Description
- The atria:
- House the sinoatrial (SA) node that initiates electrical impulses
- Are responsible for the active filling of the ventricles during diastole
- Play an important role in the neurohormonal regulation of sodium (Na+) and fluid balance
- SA node: The primary pacemaker of the heart; located at the junction of the superior vena cava (SVC) and the right atrium (RA). The action potential is initiated in the SA node which has an automaticity of 70–80 pulse per minute (ppm) and a conduction velocity of 0.05 m/s.
- Internodal bundles: There are 3 bundles that connect the SA node to the atrioventricular (AV) node (anterior internodal bundle of Bachman, middle internodal bundle of Wenckebach, and posterior internodal bundle of Thorel). The action potential is conducted via these bundles through both atria to the AV node simultaneously. The conduction velocity in these bundles is 0.8–1 m/s.
- AV node: Located in the right posterior portion of the interatrial septum (IAS). It is the only conducting pathway between the atria and the ventricles. Its conduction velocity is slower (0.02–0.05 m/s) than the rest of the heart, allowing the ventricles sufficient diastolic filling time. The AV node can act as a latent pacemaker with an automaticity of 40–60 ppm.
- His bundle: Divides at the top of the interventricular septum into the left bundle branch and right bundle branch; has an automaticity rate of 40 ppm. The left bundle divides into anterior and posterior fascicles. These bundles run subendocardially and come in contact with Purkinje fibers that spread throughout the myocardium. Conduction velocity in this system is fast (1–1.5 m/s for the bundles and 3–3.5 m/s for Purkinje fibers).
- Innervation: Embryologically, the SA node develops from the structures on the right side of the heart and the AV node from the left side of the heart. This results in the SA node being innervated by the right vagus nerve and the AV node by the left vagus nerve. Sympathetic innervations (T1–T4, cardioaccelerator fibers) follow the same distribution. The majority of sympathetic fibers come from the ipsilateral stellate ganglion.
- Endocrine physiology: Atrial myocytes are responsible for the production and release of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). ANP and BNP are polypeptides that are released from the atria in response to increases in extracellular fluid (ECF) volume due to Na+ retention. They function to increase the glomerular filtration rate (GFR) via renal glomerular afferent arteriole vasodilatation and efferent arteriole vasoconstriction; decrease the reabsorption of Na+ from the distal convoluted tubule and collecting ducts (causing a net increase in Na+ excretion and volume loss); and increase capillary permeability and relax vascular smooth muscle in arterioles and venules, causing decreases in blood pressure.
- The walls of all heart chambers consist of 3 layers: Endocardium (inner layer of the heart, comprises endothelial cells and subendocardial connective tissue), myocardium (middle layer of the heart, comprises myocardial muscle cells), and epicardium (outer layer of the heart, formed by the visceral layer of the pericardium).
- Right atrium: The chamber forming the right upper border of the heart.
- Systemic venous return from the SVC and inferior vena cava (IVC) enter the posterior, smooth wall of the RA (SVC enters at the level of the 3rd costal cartilage; IVC enters at the level of the 5th costal cartilage on the same line as the SVC). The coronary sinus (CS) carries cardiac venous return into the posterior wall between the orifice of the IVC and tricuspid valve. The IVC is protected by the Eustachian valve and the CS is protected by the Thebesian valve.
- Pectinate muscles are found on the anterior portion of the RA; they are rough, trabeculated, and made of parallel muscle bundles.
- The anterior and posterior portions are separated on the right by the sulcus terminalis externally and crista terminalis internally.
- The posteromedial wall of the RA is the IAS.
- The base of the RA is the tricuspid valve and has 3 leaflets (anterior, posterior, and septal).
- Left atrium (LA): A smooth-walled chamber that forms the base of the heart.
- Receives pulmonary venous return through the right upper and lower pulmonary veins (RUPV, RLPV) and the left upper and lower pulmonary veins (LUPV, LLPV).
- The left atrial auricle (LAA), or appendage, forms the superior part of the left border of the LA and has a rough trabeculated wall comprising pectinate muscles.
- The LA wall is slightly thicker than the RA.
- Unlike the right-sided veins, pulmonary veins do not have valves.
