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54/64 Unit 1 > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

The term used to describe the forces and mechanics of blood flow

A

Hemodynamics

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2
Q

The measurement and monitoring of the factors that influence circulation

A

Hemodynamic monitoring

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3
Q

Volume of blood ejected by the heart over 1 minute

A

Cardiac output (CO)

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4
Q

CO normal range

A

4-8 L/min

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5
Q

The volume of blood ejected from the ventricle with each beat of the heart

A

SV

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6
Q

What are the 3 components of stroke volume?

A

Preload, afterload, contractility

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7
Q

CO value adjusted for body size (BSA) that provides a more accurate measurement of adequacy of circulation

A

Cardiac Index (CI)

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8
Q

CI normal range

A

2.5-4 L/min m2

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9
Q

Equation for CI

A

CI = CO/patient’s BSA

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10
Q

BSA is calculated through what measurements?

A

Weight (Kg) and Height (cm)

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11
Q

Goal of hemodynamic monitoring

A

Tissue perfusion

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12
Q

To perfuse tissues and organs, several things must be done including

A

1) get O2 into lungs (ventilation), 2) get O2 from lungs into tissues (oxygenation), 3) get oxygenated blood to tissues (circulation), and 4) release O2 from blood into tissues

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13
Q

Factors that affect CO

A

Preload, afterload, contractility, and HR

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14
Q

Factors resulting in low cardiac output

A

Low SV, Low HR, or Both

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15
Q

Factors that decrease stroke volume

A

Low preload, high afterload, or decreased contractility

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16
Q

Component of stroke volume concerned with volume

A

Preload

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17
Q

Preload is associated with

A

Venous vasoconstriction or vasodilation

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18
Q

The initial stretching of cardiac myocytes prior to contraction

A

Preload

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19
Q

Preload is measured as ___ in the right ventricle and ___ in the left ventricle

A

CVP; PCWP/LVEDV

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20
Q

Factors that increase preload

A

Increased blood volume, pregnancy, exercise, HF, valve regurgitation, increased ventricular compliance

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21
Q

Factors that decrease preload

A

Drugs such as venous vasodilators and diuretics, loss of AV synchrony, increased HR

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22
Q

Volume of blood in the left ventricle at the end of diastole, as systole begins

A

LV end-diastolic volume

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23
Q

The ability of the heart and lungs to stretch

A

Compliance

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24
Q

How do venous vasodilators decrease preload?

A

Reduce blood return to the R side of the heart

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25
Q

How do diuretics decreased preload?

A

Reduce overall volume

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26
Q

Direct measure of preload

A

CVP

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27
Q

Premise that the greater the end-diastolic volume (preload), the greater the stretch of muscle cells, leading to greater stroke volume up to a point

A

Starling’s Law (Frank-Starling Curve)

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28
Q

Component of stroke volume associated with resistance

A

Afterload

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29
Q

Afterload is associated with

A

Arterial vasoconstriction or vasodilation

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30
Q

The pressure that must be overcome to push blood into the aorta or “what the heart has to work against”

A

Afterload

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31
Q

Factors that increase afterload

A

Vasoconstriction (medications with alpha 1 properties), hypothermia, SNS activation, aortic/pulmonic valve stenosis, HTN (systemic or pulmonary)

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32
Q

Factors that decrease afterload

A

Arterial vasodilation resulting from fever, exercise, inflammation/infection, or medications

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33
Q

Medications that cause arterial vasodilation (decreased afterload)

A

ACE inhibitors, ARBs, CCB, hydralazine (Apresoline), nipride, NTG

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34
Q

Afterload is measured through ___ in the right ventricle, and ___ in the left ventricle

A

CVP; PCWP

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35
Q

Explain resistance

A

The smaller the vessel the greater the resistance and vice versa; the greater the resistance, the harder the heart has to work to eject blood; increased resistance increases cardiac workload

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36
Q

Factors causing vasoconstriction

A

Decreased temperature, SNS activation, medications such as alpha — epi, phenylephrine, Levo (norepinephrine), vasopressin

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37
Q

Intervention to decrease afterload

A

Arterial vasodilators

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38
Q

Hormone that helps regulate BP by constricting blood vessels and triggering uptake of sodium and water

A

Angiotensin

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39
Q

Effects of increased afterload

A

Increased cardiac workload and oxygen

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40
Q

What should be administered to a smoker with HTN with narrowed, stiffened arteries?

