CSC review for NTI 5-5-11 Herrmann & Garner Herrmann, APN, CCRN, CCNS-CSC-CMC Suzanna Garner, RN,...
Transcript of CSC review for NTI 5-5-11 Herrmann & Garner Herrmann, APN, CCRN, CCNS-CSC-CMC Suzanna Garner, RN,...
5/6/2011
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Cardiac Surgery (CSC) Subspecialty Study Pearls
Cheryl Herrmann, APN, CCRN, CCNS-CSC-CMC
Suzanna Garner, RN, BSN, CCRN-CSC
Methodist Medical Center of Illinois, Peoria
www.cherylherrmann.com
www.aacn.org
CSC Exam BlueprintDownload from www.aacn.org
Patient Problems (53%)
Cardiothoracic Surgery (32%)
Pulmonary (5%)
Hematology (3%)
Neurology/ Gastrointerstinal (7%)
Renal (5%)
Nursing Interventions (48%)
24 questions
Pulmonary = 4 questions
Hematology = 2 questions
Neuro/GI = 5 questions
Renal = 4 questions
36 questions
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Study BooksConte, J. Owens, S. & Dorman, T. (2007). The Johns Hopkins Manual of Cardiac Surgical Care, 2nd ed.Mosby/Elsevier.
Hardin, S, & Kaplow, R. (2009). Cardiac Surgery Essentials for Critical Care Nursing. Jones & Bartlett.
Todd, B. (2005). Cardiothoracic Surgical Nursing Secrets. Mosby/Elsevier.
www.aacn.org
Handouts
www.pacep.org
www.pacep.org Let’s Start!
Review ofHemodynamics and
Pharmacological Interventions
Body’s Response to Low Perfusion
� Renin-Angiotensin-Aldosterone System (RAAS) Kicks in…
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Renin-Angiotensin-Aldosterone System (RAAS)
Low Cardiac Output/Hypotension/HypovolemiaDecreased Renal perfusion
↓↓↓↓Afferent Arteriole (baroreceptors)
↓↓↓↓Release Renin (a messenger)
↓↓↓↓Go to Liver to stimulate Angiotensin I production
↓↓↓↓Angiotensin I goes to the Lung
↓↓↓↓Angiotension Converting Enzyme (ACE) located in the pulmonary vascular membrane
↓↓↓↓Converts Angiotensin I to Angiotensin II
↓↓↓↓Angiotensin II
↓↓↓↓ ↓↓↓↓ ↓↓↓↓Growth Factor Potent Vasoconstrictor Adrenal Cortex
↓↓↓↓ ↓↓↓↓Increases B/P Aldosterone
↓↓↓↓ ↓↓↓↓Increases SVR Distal Renal Tubule
↓↓↓↓Increases H2O &
Na++ Reabsorption
↓↓↓↓Excretes K+ for Na+
Renin-Angiotensin-Aldosterone System (RAAS)
Low Cardiac Output/Hypotension/HypovolemiaDecreased Renal perfusion
↓↓↓↓Afferent Arteriole (baroreceptors)
↓↓↓↓Release Renin (a messenger)
↓↓↓↓Go to Liver to stimulate Angiotensin I production
↓↓↓↓Angiotensin I goes to the Lung
↓↓↓↓Angiotension Converting Enzyme (ACE) located in the pulmonary vascular membrane
↓↓↓↓Converts Angiotensin I to Angiotensin II
↓↓↓↓Angiotensin II
↓↓↓↓ ↓↓↓↓ ↓↓↓↓Growth Factor Potent Vasoconstrictor Adrenal Cortex
↓↓↓↓ ↓↓↓↓Increases B/P Aldosterone
↓↓↓↓ ↓↓↓↓Increases SVR Distal Renal Tubule
↓↓↓↓Increases H2O &
Na++ Reabsorption
↓↓↓↓Excretes K+ for Na+
X
ACE Inhibitors“Prils”
X
Angiotensin II receptor Blockers“ARBs” “Sartans”
Dilatation & Diuresis
Principles of Muscle Function
Frank-Starling Law
The longer the muscle is stretched in diastole, to a point, the stronger the
contraction in the next systole.
Cardiac Output
� A measurement of flow of the volume of blood pumped by the heart each minute.
� Cardiac Output = Stroke Volume x Heart Rate CO = SV x HR
� Normal range 4-8 liters/minute
Cardiac IndexCI = CO/BSA
� Cardiac output divided by body surface area (BSA)
� Normal range = 2.5 – 4 l/min/m2
� Subclinical: 2.2 - 2.7 l/min/m2
� Low perfusion: 1.8 - 2.2 l/min/m2
� Shock < < 1.8 l/min/m2
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Determinants of Cardiac Output
Cardiac Output =
Heart Rate x Stroke Volume
Heart Rate
� Increasing Heart Rate is the fastest way to increase CO.
� Overtime, it is not the most efficient way.
