Overview of Cardiovascular System

Cardiovascular System Cardiac Anatomy * Mediastinum * Connective tissue-lines compartment bordered by the lungs, sternum, thoracic vertebral bodies * Contains heart, aorta, PA, SVC, and IVC, trachea, esophagus, thoracic duct, and thoracic lymph nodes * RV is most anterior structure * Pericardium * Composed of fibrous outer layer and inner serous layer * Fibrous layer affixes heart to mediastinum * Serous layer consists of * Parietal * Visceral * Epicardium * Outermost layer * Right and left coronary arteries lie on epicardial surface * Myocardium * Middle layer * Composed of heart muscle * Endocardium * Innermost later that lines the heart * Heart rotates during fetal development * Cardiac base * Formed by the posterior surface of the heart * Refers to the superior aspect of the heart * Refers to where great vessels enter * Located at right and left 2ICS * Cardiac apex * Most inferior, anterior, and lateral heart * Formed by tip of LV * Palpation of PMI (not always palpable) * Located at 5ICS just medial to left MCL * Diameter of PMI is normally 1-2.5 cm ________________ Heart Chambers * Right atrium * Received deoxygenated blood from the SVC, IVC, and coronary sinus * Coronary sinus receives blood from cardiac veins and drains myocardium * Right ventricle * Comprises majority of inferior and anterior heart * Right bundle branches of AV bundle are located here * Left atrium * Received oxygenated blood from the lungs via the pulmonary vein * Left ventricle * Pumps blood to aorta Heart Valves * Atrioventricular valves * Located between the atria and ventricles (mitral and tricuspid) * S1 - Open during diastole * Semilunar valves * Leaflets are shaped like half moons * Aortic (left) and pulmonic (right) * S2 - open during systole ________________ ________________ Cardiac Arterial Blood Supply: Coronary Circulation Coronary Circulation * Right & Left Coronary arteries + branches * Supply O2 & nutrients * Branch off Ao→ wrap around heart * RCA→ supplies * RA, most of RV, variable portion of inferior wall LV * Has 1 branch* * 85 % of population are “right dominant” * *RCA→ PDA→ supplies superior interventricular septum & LV inferior wall * 15% of population are “left dominant’ * PDA- branch of LCA ________________ Cardiac Hemodynamics Cardiac Hemodynamics * SVR-calculated measure that reflects the resistance in the vascular system * Primarily influence by arterioles * Clinical indicator of afterload* * Reflects peripheral vasomotor tone, not the ventricle’s internal fiber load * SVR= MAP-CVP X 80 * ➢ CO * Mean arterial pressure-average arterial pressure throughout a cardiac cycle * Calculated by considering that the heart spends more time in diastole than in systole * MAP= 1/3 PP (Sytolic BP – Diastolic BP) + Diastolic * Laws Related to the Cardiovascular System * ➢Fick’s Principle- relates to CO; tissue O2 consumption/arterial O2 content – venous O2 consumption * ➢Law of LaPlace-describes the relationship between wall tension, internal pressure, and radius in hollow spheres or cylinders * ➢Poiseuille’s Law- flow- velocity of a liquid flowing through a capillary is directly proportional to the pressure of the liquid & the capillary radius & inversely proportional to the viscosity of a liquid & the length of the capillary * ➢Ohm’s Law-flow is proportional to the driving pressure gradient & inversely proportional to resistance * ➢ * ➢ Myocardial Oxygen Balance Cardiac Conduction System * ➢Conducting cells & muscle cells * ➢SA node- primary pacemaker * ➢AV node- relay station * ➢Bundle of His * ➢L & R Bundle Branches * ➢Purkinje fibers- ventricles * ➢ * ➢ * ➢ * ➢ Common Diseases of the Cardiovascular System * ➢Hypertensive heart disease * ➢CAD * ➢Ischemic heart disease * ➢Heart failure * ➢Cardiomyopathy * ➢Valvular heart disease * ➢Rheumatic heart disease * ➢Peripheral artery disease * ➢Arrhythmias * ➢Congenital heart disease Hypertension What is it? * ➢Persistently high pressure in the blood vessels * ➢Risk factors- older age, family history, obesity, smoking, high Na diet, physical inactivity BP Values * NORMAL BP: SBP <120; DBP < 80 * ELEVATED BP: SBP 120-129; DBP < 80 * HYPERTENSION (Stage I): SBP 130-139; DBP 80-89 * HYPERTENSION (Stage II): SBP > 140 ; DBP > 90 * UNCONTROLLED (Stage III): SBP > 180 and/or DBP > 110 When to cancel an elective surgery? * Can perioperative risk be decreased by postponement? * Will care be influenced by further preoperative examination? * ➢Patients with baseline HTN are more likely to develop intraoperative HYPOTENSION * ➢ Coronary Artery Disease * ➢~ 11 million Americans have CAD * ➢Atherosclerotic heart disease- ASHD * ➢Narrowing of epicardial coronary vessels by atherosclerotic plaque * ➢3 artery layers- intima, media, adventitia * ➢Disease progression= fatty streaks in intima, fibrous plaque formation, invasion of media * ➢Leading risk factors: * ➢Age, male gender, HTN, tobacco use * ➢Other- diabetes, obesity, personality type, lifestyle, and genetics Ischemic Heart Disease * * ➢Advanced age * ➢Smoking * ➢DM * ➢HTN * * ➢Previous MI * ➢LV dysfunction * ➢PVD * ➢Look for S & S requiring further evaluation: * ➢Fatigue * ➢angina * ➢Palpitations * ➢Syncope * ➢Dyspnea * ➢Preop Eval Objective: * ➢Determine severity, progression and functional limitations Atherosclerosis & Angina * ➢Myocardial ischemia→ * ➢myocardial O2 supply/demand