Cardiac Surgery (CSC) Subspecialty Study Pearls. CSC Exam Blueprint Download from 5/6/ questions.

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1 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 CSC Exam Blueprint Download from 24 questions Patient Problems (53%) Cardiothoracic Surgery (32%) Pulmonary (5%) Hematology (3%) Neurology/ Gastrointerstinal (7%) Renal (5%) Nursing Interventions (48%) 36 questions Pulmonary = 4 questions Hematology = 2 questions Neuro/GI = 5 questions Renal = 4 questions 1

2 Study Books Conte, J. Owens, S. & Dorman, T. (2007). The Johns Hopkins Manual of Cardiac Surgical Care, 2 nd 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. Handouts Let s Start! Body s Response to Low Perfusion Review of Hemodynamics and Pharmacological Interventions Renin-Angiotensin-Aldosterone System (RAAS) Kicks in 2

3 Renin-Angiotensin-Aldosterone System (RAAS) Low Cardiac Output/Hypotension/Hypovolemia Decreased 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/Hypovolemia Decreased 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 X Angiotensin II X Growth Factor Potent Vasoconstrictor Adrenal Cortex Dilatation & Diuresis Increases B/P Aldosterone ACE Inhibitors Prils Angiotensin II receptor Blockers ARBs Sartans Increases SVR Distal Renal Tubule Increases H2O & Na++ Reabsorption Excretes K+ for Na+ 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 Index CI = CO/BSA Cardiac output divided by body surface area (BSA) Normal range = l/min/m 2 Subclinical: l/min/m 2 Low perfusion: l/min/m 2 Shock < < 1.8 l/min/m 2 3

4 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 bpm Cardiac Medications & Effect on Cardiac Output Determinants of CO: Low Pacemaker Atropine Isuprel Dopamine Rate/Rhythm High Beta blockers Calcium channel blockers 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 Determinants of Cardiac Output Increase HR Atropine Dopamine/Intopin Epinephrine/Adrenalin Norepinephrine/Levophed Slight Increase HR Phenylephrine/ Neo-synephrine Vasopressin/Pitressin Dobutamine/Dobutrex Milrinone/Primacor Decrease HR Beta Blockers Calcium Channel Blockers Cardiac Output = Heart Rate x Stroke Volume 4

5 Know Normal Values! Parameter Normal Values Cardiac Output (CO) 4-8 l/min Cardiac Index (CI) l/min/m 2 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) dyne/sec/cm 5 Determinants of Cardiac Output Cardiac Output = Heart Rate x Stroke Volume Pulmonary vascular resistance (PVR) dyne/sec/cm 5 Stroke Volume (SV) ml/beat Stroke Volume Index (SVI) ml/beat/m 2 Arterial oxygenation saturation % Venous oxygenation saturation % Source: Sited in Cardiac Surgery Essentials, page 148 Stroke Volume (SV) Stroke Volume Index Definition: the volume of blood ejected with each beat Normal SV: ml Normal SVI: ml/beat/m2 Stroke index is defined as the amount of blood pumped with each beat indexed to BSA Normal ml s/m 2 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 Myocardial Fiber-Stretch Preload 5

6 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 Decreased Preload Inserted during surgery to measure Left atrial pressures Watch for air embolis from line Watch for tamponade after d/c 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 1 st 24 hours post op Watch for hypovolemia from rewarming and third spacing! 6

7 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/m 2 B. CVP 8 mm Hg, SVI 42 ml/beat/m 2 C. CVP 8 mm Hg, SVI 20 ml/beat/m 2 Answer Afterload C. CVP 8 mm Hg and SVI 20 ml/beat/m 2 Normal SVI: ml/beat/m2 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 = dynes/sec/cm-5 Pulmonary Vascular Resistance (PVR) reflects RV afterload Normal Range = dynes/sec/cm-5 7

