CSC review for NTI 5-5-11 Herrmann & Garner Herrmann, APN, CCRN, CCNS-CSC-CMC Suzanna Garner, RN, BSN, CCRN-CSC ... (SVR) 770 –1500 dyne/sec/cm5 Pulmonary …

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

[email protected]

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)


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


Cardiac Output =


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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


Cardiac Output =


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






Decrease Afterload

� Nitroprusside/Nipride

� Arterial vasodilator

� Nitroglycerin/Tridil

� Venous vasodilator

� Beta Blockers

� Nicardipine/Cardene

� ACE Inhibitors


Minimal effect on afterload

Slight Decrease Afterload


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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




� Phenylephrine/Neo-synephrine




� 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








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


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


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


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


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


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


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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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


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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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


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


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


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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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)


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

155

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

156

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


[email protected]

Documents

CSC review for NTI 5-5-11 Herrmann & Garner Herrmann, APN, CCRN, CCNS-CSC-CMC Suzanna Garner, RN, BSN, CCRN-CSC ... (SVR) 770 –1500 dyne/sec/cm5 Pulmonary …