imbalance * ➢Sx- aching, dull or heavy chest pressure * ➢Radiates to left jaw, arm, shoulder or back * ➢May be silent, no pain * ➢Syncope, SOB, DOE, Dysrhythmias How is Angina Diagnosed? * ➢ECG changes * ➢Hemodynamic changes * ➢↑ filling pressures- PA * ➢Regional wall motion abnormalities * ➢Angiography * ➢Patient history Canadian Cardiovascular Society Functional Classification of Angina * ➢Class 0-asymptomatic * ➢Class I – Angina during strenuous or prolonged physical activity * ➢Class II – Slight limitation→ angina only with vigorous physical activity * ➢Class III – Moderate limitation-symptoms with everyday living activities * ➢Class IV – Severe limitation- Inability to perform any activity without angina or angina at rest * ➢ * ➢ * ➢ * ➢ Stable Angina * ➢Predictable chest pain < a few minutes or less * ➢R/t or triggered by physical exertion or emotional stress * ➢Relieved by rest or medication * ➢No change in precipitating factors, frequency of pain and/or duration of pain for > 60 days * ➢Treatment * ➢Oxygen * ➢Rest * ➢Nitrates * ➢Beta Blockers * ➢Calcium Channel blockers * ➢ Acute Coronary Syndromes Unstable Angina- Acute Coronary Syndrome * ➢New symptom or change * ➢Occurs more frequently or more frequently * ➢Pain more severe or lasts longer * ➢Can be relieved with oral meds but may require more tx * ➢Unstable→ may progress to MI * ➢Medical emergency NSTEMI -Acute Coronary Syndrome * ➢NSTEMI-non- ST segment elevation MI * ➢ECG changes may not be seen * ➢Absence of ST seg ↑ * ➢Chemical markers ↑- troponins * ➢D/t partial arterial blockage * ➢Sx-chest pain/pressure/discomfort, SOB, dizziness, nausea, sweating * ➢May progress to STEMI * ➢Requires immediate attention STEMI Acute Coronary Syndrome * ➢STEMI- ST elevation MI * ➢Abrupt, prolonged blockage * ➢Large area of myocardium involved * ➢ECG changes * ➢↑ chemical markers- troponins * ➢Stunned myocardium * ➢Hibernating myocardium Cardiomyopathy * ➢Diseases of the heart muscle * ➢Can become enlarged, thickened, or stiff * ➢Disruption of pumping ability & flow * ➢Can cause heart failure * ➢3 main types * ➢Dilated cardiomyopathy-enlarged * ➢Hypertrophic cardiomyopathy-thickened * ➢Restrictive cardiomyopathy- stiff * ➢Other less common types * ➢Arrhythmogenic RV dysplasia * ➢LV non compaction * ➢Peripartum cardiomyopathy Heart Failure * Heart is unable to pump enough blood to meet body needs * Causes * Cardiomyopathy, HBP, valvular heart disease, etc. * Symptoms * CHF, Pulmonary edema, Paroxysmal nocturnal dyspnea * Clinical Findings * S3 gallop, rales, tachypea, resting tachycardia, JVD, peripheral edema * HFpEF: Heart failure with preserved EF * Ejection fraction greater than or equal to 50% * Although HFpEF patients do better than HFrEF patients, ANY heart failure diagnosis places patients at significantly higher risk! * HFrEF: Heart failure with reduced EF * Ejection fraction < 49% * Valvular Heart Disease Tricuspid, Pulmonic Mitral, Aortic Mitral valve stenosis Mitral regurgitation Aortic valve stenosis What is it? * Narrowing of aortic valve → LV outflow obstruction, ↓ CO & cardiac compliance, ↑ LVEDP What does it cause? * ↑Myocardial oxygen demand * Significant risk for perioperative cardiac morbidity How to manage? * Avoid hypotension & decreases in SVR * Maintain NSR (need atrial kick) and preload * Severe Ao stenosis ↑risk of perioperative sudden death by 14X * Normal aortic valve area= 2.5-3.5 cm2 * Severe-- < 1 cm2 * Critical- 0.5-0.7 cm 2 Aortic valve regurgitation Tricuspid Stenosis What is it? * ➢Narrowing of the tricuspid valve What causes it? Primary cause is rheumatic valvulitis * ➢Other causes: SLE, carcinoid heart dz, trauma, congenital defects, damage from pacemaker, Ao and MV disease Isolated tricuspid stenosis → signs/symptoms of R heart failure * ➢Hepatomegaly- hepatic dysfunction * ➢Ascites * ➢Edema * ➢JVD * ➢Giant a waves on CVP * ➢Takes years to develop- valve replacement usually uncommon Tricuspid Valve Regurgitation What causes it? * ➢Isolated tricuspid regurgitation - →drug abuse, endocarditis, carcinoid syndrome, or chest trauma. * ➢More commonly associated with other cardiac abnormalities- end stage AO or mitral valve disease. * ➢Congenital cause: Ebstein’s anomaly (congenital cause) -the downward displacement of the valve because of abnormal attachment of the valve leaflets * ➢TR (clinically significant)-→ dilation of the RV → pulmonary hypertension (associated with chronic RV failure) * ➢ Pulmonary Valve Stenosis What is it? * ➢A dynamic or fixed obstruction to flow from the RV to the PA * ➢Leads to RVH and CHF (severe) * ➢Usually diagnosed in childhood What causes it? * ➢Isolated valvular obstruction, may be due to sub valvular or supravalvular obstruction * ➢May occur in complicated congenital heart disorders How to manage? * ➢Treatment- valvuloplasty or replacement Pulmonary regurgitation What is it? * ➢Backward flow of blood from PA to the RV * ➢Usually, a result of a CHD and is diagnosed in childhood- TOF, congenital absence of pulmonary valve * ➢Mild cases of PR may be asymptomatic and be detectable by Echo only- no treatment needed * ➢RVH & RHF in severe cases What causes it? * ➢ Pulm. HTN, endocarditis, rheumatic heart disease, carcinoid syndrome, IE, chest trauma * ➢Asymptomatic disease- no treatment How to manage? * ➢Treatment- address underlying condition, valve replacement if needed Peripheral