� Optimal HR is 60 – 80 bpm
Determinants of CO:
Rate/Rhythm
Low
Pacemaker
Atropine
Isuprel
Dopamine
High
Beta blockers
Calcium channel blockers
Cardiac Medications & Effect on Cardiac Output
Medication Heart Rate Preload Afterload Vasodilator Vasopressor Contractility
Dopamine Hydrochloride (Intropin)
Epinephrine (Adrenalin)
Norepinephrine bitartrate (Levophed)
Phenylephrine (Neo-Synephrine)
Vasopressin (Pitressin)
Nitroprusside (Nipride)
Nitroglycerin (Tridil)
Dobutamine hydrochloride (Dobutrex)
Digitalis (Digoxin, Lanoxin)
Milrinone (Primacor)
Calcium Chloride
Amiodarone hydrochloride (Cordarone)
Lidocaine (Xylocaine)
Atropine sulfate
ACE Inhibitors
Beta Blockers
Diltiazem (Cardizem)
Nicardipine (Cardene)
www.cherylherrmann.com
The Effect of Cardiac Meds on Heart Rate
Increase HR
� Atropine
� Dopamine/Intopin
� Epinephrine/Adrenalin
� Norepinephrine/Levophed
Decrease HR
� Beta Blockers
� Calcium Channel Blockers
� Phenylephrine/ Neo-synephrine
� Vasopressin/Pitressin
� Dobutamine/Dobutrex
� Milrinone/Primacor
Slight Increase HR
Determinants of Cardiac Output
Cardiac Output =
Heart Rate x Stroke Volume
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Know Normal Values!Parameter Normal Values
Cardiac Output (CO) 4 - 8 l/min
Cardiac Index (CI) 2.5 – 4.2 l/min/m2
Right atrial pressure (CVP) 0 – 8 mmHg
Pulmonary artery pressure (PAS/PAD) 15 - 30/6 -12 mmHg
Pulmonary artery occlusive pressure 4 – 12 mmHg
Systemic vascular resistance (SVR) 770 – 1500 dyne/sec/cm5
Pulmonary vascular resistance (PVR) 20 – 120 dyne/sec/cm5
Stroke Volume (SV) 60 -130 mL/beat
Stroke Volume Index (SVI) 30 – 65 mL/beat/m2
Arterial oxygenation saturation 95 – 100 %
Venous oxygenation saturation 60 – 80 %
Source: Sited in Cardiac Surgery Essentials, page 148
Determinants of Cardiac Output
Cardiac Output =
Heart Rate x Stroke Volume
Stroke Volume (SV)
� Definition: the volume of blood ejected with each beat
� Normal SV: 60 – 100ml
� Normal SVI: 35 – 65 ml/beat/m2
Stroke Volume Index
� Stroke index is defined as the amount of blood pumped with each beat indexed to BSA
� Normal 35-45 ml’s/m2
� Very powerful indicator of ventricular function
Interpretation of SV/SVI� If low, the cause may be:
� Inadequate fluid volume: bleeding
� Impaired ventricular contractility: MI
� Increased SVR (afterload or resistance to
ejection)
� Cardiac valve dysfunction: mitral regurgitation
� If high, the cause may be:
� Fluid overload
� Low vascular resistance: sepsis
Preload
Myocardial Fiber-Stretch
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How full is the tank (heart)?Clinical Measurement of PRELOAD
� LEFT VENTRICLE = LVEDP
� Pulmonary Artery Wedge Pressure: 8-12 mm Hg
� Pulmonary Artery Diastolic: 8-15 mm Hg
� RIGHT VENTRICLE = RAP
� Right Atrial Pressure measures the pre-load of RV [normal range 2-5 mm Hg]
� CVP 4 to 10mm Hg
Left Atrial Catheter
� Inserted during surgery to measure Left atrial pressures
� Watch for air embolis from line
� Watch for tamponade after d/c
Decreased Preload
Etiology
� Hypovolemia
� Arrhythmias
� Loss of “Atrial Kick”
� Venous Vasodilation
Cardiac Surgery Specific
� Underlying cardiac disease
� Medications
� Preop medications
� Anesthesia
� Vasoactive agents
� Procedural induced hypothermia
� Rewarming
� Bleeding
Preload
Low
� Volume
High
� Diuretics
� Venous vasodilators
� Anticipate that Cardiac Surgery patients will have a decrease in blood and plasma volume (preload) within the 1st 24 hours post op
� Watch for hypovolemia from rewarming and third spacing!
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Interpretation of the CVP
� Reflects right-sided heart diastolic function and volume status
� Normal 2 - 6 mm Hg
� Assess with SV/SI
� > 6 mm Hg usually reflects right ventricular failure if the SV/SI is low
� < 2 mm Hg usually reflects hypovolemia if SV/SI is low
Which CABG patient needs volume?
A. CVP 8 mm Hg, SVI 35 ml/beat/M2
B. CVP 8 mm Hg, SVI 42 ml/beat/M2
C. CVP 8 mm Hg, SVI 20 ml/beat/M2
Answer
C. CVP 8 mm Hg and SVI 20 ml/beat/M2
� Normal SVI: 35 – 65 ml/beat/m2
Afterload
� Afterload is the pressure the ventricle has to generate to overcome resistance to ejection.
� Any resistance against which the ventricle must pump in order to eject its volume
Afterload;
pushing…
Afterload is measured as SVR and PVR� Systemic Vascular Resistance (SVR) reflects LV afterload
� Normal Range = 800-1400 dynes/sec/cm-5
� Pulmonary Vascular Resistance (PVR) reflects RV afterload
� Normal Range = 40-220 dynes/sec/cm-5
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SVR
� < 770 = vasodilated
� > 1500 = vasoconstricted
Pulmonary Vascular Resistance (PVR)
Definition:
A measurement of impedance to right ventricular ejection.