A

Arterial vasodilator due to increased afterload

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41
Q

The force the heart can generate to eject blood, or the ability of the heart to overcome afterload

A

Contractility

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42
Q

Factors that increased contractility

A

SNS activation (catecholamine release), drugs

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43
Q

Factors that decrease contractility

A

PNS stimulation, hypoxia, ischemia/injury/infarction, acidosis, electrolyte imbalances

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44
Q

Irreversible tissue death from prolonged ischemia

A

Infarction

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45
Q

A patient with hypoxia and ischemic chest pain may have decreased

A

Contractility

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46
Q

Drugs that increase contractility

A

Digoxin, dopamine, dobutamine, epi

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47
Q

Drugs that decrease contractility

A

Negative inotropes such as beta blockers

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48
Q

The percentage of blood ejected from the ventricle

A

Ejection fraction (EF), or Left Ventricular Ejection Fraction (LVEF)

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49
Q

Ejection Fraction equation

A

EF = SV/LVEDP x 100

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50
Q

Normal EF

A

55-75%

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51
Q

Normal EF in women and men

A

Slightly higher for women (54-74%) than men (52-72%)

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52
Q

Low EF resulting in decreased ventricular function is associated with what conditions?

A

MI, CM, ischemia

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53
Q

Higher EF is associated with heart conditions like

A

Hypertrophic cardiomyopathy

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54
Q

EF less than 40% is generally considered

A

HF

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55
Q

Purpose of hemodynamic monitoring

A

Early detection, identification, and treatment of life-threatening conditions; evaluation of patient’s response to treatment; evaluate effectiveness of cardiovascular function

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56
Q

Indications for hemodynamic monitoring

A

Determine fluid volume status, measure CO, monitor/manage unstable patients, assess hemodynamic response to therapies, Dx primary pulmonary HTN, Dx shock states

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57
Q

Types of hemodynamic monitoring

A

Non-invasive, direct measurement of arterial pressure, invasive

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58
Q

Non-invasive hemodynamic monitoring includes

A

Clinical assessment and NBP

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59
Q

Non-invasive hemodynamic monitoring through clinical assessment

A

skin color/temp/mottling, HR, pulses, mental status, cap refill, UO, pulse ox, edema

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60
Q

Disadvantage of non-invasive hemodynamic monitoring

A

Susceptible to inaccuracy related to nature of measurements, impact of patient condition on results, etc.

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61
Q

Automated BP is less accurate during

A

Hypotension, arrythmias

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62
Q

Inaccurate pulse ox reading may be influenced by

A

Vasoconstriction, poor perfusion, cold extremities, skin pigmentation, motion artifact

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63
Q

A blood pressure cuff that is too small may yield a false _____ reading, while a blood pressure cuff that is too large may yield a false _____ reading

A

High; low

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64
Q

Indications for arterial BP monitoring

A

Frequent titration of vasoactive drips, unstable BP, frequent ABGs or lab draws, inability to obtain noninvasive BP

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65
Q

Sites for arterial BP monitoring

A

Radial, brachial, and femoral artery

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66
Q

Complications of arterial blood pressure monitoring

A

Hematoma, blood loss, thrombosis, distal ischemia, arterial injury, infection

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67
Q

Arterial line must remain level with patient’s

A

Phlebostatic axis (4th intercostal space, mid-axillary line)

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68
Q

An arterial line transducer that sits too low can result in a false _____ pressure, while a transducer that sits too high can result in a false _____ pressure

A

High; Low

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69
Q

Purpose of zeroing an arterial line transducer

A

Eliminates atmospheric pressure (0 mm Hg) ensuring that pressure measurements reflect only pressure values from the patient

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70
Q

Calculated pressure that closely estimates the perfusion pressure in the aorta representing average systemic arterial pressure during the entire cardiac cycle

A

Mean Arterial Pressure (MAP)

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71
Q

Normal MAP

A

70-100 mm Hg

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72
Q

MAP must be maintained above ___ mm Hg to preserve perfusion of major organs

A

60

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73
Q

Nursing implications for arterial line

A

Prevent/reduce potential complications, maintain 300 mm Hg on pressure bag, maintain continuous flow through tubing, aseptic dressing changes, sterile caps on openings

74
Q

How often should arterial line tubing be changed?

A

Every 96 hrs or per facility protocol

75
Q

How often should arterial line fluids be changed?