Artery Disease * Affects 20% of adults > 55 * Often asymptomatic * Risk factors include cigarette smoking, diabetes, hyperlipidemia, HTN and physical inactivity * PE Findings: absent or diminished pulses, abnormal skin color, poor hair growth, the presence of a femoral bruit, cool skin * ABI (Ankle Brachial Index) is a comparison of the BP in the ankle with the BP measured in the arm Arrhythmias * ➢What is baseline rhythm? * ➢Ventricular arrhythmias * Benign: unifocal PVCs * Potentially malignant: Heart disease on antiarrhythmics * Malignant: hemodynamic compromise * Is patient on antiarrhythmic treatment? * ➢12-lead EKG * ➢Electrolyte levels (potassium, magnesium) * ➢CXR to identify any structural cardiac disease Congenital Heart Disease * ➢Heart disease caused by various heart defects present at birth * ➢Defects may occur in vessels, chambers, valves * ➢Simple defects * ➢Ex: ASD, VSD, * ➢Complex defects * ➢Tetralogy of Fallot * ➢Transposition of the Great Arteries * ➢Acyanotic & cyanotic PREOPERATIVE ASSESSMENT & CARDIAC RISK FACTORS FOR MORBIDITY & MORTALITY Patients Having Non-Cardiac & Cardiac Surgical Procedures Importance of Preoperative Cardiac Assessment * ➢Why is a pre-op cardiac assessment important? * ➢CV disease * ➢Major causes of perioperative morbidity and mortality seen in anesthetic practice * ➢~25-50% of deaths following noncardiac surgery → cardiovascular complications * ➢Complication causes: * ➢Perioperative MI * ➢Dysrhythmias * ➢PE * ➢CHF * ➢Thromboembolism Head to Toe Cardiac Clues * ➢Basic skills →Inspection→ Palpation→ Percussion→ Ausculation * Focused assessment- * Past medical & surgical history * Physical exam * Physical status classification * Current Medications * ➢Labs-CBC, Chemistry, Coagulation factors, Cardiac Markers * Other testing data- 12 lead ECG, cardiac stress test, cardiac catheritization, * ➢Patient specific plan of care Collecting Past & Current Medical History * PMH and Current symptoms: * Preexisting heart disease? * CAD, previous MI, chest pain/pressure, CHF, peripheral edema, DOE, HTN * Activity & exercise level- & functional capacity * Disease severity, stability, prior treatments * Prior MI: * < 30 days highest risk * > 30 days- based on s/s and exercise tolerance * Other comorbidities- Diabetes, obesity, smoking, PAD, etc. * Related labs/tests- 12 lead ECG, Echo, stress test, cardiac catheterization * Current Activity Level & Functional Capacity Angina/Ischemia Symptoms & Medications * ➢Is the patient having Ischemia? * ➢ What do we look for? * ➢Hallmark-ST segment ↑ on ECG * ➢Level of symptoms * ➢Control of angina * ➢Associated disease * ➢CHF, Recent MI, LMC disease*-↑ risk * ➢List of medications * ➢When last taken- nitrates * ➢Effectiveness * ➢ Cardioprotective Pharmacotherapy ACC/AHA Clinical Practice Guidelines * Myocardial Infarction * Delay noncardiac surgery > 60 days after MI without coronary intervention * Coronary Balloon Angioplasty * Delay elective noncardiac surgery for 14 days after coronary balloon angioplasty * Bare Metal Stents: * Continue DAPT (aspirin and clopidogrel only) x 1 month following PCI * Postpone elective surgery x 30 days following PCI * Drug Eluting Stents: * Postpone elective surgery x 6 months after stent placement * If risk of delaying surgery > risk of thrombosis, can consider surgery 3 months following PCI * DAPT: dual antiplatelet therapy * PCI: percutaneous coronary intervention * Focused Physical Exam: Cardiovascular Assessment Focused Cardiovascular Physical Examination * General appearance * Height (cm), weight (kg), * VS- HR, BP especially in both arms, RR, SaO2, Temparature * Auscultate heart tones, carotid arteries * Assess skin color & turgor * Palpate peripheral pulses * Observe for signs of respiratory distress, cyanosis, and jugular venous distention. * Labs- * H/H, plts & Chemistry- * Na,K, Glucose, * Cardiac biomarkers * Other tests * Surgical and anesthetic history- * review old case records * Obtain the information that is most important in urgent/emergent situations * General Appearance Pectus Excavatum * Congenital chest wall deformity * Chest appears “sunken in” * Affects boys > girls * Often present at birth Pectus Carinatum * aka Pigeon Chest Deformity * breastbone and ribs are pushed outward * Affects boys > girls * Can be asymmetrical * Often worsens as child grows * Can be associated with scoliosis Peripheral & Carotid Pulse Assessment * ➢Rate, Rhythm, Contour, Amplitude * ➢Pulse wave amplification * ➢Arterial pulse changes as it travels from aorta to peripheral arteries * ➢MAP decreases & SBP increases * ➢Carotid pulse best to evaluate heart * ➢Distal pulses best to evaluate vessels * ➢Contour describes shape (onset) –upstroke, summit, downstroke * ➢Amplitude describes how strong or forceful a pulse is * ➢Contour is used for noninvasive CO measurement Carotid Auscultation * ➢Patient in supine or sitting position * ➢Have patient breathe in and hold their breath * ➢ Place bell of stethoscope over carotid artery * ➢ Bruit are systolic “blowing” sounds * ➢Usually caused by atherosclerotic luminal stenosis * ➢Other causes: tortuous carotid artery, external carotid arterial disease, aortic stenosis, hypervascularity of hyperthyroidism, and external compression from thoracic outlet syndrome * ➢Bruits do not correlate with clinically significant underlying disease * ➢Cardiac murmurs can