Cardiovascular Surgery Manual PDF

Our Lady of Fatima University College of Medicine Department of Surgery TCVS CARDIAC SURGERY I. Acquired Cardiac Diseases A. Cor...

Our Lady of Fatima University College of Medicine Department of Surgery TCVS CARDIAC SURGERY I. Acquired Cardiac Diseases A. Coronary Artery Disease (CAD) B. Valvular Heart Diseases (VHD) II. Congenital Heart Diseases (CHD) A. Left-to-Right (L-R) shunts 1. Patent Ductus Arteriosus (PDA) 2. Atrial Septal Defect (ASD) 3. Ventricular Septal Defect (VSD) B. Right-to-Left (R-L) shunts 1. Tetralogy of Fallot (TOF) III. Miscellaneous A. Permanent Pacemaker Implantation (PPI) B. Pericardial Diseases C. Tumors D. Trauma General Considerations 1. History & Physical Examination 2. Symptoms - angina, dyspnea, edema, cough or hemoptysis, palpitation, syncope 3. Differential Diagnosis (for CAD) - GERD, esophageal spasm, musculoskeletal pain, PUD, pulmonary embolus, costochondritis (Tietze’s syndrome), biliary tract disease, pleuritis, pulmonary hypertension, pericarditis, aortic dissection 4. Preop Assessment/Evaluation/Risk Stratification Tools a. American Heart Association (AHA) Guidelines - Circulation Journal; circ.ahajournal.org b. European Society of Cardiology (ESC) Guidelines - www.escardio.org c. New York Heart Association (NYHA) Functional Classification Class I - Patients with cardiac disease, but without resulting limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or angina pain. Class II - Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or angina pain. Class III - Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity results in fatigue, palpitation, dyspnea or anginal pain. Class IV - Patients with cardiac disease resulting in an inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased d. Canadian Cardiovascular Society (CCS) Angina Classification Class I - Ordinary physical activity such as walking or climbing stairs, does not cause angina. Angina may occur with strenuous, rapid, or prolonged exertion at work or recreation. Class II - There is slight limitation of ordinary activity. Angina may occur with walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals or in the cold, in the wind, or under emotional stress, or walking 1  >2 blocks on the level , or climbing >1 flight of stairs under normal conditions at a normal pace Class III - There is marked limitation of ordinary physical activity. Angina may occur after walking ≥1 block on the level, or climbing 1 flight of stairs under normal conditions at a normal pace Class IV - There is inability to carry on physical activity without discomfort; angina may be present at rest. e. EuroScore II - free downloadable app f. Society of Thoracic Surgeons (STS) - free downloadable app 5. Diagnostic Tools a. Chest X-ray (CXR) - cardiac silhouette, pulmonary congestion, associated pulmonary pathology b. 12-Lead Electrocardiogram (12-L ECG) - rate, rhythm, ventricular hypertrophy, blocks, ischemia c. 2-Dimensional Echocardiography with Doppler (2DED) - chamber size, wall motion, shunts, valve pathology, LV function, effusion d. Viability Studies (1) Radionuclide studies (a) Thallium scan (b) Positron Emission Tomography (PET) scan (2) Magnetic Resonance Imaging (MRI) - transmural infarct, ventricular scar & aneurysm e. Cardiac Catheterization/Coronary Angiography - chamber pressures, cardiac output, shunt quantification, wall motion, coronary anatomy f. Computed Tomography (CT) Coronary Angiography - intraluminal calcium ACQUIRED CARDIAC DISEASES I. Coronary