A

Every 24 hours (NS or heparin 1000 units/500 mL)

76
Q

The nurse should hold the discontinued arterial line site for at least

A

5 min

77
Q

Why does arterial line tubing need to be changed every 96 hrs?

A

To decrease opportunity for contamination of closed system

78
Q

Why is heparin not commonly used in an arterial line?

A

Risk of HIT

79
Q

Measurement of right atrial pressures reflecting preload to the right side of heart

A

Central Venous Pressure (CVP)

80
Q

CVP assesses

A

Blood volume and RV function

81
Q

CVP normal range

A

2-6 mm Hg

82
Q

Causes of low CVP

A

Inadequate preload, hypovolemia (or bleeding), vasodilation

83
Q

Causes of high CVP

A

Hypervolemia, RV failure, cardiac tamponade, tricuspid valve disease, pulmonary HTN, chronic LV failure, ventricular septal defect, constrictive pericarditis, PEEP > 10

84
Q

CVC/PAC nursing care

A

Sterile insertion and dressing changes, hand hygiene, avoid kinking, periodic flushing for patency, maintain sterile port, prompt removal if no longer required, NOT routinely replaced, replace tubing every 96 hrs, monitor for infection

85
Q

Hand hygiene is the most crucial step in nursing care for CVC to avoid

A

HAI such as CLABSI

86
Q

Why are CVCs not routinely replaced?

A

Risk of complications and infections

87
Q

CVC ports nursing care

A

Vigorous scrubbing before use (CHG, alcohol), use only sterile devices to access, lumens capped at all times

88
Q

Placement of swan gang (pulmonary artery) catheter

A

Internal jugular vein, subclavian vein, femoral vein

89
Q

What does a swan ganz catheter measure?

A

Pulmonary artery pressure (PAP), central venous pressure (CVP), core body temp, and allows for measurement of CO

90
Q

Where does the tip of the swan ganz catheter lie?

A

Pulmonary artery

91
Q

Indications for PA catheter

A

Dx and management of PAH, HF management, shock differentiation

92
Q

Pulmonary artery pressure (PAP) normal range

A

20-30 / 6-12 mm Hg

93
Q

Reasons for increased PAP

A

L-sided HF, increased pulmonary blood flow, increased pulmonary arteriolar resistance

94
Q

Reasons for decreased PAP

A

Hypovolemia, increased pulmonary resistance (ex: pulmonary HTN)

95
Q

Normal range for wedge pressure (PAWP/PCWP)

A

4-12 mm Hg

96
Q

Indirect measure of left atrial filling pressure

A

Wedge pressure (PAWP/PCWP)

97
Q

What does PAWP/PCWP indicate?

A

Intravascular fluid volume status

98
Q

Wedge pressure should be roughly equal to

A

Left ventricular end diastolic pressure (LVEDP)

99
Q

Why should PAP and PAWP be measured at end-expiration?

A

Respiratory pressure changes (ventilation) affect PAP and PAWP; intrathoracic pressure approaches atmospheric pressure and has the least effect on hemodynamic pressures at end-expiration

100
Q

Swan and Wedge ports should be inflated with no more than ___ mL of air

A

1.5

101
Q

How is wedge pressure measured?

A

By advancing a PA or swan ganz catheter in small branch of pulmonary artery

102
Q

PA catheter puncture site complications

A

Infection, hematoma, bleeding, pneumothorax (IJ/SCV access)

103
Q

PA catheter rhythm disorder complications

A

PAC/PVC, VT, VF

104
Q

PA Catheter conduction disorders complications

A

Right bundle branch block (particularly danger in preexisting LBBB)

105
Q

PA catheter complications

A

Damage to pulmonic or tricuspid valve (caused by pullback with inflated balloon), pulmonary artery rupture, pulmonary infarction/thromboembolism

106
Q

Measures of preload

A

CVP, wedge pressure, PAD

107
Q

Measures of afterload

A

ABP, SVR, PVR, valvular dysfunction

108
Q

Measures of contractility

A

LVEF, RVEF

109
Q

PAD can be a substitute measure for preload EXCEPT in patients with any degree of

A

Pulmonary hypertension (ex: smokers)

110
Q

How does a defibrillator work?