be transmitted to carotids so be sure to perform a complete precordial exam * ➢Thrills (like throat vibrations of a cat when it purrs) of aortic stenosis are transmitted to the carotid arteries from the suprasternal notch or second right intercostal space. Pulse Abnormalities Orthostatic Hypotension Orthostatic hypotension (aka Postural Hypotension) is * ➢BP falls when standing up or stretching * ➢Drop of SBP by 20 mm Hg or more * ➢Drop of DBP of 10 mm Hg or more * ➢Within 3 min of standing * ➢Caused by blood pooling in the lower extremities * ➢Defined as: a 20 mm Hg decrease in SBP or 10 mm Hg decrease in DBP within three minutes of standing Measuring Jugular Venous Pressure * ➢Find highest point of oscillation in the internal jugular vein * ➢Measure vertical distance above the sternal angle (angle of Louis) * ➢If no jugular pulsation is noted, it may lie below the level of the sternum venous pressure is not elevated. * ➢JVP > 3 cm suggests elevated CVP * ➢JVP < 3 cm suggests normal heart pressure Palpation of the Heart * ➢Cardiac apex is formed by tip of the LV * ➢Place whole hand flat over precordium * ➢Palpate PMI at 5th ICS at/ just medial to MCL * ➢Normal: 2.5 cm in diameter * ➢Not palpable in some individuals Abnormal Findings * ➢Dextrocardia: PMI is located on the right side of the chest * ➢Cardiomegaly: Lateral shift of PMI * ➢LVH: PMI >2.5 cm and/or shifted lateral to MCL (left) * ➢RVH (COPD): PMI shifts to xiphoid or epigastric area (right/down) * ➢ASCITES, PREGNANCY, ABDOMINAL DISTENTION: displace apex upwards and to the left * ➢ Evaluating Heart Murmurs Timing in cardiac cycle * ➢Early, Mid, or Late Systole * ➢Early, Mid, or Late Diastole * ➢Throughout Systole or Diastole * ➢Intensity- Grades 1-4 * ➢Pitch- high, medium, low * ➢Pattern-crescendo, decrescendo, crescendo-decrescendo * ➢Quality-click, snap, musical, blowing, harsh, rumbling * ➢Location- maximum intensity location * ➢Radiation- sound is transmitted direction of blood * ➢ Peripheral Vascular Exam Edema * 1+ Mild pitting with only slight indentation and no appreciable extremity edema * 2+ Moderate pitting, thumb indentation resolves rapidly * 3+ Deep pitting, indentation briefly remains, extremity edema present * 4+ Severe pitting, indentation remains, extremity is obviously swollen * Peripheral Pulses * 3+ Bounding * 2+ Normal * 1+ Weak * 0 Absent Cardiac Tamponade * ➢Increased intrapericardial pressure causes impaired diastolic filling * masses, pericarditis * ➢SYMPTOMS: * ➢BECK’s TRIAD: Hypotension, JVD, Muffled heart sounds * ➢PULSUS PARADOXUS: Exaggerated decrease in SBP (>10 mmHg) with inspiration * ➢Enlarged cardiac silhouette on CXR * ➢Decreased voltage across all leads on EKG * ➢DIAGNOSIS: ECHOCARDIOGRAPHY is best method for detection * ➢TREATMENT: PERICARDIOCENTESIS/ PERICARDIAL WINDOW Lab Results Troponin I or T * ➢Structural protein in cardiac myocytes * ➢Regulates muscle contraction * ➢Indicates myocardial necrosis in blood * ➢Cardiomyocytes release intracellular enzymes inc. troponin when damaged * ➢Troponin levels – 3X SD from normal * ➢Serial * ➢Normal 0-0.04 ng/mL B type Natriuretic Peptide (BNP) * ➢Type of protein hormone that help regulate the circulation * ➢Act on blood vessels causing vasodilation * ➢Act on kidneys- ↑excretion of Na and H2O * ➢Reduce various hormones that narrow blood vessels, ↑HR, or affect fluid retention * ➢Ex: adrenaline, angiotension, aldosterone Creatine Kinase & Myoglobin * Creatine kinase- enzyme found in muscle, brain, heart tissue- ↑levels = heart muscle damage * 3 main forms- CK-MB, CK MM, CK BB * ↑CK MB- indicative of MY * Myoglobin- protein in heart & skeletal muscle that stores oxygen * Released in the blood when the muscle is damaged * Can be indicative of MI or other muscle injury * Not specific to MI- used with other cardiac biomarkers Cardiovascular Electronic Implantable Devices Cardiac Risk Factors for Morbidity & Mortality- Major & Intermediate * ➢Intermediate:- * ➢Mild angina pectoris ( Class I or II) * ➢Previous MI (history or Q waves on EKG) * ➢Compensated or hx of CHF * ➢DM- particularly IDDM * ➢Renal Insufficiency Minor Cardiac Risk Factors for Morbidity & Mortality * ➢Minor- * ➢Advanced age * ➢Abnormal ECG- * * ➢Abnormal rhythm * ➢Low functional capacity/cardiac reserve * ➢Hx of CVA * ➢Hypertension* Indicators of Poor LV Function * ➢Poor LV may be associated with: * ➢EF <40% * ➢Resting LVEDP >18mmHg * ➢Significant LV wall motion abnormality * ➢Hx of CHF * ➢Recent MI * ➢Severe valvular disease Predictors for post CPB circulatory assistance: Pre-op * ➢Ejection fraction- EF * ➢Measurement of % of blood pumped out by LV per contraction * ➢Normal ~ 60% * ➢Pre-op LV function < 30% * ➢End stage myocardial impairment from severe valvular heart disease (regurgitation) * ➢CAD that can only be partially bypassed * ➢Anticipated long CPB run Developing the Patient Specific Anesthetic Plan * ➢Review all patient findings * ➢Identify risk factors * ➢Select type of anesthesia * ➢Airway management * ➢Drug selection * ➢Monitoring * ➢Fluid management * ➢Calculating allowable blood loss * ➢Positioning * ➢Complications/Potential complications * ➢Post op care * ➢ Anesthetic Goals * ➢Maintain myocardial oxygen supply and reduce the demand * ➢Maintain adequate anesthetic depth * ➢Maintain hemodynamics to ensure organ perfusion during induction, maintenance, and emergence * ➢ *

