Source
Branch #1
Branch #2
Supply
Left main
Circumflex
Obtuse marginal branches
Left ventricle lateral & posterior walls
Left anterior descending (LAD)
Septal branches
Majority of interventricular septum
Diagonal branches
Left ventricular surface, especially anterior wall
Right main
Acute marginal branches
Right ventricle
AV nodal & SA nodal
AV & SA nodes
Posterior descending
Inferior & posterior wall of left ventricle, right ventricle
The venous supply from the heart follows the arterial supply and the coronary veins drain into the coronary sinus which then drains into the right atrium. Thebesian veins, which connect directly from the left ventricular cavity also provide a route for venous drainage.
There are 4 heart valves that promote unidirectional flow (see Fig. 18.1). They open and close based on pressure changes that occur on either side of the valve. The heart’s atrioventricular valve on the left side is the mitral valve (between the left atrium and ventricle), which has two leaflets: anterior and posterior. The atrioventricular valve that connects the right atrium and right ventricle is the tricuspid valve, which has three leaflets: anterior, posterior, and septal. The left ventricle pumps blood into the aorta via the aortic valve. The right ventricle pumps blood into the pulmonary artery via the pulmonary or pulmonic valve . Both of these valves are semilunar valves and have three cusps.
The cardiac conduction system is comprised of autorhythmic cells that initiate and conduct action potentials. In a normal heart, the sinoatrial (SA) node is the heart’s pacemaker. After an impulse is generated here, it conducts to the atrioventicular (AV) node , where it splits into the Bundle of His down the left bundle branch and right bundle branch. Eventually, the ventricular muscle is innervated when the impulse reaches the Purkinje fibers . Sympathetic and parasympathetic nerves innervate the heart. β-adrenergic stimulation increases cyclic AMP levels and enhances Ca2+ influx which causes depolarization of conduction cells. Cholinergic signals, via parasympathetics (vagus nerve), oppose β-adrenergic stimulation and slow down the heart.
The Cardiac Cycle
The cardiac cycle is a highly coordinated series of events that requires the participation of the cardiac conduction system, valves, and muscle to orchestrate the movements of systole and diastole (see Fig. 18.2). Systole is isovolumic ventricular contraction and ejection of blood from the heart. Diastole is isovolumic ventricular relaxation and filling of the heart.
Blood returns from the systemic vasculature through the superior vena cava (SVC) and inferior vena cava (IVC) into the right atrium. Pulmonary veins drain into the left atrium. Filling of each atrium occurs continuously. Once atrial pressure exceeds ventricular diastolic pressure, the atrio-ventricular valves open and the ventricles fill (early ventricular filling). Contraction of the atrium comprises late ventricular filling and is often called the “atrial kick”. As the ventricles begin to contract, the mitral and tricuspid valves close (S1 heart sound). Isovolumetric ventricular contraction occurs when atrio-ventricular valves are closed but pressure in the ventricles has not yet exceeded pulmonary artery or aortic pressure. Intraventricular pressure continues to rise, but volume remains constant. As ventricular pressure exceeds pressure in the respective great vessel, the semilunar valves open and blood is ejected. After ejection, ventricular pressure falls below aortic and pulmonary artery pressure, causing the aortic and pulmonic valves, respectively, to close (S2 heart sound). Ventricular isovolumetric relaxation occurs when aortic and pulmonic valves are closed and the volume in the ventricles remains constant while the ventricle relaxes. When the ventricular pressure falls below atrial pressures, early diastolic filling occurs and the cycle repeats.
Definitions for cardiac output, stroke volume, and several other important components of the cardiac cycle are listed in Table 18.2.
Table 18.2
Other cardiac cycle definitions and equations
Cardiac output (CO) | Volume of blood pumped per minute. |
CO = heart rate × stroke volume | |
Stroke volume | Amount of blood pumped with each contraction |
Preload | Volume of blood in the ventricle before systole. Usually measured as left ventricular end-diastolic pressure (LVEDP), which estimates left ventricular end-diastolic volume (LVEDV) |
Afterload | Resistance to ejection of blood by each ventricle |
Starling’s Law | Contractility depends on muscle fiber length |
Coronary perfusion pressure | CPP = Aortic diastolic blood pressure – LVEDP |
Left ventricular wall tension | Wall tension = (interventricular pressure × chamber radius)/(thickness × 2) |
Fick equation | C.O. = O2 Consumption/([Arterial O2 content] – [Venous O2 content]) |
Common Disease States Affecting the Heart
Ischemic Heart Disease
There are many manifestations of ischemic heart disease (see Table 18.3). Determinants of myocardial perfusion depend on the relationship of supply and demand. Myocardial supply is provided by coronary perfusion pressure, heart rate, PaO2, and coronary diameter. Myocardial demand parameters are myocardial oxygen consumption, heart rate, left ventricular wall tension, contractility, conduction, and relaxation.