Artery Disease (CAD) A. Anatomy of coronary arteries 1. Left Main (LM) Coronary - branches into a. Left Anterior Descending (LAD) - diagonal, septal branches b. Left Circumflex (LCx) - obtuse marginal branches - supplies RVFW, septum, LVFW, apex of RV and LV 2. Right Coronary Artery - branches into a. Right Posterolateral (RPL) - supplies AV node b. Right Posterior Descending (RPDA) - septal, RV and LV branches, SA node B. Etiology: atherosclerosis, multifactorial C. Risk Factors: hyperlipidemia, smoking, obesity, sedentary lifestyle, male gender, elevated levels of CRP, lipoprotein and homocysteine D. S/S: angina pectoris, MI, CHF, arrhythmias, sudden death; MI is the most common serious complication E. Treatment Options 1. Coronary Artery Bypass Graft (CABG) Surgery - indications (AHA Guidelines) a. Chronic angina b. unstable angina c. postinfarction angina d. asymptomatic patients with atypical symptoms developing ischemia during stress test - 1-3% O.R. mortality rate 2. Percutaneous coronary intervention (PCI)/ Percutaneous Transluminal Coronary Angioplasty (PTCA) 3. Thrombolysis - 6 hours golden period; streptokinase, urokinase F. Acute Myocardial Infarction (AMI) 2  1. PCI or thrombolysis - preferred method of emergent revascularization for uncomplicated MI 2. subendocardial MI + LM disease or postinfarction angina & multivessel involvement - CABG surgery 3. Primary indications for surgery after acute transmural MI a. Postinfarction VSD b. Postinfarction LV aneurysm c. Papillary muscle rupture with mitral insufficiency d. LV rupture G. Surgical Considerations 1. Incision - mid sternotomy; thigh & legs [island incisions or endovascular harvest (EVH)] 2. Grafts/ conduits - a. arterial grafts - internal mammary/thoracic artery (IMA/ITA), radial artery, right gastroepiploic artery, free inferior epigastric artery, splenic artery b. venous grafts - greater saphenous vein, lesser saphenous vein 3. Cardio-Pulmonary Bypass (CPB) Machine - Heart-Lung Machine 3  a. Components: venous drainage line & reservoir, pump, oxygenator-heat exchanger, arterial filter, arterial inflow line b. Agents of Damage/ Side Effects (1) shear stress (2) incorporation of foreign substances (3) heparin and protamine side effects (4) trauma to the blood - RBC hemolysis (5) low-grade coagulopathy (6) systemic inflammatory response (7) end-organ dysfunction 4. Myocardial protection a. chemical cardioplegia (antegrade; retrograde) - solution with high K+ content b. hypothermia - decreases O2 requirement and allows lower flow rates without producing lactic acidosis; metabolic activity decreases with lower body temperature H. Off-Pump Coronary Artery Bypass (OPCAB) Surgery - beating heart 1. mortality rate (6.5 vs 11.4%) 2. stroke (1.6 vs 5.7%) 3. decreased perioperative complications 4. less myocardial injury 5. fewer blood transfusions 6. earlier postoperative extubation 7. earlier hospital discharge I. Other treatment options 1. Minimally invasive direct coronary artery bypass (MIDCAB) a. L anterior minithoracotomy b. beating heart c. single-vessel disease : LAD or diagonal d. late results better than PCI 2. Transmyocardial Laser Revascularization (TMR) a. carbon dioxide, holmium;yttrium-aluminum-garnet laser b. drill multiple holes through the myocardium into ventricular cavity which stimulates angiogenesis in the area of injury c. for patients with refractory angina who are unsuitable candidates for standard CABG due to poor distal coronary artery anatomy J. The future of CAD 1. Total endoscopic coronary