Cardiovascular System

Cardiac Anatomy
* Mediastinum
   * Connective tissue-lines compartment bordered by the lungs, sternum, thoracic vertebral bodies
   * Contains heart, aorta, PA, SVC, and IVC, trachea, esophagus, thoracic duct, and thoracic lymph nodes
   * RV is most anterior structure
* Pericardium
   * Composed of fibrous outer layer and inner serous layer
      * Fibrous layer affixes heart to mediastinum
      * Serous layer consists of
         * Parietal
         * Visceral 
* Epicardium
   * Outermost layer
   * Right and left coronary arteries lie on epicardial surface
* Myocardium
   * Middle layer
   * Composed of heart muscle 
   * Endocardium
      * Innermost later that lines the heart
* Heart rotates during fetal development
* Cardiac base
   * Formed by the posterior surface of the heart
   * Refers to the superior aspect of the heart
   * Refers to where great vessels enter
   * Located at right and left 2ICS
* Cardiac apex
   * Most inferior, anterior, and lateral heart
   * Formed by tip of LV
   * Palpation of PMI (not always palpable)
      * Located at 5ICS just medial to left MCL
      * Diameter of PMI is normally 1-2.5 cm
________________

Heart Chambers
* Right atrium
   * Received deoxygenated blood from the SVC, IVC, and coronary sinus
   * Coronary sinus receives blood from cardiac veins and drains myocardium
* Right ventricle
   * Comprises majority of inferior and anterior heart
   * Right bundle branches of AV bundle are located here
* Left atrium
   * Received oxygenated blood from the lungs via the pulmonary vein
* Left ventricle
   * Pumps blood to aorta

Heart Valves
* Atrioventricular valves
   * Located between the atria and ventricles (mitral and tricuspid)   
   * S1 - Open during diastole
* Semilunar valves
   * Leaflets are shaped like half moons
   * Aortic (left) and pulmonic (right) 
   * S2 - open during systole

________________

Cardiac Arterial Blood Supply: Coronary Circulation

Coronary Circulation
* Right & Left Coronary arteries + branches
* Supply O2 & nutrients
* Branch off Ao→ wrap around heart
* RCA→ supplies
   * RA, most of RV, variable portion of inferior wall LV
   * Has 1 branch*
* 85 % of population are “right dominant”
   * *RCA→ PDA→ supplies superior interventricular septum & LV inferior wall
* 15% of population are “left dominant’
   * PDA- branch of LCA

________________

Cardiac Hemodynamics

Cardiac Hemodynamics
* SVR-calculated measure that reflects the resistance in the vascular system
   * Primarily influence by arterioles
   * Clinical indicator of afterload*
   * Reflects peripheral vasomotor tone, not the ventricle’s internal fiber load
* SVR= MAP-CVP X 80
*         ➢                CO
* Mean arterial pressure-average arterial pressure throughout a cardiac cycle
* Calculated by considering that the heart spends more time in diastole than in systole
* MAP= 1/3 PP (Sytolic BP – Diastolic BP) + Diastolic
   * Laws Related to the Cardiovascular System
*         ➢Fick’s Principle- relates to CO; tissue O2 consumption/arterial O2 content – venous O2 consumption
*         ➢Law of LaPlace-describes the relationship between wall tension, internal pressure, and radius in hollow spheres or cylinders
*         ➢Poiseuille’s Law- flow- velocity of a liquid flowing through a capillary is directly proportional to the pressure of the liquid & the capillary radius & inversely proportional to the viscosity of a liquid & the length of the capillary
*         ➢Ohm’s Law-flow is proportional to the driving pressure gradient & inversely proportional to resistance
*         ➢
*         ➢
Myocardial Oxygen Balance
Cardiac Conduction System
*         ➢Conducting cells & muscle cells
*         ➢SA node- primary pacemaker
*         ➢AV node- relay station
*         ➢Bundle of His
*         ➢L & R Bundle Branches
*         ➢Purkinje fibers- ventricles 
*         ➢
*         ➢
*         ➢
*         ➢
Common Diseases of the Cardiovascular System
*         ➢Hypertensive heart disease
*         ➢CAD
*         ➢Ischemic heart disease
*         ➢Heart failure
*         ➢Cardiomyopathy
*         ➢Valvular heart disease
   *         ➢Rheumatic heart disease
*         ➢Peripheral artery disease
*         ➢Arrhythmias
*         ➢Congenital heart disease
Hypertension

What is it?
*         ➢Persistently high pressure in the blood vessels 
*         ➢Risk factors- older age, family history, obesity, smoking, high Na diet, physical inactivity
BP Values
* NORMAL BP: SBP <120;  DBP < 80
* ELEVATED BP: SBP 120-129;  DBP < 80
* HYPERTENSION (Stage I): SBP 130-139;         DBP  80-89
* HYPERTENSION (Stage II): SBP > 140 ; DBP > 90
* UNCONTROLLED (Stage III): SBP > 180   and/or        DBP > 110
When to cancel an elective surgery?
   * Can perioperative risk be decreased by postponement?
   * Will care be influenced by further preoperative examination?
*         ➢Patients with baseline HTN are more likely to develop intraoperative HYPOTENSION
*         ➢
Coronary Artery Disease
*         ➢~ 11 million Americans have CAD
*         ➢Atherosclerotic heart disease- ASHD
*         ➢Narrowing of epicardial coronary vessels by atherosclerotic plaque
*         ➢3 artery layers- intima, media, adventitia
*         ➢Disease progression= fatty streaks in intima, fibrous plaque formation, invasion of media
*         ➢Leading risk factors:
   *         ➢Age, male gender, HTN, tobacco use
   *         ➢Other- diabetes, obesity, personality type, lifestyle, and genetics
Ischemic Heart Disease

*    *         ➢Advanced age
   *         ➢Smoking
   *         ➢DM
   *         ➢HTN
   *         
   *         ➢Previous MI
   *         ➢LV dysfunction
   *         ➢PVD
*         ➢Look for S & S requiring further evaluation: 
   *         ➢Fatigue
   *         ➢angina 
   *         ➢Palpitations
   *         ➢Syncope
   *         ➢Dyspnea
*         ➢Preop Eval Objective: 
*         ➢Determine severity, progression and functional limitations
Atherosclerosis & Angina
*         ➢Myocardial ischemia→
   *         ➢myocardial O2 supply/demand imbalance
*         ➢Sx- aching, dull or heavy chest pressure
*         ➢Radiates to left jaw, arm, shoulder or back
*         ➢May be silent, no pain
*         ➢Syncope, SOB, DOE, Dysrhythmias
How is Angina Diagnosed?
*         ➢ECG changes
*         ➢Hemodynamic changes
*         ➢↑ filling pressures- PA
*         ➢Regional wall motion abnormalities
*         ➢Angiography
*         ➢Patient history