A

randomized shock delivery to myocardium making all electrical activity stop. Goal is that patient’s own pacemaker will kick in and restore a normal rhythm

111
Q

Defibrillators that decrease the amount of energy needed to convert rhythm resulting in less myocardial damage

A

Biphasic (150j - 200j)

112
Q

Monophonic defibrillator range

A

200j - 360j

113
Q

Shock synchronized with the patient’s R wave on EKG to avoid delivery of electricity during the refractory or repolarization phase

A

Cardioversion (synchronized shock)

114
Q

Indications for cardioversion

A

Convert arrhythmias back to Sinus Rhythm, used for rapid rhythms WITH pulse (SVT, Afib, Aflutter, VT (pulse))

115
Q

What causes ventricular tachycardia?

A

Low magnesium level

116
Q

Preparing the patient for cardioversion

A

Ensure understanding, remove all metal objects from pt to prevent burns, do not shock over transdermal medication (remove or avoid), ensure pt and environment dry, remove hair from chest if necessary, confirm asystole in 2 leads; no need to turn to side

117
Q

Defibrillator pad placement

A

To right of sternum just below clavicle, to left anterior axillary line 5th-6th intercostal space; NOT placed over permanent pacemaker

118
Q

Additional patient preparation for cardioversion

A

Informed consent, time-out, obtain 12-lead EKG, NPO, supine position, remove dentures/partial plates, pre oxygenate and maintain oxygenation throughout procedure (NRB or oxymask; ambu-bag on standby), ensure suction set up, sedation and analgesia as prescribed, set defibrillator on “synchronize”

119
Q

Synchronizing a defibrillator

A

Synchronized to R wave of patient’s EKG rhythm; marker indicates synchronization and beeping sound for each R wave (note: this procedure hurts!)

120
Q

Post defibrillation care

A

Assess VS, LOC, pulmonary and cardiovascular status; antidysrhythmic meds if needed; evaluate for burns; emotional support

121
Q

Treatment of choice for ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT)

A

Defibrillation

122
Q

Synchronized v. Unsynchronized defibrillation for V -tach

A

Stable v. Unstable

123
Q

Defibrillator strips for ventricular tachycardia vs. ventricular fibrillation

A

Monomorphic for VT and fine VF

124
Q

Post unsynchronized shock monitoring and care

A

Evaluate LOC, VS, burns, and electrolytes; monitor airway (may be intubated during code), IV fluids (vasopressors for BP) antidysrhytmic medications (IV drip, amiodarone), consider possible causes

125
Q

Defibrillation education

A

Explain S/S and problems associated with the dysrhythmia, discuss need for long term drug therapy, lifestyle changes, possible implanted cardiac defibrillator (ICD), need for an emergency communication system

126
Q

Types of pacemakers

A

Transdermal, transvenous, epicardial, permanent

127
Q

Transdermal pacemaker

A

Emergency, painful, very temporary

128
Q

Transvenous pacemaker

A

Temporary, usually via IJ or femoral vein, sits in RV

129
Q

Epicardial pacemaker

A

After cardiac surgery, use gloves to handle

130
Q

What should patients with pacemakers avoid?

A

Strong magnets (turn off pacemaker and stop function), MRI

131
Q

Permanent pacemaker

A

For complete heart block or other severe blocks, single/double/or triple chamber options, few restrictions after recovery (exercise, sexual activity, etc. are OK)

132
Q

Permanent pacemaker post-procedure care

A

CXR, Monitor for bleeding/swelling at insertion site, pain/comfort, and assess EKG for appropriate function

133
Q

Function of implantable cardiac defibrillator (ICD)

A

Shocks the patient internally for VT or VF

134
Q

ICD education

A

OK to do chest compressions, magnet turns off defib (no MRI w/o consult), can have pacemaker and defib in one (most ICDs are also pacemakers), batteries replaced in several years (~10)

135
Q

Where to listen during cardiac assessment

A

Aortic area, pulmonic area, Erb’s point, tricuspid area, mitral area/apex

136
Q

Aortic area

A

2nd intercostal space, right sternal border

137
Q

Pulmonic area

A

2nd intercostal space, left sternal border

138
Q

Erb’s point

A

3rd intercostal space, left sternal border

139
Q

Tricuspid area

A

4th intercostal space, left sternal border

140
Q

Mitral area/Apex

A

5th intercostal space, midclavicular line

141
Q

Area in which S2 (dub) sound is loudest

A

Aortic area

142
Q

Area in which S1 (lub) sound in loudest

A

Mitral area

143
Q

S2 (dub) sound is associated with

A

Closure of pulmonic and aortic valves

144
Q

S1 (lub) sound is associated with

A

Closure of mitral and tricuspid valves

145
Q

S3 heart sound

A

Follows S2, ventricular gallop (“Ken-tuck-y”), common in children, cardinal sign of HF, pulmonary edema, atrial septal defect

146
Q

S4 heart sound

A

Occurs just before S1, Atrial gallop (“ten-nes-see”), indicates increased resistance to ventricular filling, MI after effect, elderly, HTN, aortic stenosis

147
Q

Murmurs are caused by

A

Turbulent blood flow (d/t stenosis, regurgitation, structural defects such as septal defects, ruptured papillary muscle, etc.)