artery bypass (TECAB) - robotics 2. Biomolecular therapy and tissue engineering 3. Anastomotic devices - proximal & distal anastomotic devices (staplers) K. CABG Outcome 1. mortality rate a. elective CABG for stable angina w/ good LV function 40% 2. saphenous vein graft a. patency rate 65-75% in 10 years b. 10-15% occlude within the 1st year c. 2-5%/yr occlude thereafter 3. IMA graft - in-situ patency rate 90-95% in 10 yrs; 70-80% if free graft 4  4. recurrent angina occurs in 35% 2o to vein graft occlusion & progression of disease in non bypassed vessels or in bypassed vessels beyond the site of distal anastomosis 5. angina symptoms treated medically w/ only 10% requiring reop at 10 yrs 6. Peri-op MI a. 2-3% in stable angina b. 5-10% UA c. 30-50% in “E’ CABG after a failed PTCA d. thereafter, late MI rate is 1-3%/yr 7. mortality rate in reop 2-3x higher 8. long-term survival rate a. all vein graft 80% & 65% ( 5 & 10 yrs respectively) b. IMA 90% & 75% 9. the most important predictor adversely predicting long-term prognosis is LV dysfunction L. PTCA Outcome 1. 90% 10-yr survival rate (SR) in single vessel PTCA 2. additional angioplasty required in 30%, bypass surgery in another 25% 3. results favourable for vein graft stenosis in the distal anastomotic site 4. recurrent stenosis rate 25-30%, earliest 6 mos Freedom from subsequent bypass grafting or repeat angioplasty is significantly higher for those undergoing CABG II. Valvular Heart Diseases A. Mitral Stenosis (MS) 1. Etiology: rheumatic heart disease (RHD), congenital 2. normal mitral valve area (MVA) : 4-6cm2 mild stenosis: 1-1.5 cm2 severe stenosis: 1.5 cm2 severe AS: 50mmHg critical AS: 1.5cm2 1-1.5cm2 RA>LV & RV (87%, 6%, 4%, 2%) (4) Diagnostics - 2DEcho, CT scan, MRI (5) Treatment - excision under CPB 2. Malignant - 25% (angiosarcoma - most common; rhabdomyosarcoma, fibrosarcoma, leiomyosarcoma, liposarcoma, lymphoma) B. Metastatic - most common, 4-12%(lung, breast, melanoma, lymphoma) C. Diagnostics: 2DE, TEE, MRI, cardiac cath D. Treatment: excision, chemotherapy, RT IV. Trauma A. Penetrating Cardiac Trauma - 60-70% of penetrating chest injuries 2° to stab wounds - RV frequently injured, 40-45% (RV>LV>RA>LA) - LA least injured, 5% - simultaneous injury of >1 chamber in 30% - Beck's triad (hypotension, venous pressure, muffled heart sounds) in only MV>TV - ventricular septal rupture occurs in the muscular portion near the apex - pericardial tear: L>R herniation - Diagnostics: ECG, CXR, cardiac enzymes - Tx: ICU - treat as MI 14  Normal Values Formulas CO 4-8 L/min CO SV x HR CI 2.5-4 L/min SV LVEDV - LVESV SV 1 mg/kg/beat PCWP = LAP = LVEDP SVI 33-47 mL/beat/m2 CVP = RAP = RVEDP MAP 70-100 mmHg Pulse P SBP - DBP PAWP 10-15 mmHg MAP DBP + ½ of pulse P SVR 800-1200 dynes sec/cm5 MAP CI x SVRI SVRI 1600-2400 dynes sec m2/cm5 SVRI [(MAP-RAP)x 80]/CI PVS 50-250 BSA wt(kg) x 0.02 +0.4 LVSWI 45-75 mg/m/beat m2 Determinants of SV 1. Preload - LVEDP or LVED fiber length 2. Afterload - LV systolic wall tension determined by preload & SVR 3. Contractility - can be improved by inotropes, ng preload or HR, ↓ng afterload Normal Dimensions/Values Size (cm) P (mmHg) Mean P (mmHg) RA 3.5-4.5 2-8 3 RV 2.2-4 15-30 25/4 LA 3-3.5 6-8 8 LV 4.5-5.2 LA diastolic 130/8 PCWP = LAP (8-15) Cardiac Drugs and Dosages INOTROPES Dopa (DA) 2-20 µg/kg/min (2-3 renal dose) Dobu 2-20 µg/kg/min Epi 1-4 µg/min NE (Levo) 2-100 µg/min Milrinone 500 µg/kg bolus 0.5 µg/kg/min ANTI-HYPERTENSIVES NTG 0.1-10 µg/kg/min Nicard 2.5 mg over 5 min, rpt x 4 at 10min