Canadian Cardiovascular Society Functional Classification of Angina
*         ➢Class 0-asymptomatic
*         ➢Class I – Angina during strenuous or prolonged physical activity
*         ➢Class II – Slight limitation→ angina only with vigorous physical activity
*         ➢Class III – Moderate limitation-symptoms with everyday living activities
*         ➢Class IV – Severe limitation- Inability to perform any activity without angina or angina at rest
*         ➢
*         ➢
*         ➢
*         ➢
Stable Angina
*         ➢Predictable chest pain < a few minutes or less
*         ➢R/t or triggered by physical exertion or emotional stress
*         ➢Relieved by rest or medication 
*         ➢No change in precipitating factors, frequency of pain and/or duration of pain for > 60 days
*         ➢Treatment
   *         ➢Oxygen
   *         ➢Rest
   *         ➢Nitrates
   *         ➢Beta Blockers
   *         ➢Calcium Channel blockers
   *         ➢
Acute Coronary Syndromes
Unstable Angina- Acute Coronary Syndrome
*         ➢New symptom or change
*         ➢Occurs more frequently or more frequently
*         ➢Pain more severe or lasts longer
*         ➢Can be relieved with oral meds but may require more tx
*         ➢Unstable→ may progress to MI
*         ➢Medical emergency
NSTEMI -Acute Coronary Syndrome
*         ➢NSTEMI-non- ST segment elevation MI
*         ➢ECG changes may not be seen
*         ➢Absence of ST seg ↑
*         ➢Chemical markers ↑- troponins
*         ➢D/t partial arterial blockage
*         ➢Sx-chest pain/pressure/discomfort, SOB, dizziness, nausea, sweating
*         ➢May progress to STEMI
*         ➢Requires immediate attention
STEMI Acute Coronary Syndrome
*         ➢STEMI- ST elevation MI
*         ➢Abrupt, prolonged blockage
*         ➢Large area of myocardium involved
*         ➢ECG changes
*         ➢↑ chemical markers- troponins
*         ➢Stunned myocardium
*         ➢Hibernating myocardium
Cardiomyopathy
*         ➢Diseases of the heart muscle
   *         ➢Can become enlarged, thickened, or stiff
   *         ➢Disruption of pumping ability & flow
   *         ➢Can cause heart failure
*         ➢3 main types
   *         ➢Dilated cardiomyopathy-enlarged
   *         ➢Hypertrophic cardiomyopathy-thickened
   *         ➢Restrictive cardiomyopathy- stiff
*         ➢Other less common types
   *         ➢Arrhythmogenic RV dysplasia
   *         ➢LV non compaction
   *         ➢Peripartum cardiomyopathy
Heart Failure

* Heart is unable to pump enough blood to meet body needs
* Causes
   * Cardiomyopathy, HBP, valvular heart disease, etc.
* Symptoms         
   * CHF, Pulmonary edema, Paroxysmal nocturnal dyspnea
* Clinical Findings 
   * S3 gallop, rales, tachypea, resting tachycardia, JVD, peripheral edema
   * HFpEF: Heart failure with preserved EF
      * Ejection fraction greater than or equal to 50%
      * Although HFpEF patients do better than HFrEF patients, ANY heart failure diagnosis places patients at significantly higher risk!
   * HFrEF: Heart failure with reduced EF
      * Ejection fraction < 49%
* Valvular Heart Disease
Tricuspid, Pulmonic
Mitral, Aortic
Mitral valve stenosis
Mitral regurgitation
Aortic valve stenosis
What is it?
* Narrowing of aortic valve → LV outflow obstruction, ↓ CO & cardiac compliance, ↑ LVEDP 
What does it cause?
* ↑Myocardial oxygen demand
* Significant risk for perioperative cardiac morbidity
How to manage?
* Avoid hypotension & decreases in SVR
* Maintain NSR (need atrial kick) and preload
* Severe Ao stenosis ↑risk of perioperative sudden death by 14X
* Normal aortic valve area= 2.5-3.5 cm2
* Severe-- < 1 cm2
* Critical- 0.5-0.7 cm 2
Aortic valve regurgitation
Tricuspid Stenosis
What is it?
*         ➢Narrowing of the tricuspid valve
What causes it?
Primary cause is rheumatic valvulitis
*         ➢Other causes: SLE, carcinoid heart dz, trauma, congenital defects, damage from pacemaker, Ao and MV disease
Isolated tricuspid stenosis → signs/symptoms of R heart failure
   *         ➢Hepatomegaly- hepatic dysfunction
   *         ➢Ascites
   *         ➢Edema
   *         ➢JVD
   *         ➢Giant a waves on CVP
*         ➢Takes years to develop- valve replacement usually uncommon
Tricuspid Valve Regurgitation
What causes it?
*         ➢Isolated tricuspid regurgitation - →drug abuse, endocarditis, carcinoid syndrome, or chest trauma.  
*         ➢More commonly associated with other cardiac abnormalities- end stage AO or mitral valve disease.  
*         ➢Congenital cause: Ebstein’s anomaly (congenital cause) -the downward displacement of the valve because of abnormal attachment of the valve leaflets
*         ➢TR (clinically significant)-→ dilation of the RV → pulmonary hypertension (associated with chronic RV failure)  
*         ➢
Pulmonary Valve Stenosis
What is it?
*         ➢A dynamic or fixed obstruction to flow from the RV to the PA
*         ➢Leads to RVH and CHF (severe)
*         ➢Usually diagnosed in childhood
What causes it?
*         ➢Isolated valvular obstruction,  may be due to sub valvular or supravalvular obstruction
*         ➢May occur in complicated congenital heart disorders
How to manage?
*         ➢Treatment- valvuloplasty or  replacement 
Pulmonary regurgitation
What is it?
*         ➢Backward flow of blood from PA to the RV
*         ➢Usually, a result of a CHD and is diagnosed in childhood- TOF, congenital absence of pulmonary valve
*         ➢Mild cases of PR may be asymptomatic and be detectable by Echo only- no treatment needed
*         ➢RVH & RHF in severe cases
What causes it?
*         ➢ Pulm. HTN, endocarditis, rheumatic heart disease, carcinoid syndrome, IE, chest trauma
*         ➢Asymptomatic disease- no treatment
How to manage?
*         ➢Treatment- address underlying condition, valve replacement if needed
Peripheral Artery Disease
* Affects 20% of adults > 55
* Often asymptomatic
* Risk factors include cigarette smoking, diabetes, hyperlipidemia, HTN and physical inactivity
* PE Findings: absent or diminished pulses, abnormal skin color, poor hair growth, the presence of a femoral bruit, cool skin
* ABI (Ankle Brachial Index) is a comparison of the BP in the ankle with the BP measured in the arm
Arrhythmias
*         ➢What is baseline rhythm?
*         ➢Ventricular arrhythmias
   * Benign: unifocal PVCs
   * Potentially malignant: Heart disease on antiarrhythmics
   * Malignant: hemodynamic compromise
   * Is patient on antiarrhythmic treatment?
*         ➢12-lead EKG
*         ➢Electrolyte levels (potassium, magnesium)
*         ➢CXR to identify any structural cardiac disease
Congenital Heart Disease
*         ➢Heart disease caused by various heart defects present at birth
*         ➢Defects may occur in vessels, chambers, valves
*         ➢Simple defects
   *         ➢Ex: ASD, VSD,
*         ➢Complex defects
   *         ➢Tetralogy of Fallot
   *         ➢Transposition of the Great Arteries
*         ➢Acyanotic & cyanotic

