60 minutes after injury

149

Cardiac enzymes: CK-MB

4 to 8hrs- after injury

peaks: 18 to 24hrs

150

Cardiac enzymes: Troponin I and T

As early as 1hr after injury

151

Cholesterol in CAD

HDL- considered GOOD

LDL- is BAD

152

LDL target levels (NIH)

* No CHD & fewer than 2 risk factors

- 160 mg/dL

* No CHD & 2 or more risk factors

- 130 mg/dL

* CAD

- <100 mg/dL

153

↑ Cholesterol treatment

  1. Diet: Low cholesterol, low salt
  2. Exercise: aerobic
  3. Medications: Lipid-lowering agents

- Various types: weigh advantages & disadvantages of each

154

Medications for hyperlipidemia

* HmG CoA reductase inhibitors; slow production: most effective:

- Statins

* Bile acid resins bind & are excreted via bowel

- Cholestyramine

- Colestipol

* Nicotinic acid; inhibits LDL synthesis & increases HDL; many side effects

* Fibric acid derivatives; increase VLDL clearance

- Gemfibrozil

155

Hyperlipidemia: Medications Affecting Platelets

- ASA

- Others: dipyridamole, ticlopidine, and clopidogrel

156

Chest pain

  • Classic symptom
  • Often midsternal
  • May radiate to arms, jaw, or back
157

Angina

Myocardial ischemia: demand higher than supply

158

Types of Angina: Stable

Chronic, exertional= Effort, classic

T-wave inversion on ECG

Treatment: rest & nitroglycerin

159

Types of Angina: Unstable

Crescendo (starts off mild, then increases)

- More often & severe, less relief

* May see ST elevation on ECG

* Treatment: Rest and nitroglycerin; drugs affecting platelets; revascularization

160

Types of Angina: Variant

Prinzmetal's (vasospasms)

* ST elevation during pain episodes

* Treatment: Calcium channel blockers

161

Nursing management: Angina

Maintain cardiac output

Pain relief

Self-care; risk-factor modification

162

Nursing management of the patient w/angina is directed toward

A. Immediate administration of nitrates

B. Assessment of history of previous angina episodes

C. Assessment & documentation of chest pain episodes

D. Administration of prophylactic lidocaine for ventricular ectopy

C. Assessment & documentation of chest pain episodes

163

Acute myocardial infarction (AmI)

  • Ischemia w/myocardial cell death
  • Imbalance of oxygen supply & demand
  • Causes
    • Atherosclerosis
    • Emboli
    • Blunt trauma
    • Spasm
164

Acute myocardial infarction (AmI): Types

  • Q wave: total occlusion of coronary artery w/ thrombus
  • Non Q wave: partial occlusion of coronary artery

Collateral circulaion

165

Assessment of AMI

~ Midsternal chest pain

- Severe, crushing, and squeezing pressure

- May radiate

- Unrelieved w/nitrates

~ Pale & diaphoretic

~ Dyspnea & tachypnea

~ Syncope

~ Nausea & vomiting

~ Dysrhythmias

166

Describing factors of AMI midsternal chest pain:

  1. Severe, crushing, and squeezing pressure
  2. May radiate
  3. Unrelieved w/nitrates
167

Diagnosis of AMI

  • Signs & symptoms- often atypical symptoms in women
  • 12 lead:

- ST elevation followed by Q wave (Q wave myocardial infarction)

- ST depression (non-Q-wave myocardial infarction)

  • Elevated cardiac enzymes

- CPK-MB

  • Elevated serum troponin I/T, myoglobin
168

Which finding on the ECG is most conclusive for infarction?

