Cardiac Physiology Flashcards

Cardiac Physiology

Introduction

• Every anesthetic agent has a direct or indirect effect on the cardiovascular system.
• Patients in the perioperative period often receive agents that affect hemodynamic variables.
  • Heart rate
  • Rhythm
  • Blood pressure
  • Cardiac output
• The effects of these agents are predominantly governed by transmembrane ion fluxes.
• Drugs used for rhythm and rate control act by modulating Na^+, K^+, and Ca^{+2} currents.
• Intracellular calcium is a key mediator in coupling electrical excitation to mechanical contraction.
• Calcium is an important determinant of the contractile state of the myocardium.

Cardiac Function and Pericardium

• Blood tends to flow from areas of high pressure to areas of lower pressure.
• Opening and closing of cardiac valves is a function of the pressure gradients across those valves at any point in time.
• Normal cardiac function can occur in the absence of the pericardium; it is non-essential for survival.

Functions of the Pericardium:

1. Reduces friction between the heart and surrounding structures.
2. Limits acute dilatation of cardiac chambers.
3. Provides a barrier to infection.
4. Limits excessive movement of the heart in the chest cavity.

• The pericardium is metabolically active and secretes prostaglandins that affect coronary artery tone and cardiac reflexes.
• The pericardium is a highly innervated structure via the vagus nerve, phrenic nerve, and sympathetic trunks.
• Pericardial inflammation or manipulation may produce pain or vagally mediated reflexes.

Cardiac Muscle Structure

• Functional Syncytium:
  • Cardiac muscle cells are electrically connected through intercalated discs, allowing them to contract simultaneously (Figure 15.13).

Differences Between Cardiac Muscle and Skeletal Muscle:

• Myocardial fibers have a more branching, interconnected structure, with gap junctions facilitating the conduction of the action potential from one cell to another.
• Myocardial sarcomeres contain a higher concentration of mitochondria due to the heart's high metabolic rate.
• The myocardial sarcomere system has a rich capillary blood supply (one capillary per fiber) that allows for efficient diffusion and perfusion.
• Myocardial cells have a more extensive sarcoplasmic reticulum and T-tubule system, to allow for rapid release and reabsorption of calcium.

Fibrous Skeleton of the Heart

• The heart has a skeleton composed of fibrous rings.
• Left fibrous trigone
• Fibrous ring of the pulmonary valve
• Left atrioventricular ring
• Fibrous ring of the aortic valve
• Right atrioventricular ring
• Right fibrous trigone

Plays a vital role in supporting the structure and function of the heart:

• Composed of 4 fibrous rings (around the MV, TV, the pulmonary trunk, and the aortic orifice) and the membranous portions of the interatrial, interventricular, and atrioventricular septa.
• Provides attachment points for valve leaflets and cusps.
• Provides a framework for attachment of myocardial fibers.
• Acts as an electrical insulator between the atria and the ventricles.
• Provides a passageway for the AV Bundle (bundle of His).

Atrial Septal Defects (ASDs)

• Most common congenital heart lesion diagnosed in adults.
• Four types:
  • Secundum defect (75%) (central)
  • Primum defect (above AV valves)
  • Sinus venosus defect (at either the SVC or IVC junction)
  • Unroofed coronary sinus
• Allows left-to-right shunt and leads to elevated pulmonary and right heart pressures.
• Size of defect and amount of shunt dictates whether repair is necessary.

Interventricular Septum

• Composed of a membranous septum (upper and posterior) and a muscular septum (anterior).
• Under normal physiologic pressure and filling conditions, its convexity is bowing into the right ventricle.

Heart Chambers and Valves

Left Heart

• Aortic Valve
  • Part of the aortic root (annulus, AV cusps, the sinuses of Valsalva, and the proximal ascending aorta).
  • Trileaflet semilunar valve.
  • Left, right, and non-coronary cusps.
  • Right and Left cusps give rise to RCA and Left Main coronary artery.

Valves

• Atrioventricular (AV) valves
  • Tricuspid valve

Coronary Artery & Vein Anatomy

Cardiac Conduction System

• Sinoatrial (SA) node
• Anterior internodal tract
• Middle internodal tract
• Posterior internodal tract
• Bachman's bundle
• Atrioventricular (AV) node
• Atrioventricular (AV) bundle (bundle of His)
• Left and right bundle branches
• Purkinje fibers

Neural Control of Cardiac Function

• Parasympathetic (Vagus nerves)
• Sympathetic Chain (T1-T4) 'cardioaccelerator fibers'
• The atria are innervated by both the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS), while the ventricles are supplied principally by the SNS.
  • The PNS, acting via acetylcholine (Ach) and muscarinic receptors (via vagal nerve), reduces heart rate (HR), AV node conduction, and contractility.
  • The SNS, acting through adrenergic receptors (via norepinephrine), has positive ionotropic, chronotropic, and lusitropic effects on the heart.
  • Maximal SNS stimulation can increase cardiac output by 100% above normal.
  • Strong PNS stimulation can cause a period of asystole.