8 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: 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) Decreased Vasodilation Vasodilation from rewarming Vasodilator therapies Preop beta blockers Sepsis Afterload Right Increased Pulmonary hypertension Hypoxemia Pulmonic stenosis Left Severe LV dysfunction Vasoconstriction Vasopressors Hypothermia catecholamine simulation from surgery Afterload The Effect of Cardiac Meds on Afterload Low Vasopressors High Warming blanket Vasodilators Calcium channel blockers IABP Increase Afterload Dopamine/Intopin Epinephrine/Adrenalin Norepinephrine/Levophed Phenylephrine/ Neo-synephrine Vasopressin/Pitressin Minimal effect on afterload Dobutamine/Dobutrex Decrease Afterload Nitroprusside/Nipride Arterial vasodilator Nitroglycerin/Tridil Venous vasodilator Beta Blockers Nicardipine/Cardene ACE Inhibitors Slight Decrease Afterload Milrinone/Primacor 8

9 Contractility Increased Contractility Inotropic state of muscle Not directly measurable Independent of Starling mechanism Sympathetic stimulation Metabolic states: Hypercalcemia Calcium Inotropic therapies: Epinephrine Dopamine/Intopin Epinephrine/Adrenalin Norepinephrine/Levophed Phenylephrine/Neosynephrine 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 The Effect of Cardiac Meds on Contractility Optimize preload & afterload Treat underlying causes Inotropes IABP Ventricular assist devices 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 9

10 Let s Practice! Draw arrows to indicated if the hemodynamic parameters would be increased, decreased or normal. CO/CI CVP PAD SV/SVI SVR/SVRI PVR/PVRI Hypovolemia Fluid Overload LV failure RV failure RV & LV failure Sepsis Hypovolemia Hypovolemia Fluid Overload CO/CI CO/CI Nx or CVP CVP PAD PAD SV/SVI SV/SVI SVR/SVRI Normal SVR/SVRI Normal Normal PVR/PVRI Normal PVR/PVRI Normal Normal Hypovolemia Fluid Overload LV failure Hypovolemia Fluid Overload LV failure RV failure CO/CI Nx or CO/CI Nx or CVP Normal PAD SV/SVI SVR/SVRI Normal Normal PVR/PVRI Normal Normal Normal CVP Normal PAD Normal SV/SVI SVR/SVRI Normal Normal Normal PVR/PVRI Normal Normal Normal 10

11 Hypovolemia Fluid Overload LV 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 Overload LV 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 admission Dopamine 2.5 mcg/kg/min CO/CI 3.7/1.8 SBP/DBP 115/53 MAP 71 HR 85 Sv CVP 9 PAS/PAD 26/16 PAM 21 PAW 20 SV 44 SVR 1339 SVRI 2779 PVR 22 PVRI 45 CABG on admission Dopamine 2.5 mcg/kg/min CO/CI 3.7/1.8 SBP/DBP 115/53 MAP 71 HR 85 Sv CVP 9 PAS/PAD 26/16 PAM 21 PAW 20 SV 44 SVR 1339 SVRI 2779 PVR 22 PVRI 45 CABG on admission Dopamine 2.5 mcg/kg/min CO/CI 3.7/ /2.4 SBP/DBP 115/53 123/55 MAP HR Sv CVP 9 10 PAS/PAD 26/16 29/18 PAM PAW SV SVR SVRI PVR PVRI minutes later after 250 ml 5% albumin CABG on admission Dopamine 2.5 mcg/kg/min CO/CI 3.7/ /2.4 SBP/DBP 115/53 123/55 MAP HR Sv CVP 9 10 PAS/PAD 26/16 29/18 PAM PAW SV SVR SVRI PVR PVRI minutes later after 250 ml 5% albumin 11

12 CABG on admission Dopamine 2.5 mcg/kg/min 30 minutes later after 250 ml 5% albumin CO/CI 3.7/ / /3.1 SBP/DBP 115/53 123/55 133/40 MAP HR Sv CVP PAS/PAD 26/16 29/18 40/19 PAM PAW SV SVR SVRI PVR PVRI hours later 500 ml 5% albumin & Dopamine 1 mcg/kg/min 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? 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 SVO 2 32 CO 3.8 CI 1.6 SVR 1031 SpO 2 92 SV 30 UO 30 T 2300 Art BP 92/57 MAP 68 HR 125 PAS/PAD 37/26 CVP 19 SVO 2 32 CO 3.8 CI 1.6 SVR 1031 SpO 2 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 12