Equation: PVR = MPA – PCW x 80
CO
Normal Range: 40 - 220 dyne.sec.cm5
Factors That Decrease Pulmonary Vascular Resistance
Pharmacologic Agents•Oxygen•Isoproterenol•Aminophylline•Calcium channel blocking agents•Nitrous Oxide
Humoral Substances•Acetylcholine•Bradykinin•Prostaglandin E•Prostacyclin•Sildenafil (Viagra)
AfterloadDecreased
� Vasodilation� Vasodilation from rewarming
� Vasodilator therapies
� Preop beta blockers
� Sepsis
Increased
� Right� Pulmonary hypertension
� Hypoxemia
� Pulmonic stenosis
� Left� Severe LV dysfunction
� Vasoconstriction
� Vasopressors
� Hypothermia
� ↑ catecholamine simulation from surgery
Afterload
Low
� Vasopressors
High
� Warming blanket
� Vasodilators
� Calcium channel blockers
� IABP
The Effect of Cardiac Meds on Afterload
Increase Afterload
� Dopamine/Intopin
� Epinephrine/Adrenalin
� Norepinephrine/Levophed
� Phenylephrine/ Neo-synephrine
� Vasopressin/Pitressin
Decrease Afterload
� Nitroprusside/Nipride
� Arterial vasodilator
� Nitroglycerin/Tridil
� Venous vasodilator
� Beta Blockers
� Nicardipine/Cardene
� ACE Inhibitors
� Dobutamine/Dobutrex
Minimal effect on afterload
Slight Decrease Afterload
� Milrinone/Primacor
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Contractility
� Inotropic state of muscle
� Not directly measurable
� Independent of Starling
mechanism
Increased Contractility
� Sympathetic stimulation
� Metabolic states:
� Hypercalcemia
� Calcium
� Inotropic therapies:
� Epinephrine
� Dopamine/Intopin
� Epinephrine/Adrenalin
� Norepinephrine/Levophed
� Phenylephrine/Neo-synephrine
� Vasopressin/Pitressin
� Dobutamine/Dobutrex
� Milrinone/Primacor
� Digoxin
Decreased Contractility
� Parasympathetic stimulation
� Negative inotropic therapies� Beta blockers
� Calcium channel blockers
� Metabolic states:� Acidosis
� Hyperkalemia
� Myocardial ischemia/infarct
Etiology of ↓ contractility
Cardiac surgery
� ↑ or ↓ preload
� ↑ afterload
� Factors that affect myocardial contractility directly
� Ischemia
� RV or LV failure
� Aneurysms
� Electrolyte imbalances
� Tamponade
Treating Low Contractility
� Optimize preload & afterload
� Treat underlying causes
� Inotropes
� IABP
� Ventricular assist devices
The Effect of Cardiac Meds on Contractility
Increase Contractility
� Calcium
� Dopamine/Intopin
� Epinephrine/Adrenalin
� Norepinephrine/Levophed
� Phenylephrine/ Neo-synephrine
� Vasopressin/Pitressin
� Dobutamine/Dobutrex
� Milrinone/Primacor
Decrease Contractility
� Beta Blockers
� Calcium Channel Blockers
� Nicardipine/Cardene
� Lidocaine/Xylocaine
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Let’s Practice! Draw arrows to indicated if the hemodynamic parameters
would be increased, decreased or normal.
Hypovolemia Fluid
OverloadLV failure
RV failure
RV & LV failure
Sepsis
CO/CI
CVP
PAD
SV/SVI
SVR/SVRI
PVR/PVRI
Hypovolemia
CO/CI �
CVP �
PAD �
SV/SVI �
SVR/SVRI Normal
PVR/PVRI Normal
Hypovolemia Fluid Overload
CO/CI � Nx or �
CVP � �
PAD � �
SV/SVI � �
SVR/SVRI Normal Normal
PVR/PVRI Normal Normal
Hypovolemia Fluid
OverloadLV failure
CO/CI � Nx or � �
CVP � � Normal
PAD � � �
SV/SVI � � �
SVR/SVRI Normal Normal �
PVR/PVRI Normal Normal Normal
Hypovolemia Fluid
OverloadLV failure RV failure
CO/CI � Nx or � � �
CVP � � Normal �
PAD � � � Normal
SV/SVI � � � �
SVR/SVRI Normal Normal � Normal
PVR/PVRI Normal Normal Normal �
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Hypovolemia Fluid
OverloadLV failure
RV failure
RV & LV failure
CO/CI � Nx or � � � �
CVP � � Normal � �
PAD � � � Normal �
SV/SVI � � � � �
SVR/SVRI Normal Normal � Normal �
PVR/PVRI Normal Normal Normal � �
Hypovolemia Fluid
OverloadLV failure
RV failure
RV & LV failure
Sepsis
CO/CI � Nx or � � � � �
CVP � � Normal � � �
PAD � � � Normal � �
SV/SVI � � � � � �
SVR/SVRI Normal Normal � Normal � �
PVR/PVRI Normal Normal Normal � � �
CABG on
admissionDopamine 2.5 mcg/kg/min
CO/CI 3.7/1.8
SBP/DBP 115/53
MAP 71
HR 85
Sv02 38
CVP 9
PAS/PAD 26/16
PAM 21
PAW 20
SV 44
SVR 1339
SVRI 2779
PVR 22
PVRI 45
CABG on
admissionDopamine 2.5 mcg/kg/min
CO/CI 3.7/1.8
SBP/DBP 115/53
MAP 71
HR 85
Sv02 38
CVP 9
PAS/PAD 26/16
PAM 21
PAW 20
SV 44
SVR 1339
SVRI 2779
PVR 22
PVRI 45
CABG on
admissionDopamine 2.5 mcg/kg/min
30 minutes later
after 250 ml 5%
albumin
CO/CI 3.7/1.8 4.9/2.4
SBP/DBP 115/53 123/55
MAP 71 74
HR 85 88
Sv02 38 39
CVP 9 10
PAS/PAD 26/16 29/18
PAM 21 23
PAW 20 21
SV 44 56
SVR 1339 1055
SVRI 2779 2166
PVR 22 33
PVRI 45 68
CABG on
admissionDopamine 2.5 mcg/kg/min
30 minutes later
after 250 ml 5%
albumin
CO/CI 3.7/1.8 4.9/2.4
SBP/DBP 115/53 123/55
MAP 71 74
HR 85 88
Sv02 38 39
CVP 9 10
PAS/PAD 26/16 29/18
PAM 21 23
PAW 20 21
SV 44 56
SVR 1339 1055
SVRI 2779 2166
PVR 22 33
PVRI 45 68
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CABG on
admissionDopamine 2.5 mcg/kg/min
30 minutes later
after 250 ml 5%
albumin
36 hours later500 ml 5% albumin
& Dopamine 1 mcg/kg/min
CO/CI 3.7/1.8 4.9/2.4 6.5/3.1
SBP/DBP 115/53 123/55 133/40
MAP 71 74 69
HR 85 88 75
Sv02 38 39 55
CVP 9 10 12
PAS/PAD 26/16 29/18 40/19
PAM 21 23 27
PAW 20 21 26
SV 44 56 86
SVR 1339 1055 701
SVRI 2779 2166 1455
PVR 22 33 12
PVRI 45 68 26
Answer
� CABG on admission: CO/CI, SVO2, CVP, PAD, SV low so would give fluids. LVSWI and RVSWI also low but most likely due to hypovolemia.