interval, then 2-3mg/h Esmolol 0.25-0.5 mg/kg bolus over 1 min, then 50-200 µg/kg/min 15 INOTROPES ANTI-ARRHYTHMICS Amio 150 mg in 15-30min 1mg/min x 6 h 1 g/d; 300 mg IV bolus 600mg x 24h Digoxin 0.25 mg IV q 6h x 4 0.25 mg QID Lidocaine Load: 1mg/kg 0.5mg/kg 1-2x x 10min apart; Drip: 2-4mg/min (15/250 mL) Adenosine 6mg IV rapid push central line fed by saline flush rpt 12 mg after 2 min Cardiac Drugs & Mechanism of Action INOTROPRES DA (2-3 µg) selective “dopaminergic” effect, dilates renal a; mild ß2 effect, ↓periph resis, ↓BP, profound tachy; (3-8µg) strong ß1 inotropic effect, improve contractility, HR, potential arrhythmogenesis; (>8µg) ng inotropic effect, predom α effect, SVR, systemic BP. filling P; may AV condxn in AF or flutter Dobu positive inotrope, strong ß1 effect, contrac & HR, mild ß2 effect, ↓vasc resistance, min α1 effect, ↓ preload & afterload Epi strong ß1 effect, contrac & HR, CO, α-agonist effect at dose ( SVR) NE (Levo) SVR, contrac, HR, strong α & ß adrenergic fx Milrinone phosphodiesterase inhibitor, ↓SVR, modest inotropic effect Phenyleprine pure α agonist, SVR, no direct cardiac effect ANTI-HYPERTENSIVES NTG ventilator, preload, filling P, SV & CO; dilates coronary conductance vessels & improve coronary blood flow to isch zones; arterial vasodil at high doses 16  VASCULAR SURGERY I. Aortic Diseases A. Aneurysmal Disease - dilatation of an artery >1.5x its normal diameter; most common in the abdominal aorta, thoracic aorta, cerebral vessels, iliac, popliteal, and femoral aa; rarely visceral aa - Law of Laplace; T = Pr - Classification: a. Shape - fusiform, saccular b. Wall constituents - true aneurysm; pseudoaneurysm c. Etiology - dissecting aneurysm, mycotic, traumatic 1. Abdominal Aortic Aneurysm (AAA) a. Etiology: degenerative, atherosclerosis, progressive loss of elastin, metalloprotease activity b.Incidence: >50y/o, M>F = 5:1 c. Risk factors: older age, male, white, (+) family history, smoking, hypertension, hypercholesterolemia, PVOD, CAD d. S/S: mostly asymptomatic, nausea and vomiting, pulsatile mass, abdominal/low- back pain, hypotension e. average growth 0.4cm/yr f. Dx: UTZ, CT scan w/contrast, MRI, MRA, angiography g. Summary of Imaging Modalities Studies Overview Pros Cons X-rays Calcified aortic wall Simple, inexpensive Lower specificity; detects 60% of AAAs; calcified wall B-mode Good screening tool Accurate (80-90%); Bowel gas interference; ultrasound inexpensive operator-dependent CT scan Most accurate study Accurate; define Expensive; ionizing for AAA diameter anatomy & anomalies radiation CT New modality; 3-D images; avoids Expensive; same contrast angiogram combine CT and radiation & invasive load as angiogram; special angio angiogram protocol MRA New modality 3-D images; avoids Expensive; limited radiation & invasive resolution; patient angiogram contraindications Angiogram Popular due to Shows visceral & Expensive; invasive; endografting occlusive disease contrast load h. Tx: conservative/selective management if small (1cm/yr expansion or with symptoms) : Aortic Endografting, EndoVascular Aneurysm Repair (EVAR) - cutdown on bilateral CFA, Seldinger technique, Bentsen guidewire w/ fluoroscopy (1) Ideal characteristics of an aneurysm for endovascular abdominal aneurysm repair (CT scan findings) (a) neck length >15mm (b) neck diameter >18mm, 1cm in 1-yr (for chronic phase) d. Endovascular treatment - 9% operative mortality rate - 7% stroke rate - 3% paraplegia/paraparesis rate - 20-25% endoleak - other cxs: stent-graft misdeployment, device