- Interatrial septum: Separates the 2 chambers and extends posteriorly and to the right causing most of the LA to be posterior to the RA.
- Embryologically, the IAS is formed by the septum primum and septum secundum (1).
- The septum primum starts to develop in the 5th week of gestation and grows towards the endocardial cushion (1).
- The septum secundum, at the same time, develops to the right of the septum primum as an invagination of the atrial wall. It stops growing in the 7th week of gestation. It leaves a posterior inferior gap called the "fossa ovalis (1)."
- The lower portion of the septum primum persists into adulthood as the "flap valve." Upon birth and expansion of the lungs, right-sided pressures drop below left-sided pressures and the flap valve is pressed against the septum secundum. In 66% of people they fuse together forming the "fossa ovalis." In 33% they fail to fuse resulting in a "patent foramen ovale" (PFO) (1).
Physiology/Pathophysiology
- Abnormal pulmonary venous return (congenital defect): One or more pulmonary veins that carry oxygenated blood from the lungs enter the RA instead of the LA; this can be partial anomalous pulmonary venous return (PAPVR) or total anomalous pulmonary venous return (TAPVR). PAPVR presents with symptoms of right-sided volume overload, pulmonary hypertension, and right heart failure. TAPVR is a cyanotic disorder and a true surgical emergency needing an atrial septostomy in the newborn. Since all of the pulmonary venous flow returns to the RA, presence of an atrial septal defect (ASD) or patent ductus arteriosus (PDA) is essential to sustain life after birth.
- Atrial septal defect: An abnormal connection between the LA and RA that is associated with a left-to-right shunt. Patients present with symptoms of right-sided volume overload (JVP elevation, hepatic congestion, lower extremity edema, shortness of breath, pulmonary congestion). Over time, if not corrected, it can cause right ventricle (RV) failure and elevation of RA pressures with resultant shunt reversal (right-to-left shunt; Eisenmenger's syndrome). This will lead to hypoxemia and cyanosis. There are 4 major types:
- Septum secundum ASD: Results from inadequate growth of the septum secundum, enlarged foramen ovale, or excessive absorption of the septum primum. Most common ASD (80–90%), usually seen in women in the 5th or 6th decade of life, and rarely associated with other cardiac defects (1).
- In addition to the septum primum, the endocardial cushion is responsible for the development of the medial portion of the mitral and tricuspid valves, and the inlet portion of the interventricular septum. A complete endocardial cushion defect is associated with a septum primum ASD, a common AV valve, and an inlet VSD. It comprises 2–3% of all ASDs and can be associated with a mitral (anterior leaflet) or tricuspid valve (septal leaflet) cleft (1).
- Sinus venosus ASD: The failure in separation between the right-sided pulmonary veins and the SVC, IVC, or RA. It comprises 2–10% of all ASDs. The superior type is a defect at the junction of the SVC and RA leading to anomalous pulmonary venous return of the RUPV into the RA. The inferior type is a defect in the junction of the IVC and RA leading to anomalous pulmonary venous return of the RLPV into the RA (1).
- Coronary sinus ASD: Results from the unroofing of the CS which leads to a connection between the inferior part of the LA and CS; associated with left-sided SVC. It is the least common form.
- Atrial bradycardia: Sinus bradycardia (SB) is a heart rate <60 bpm. It can be seen normally in athletes due to preconditioning and increased stroke volume due to exercise. SB can also result from conditions involving the SA node such as inferior myocardial infarction; medications (beta-blockers, inhalational anesthetic agents, narcotics, anticholinesterase agents, and succinylcholine); and vagus nerve stimulation from carotid sinus message, tension on the extra-ocular muscles (oculocardiac reflex) or omentum. Additionally, reflex bradycardia can result from a sudden rise in BP that is detected by the carotid sinus. Causes include a rise in intracranial pressure (Cushing's reflex from tumors, intracranial bleed), use of alpha-agonists (phenylephrine, norepinephrine), and increases in cardiac output.
- Atrial tachycardia is a heart rate >100 bpm with a narrow complex QRS on ECG.