PREOPERATIVE ASSESSMENT & CARDIAC RISK FACTORS FOR MORBIDITY & MORTALITY
Patients Having Non-Cardiac & Cardiac Surgical Procedures
Importance of  Preoperative Cardiac Assessment
*         ➢Why is a pre-op cardiac assessment important?
*         ➢CV disease 
*         ➢Major causes of perioperative morbidity and mortality seen in anesthetic practice
*         ➢~25-50% of deaths following noncardiac surgery → cardiovascular complications
*         ➢Complication causes:
   *         ➢Perioperative MI 
   *         ➢Dysrhythmias
   *         ➢PE
   *         ➢CHF
   *         ➢Thromboembolism
Head to Toe Cardiac Clues
*         ➢Basic skills →Inspection→ Palpation→ Percussion→ Ausculation
* Focused assessment- 
* Past medical & surgical history
* Physical exam
* Physical status classification
* Current Medications
*         ➢Labs-CBC, Chemistry, Coagulation factors, Cardiac Markers
* Other testing data- 12 lead ECG, cardiac stress test, cardiac catheritization, 
*         ➢Patient specific plan of care
Collecting Past & Current Medical History
* PMH and Current symptoms:
* Preexisting heart disease?
   * CAD, previous MI, chest pain/pressure, CHF, peripheral edema, DOE, HTN
* Activity & exercise level- & functional capacity
* Disease severity, stability, prior treatments
* Prior MI:
   * < 30 days highest risk
   * > 30 days- based on s/s and exercise tolerance
* Other comorbidities- Diabetes, obesity, smoking, PAD, etc.
* Related labs/tests- 12 lead ECG, Echo, stress test, cardiac catheterization
* Current Activity Level & Functional Capacity
Angina/Ischemia Symptoms & Medications
*         ➢Is the patient having Ischemia?
*         ➢ What do we look for?
*         ➢Hallmark-ST segment ↑ on ECG
*         ➢Level of symptoms
   *         ➢Control of angina
   *         ➢Associated disease
      *         ➢CHF, Recent MI, LMC disease*-↑ risk
*         ➢List of medications 
   *         ➢When last taken- nitrates
   *         ➢Effectiveness
   *         ➢
Cardioprotective Pharmacotherapy
ACC/AHA
Clinical Practice Guidelines
* Myocardial Infarction
   * Delay noncardiac surgery > 60 days after MI without coronary intervention
* Coronary Balloon Angioplasty
   * Delay elective noncardiac surgery for 14 days after coronary balloon angioplasty 
* Bare Metal Stents:
   * Continue DAPT (aspirin and clopidogrel only) x 1 month following PCI
   * Postpone elective surgery x 30 days following PCI
* Drug Eluting Stents: 
   * Postpone elective surgery x 6 months after stent placement
   * If risk of delaying surgery > risk of thrombosis, can consider surgery 3 months following PCI   
* DAPT: dual antiplatelet therapy
* PCI:  percutaneous coronary intervention
   * Focused Physical Exam:
Cardiovascular Assessment
Focused Cardiovascular Physical Examination
* General appearance
* Height (cm), weight (kg),
* VS- HR, BP especially in both arms, RR, SaO2, Temparature
* Auscultate heart tones, carotid arteries
* Assess skin color & turgor
* Palpate peripheral pulses
* Observe for signs of respiratory distress, cyanosis, and jugular venous distention. 
* Labs-
   * H/H, plts & Chemistry- 
   * Na,K, Glucose, 
   * Cardiac biomarkers
* Other tests
* Surgical and anesthetic history- 
   * review old case records
* Obtain the information that is most important in urgent/emergent situations
* General Appearance
Pectus Excavatum
* Congenital chest wall deformity
* Chest appears “sunken in”
* Affects boys > girls
* Often present at birth
Pectus Carinatum
* aka Pigeon Chest Deformity
* breastbone and ribs are pushed outward
* Affects boys > girls
* Can be asymmetrical
* Often worsens as child grows
* Can be associated with scoliosis
Peripheral & Carotid Pulse Assessment
*         ➢Rate, Rhythm, Contour, Amplitude
*         ➢Pulse wave amplification
*         ➢Arterial pulse changes as it travels from aorta to peripheral arteries
*         ➢MAP decreases & SBP increases
*         ➢Carotid pulse best to evaluate heart
*         ➢Distal pulses best to evaluate vessels
*         ➢Contour describes shape (onset) –upstroke, summit, downstroke
*         ➢Amplitude describes how strong or forceful a pulse is
*         ➢Contour is used for noninvasive CO measurement
Carotid Auscultation
*         ➢Patient in supine or sitting position
*         ➢Have patient breathe in and hold their breath
*         ➢ Place bell of stethoscope over carotid artery
*         ➢ Bruit are systolic “blowing” sounds 
*         ➢Usually caused by atherosclerotic luminal stenosis
*         ➢Other causes: tortuous carotid artery, external carotid arterial disease, aortic stenosis, hypervascularity of hyperthyroidism, and external compression from thoracic outlet syndrome
*         ➢Bruits do not correlate with clinically significant underlying disease
*         ➢Cardiac murmurs can be transmitted to carotids so be sure to perform a complete precordial exam
*         ➢Thrills (like throat vibrations of a cat when it purrs) of aortic stenosis are transmitted to the carotid arteries from the suprasternal notch or second right intercostal space.