� 30 minutes later, pt still needs fluid. Gave another 500 ml 5% albumin
� 36 hours later: Patient is now normovolumic….. With SvO2 low, low SVR/PVR, nx SV, give a positive inotrope. RV is okay but LV needs some help with contractility as evidenced by LVSWI low and normal SV.
Case 1: Identify abnormal hemodynamic parameters and what you would do?
2300
Art BP 92/57
MAP 68
HR 125
PAS/PAD 37/26
CVP 19
SVO2 32
CO 3.8
CI 1.6
SVR 1031
SpO2 92
SV 30
UO 30
T
Case 1: Identify abnormal hemodynamic parameters and what you would do?
2300
Art BP 92/57
MAP 68
HR 125
PAS/PAD 37/26
CVP 19
SVO2 32
CO 3.8
CI 1.6
SVR 1031
SpO2 92
SV 30
UO 30
T
Case 1 Answer: Tamponade. If cardiogenic shock would expect a higher SVR and CVP would be lower. Treatment– reexploration of chest
2300
Art BP 92/57
MAP 68
HR 125
PAS/PAD 37/26
CVP 19
SVO2 32
CO 3.8
CI 1.6
SVR 1031
SpO2 92
SV 30
UO 30
Case 2: Identify abnormal hemodynamic parameters and what you would do?
1300
Art BP 118/71
MAP 80
HR 107
PAS/PAD 37/26
CVP 23
SVO2 45
CO 4.2
CI 1.8
SVR 1316
SpO2 95
SV 39
UO 60
T2
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Case 2: Identify abnormal hemodynamic parameters and what you would do?
1300
Art BP 118/71
MAP 80
HR 107
PAS/PAD 37/26
CVP 23
SVO2 45
CO 4.2
CI 1.8
SVR 1316
SpO2 95
SV 39
UO 60
T2
Case 2 Answer: Tamponade. If cardiogenic shock would expect a higher SVR and CVP would be lower. Treatment– reexploration of chest. Note same patient as before only 11 hours later & did not go for reexploration and was treated with intropes :Dopamine 2.5 mcgkg/min, Epi 3.07 mcg/min Milrinone 0.5 mcg/kg/min . Did it help?
1300
Art BP 118/71
MAP 80
HR 107
PAS/PAD 37/26
CVP 23
SVO2 45
CO 4.2
CI 1.8
SVR 1316
SpO2 95
SV 39
UO 60
Case 3: Identify abnormal hemodynamic parameters and what you would do? Patient is on Dopamine 2.5 mcgkg/min, Epi 3.07 mcg/min Milrinone 0.5 mcg/kg/min
1600
Art BP 126/59
MAP 75
HR 125
PAS/PAD 29/20
CVP 17
SVO2 72
CO 7.9
CI 3.3
SVR 831
SpO2 99
SV 66
T3
Case 3: Identify abnormal hemodynamic parameters and what you would do? Patient is on Dopamine 2.5 mcgkg/min, Epi 3.07 mcg/min Milrinone 0.5 mcg/kg/min
1600
Art BP 126/59
MAP 75
HR 125
PAS/PAD 29/20
CVP 17
SVO2 72
CO 7.9
CI 3.3
SVR 831
SpO2 99
SV 66
T3
Case 3 Answer: This is the same patient post removal of tamponade. SV is borderline low – may need some fluid even with high CVP. Wean intropes as HR ↑
1600
Art BP 126/59
MAP 75
HR 125
PAS/PAD 29/20
CVP 17
SVO2 72
CO 7.9
CI 3.3
SVR 831
SpO2 99
SV 66
Case 4: Identify abnormal hemodynamic parameters and what you would do?
2200
Art BP 106/38
MAP 62
HR 83
Temp 99 F
PAS/PAD 29/14
CVP 13
SVO2 64
CO 3.3
CI 1.7
SVR 1186
SpO2 100
SV 39
UO 375 per hour
CT 60 H
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Case 4: Identify abnormal hemodynamic parameters and what you would do?
2200
Art BP 106/38
MAP 62
HR 83
Temp 97 F
PAS/PAD 29/14
CVP 13
SVO2 64
CO 3.3
CI 1.7
SVR 1186
SpO2 100
SV 39
UO 375 per hour
CT 60 H
Case 4 Answer: Hypovolemia. Give fluids – 250 ml 5% AlbuminBe careful when warming patient
2200
Art BP 106/38
MAP 62
HR 83
Temp 99 F
PAS/PAD 29/14
CVP 13
SVO2 64
CO 3.3
CI 1.7
SVR 1186
SpO2 100
SV 39
UO 375 per hour
CT 60
Case 5: Identify abnormal hemodynamic parameters and what you would do?