148
Q

Assessment of abnormal or extra heart sounds

A

Location, degree (loudness), character, timing

149
Q

Extra heart sounds

A

S3 and S4

150
Q

Extra heart sounds indicate

A

Decreased ventricular compliance to filling

151
Q

Extra heart sound associated with early diastole (passive filling phase)

A

S3

152
Q

Extra heart sound associated with late diastole (caused by blood in active filling phase working against higher pressure (non-compliant LV))

A

S4

153
Q

Best way to hear abnormal or extra heart sounds

A

With bell of stethoscope (low-pitched sound), patient on L side

154
Q

Flow of blood through a valve that is supposed to be open, but is narrowed d/t calcium, clots, congenital defects, etc.

A

Stenosis

155
Q

Backward flow of blood through a valve

A

Regurgitation

156
Q

Regurgitation characteristics

A

Blowing, harsh, musical sound

157
Q

S3 may be normal in patients…

A

Under 40 or some athletes (should disappear before middle age)

158
Q

S4 is nearly always

A

Pathologic

159
Q

Pulses to assess

A

Carotid, brachial, radial, ulnar, femoral, popliteal, posterior tibial, dorsalis pedis

160
Q

Assessment of pulses

A

Note symmetry and strength, start distal and move up if not felt, if you think you feel it —> confirm w/ Doppler

161
Q

Indications of poor CO and tissue perfusion

A

Cyanosis, pallor, cold skin

162
Q

Characteristics of arterial insufficiency

A

Skin cool, pale, and shiny; ulcerations on toes and heels; foot usually turns deep red when dependent; nails may be thick and ridged

163
Q

Characteristics of chronic venous insufficiency

A

Ulcerations around ankles, foot cyanosis when dependent, edema

164
Q

Visible JVD can indicate

A

R-sided HF (occurs any time venous return is greater than hearts ability to pump the blood back out)

165
Q

Partially occluded blood vessels

A

Bruits

166
Q

Assessment of carotid artery bruit

A

Auscultate upper, middle, and lower carotid artery; have patient hold breath while auscultating each spot (eliminates high tracheal breath sounds)

167
Q

Factors for monitoring perfusion

A

Noninvasive BP, HR, pulses, mental status, skin temp, mottling, cap refill, UO, pulse ox

168
Q

Structures responsible for nutrient and oxygen delivery

A

Arteries and capillaries

169
Q

Characteristics of ischemia

A

Blood is available but reduced (thrombus, stenosis, vasospasm), always results in hypoxia, leads to pain

170
Q

Reduced oxygenation (turning blue) as a result of uncorrected ischemia

A

Hypoxia

171
Q

Total lack of oxygen in body tissues resulting in cell death (infarction)

A

Anoxia

172
Q

Insufficient flow of oxygenated blood to tissues that may result in hypoxia and subsequent cellular injury and death

A

Ischemia

173
Q

The death of tissue with an inability to regenerate

A

Infarction

174
Q

The death of an area of heart muscle or myocardium

A

Myocardial infarction

175
Q

Chest pain assessment scale

A

APQRST: associated symptoms, palliative/provoking, quality (dull/sharp/crushing), radiate, severity (0-10), timing (before/after exercise, etc.)

176
Q

Cardiac laboratory testing for diagnosis

A

Enzymes such as CK, CK-MB; troponin (elevation indicates MI/infarction); BNP (elevation indicates HF)

177
Q

Laboratory tests for cardiac risk factors

A

Cholesterol/lipids (HDL/LDL), triglycerides

178
Q

Cardiac enzyme that measure possible brain, heart, skeletal mm injury

A

CK

179
Q

Cardiac enzyme specific to cardiac injury

A

CK-MB

180
Q

Peptide that helps regulate circulation by promoting urine excretion, relaxing blood vessels, lowering BP, and reducing cardiac workload

A

BNP

54/64 Unit 1 (9 decks)

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