migration, endograft kinking II. Peripheral Arterial Occlusive Disease A. Lower extremity acute ischemia/Acute Limb Ischemia (ALI) - heart is the most common source of distal emboli (70%) - atrial thrombus fr AF is the most common cause - mural thrombus from LV aneurysm are the most common cause of a saddle embolus - 6P’s - pain, pallor, paresthesia, paralysis, pulselessness, poikilothermic or “perishing cold” - /s: foot and calf pain - most common location for an embolus to lodge is common femoral artery (CFA) - Tx: A. Medical - anticoagulation, heparin B. Lysis - urokinase, rtPA C. Surgery - embolectomy, thrombectomy - Clinical Categories - TransAtlantic Inter-Society Consensus (TASC) Findings Doppler signals Category Description/ Sensory Muscle Arterial Venous Prognosis loss weakness I Viable Not immediately (-) (-) Audible Audible threatened II Threatened a. Marginally Salvageable if Minimal (-) Often Audible promptly treated (toes) or - inaudible 23  Findings Doppler signals Category Description/ Sensory Muscle Arterial Venous Prognosis loss weakness b. Immediately Salvageable w/ >toes, Mild, mod usually Audible immediate revasc assoc’d w/ inaudible rest pain III Irreversible Major tissue loss Profound Profound Inaudible Inaudible or permanent anaesthesia paralysis nerve damage (rigor) - Complications of Revascularization A. Reperfusion syndrome - hypotension, hyperkalemia, myoglobinuria, renal failure B. Compartment syndrome C. Ischemic neuropathy D. Muscle necrosis E. Recurrent thrombosis 1. recurrent embolization 2. inadequate thrombus removal 3. arterial injury from thrombectomy catheter 4. failure to treat critical lesion-causing thrombosis 5. extensive muscle edema precluding distal flow 6. underlying hypercoagulable state 7. technical problem w/ bypass graft/arteriotomy closure - Fontaine/Rutherford Classification - Ankle-Brachial Index (ABI) = ankle systolic pressure/brachial systolic pressure - 95% sensitivity, 99% specificity - normal ABI 0.9-1.0 mild 0.8-0.89 mod 0.5-0.79 severe 0-0.49 - a pressure drop of 30mmHg between 2 adjacent levels identifies site of most proximal occlusion ( in segmental pressure wave studies) - rest pain = toe pressure 30mmHg B. Thromboangiitis Obliterans (TAO) - aka Buerger’s Disease - non atherosclerotic, segmental inflammatory dse of small & medium-sized aa & vv, in UE & LE 24  - Etio: unknown; cigarette smoking, HLA, hypercoagulable state - Patho: endarteritis, endophlebitis - S/S: foot claudication, trophic changes, gangrenous ulcers - M>F (F=1-2%) - immunologic markers are N or negative (CRP, WSR, ANA, RF, complement) - unusual locations : aorta, iliac, pulmo aa - Dx: Labs: CBC, LFT, renal function, FBS, UA, acute phase reactants (WSR,CRP), ANA, RF, complements, hypercoag screening : arteriography - “corkscew collaterals” - Tx: cornerstone = complete D/C of cig smoking! avoid passive smoking wound care Ca channel blockers, anti platelet, pentoxifylline Iloprost analgesic sympathectomy bypass implantable SC stimulator thrombolytic therapy - streptokinase, urokinase amputation if all else fails - surgical revasc is NOT usually a viable alternative owing to diffuse segmental involvement & extreme distal nature of the dse; other option - omental transfer C. Takayasus Arteritis - aka “great imitator”, “obliterative brachiocephalic arteritis” - progressive visual loss, vertigo, syncope & conjunctival injection, retinal A-V changes associated with absent pulses in upper ext (“pulseless dse”), & alopecia - all race & age group.M