13 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 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 T 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 13

14 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% Albumin Be 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 CT per hour 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

15 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? Case 7: After two units of prbcs. Did it help? What would you? 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 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 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 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 Case 7 Answer: Still hypovolemic needs more blood/surgery to find bleeder 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! 15

16 Cardiac Medications & Effect on Cardiac Output Volume Vasopressors LOW Optimize preload Inotropes Calcium Ventricular Assist Devices Pacemaker Atropine Isuprel Dopamine CARDIAC OUTPUT Treatment Options PRELOAD CVP, PAD, PAOP AFTERLOAD SVR,PVR CONTRACTILITY CO/CI indirect measurement RATE/RHYTHM HIGH Diuretics Venous Vasodilation Vasodilators Calcium Channel Blockers IABP Valve Surgery Beta Blockers Calcium Channel Blockers 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 16

17 Cardiac Tamponade: Signs & Symptoms Hypotension Low urine output Rising & equalization of CVP & PAD Falling SVO 2, 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 Triad Hypotension 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 DOS POD #1 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 tamponading Started on Dopamine 2.5 mcgkg/min Epi 3.07 mcg/min Milrinone 0.5 mcg/kg/min 1300 back to OR 1600 back to CVICU post removal of blood Note SV changes POD #2 17

18 DOS post op POD POD 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) Causes Bleeding from suture lines Clip comes off graft Aortic or ventricular rupture Chest wall bleeders Non Surgical --Abnormal clotting factors due to: Preop anticoagulant meds Systemic heparinization during CPB Breakdown of factors (platelets) during CPB 18

19 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 > cc/hr Low or labile B/P Low CVP or PAD Falling SVO 2 and CO/CI Abnormal clotting Factors Bleeding from line sites, incisions Treatments Monitor CT output. May need to replace CT output cc for cc with packed cells Keep sedated and B/P < 140 to prevent stress on suture lines Keep 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 products FFP for PT or PTT Platelet Phoresis for Platelet count Cryoprecipitate for Fibrinogen level Packed cells for H & H 19

20 Normal Values ACT < 130 seconds PT seconds APTT seconds Platelets 150, ,000 Fibrinogen Rule of thumb Replace CT output ml for ml After every 4 th unit prbcs Calcium Chloride FFP Treatments Pharmacological Interventions Protamine to reverse effects of systemic heparinization Aminocaproic Acid (Amicar) to inhibit conversion of plasminogen to plasmin Desmopressin (DDAVP) to improve platelet function Factor 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 20

21 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 Pathophysiology Tissue 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 Findings Test 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 21

22 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) Diagnosis ELISA 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 Protamine Reactions 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 Minor Hypotension Elevated PA pressures Hemodynamic profile Bradycardia Decreased CO Elevated PAP Elevated SVR & PVR Severe Massive systemic vasodilation Hypotension Decreased SVR Increased CO Acute pulmonary vasoconstriction Increased PAP RV failure 22

23 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 Potassium Flattened T waves, u waves, PVCs, V-tach High Potassium Tall, 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 Magnesium Peaked T waves, bradycardia, hyporelexia Low Sodium Fluid excess Sodium Deficit/mental changes/confusion Electrolytes in a Nutshell (2) Low Phosphorus Associated with resp alkalosis High Phosphorus Associated 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 Calcium Shortened QT interval, depressed T wave. Mental changes 23