Pulse Abnormalities

Orthostatic Hypotension
Orthostatic hypotension (aka Postural Hypotension) is         
   *         ➢BP falls when standing up or stretching
   *         ➢Drop of SBP by 20 mm Hg or more
   *         ➢Drop of DBP of 10 mm Hg or more
   *         ➢Within 3 min of standing
   *         ➢Caused by blood pooling in the lower extremities
   *         ➢Defined as: a 20 mm Hg decrease in SBP or 10 mm Hg decrease in DBP within three minutes of standing
Measuring Jugular Venous Pressure
   *         ➢Find highest point of oscillation in the internal jugular vein 
   *         ➢Measure vertical distance above the sternal angle (angle of Louis)
   *         ➢If no jugular pulsation is noted, it may lie below the level of the sternum  venous pressure is not elevated. 
   *         ➢JVP > 3 cm suggests elevated CVP
   *         ➢JVP < 3 cm suggests normal heart pressure

Palpation of the Heart
   *         ➢Cardiac apex is formed by tip of the LV
   *         ➢Place whole hand flat over precordium
   *         ➢Palpate PMI at 5th ICS at/ just medial to MCL
   *         ➢Normal: 2.5 cm in diameter
   *         ➢Not palpable in some individuals
Abnormal Findings
   *         ➢Dextrocardia: PMI is located on the right side of the chest   
   *         ➢Cardiomegaly: Lateral shift of PMI
   *         ➢LVH:  PMI >2.5 cm and/or shifted lateral to MCL (left)
   *         ➢RVH (COPD): PMI shifts to xiphoid or epigastric area (right/down)
   *         ➢ASCITES, PREGNANCY, ABDOMINAL DISTENTION: displace apex upwards and to the left
   *         ➢
Evaluating Heart Murmurs
Timing in cardiac cycle
   *         ➢Early, Mid, or Late Systole
   *         ➢Early, Mid, or Late Diastole
   *         ➢Throughout Systole or Diastole
   *         ➢Intensity- Grades 1-4
   *         ➢Pitch- high, medium, low
   *         ➢Pattern-crescendo, decrescendo, crescendo-decrescendo
   *         ➢Quality-click, snap, musical, blowing, harsh, rumbling
   *         ➢Location- maximum intensity location
   *         ➢Radiation- sound is transmitted direction of blood 
   *         ➢
Peripheral Vascular
Exam
Edema
   * 1+ Mild pitting with only slight indentation and no appreciable extremity edema
   * 2+ Moderate pitting, thumb indentation resolves rapidly
   * 3+ Deep pitting, indentation briefly remains, extremity edema present
   * 4+ Severe pitting, indentation remains, extremity is obviously swollen
   * Peripheral Pulses
   * 3+ Bounding
   * 2+ Normal
   * 1+ Weak
   * 0 Absent
Cardiac Tamponade
   *         ➢Increased intrapericardial pressure causes impaired diastolic filling
   *   masses, pericarditis
   *         ➢SYMPTOMS:
   *         ➢BECK’s TRIAD: Hypotension, JVD, Muffled heart sounds
   *         ➢PULSUS PARADOXUS: Exaggerated decrease in SBP (>10 mmHg) with inspiration
   *         ➢Enlarged cardiac silhouette on CXR
   *         ➢Decreased voltage across all leads on EKG
   *         ➢DIAGNOSIS: ECHOCARDIOGRAPHY is best method for detection
   *         ➢TREATMENT: PERICARDIOCENTESIS/ PERICARDIAL WINDOW
Lab Results
Troponin I or T
   *         ➢Structural protein in cardiac myocytes
   *         ➢Regulates muscle contraction
   *         ➢Indicates myocardial necrosis in blood
   *         ➢Cardiomyocytes release intracellular enzymes inc. troponin when damaged
   *         ➢Troponin levels – 3X SD from normal
   *         ➢Serial 
   *         ➢Normal 0-0.04 ng/mL
B type Natriuretic Peptide (BNP) 
   *         ➢Type of protein hormone that help regulate the circulation
   *         ➢Act on blood vessels causing vasodilation
   *         ➢Act on kidneys- ↑excretion of Na and H2O
   *         ➢Reduce various hormones that narrow blood vessels, ↑HR, or affect fluid retention
   *         ➢Ex: adrenaline, angiotension, aldosterone
Creatine Kinase & Myoglobin
   * Creatine kinase- enzyme found in muscle, brain, heart tissue- ↑levels = heart muscle damage
   * 3 main forms- CK-MB, CK MM, CK BB
   * ↑CK MB- indicative of MY
   * Myoglobin- protein in heart & skeletal muscle that stores oxygen 
   * Released in the blood when the muscle is damaged
   * Can be indicative of MI or other muscle injury
   * Not specific to MI- used with other cardiac biomarkers
Cardiovascular Electronic Implantable Devices
Cardiac Risk Factors for Morbidity & Mortality- Major & Intermediate
   *         ➢Intermediate:- 
   *         ➢Mild angina pectoris ( Class I or II)
   *         ➢Previous MI (history or Q waves on EKG)
   *         ➢Compensated or hx of CHF
   *         ➢DM- particularly IDDM
   *         ➢Renal Insufficiency
Minor Cardiac Risk Factors for Morbidity & Mortality
   *         ➢Minor- 
   *         ➢Advanced age
   *         ➢Abnormal ECG- *
   *         ➢Abnormal rhythm
   *         ➢Low functional capacity/cardiac reserve
   *         ➢Hx of CVA
   *         ➢Hypertension*

Indicators of Poor LV Function
   *         ➢Poor LV may be associated with:
   *         ➢EF <40%
   *         ➢Resting LVEDP >18mmHg
   *         ➢Significant LV wall motion abnormality
   *         ➢Hx of CHF
   *         ➢Recent MI 
   *         ➢Severe valvular disease
Predictors for post CPB circulatory assistance: Pre-op
   *         ➢Ejection fraction- EF
   *         ➢Measurement of % of blood pumped out by LV per contraction
   *         ➢Normal ~ 60%
   *         ➢Pre-op LV function < 30%
   *         ➢End stage myocardial impairment from severe valvular heart disease (regurgitation)
   *         ➢CAD that can only be partially bypassed
   *         ➢Anticipated long CPB run
Developing the Patient Specific Anesthetic Plan
   *         ➢Review all patient findings
   *         ➢Identify risk factors
   *         ➢Select type of anesthesia 
   *         ➢Airway management
   *         ➢Drug selection
   *         ➢Monitoring
   *         ➢Fluid management
   *         ➢Calculating allowable blood loss
   *         ➢Positioning
   *         ➢Complications/Potential complications
   *         ➢Post op care
   *         ➢
Anesthetic Goals
   *         ➢Maintain myocardial oxygen supply and reduce the demand
   *         ➢Maintain adequate anesthetic depth
   *         ➢Maintain hemodynamics to ensure organ perfusion during induction, maintenance, and emergence
   *         ➢
   *

Transcript for:Overview of Cardiovascular System

Transcript for:
Overview of Cardiovascular System