A. Q waves

B. Inverted T waves

C. Tall, peaked T waves

D. ST-segment depression

A. Q waves

169

Nursing goals AMI

  • Maintain cardiac output
  • Treat pain
  • Assess for complications
  • Increase activity tolerance
  • Relieve anxiety
  • Ongoing & discharge teaching
170

Complications of AMI

  • Dysrhythmias
  • Sudden death
  • Congestive heart failure, cardiogenic shock
  • Ventricular aneurysm or rupture
  • Papillary muscle dysfunction
  • Pericarditis
171

Medical management: AMI

* Pain relief: morphine, nitroglycerin

* Oxygen

* Drugs affecting platelets- ASA glycoprotein IIb/IIIa inhibitors

* Beta-blockers

* Nitrates

* ACE inhibitors

* Antidysrhythmics

172

Primary Angioplasty

  • Get pt. to catheterization lab for emergent percutaneous intervention or stenting if facilities are available
  • Better outcomes than thrombolytics
173

Thrombolytic therapy

  • Time is muscle; 6hr window
  • Several thrombolytic agents available, such as:
    • Tissue plasminogen activator (t-PA)
    • Streptokinase
    • Retaplase
  • Heparin & glycoprotein IIb/IIIa inhibitors
174

Interventional cardiology

* Variety of procedures

- Percutaneous transluminal coronary angioplasty (PTCA)

- Intracoronary stenting

* Drug-eluting stents

175

PTCA: Goal

To increase blood flow to myocardium

176

PTCA: criteria

  • Uncompromised collateral flow
  • Noncalcified lesions
  • Lesions not on bifurcations of vessels

* Balloon catheter is inflated

177

Intracoronary Stents

  1. Tubes placed in conjunction w/angioplasty to keep vessel patent
  2. Help prevent the restenosis associated w/angioplasty
  3. Similar procedure as PTCA
  4. Anticoagulation therapy
178

New Interventional techniques: Nuclear

* Excimer laser angioplasty

- Xenon chloride laser

* Radiation therapy

- Beta or gamma radiation

179

Surgical Revascularization

  • Coronary artery graft (CABG) surgery
  • Minimally invasive direct coronary artery bypass (MIDCAB) surgery
  • Transmyocardial revascularization (TMR)
180

CABG surgery

  • Provides additional conduits for blood flow
    • Saphenous vein
    • Internal mammary artery
    • Radial artery
  • Arteries longer patency
181

Indications for CABG

  1. Unstable angina
  2. AMI
  3. Failure of percutaneous interventions
182

Risks associated with CABG

~ Increased mortality associated with:

  1. Left ventricle dysfunction
  2. Emergency surgery
  3. Age
  4. Sex (female)
  5. Number of diseased vessels
  6. Decreased ejection fraction w/congestive heart failure
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Traditional CABG

  • Median sternotomy or sternum split
  • Excision of pericardium
  • Cardiopulmonary bypass
  • Myocardial preservation or cardioplegia
  • Grafts
  • Wean bypass; defibrillate if needed
  • Mediastinal and chest tubes
  • Epicardial pacing wires
  • Wire sternum
184

Goals of CABG surgery

  1. Increases blood flow to myocardium
  2. Relieve symptoms
  3. Prolong survival
  4. Improve quality of life
185

Minimally invasive direct coronary artery bypass surgery: Port-access coronary artery bypass

  • Cardiopulmonary bypass
  • Incisions (ports)
186

Minimally invasive direct coronary artery bypass surgery

  • No cardiopulmonary bypass
  • Heart still beating
  • One or two bypasses

* Heart stays beating

187

Cardiac surgery complications

  • Low cardiac output
    • Renal impairment
    • Gastrointestinal dysfunction
    • Impaired peripheral circulation
  • Mediastinal bleeding
    • Infection: very serious if sternal
  • Atrial dysrhythmias
  • Hypovolemia
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Complications of CABG

  1. Dysrhythmias
  2. Impaired contractility; low cardiac output
  3. Intraoperative myocardial infarction
  4. Pericardial tamponade
  5. Respiratory insufficiency
  6. Pain
  7. Emboli; stroke
  8. Death
189

Pericardial tamponade

Fluid, pus, blood, clots, or gas accumulates in the pericardium (the sac in which the heart is enclosed), resulting in slow or rapid compression of the heart.