Admission
Art BP 142/52
MAP 83
HR 68
Temp 97
PAS/PAD 32/17
CVP 14
SVO2 69
CO 3.5
CI 1.8
SVR 1685
SpO2 97
SV 51
UO 750
CT 210
Case 5: Identify abnormal hemodynamic parameters and what you would do?
Admission
Art BP 142/52
MAP 83
HR 68
Temp 97
PAS/PAD 32/17
CVP 14
SVO2 69
CO 3.5
CI 1.8
SVR 1685
SpO2 97
SV 51
UO 750
CT 210
Case 5 Answer: Warm to decrease SVR. Fluids (check Hbg) for low SV, CI
Admission
Art BP 142/52
MAP 83
HR 68
Temp 97
PAS/PAD 32/17
CVP 14
SVO2 69
CO 3.5
CI 1.8
SVR 1685
SpO2 97
SV 51
UO 750
CT 210
Case 6: Identify abnormal hemodynamic parameters and what you would do?
0500
Art BP 91/38
MAP 58
HR 108
Temp 99
PAS/PAD 20/12
CVP 6
SVO2 59
CO 3.6
CI 1.8
SVR 1006
SpO2 93
SV 33
UO 40
CT 200
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Case 6: Identify abnormal hemodynamic parameters and what you would do?
0500
Art BP 91/38
MAP 58
HR 108
Temp 98
PAS/PAD 20/12
CVP 6
SVO2 59
CO 3.6
CI 1.8
SVR 1006
SpO2 93
SV 33
UO 40
CT 200
Case 6 Answer: Hypovolemia from bleeding. Give blood, check coags
0500
Art BP 91/38
MAP 58
HR 108
Temp 99
PAS/PAD 20/12
CVP 6
SVO2 59
CO 3.6
CI 1.8
SVR 1006
SpO2 93
SV 33
UO 40
CT 200
Case 7: After two units of pRBCs. Did it help? What would you?
0700
Art BP 109/42
MAP 67
HR 101
Temp 99
PAS/PAD 43/16
CVP 8
SVO2 61
CO 4.2
CI 2.1
SVR 1180
SpO2 95
SV 43
UO 75
CT 300
0500
Art BP 91/38
MAP 58
HR 108
Temp 99
PAS/PAD 20/12
CVP 6
SVO2 59
CO 3.6
CI 1.8
SVR 1006
SpO2 93
SV 33
UO 40
CT 200
Case 7: After two units of pRBCs. Did it help? What would you?
0700
Art BP 109/42
MAP 67
HR 101
Temp 99
PAS/PAD 43/16
CVP 8
SVO2 61
CO 4.2
CI 2.1
SVR 1180
SpO2 95
SV 43
UO 75
CT 300
0500
Art BP 91/38
MAP 58
HR 108
Temp 99
PAS/PAD 20/12
CVP 6
SVO2 59
CO 3.6
CI 1.8
SVR 1006
SpO2 93
SV 33
UO 40
CT 200
Case 7 Answer: Still hypovolemic – needs more blood/surgery to find bleeder.
0700
Art BP 109/42
MAP 67
HR 101
Temp 99
PAS/PAD 43/16
CVP 8
SVO2 61
CO 4.2
CI 2.1
SVR 1180
SpO2 95
SV 43
UO 75
CT 300
What if you have one hemodynamic value you can’t remember the normal?
Don’t PANIC!
GO WITH WHAT YOU KNOW!
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LOW
CARDIAC OUTPUTTreatment Options
HIGH
Volume PRELOADCVP, PAD, PAOP
DiureticsVenous Vasodilation
Vasopressors AFTERLOADSVR,PVR
VasodilatorsCalcium Channel BlockersIABPValve Surgery
Optimize preloadInotropesCalciumVentricular Assist Devices
CONTRACTILITYCO/CI indirect measurement
-----
PacemakerAtropineIsuprelDopamine
RATE/RHYTHM Beta BlockersCalcium Channel Blockers
Cardiac Medications & Effect on Cardiac Output
Medication Heart Rate Preload Afterload Vasodilator Vasopressor Contractility
Dopamine Hydrochloride (Intropin)
Epinephrine (Adrenalin)
Norepinephrine bitartrate (Levophed)
Phenylephrine (Neo-Synephrine)
Vasopressin (Pitressin)
Nitroprusside (Nipride)
Nitroglycerin (Tridil)
Dobutamine hydrochloride (Dobutrex)
Digitalis (Digoxin, Lanoxin)
Milrinone (Primacor)
Calcium Chloride
Amiodarone hydrochloride (Cordarone)
Lidocaine (Xylocaine)
Atropine sulfate
ACE Inhibitors
Beta Blockers
Diltiazem (Cardizem)
Nicardipine (Cardene)
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Assessment & Treatment of Cardiac Surgery Complications
Cardiac Tamponade
Postop Bleeding
Coagulopathy
Fluid & Electrolyte Shifts
Compression of the heart due to collection of fluid or blood in the pericardial space
Cardiac Tamponade
Typically occurs within first 12 hours post op
Difficult to diagnose as hypotension, tachycardia and elevated filling pressures are common in the post op period.