Table 18.3
Ischemic cardiac disease
Disease | Definition |
|---|---|
Coronary artery disease | Narrowing of coronary arteries from atherosclerosis |
Ischemic heart disease | Myocardial O2 demand not met by coronary blood flow |
Acute coronary syndrome/myocardial ischemia | Term that includes any of the life threatening conditions below which represent acute myocardial ischemia |
Angina pectoris | Myocardial ischemia with chest discomfort |
Stable angina | Exercise induced chronic angina pectoris |
Unstable angina | Myocardial ischemia at rest or with minimal exertion |
Variant angina | Discomfort from coronary artery vasospasm |
Non-ST-segment elevation myocardial infarction (NSTEMI) | Myocardial ischemia from a partially occlusive coronary thrombus |
ST-segment elevation myocardial infarction (STEMI) | Myocardial ischemia from a totally occlusive coronary thrombus |
Myocardial revascularization procedures such as percutaneous coronary interventions (i.e. coronary stenting) and coronary artery bypass graft surgery (CABG) are performed to relieve symptoms, or prevent future morbidity and mortality related to myocardial ischemia and infarction. The specific indications of when to use each of these techniques is complex, and the literature is evolving as new information comparing the two modalities becomes available. Coronary revascularization may be indicated for patients symptomatic with persistent anginal episodes, unstable angina, NSTEMI, STEMI, and patients in cardiogenic shock. Indications also include significant stenosis of multiple coronary arteries, significant left anterior descending, left main disease, or left main equivalent disease (left anterior descending and left circumflex artery disease).
Valvular Disease
Common causes for mitral stenosis (MS) are rheumatic fever and congenital stenosis. It can lead to pulmonary edema and left ventricular failure. Mild MS is a valve area of ≤2 cm2 and critical MS is ≤1 cm2. Treatment is medical therapy, balloon mitral valvuloplasty, open mitral commissurotomy, or mitral valve replacement. During anesthesia it is important to maintain sinus rhythm (atrial kick provides 40 % of ventricular filling), preload, stroke volume, and low/normal heart rate (to allow time for filling). Avoid drops in SVR and prevent increases in PVR by preventing hypoxia, hypercarbia, and acidosis.
Mitral regurgitation (MR) can be caused by myxomatous mitral valve disease resulting in prolapse, ruptured chordae, chordal elongation, perforations in mitral valve leaflets, or flail segments of the mitral valve. Other causes of mitral regurgitation include ischemic heart disease, which can result in left ventricular enlargement with restriction of mitral valve leaflets, mitral annulus abnormalities, or necrosis of papillary muscle structures. Other less common etiologies include endocarditis, rheumatic heart disease, congenital clefts, and hypertrophic cardiomyopathy, which can lead to systolic anterior motion (SAM) of the anterior leaflet of the mitral valve. Acute MR leads to high pulmonary pressures and pulmonary congestion, whereas chronic MR can be more compensated with lower pulmonary artery pressures but a low cardiac output. Medical treatment includes inotropic agents and vasodilators. Surgical treatment is with mitral valve repair or replacement, or a percutaneously placed clip which holds the posterior and anterior leaflets together. During anesthesia, avoid myocardial depression and increases in SVR (will worsen regurgitation), while maintaining a normal/high heart rate (less time for regurgitation).
Aortic stenosis (AS) is caused by senile degenerative disease, congenital bicuspid aortic valve, or rheumatic heart disease. Male gender, hypercholesterolemia, and smoking are risk factors. Blood flow is obstructed during systole which results in concentric left ventricular hypertrophy. There is a fixed stroke volume and filling is 40 % dependent on the atrial kick. AS is a valve area great than 1.5 cm2, moderate is 1.0–1.5 cm2, severe is 0.7–0.99 cm2, and critical is <0.7 cm2. Treatment is percutaneous balloon valvuloplasty, transcatheter aortic valve replacement (TAVR) , or surgical aortic valve replacement. Anesthetic management includes maintaining sinus rhythm (need atrial kick) and slow to normal heart rate (allows for filling time). Also, avoid decreases in SVR because stroke volume is fixed (and thus cardiac output without a rise in heart rate) and the coronary perfusion pressure will fall. Chest compressions during cardiopulmonary resuscitation are usually ineffective.
Aortic regurgitation (AR) is usually caused by leaflet abnormalities (rheumatic disease, endocarditis, and congenital bicuspid valve) or dilation of the aortic root (aortic aneurysm/dissection, Marfan’s syndrome, syphilis-cystic medial necrosis). Acute AR is a surgical emergency manifested by a sudden increase in LV diastolic pressure which causes acute pulmonary congestion, hypertension, and pulmonary edema. In chronic AR, the LV compensates with dilation and hypertrophy which leads to heart failure. Asymptomatic AR can be treated with medical management until the left ventricular dilation causes ventricular dysfunction or symptoms of heart failure. Asymptomatic disease in the presence of LV dysfunction or symptomatic AR should be treated with an aortic valve replacement. Anesthetic management includes maintaining sinus rhythm and normal to high heart rate. Avoid myocardial depression and increases in SVR which will worsen the regurgitant fraction. Consider using afterload reduction which decreases the regurgitant fraction.
Arrythmia Management
Cardiovascular Implantable Electronic Devices (CIEDs) include pacemakers that Pacemakers are indicated in sick sinus syndrome , tachy-brady syndrome , advanced second degree or third degree heart block, and symptomatic bifascicular block. In general, pacemakers can be left as programmed during a surgical procedure, but electrocautery may inhibit their function. Thus, in patients who are pacemaker-dependent, the pacemaker should be converted to an asynchronous mode of pacing with a magnet or programming (preferred). Exposure to an MRI can convert pacemakers to asynchronous mode. Consider interrogating a patient’s pacemaker at the end of the procedure to ensure proper functioning.
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