24 Valvular Surgery Aortic Valve Preop Post op Aortic Stenosis LV hypertrophy SVR s/s heart failure LV may not anticipate in SVR and continue to pump hard Avoid hypertension and stress on suture line Aortic Regurgitation LV hypertrophy IV vasodilators to SVR Inotropic support to promote empting LV: Milrinone/Dobutamine IABP Valvular Surgery Mitral Valve Preop Post op Mitral Stenosis Nx LV function Pulmonary Hypertension RV failure High atrial & pulmonary pressures Pulmonary congestion Assess pulmonary hypertension (PVR) Dobutamine or Milrinone + Norepinephrine to contractility of RV & PVR Fluids CVP may indicate RV decompression Treat atrial fibrillation Mitral Regurgitation Enlarged left atrium Both common to have atrial fibrillation Immediate SVR due to no backflow of blood in LA Pulmonary hypertension & myocardial hibernation take time to reverse Inotropes (Milrinone, Dobutamine) + epinephrine IABP Monitor for RV failure Treat atrial fibrillation Mechanical versus Prosthetic IABP Intraaortic Balloon Pump Counterpulsation Mechanical valves are more durable than prosthetic valves Mechanical valves require life long anticoagulation Look at patient s age and med compliancy Inflation Coronary artery perfusion Deflation Decrease afterload Datascope Corp. Contraindications 1. Inflate at the beginning of diastole (dicrotic notch) 2. Deflate before ventricular systole 1. Severe aortic insufficiency 2. Abdominal or aortic aneurysm 3. Severe calcified aorta-iliac disease or peripheral vascular disease mm Hg B C Increased Coronary Artery Perfusion D B F 80 E A Reduced Myocardial O 2 Demand Datascope Corp. Datascope Corp. 24

25 Timing just like going to a party It s rude to come too early and It s rude to stay too late! Timing Errors - Early Inflation Unassisted Systole Diastolic Augmentation Assisted Systole Assisted Aortic End- Diastolic Pressure Datascope Corp. Datascope Corp. Timing Errors - Late Deflation Unassisted Systole Diastolic Augmentation Widened Appearance Assisted Aortic End-Diastolic Pressure Prolonged Rate of Rise of Assisted Systole Potential Side Effects and Complications Limb ischemia Bleeding at the insertion site Thrombocytopenia Migration of the balloon catheter Balloon leak Infection Aortic dissection Compartment syndrome Datascope Corp. Datascope Corp. 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

26 Phrenic Nerve Injury Causes Cold injury to nerve from cardioplegia solution Surgical trauma during takedown of IMA Air Leak Syndromes Pneumothorax Pneumopericardium Pneumomediastinum 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 Sp0 2 & p0 2 Subcutaneous emphysema Black area over lung field with no lung markings on CXR 153 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 % If tension pneumothorax ---- it is a medical EMERGENCY and needs immediate needle decompression 155 Tension Pneumothorax Distended neck veins Hypotension Tracheal deviation Note swan

27 Pneumomediastinum Air in the mediastinal soft tissues Cause: Rupture of alveoli Pneumopericardium Air in the pericardial sac Same hemodynamic instability as tamponade NORMAL ABG VALUES Management of Recovery from Anesthesia Know general effects of anesthetic agents 159 ROMS for ph and pco2 R = Respiratory O = Opposite M = Metabolic S = Same

28 ABGs What would you do? Respiratory Acidosis Patient A Patient B ph pco p TCO O 2 % BE -1-6 Cause: Result of Hypoventilation ph pco 2 Reasons: Sedation: Anesthesia, pain meds COPD, Pulm Edema, Pneumonia Chest trauma: flail chest or fx ribs Metabolic Acidosis Metabolic Acidosis ph HCO 3 Cause: Retention of Acid OR Loss Base Reasons: Hyperglycemia Shock, Sepsis (anaerobic metabolism) Renal Failure 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 Acidosis Ongoing 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 mmol/L (mortality 25-35%) Moderate acidosis mmol/L (mortality 60-75%) Severe acidosis > 10mmol/L (mortality > 95%) Shoemaker, WC et al. Textbook of critical care WB Saunders 28

29 Brush Up on.. Postop Cardiac Surgery Arrhythmias Atrial arrhythmias Maze procedure Antiarrhythmic meds Ventricular arrhythmias Bradyarrhythmia Pacemakers 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! Cardiac Surgery (CSC) Subspecialty Study Pearls You can pass CSC! Contact Cheryl Herrmann if you are interested in a longer CSC review class cherrmann@frontier.com 29