- Sinus tachycardia is due to an increase in output (automaticity rate) of the SA node. Heart rate is usually 100–180 bpm with a "P" wave seen on the ECG. Common causes include sympathetic stimulation (hypoxia, hypercarbia, acidosis, ischemia), hypotension or hypovolemia, anemia, anxiety, fever, anaphylactic reactions, sepsis, medications (dopamine, epinephrine), hyperthyroidism, and physical activity.
- Supraventricular tachycardia (SVT) includes all forms of tachycardia originating above the bifurcation of the His bundle. They have a regular rate of 150–220 bpm. The most common type is AV nodal re-entrant tachycardia (60%). Another 30% are due to an AV re-entry pathway connecting the atria to the ventricles. The remaining etiologies include pre-excitation syndromes such as Wolff–Parkinson–White and paroxysmal atrial tachycardia.
- Atrial flutter occurs at a rate of 200–350 bpm. It is usually associated with a circuit movement of the right atrial tissue causing the saw tooth pattern on ECG. Atrial flutter is almost always associated with a 2:1 or greater AV block because the AV node is not able to conduct more than 220 bpm.
- Atrial fibrillation occurs at a rate of 300–500 bpm in a completely irregular and disorganized fashion. It is the result of multiple, concurrent, circulating re-entrant excitation waves in both atria; seen as an irregular pattern of AV node conduction at irregular intervals about 80–160 bpm. A-fib can be acute, chronic, or paroxysmal. Most of the foci responsible for a-fib appear to originate from atrial smooth muscle at the junction of the pulmonary veins and the LA. Other foci that can be involved include the mitral valve isthmus, orifice of CS, and SVC.
- Conduction abnormalities:
- First-degree heart block: All impulses are conducted to the ventricles but the PR interval on the ECG is prolonged.
- Second-degree heart block (2 types): Type 1 (Wenckebach) is associated with gradual prolongation of the PR interval and eventual drop of a ventricular beat. Type 2 has a normal PR interval with sudden dropped ventricular beats; it has the potential to progress into complete heart block.
- Third-degree (complete) heart block is associated with total dissociation of the atria and ventricles. The ventricles beat at a rate lower than the atrial rhythm. The block can be at the level of the AV node (nodal block) or lower (infranodal). In nodal block the remaining AV node becomes the pacemaker of the ventricles at a rate of 40–50 bpm. In infranodal block the pacemaker will be further down the conduction system with a lower rate of 15–30 bpm which can result in significant hypotension, dizziness, and syncope. Complete heart block usually occurs due to myocardial infarction, cardiac surgery, or ventricular septal defects.
- Right or left bundle branch block (RBBB, LBBB): Impulse is conducted through the intact bundle into the normal side and then through the ventricular myocardium to the blocked side. Ventricular rate is normal but there is a wide QRS complex on the ECG.
- Sinus bradycardia: Intraoperative medical management should be administered when associated with hemodynamic changes; treatment may include anticholinergic agents (atropine, glycopyrrolate), beta-agonists (isoproterenol), and volume resuscitation. If medical management fails, the use of temporary pacing devices should be considered, such as cutaneous pacing pads, esophageal pacing leads, intravenous pacing wires and pacing pulmonary artery catheters (PAC, or epicardial pacing placed prior to closure of the chest in cardiac surgery).
- LBBB: Avoid placement of a PAC due to the risk of complete heart block. Detection of a new onset LBBB in the perioperative period is suggestive of an ischemic event.
- Atrial contraction (P wave on ECG) is responsible for 20% of LV filling during diastole. This percentage increases in patients with mitral stenosis (30%) and aortic stenosis (40%), so maintaining sinus rhythm in these patients is of utmost importance. If a-fib or atrial flutter occurs, medical or electrical cardioversion should be attempted. If attempts for cardioversion are unsuccessful, ventricular response rate should be controlled to allow for adequate ventricular filling.
- Atrial tachycardias in the perioperative period should be managed based upon the appropriate ACLS protocols.
- Serum BNP level is an indicator of heart failure. Normal serum BNP levels are <100 pg/dL. Levels >100 pg/dL suggest heart failure. Its sensitivity, specificity, and positive predictive value are higher than cardiomegaly on CXR or rales on physical exam in diagnosing heart failure. It also serves as an objective means to assess treatment.