190

Transmycardial revascularization

  • Laser channels into ventricle
  • Goal is to increase perfusion of heart muscle
  • Relief of symptoms occurs over time
  • Poor candidates for CABG Mixed results from clinical trials
191

Dysrhythmias

  • Radiofrequency catheter ablation
  • Permanent pacemakers
  • Implantable cardioverter-defibrillator
192

Ablation

  • Supraventricular tachycardia
  • Interrupt electrical conduction or activity
  • Radiofrequency used
  • Electrophysiology
193

Implantable cardioverter-defribrillator (ICD)

  • Used to treat survivors of sudden cardiac arrest
  • Some have built-in pacemakers
  • Delivers high-energy shock
  • Patient education
  • Emergency procedures
194

Heart failure

  • Inability to generate adequate flow
  • Systolic (impaired contractility)
  • Diastolic (Impaired filling)
195

Heart failure: Etiology

  • AMI
  • Hypertension
  • Idiopathic; cardiomyopathy
  • Valvular disease
196

Left heart failure: Patho

  1. Decreased pumping action
  2. Back-up of blood from left ventricle
  3. Fluid build-up in lungs
  4. Backflow leads to right heart failure
  5. Fail to meet metabolic demands
  6. Compensatory mechanisms

* Renin-angiotensin- aldosterone system

* Sympathetic nervous system

7. Right heart failure

* Leads to system symptoms

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Heart failure treatment

Improve pump function

  • Diuretics
  • ACE inhibitors/angiotensin receptor blockers
  • Digoxin
  • Beta-blockers (carvedilol [Coreg])
  • BNP- nesiritide citrate (Natrecor)
198

Heart failure treatment: Reduce cardiac workload

  • Intraaortic balloon pump
    Ventricular assist device
  • Biventricular pacing
  • Nursing interventions
199

Heart failure treatment: Optimization of gas exchange

  • Airway
  • Diuresis
  • VTE prophylaxis
  • Control sodium & fluid retention
200

Heart failure complications

Pulmonary edema

  • Dyspnea
  • Cyanosis
  • Gurgles
  • Pink, frothy sputum
  • Hypoxemia

Cardiogenic shock

201

Inflammatory heart disease

  • Pericarditis- inflammation of the pericardium
  • Endocarditis- inflammation of the endocardium
202

Pericarditis: Etiology

  • After myocardial infarction
  • Uremia
  • Cancers

Can lead to infusion, tamponade, and scarring

203

Hallmarks of Pericarditis

  • Friction rub
  • Pulsus paradoxus
  • Initial ST elevation
204

Pericarditis: Procedures

- Pericardiocentesis
- Pericardial window

205

Endocarditis

  • Endocardium continuous w/valves
  • Vegetation
  • Embolization
  • Valvular dysfunction
206

Endocarditis: Diagnosis

  1. Echocardiogram
  2. Transesophageal
  3. Echocardiography
207

Endocarditis: Treatment

Antibiotics & rest

208

Endocarditis: Prevention

Antibiotic prescription before treatments (e.g., dentist)

- Heart valve

- History of endocarditis

- Microvascular pressure w/regurgitation

209

Vascular alterations: Aortic aneurysms

  • Dilation or thinning of wall
  • Thoracic aortic
  • Thoracoabdominal aortic
  • Abdominal aortic
  • Treat based on size & symptoms
  • False versus true
210

Vascular alterations: Aortic dissection

  1. Tear of intimal layer of the vessel
  2. Sudden
  3. Sharp
  4. Shifting pain
  5. Marfan syndrome
211

Signs of Marfan syndrome

  • Long arms, legs and fingers
  • Tall and thin body type
  • Curved spine
  • Chest sinks in or sticks out
  • Flexible joints
  • Flat feet
  • Crowded teeth
  • Stretch marks on the skin that are not related to weight gain or loss
212

Marfan syndrome:

Marfan syndrome is a genetic disorder that affects the body’s connective tissue. Connective tissue holds all the body’s cells, organs and tissue together.

213

Vascular alterations: Surgical treatment

  • Open approach
  • Endovascular approach