Cardiac Tamponade: Causes
Blood accumulated in the chest from:CTs clotted off and unable to drain excess blood
Epicardial wire removal
May occur quickly within minutes of hours or may occur slowly over days or weeks
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Cardiac Tamponade:Signs & Symptoms
Hypotension
Low urine output
Rising & equalization of CVP & PAD
Falling SVO2, CO/CI
Sudden decrease in CT output
Widening mediastinum on CXR
Neck Vein Distention
Tachycardia
Pulses Paradox > 20 mmHG
Diminished heart sounds
For tamponade that occurs slowly may also see these S/S:
Shortness of Breath
Chest Pain
Ischemic changes on EKG
Nausea
Cardiac Tamponade
Beck’s TriadHypotension
Neck vein distention
Muffled heart sounds
Suspect Tamponade if…
Continuous hypotension that does not respond to fluids AND the presence of the listed S/S,
Equalization of pressures
Cardiac Tamponade: Treatment
Urgent surgical exploration to evacuate excess blood & correct cause of the tamponade
Bedside echo may be used to make differential diagnosis between tamponade & LV failure
Administer fluids & inotropes or Calcium Chloride until patient can be returned to OR
Prepare for possible exploration of chest at bedside
2300 – started tamponadingStarted on Dopamine 2.5 mcgkg/minEpi 3.07 mcg/min Milrinone 0.5 mcg/kg/min1300 – back to OR1600 – back to CVICU post removal of blood
Note SV changes
DOS POD #1
POD #2
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DOS post op POD 1 2300 POD 2 1230 POD 3 post evacuation 0600
Cardiac tamponade
Low CO/CI
High CVP
All RA/PA pressures equal
SV low
Bleeding risk factors
Greater risk if CPB – more heparin
Hemodilution
Fibrinolysis
Hypothermia
If off pump patient is bleeding it is usually surgical in nature
Dark blood = venous or older blood
Bright red (warm) blood = arterial or fresh blood
Causes
Surgical (Mechanical) CausesBleeding from suture linesClip comes off graftAortic or ventricular ruptureChest wall bleeders
Non Surgical --Abnormal clotting factors due to:
Preop anticoagulant medsSystemic heparinization during CPBBreakdown of factors (platelets) during CPB
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Potential causes of post op bleeding
Surgical bleeding
Platelet dysfunction/depletion
Hypotension
Deficiency/depletion of plasma clotting factors
Residual effects of heparin due to incomplete reversal with protamine
Hemodilution
Hypothermia
Increased fibrinolytic activity
Consumption coagulopathy
Excessive Bleeding
More than 500 ml blood in first post op hour
Greater than 200 ml/hour x 2 hours
Signs & Symptoms
CT bleeding > 100 – 200 cc/hr
Low or labile B/P
Low CVP or PAD
Falling SVO2 and CO/CI
Abnormal clotting Factors
Bleeding from line sites, incisions
TreatmentsMonitor CT output. May need to replace CT output cc for cc with packed cellsKeep sedated and B/P < 140 to prevent stress on suture linesKeep CT patent by gently milking.Use warming blanket to keep normal thermic.
Hypothermia interferes with clotting factors
Hypothermia more common with CPB
Bleeding, platelet dysfunction and impairment of the coagulation cascade
May stimulation the SNS leading to: Hemodynamic instability
Dysrrhythmias
Vasoconstriction, hypertension, and increased SVR
Shivering Increased oxygen consumption (� SVO2) and CO2 production
Adrenergic stimulation
Use Demerol to treat
Treatment: Blood and Blood Products
Give blood and blood productsFFP for ↑ PT or PTTPlatelet Phoresis for ↓ Platelet countCryoprecipitate for ↓ Fibrinogen levelPacked cells for ↓ H & H
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Normal Values
ACT < 130 seconds
PT 10 – 13 seconds
APTT 25 – 40 seconds
Platelets 150,000 – 400,000
Fibrinogen 150 - 400
Rule of thumb
Replace CT output ml for ml
After every 4th unit pRBCsCalcium Chloride
FFP
Treatments
Pharmacological InterventionsProtamine to reverse effects of systemic heparinizationAminocaproic Acid (Amicar) to inhibit conversion of plasminogen to plasminDesmopressin (DDAVP) to improve platelet functionFactor VIIa: expediting platelet activation and ultimate fibrin clot formation
May need to return to surgery to repair mechanical cause of bleeding
DDAVP 1 Desamino-8-o-Arginine Vasopressin
Does not have the vasoconstrictive properties of vasopressin and yet maintains antidiuretic and hemostatic actions
Improves hemostatsis by increasing the plasma concentration of von Willebrand’s factor (vWF) and Factor VIII
Half life 1 – 2 hours
Dose 0.3 mcg/kg
Use for hemophilia A and von Willebrand’s Disease
Based on these coag values, what blood products do you expect to be ordered?
With excessive bleeding or tamponade….
Be Prepared to Emergently open the chest at the
bedside
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Coagulopathy
DIC
HIT
ReoPro Induced
Heparin Rebound
Disseminated Intravascular Coagulation (DIC)
Secondary disorder resulting from a primary pathophysiologic state or disease
Complex disease with overstimulation of both bleeding and thrombosis
Microvascular thrombi and bleeding occur simultaneously
DIC Common Physiologic Responses
Tissue damage
Platelet damage
Endothelial damage
DIC PathophysiologyTissue damage occurs
Healing (clotting) is stimulated
Hemopoietic chaos
Fibrinolytic mediators released
Initially microvascular thrombi
Consumption exceeds synthesis
Ability to clot is lost
Fibrinolyitc mediators “run a muck”
Lyse all clots
Bleeding State
Consumption Coagulopathy
DIC Laboratory FindingsTest Elevated Decreased
Hgb ↓
HCT ↓
Platelet Count ↓
PT ↑
PTT ↑
Fibrinogen ↓
FDP/FSP ↑
D-Dimer ↑
•H/H and platelets ↓ as they are used up in clots and lost from bleeding
•PT/PTT ↑ as clotting factors are being used up in clots
•Fibrinogen is used up when thrombin slips it to make clots so it ↓
•FSP/FDP ↑ as the clots are breaking up
•D-Dimer ↑ as there fibrin has cross linked with the type of clots you get from DIC
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DIC Treatment
No definite treatment– support/treat primary disorder
Early Recognition
Decrease bleeding risk
Treat pain
Transfusion therapy – pRBC, FFP, Platelets, cryo
Vitamin K
Anticoagulation therapy – Heparin
General Critical Care Support
Heparin Induced Thrombocytopneia (HIT)
Acquired allergy to Heparin
Antibodies are produced to Heparin
With Heparin administration the antibodies attack heparin and thrombocytes
Platelet count drops: 50% drop from baseline typically between day 5 – 14 of heparin administration
In Cardiac Surgery: Higher risk secondary to large systemic dose and long exposure to unfractionated heparin during CPB.
Heparin Induced Thrombocytopneia (HIT)
DiagnosisELISA assay antibody to identify if antibiodies are present
Treatment:Stop all heparin
Administer non-heparin anticoagulant• Argatroban – a direct thrombin inhibitor to prevent further
thrombosis
• Angiomax
Administer platelets ONLY if needed
Reopro (Abciximab) Induced Coagulopathy
Reopro is bound to platelet receptor sites immediately upon admission
Most platelets recover within 48 hours
Low levels of platelet blockade occurs up to 10 days post administration
Transfuse platelets to achieve hemostasis if bleeding from Reopro
Heparin Rebound
Heparin is reversed with protamine in 1:1 ratio at the end of CPB
The longer the CPB, more protamine is needed.
Heparin Rebound: hypocoagulable state may occur several hours after successful neutralization
Protamine metabolism
Release of heparin from tissue stores
ACT or PTT will be elevated
Treat with additional doses of protamine
Protamine Reactions
Minor
Hypotension
Elevated PA pressures
Severe
Massive systemic vasodilation
Hypotension
Decreased SVR
Increased CO
Acute pulmonary vasoconstriction
Increased PAP
RV failure
Hemodynamic profile•Bradycardia
•Decreased CO
•Elevated PAP•Elevated SVR & PVR
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Protamine Reaction Risk Factors
Allergy to fish
Use of NPH insulin – Diabetic patient
Protamine Reaction Treatment• Calcium Chloride 500 mg to support systemic
resistance and provide some inotropic support• a-agents (phenylephrine, norepinephrine) to
support systemic resistance• B-agents for inotropic support that can also
reduce pulmonary resistance (low dose epi, dobutamine)
• Aminophylline to manage wheezing• Heparin to reverse protamine reaction
Fluid & Electrolyte Shifts Fluid Shifts with Rewarming
Causes vasodilation � � BP and filling pressures
Use volume and pressors
May get postop cognitive impairment due to cerbral hyperthermia if warmed too fast
Electrolytes in a Nutshell
Low PotassiumFlattened T waves, u waves, PVCs, V-tach
High PotassiumTall, peaked T waves, absent p waves, wide QRS, ventricular escape/Asystole
Low Magnesium (Potassium’s little brother)Flattened T waves, prolonged QT, PVCs, V Tach,
Positive Trousseau’s and Chvostek’s
High MagnesiumPeaked T waves, bradycardia, hyporelexia
Low SodiumFluid excess – Sodium Deficit/mental changes/Confusion
Electrolytes in a Nutshell (2)
Low PhosphorusAssociated with resp alkalosis
High PhosphorusAssociated with resp acidosis, Positive Trousseau’s and Chvostek’s signs
Watch for heart block or flaccid paralysis with infusion of phosphorus as these are signs of rebound hyperphosphatemia. Stop infusion immediately!
Low Calcium↓CO, ↓ contractility, hypotension, Prolonged QT interval, hyperactive BS
Positive Trousseau’s and Chvostek’s signs
High CalciumShortened QT interval, depressed T wave. Mental changes
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Valvular SurgeryAortic Valve
Aortic Stenosis Aortic Regurgitation
Preop LV hypertrophy↑ SVRs/s heart failure
LV hypertrophy
Post op LV may not anticipate ↓ in SVR and continue to pump hardAvoid hypertension and stress on suture line
IV vasodilators to ↓ SVRInotropic support to promote empting LV: Milrinone/DobutamineIABP
Valvular SurgeryMitral Valve
Mitral Stenosis Mitral RegurgitationPreop Nx LV function
Pulmonary HypertensionRV failureHigh atrial & pulmonary pressuresPulmonary congestion
Enlarged left atriumBoth common to have atrialfibrillation
Post op Assess pulmonary hypertension (PVR)Dobutamine or Milrinone + Norepinephrine to ↑ contractility of RV & ↓ PVRFluids↑ CVP may indicate RV decompressionTreat atrial fibrillation
Immediate � SVR due to no backflow of blood in LAPulmonary hypertension & myocardial hibernation take time to reverseInotropes (Milrinone, Dobutamine) + epinephrineIABPMonitor for RV failureTreat atrial fibrillation
Mechanical versus Prosthetic
Mechanical valves are more durable than prosthetic valves
Mechanical valves require life long anticoagulation
Look at patient’s age and med compliancy
© Datascope Corp.
IABP Intraaortic Balloon Pump CounterpulsationIABP Intraaortic Balloon Pump Counterpulsation
Inflation↑ Coronary artery perfusion
Inflation↑ Coronary artery perfusion
DeflationDecrease afterload
DeflationDecrease afterload
© Datascope Corp.
ContraindicationsContraindications
1. Severe aortic insufficiency2. Abdominal or aortic aneurysm3. Severe calcified aorta-iliac disease or
peripheral vascular disease
1. Severe aortic insufficiency2. Abdominal or aortic aneurysm3. Severe calcified aorta-iliac disease or
peripheral vascular disease
© Datascope Corp.
Increased CoronaryArtery Perfusion
mmHg
C
D
A
B
E
F
Reduced MyocardialO2 Demand
120
100
80
B
© Datascope Corp.
1. Inflate at the beginning of diastole (dicrotic notch)2. Deflate before ventricular systole1. Inflate at the beginning of diastole (dicrotic notch)2. Deflate before ventricular systole
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© Datascope Corp.
Timing – just like going to a partyTiming – just like going to a party
It’s rude to come too early and
It’s rude to stay too late!
It’s rude to come too early and
It’s rude to stay too late!
© Datascope Corp.
Timing Errors - Early Inflation
AssistedSystole
Diastolic Augmentation
Assisted Aortic End-Diastolic Pressure
Unassisted Systole
Timing Errors - Late Deflation
Diastolic Augmentation
Assisted Aortic End-Diastolic
Pressure
Unassisted Systole
Widened Appearance
Prolonged Rate of Rise of
Assisted Systole
© Datascope Corp. © Datascope Corp.
Potential Side Effects and ComplicationsPotential Side Effects and Complications
• Limb ischemia• Bleeding at the insertion site• Thrombocytopenia• Migration of the balloon catheter• Balloon leak• Infection• Aortic dissection• Compartment syndrome
• Limb ischemia• Bleeding at the insertion site• Thrombocytopenia• Migration of the balloon catheter• Balloon leak• Infection• Aortic dissection• Compartment syndrome
149
Pulmonary 5%4 questions
Acute Resp Failure R/T phrenic nerve injury
• Phrenic nerve is responsible for diaphragmatic contraction
• Phrenic nerve injury may be associated with unilateral or bilateral neuropathy or paralysis
• With partial injury of one or both phrenic nerves lower lobe atelectasis may occur – esp on the left side
– Delay of weaning
– Decreased ability to clear secretions
150
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Phrenic Nerve Injury Causes
• Cold injury to nerve from cardioplegia solution
• Surgical trauma during takedown of IMA
151
Air Leak Syndromes
Pneumothorax
Pneumopericardium
Pneumomediastinum
152
153
• Air in the pleural space that inhibits complete lung expansion
• A thin, white line represents the displaced visceral pleura
Pneumothorax
• Diminished or absent lung sounds over the affected lung
• Dyspnea
• Tachypnea
• Acute pain on affected side of the chest
• Decreased Sp02 & p02
• Subcutaneous emphysema
• Black area over lung field with no lung markings on CXR
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Pneumothorax
• Causes:– Direct injury to the lung during surgery
– Line insertion causing tear in lung
– Baratrauma during positive pressure ventilation
– Occurs more on left due to LIMA disection
• Treatment:– Chest tube insertion if greater than 10 – 15 %
– If tension pneumothorax ---- it is a medical EMERGENCY and needs immediate needle decompression
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Tension Pneumothorax
• Distended neck veins
• Hypotension
• Tracheal deviation
Note swan
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Pneumomediastinum
• Air in the mediastinal soft tissues
• Cause: Rupture of alveoli
157
Pneumopericardium• Air in the pericardial sac
• Same hemodynamic instability as tamponade
158
Management of Recovery from Anesthesia
Know general effects of anesthetic agents
159
NORMAL ABG VALUES
ROMS for ph and pCO2
• R = Respiratory
• O = Opposite
• M = Metabolic
• S = Same
161 162
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ABGsWhat would you do?
Patient A Patient B
ph 7.29 7.31
pCO2 60 38
p02 132 100
TCO2 31 19
O2 % 98 98
BE -1 -6
Respiratory Acidosis
pH pCO2
Cause: Result of Hypoventilation
Reasons:
Sedation: Anesthesia, pain meds
COPD, Pulm Edema, Pneumonia
Chest trauma: flail chest or fx ribs
Metabolic AcidosisCause: Retention of Acid OR Loss
BasepH
HCO3Reasons:
Hyperglycemia
Shock, Sepsis (anaerobic metabolism)
Renal Failure
Metabolic Acidosis
• Type B Lactic Acidosis
– Occurs in the absence of tissue hypoxia
– May be catecholamine-induced metabolic effect (especially with epinephrine)
– May be caused by hyperglycemia & alterations in fatty acid metabolism
Metabolic AcidosisOngoing Metabolic Acidosis means something is not being perfused
• Type A Lactic Acidosis
– Reflects impaired tissue oxygenation & anaerobic metabolism resulting from circulatory failure
– The lactate ion more than the acidemia contributes to potential cardiovascular dysfunction
The Value of Lactate
Serial lactate levels predictor of perfusion
– Normal <2.5mmol/L
– Mild acidosis 2.5-4.9mmol/L (mortality 25-35%)
– Moderate acidosis 5.0-9.9mmol/L
(mortality 60-75%)
– Severe acidosis > 10mmol/L
(mortality > 95%)
Shoemaker, WC et al. Textbook of critical care. 1995. WB Saunders
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Postop Cardiac
Surgery
Arrhythmias
Atrial arrhythmias
Maze procedure
Antiarrhythmic meds
Ventricular arrhythmias
Bradyarrhythmia
Pacemakers
Brush Up on….. Next Steps
Make a study action plan
Set the target test date
Get a study partner
If WE can do it, YOU can do it!
You can pass CSC!
Cardiac Surgery (CSC) Subspecialty Study Pearls
Contact Cheryl Herrmann if you are interested in a longer CSC review class
www.cherylherrmann.com