Hormonal Control of Cardiac Function

• Atrial Natriuretic Peptide (ANP) and B-type Natriuretic Peptide (BNP) are released from atria and ventricle in response to increased stretch of the chamber wall; they help the myocardium by inducing diuresis, natriuresis, and vasodilation.
• Adrenomedullin is a peptide hormone that acts by increasing cAMP levels and has positive ionotropic and chronotropic effects, as well as vasodilation.
• Angiotensin II stimulates AT1 receptors and has positive ionotropic and chronotropic effects.

12 Lead ECG EKG Lead Placement

• V1
• V2
• V3
• V4
• V5
• V6

Ionic Content and Resting Membrane Potential

• Major ionic content inside and outside a cell:
  • Inside: K^+, negatively charged proteins (A-)
  • Outside: Na^+, Cl^-
• Under normal conditions at rest, membrane potentials are negative, meaning that the voltage is more negative within the cell than outside of it.

Cardiac Action Potential

• Phase 0 (Depolarization):

  • Sodium channels open.
  • Rapid influx of Na^+ causes rapid depolarization.

• Phase 1 (Initial Repolarization):

  • Sodium channels close.
  • Cell begins to repolarize.

• Phase 2 (Plateau):

  • Calcium channels open, allowing Ca^{2+} influx.
  • Potassium channels open, allowing K^+ efflux.
  • Balance of influx and efflux creates a plateau.

• Phase 3 (Rapid Repolarization):

  • Calcium channels close.
  • Potassium channels remain open, causing rapid repolarization.

• Phase 4 (Resting Potential):

  • Leaky potassium channels maintain the resting membrane potential.

• Prolonged depolarization distinguishes cardiac muscle cells from skeletal muscle cells.

• Absolute Refractory Period: Stimulus cannot depolarize the cell.

Drugs Affecting the Cardiac Action Potential

• Class 1: Sodium Channel Blockers

  • 1a (moderate): Quinidine, Procainamide
  • 1b (weak): Lidocaine, Phenytoin
  • 1c (strong): Flecainide, Propafenone

• Class 2: Beta-blockers

  • Propranolol, Metoprolol

• Class 3: Potassium Channel Blockers

  • Amiodarone, Sotalol

• Class 4: Calcium Channel Blockers

  • Verapamil, Diltiazem

Importance of Calcium in Cardiac Function

• Plays a dual role in cardiac function:
  • Key ion involved in cell membrane depolarization and action potential propagation.
  • Major ion involved in excitation-contraction coupling and muscle contraction.

Excitation-Contraction Coupling:

1. Influx of Ca^{2+} from the interstitial fluid during excitation triggers the release of Ca^{2+} from the sarcoplasmic reticulum (SR).
2. Free cytosolic Ca^{2+} activates contraction of the myofilaments (systole).
3. Relaxation (diastole) occurs as a result of uptake of Ca^{2+} by the sarcoplasmic reticulum and extrusion of intracellular Ca^{2+} by Na^+-Ca^{2+} exchange.

Actin-Myosin Dependence:

• Actin-myosin binding depends on Ca^{2+}-troponin binding for tension development to occur.

Sarcomere Length and Tension Development

• The fibrous cardiac skeleton inhibits sarcomere stretch from approaching a sarcomere length of 2.8 μm.

Frank-Starling Mechanism

• The Frank-Starling curve shows how changes in venous return cause the ventricle to move up or down along a single Frank-Starling curve.
• The slope of that curve is defined by the existing conditions of afterload and inotropy.

Factors Determining LV Performance:

• Preload: Venous return, end-diastolic volume
• Afterload: Systemic vascular resistance, ventricular wall stress
• Contractility: The force generated at any given end-diastolic volume

Left Ventricular Pressure-Volume Loop

• Phases:
  • Ventricular filling
  • Isovolumetric contraction
  • Ventricular ejection
  • Isovolumetric relaxation

Effects of Changes in Preload, Afterload, and Inotropy:

• Preload: Increased preload shifts the curve to the right.
• Afterload: Increased afterload increases pressure and reduces stroke volume.
• Inotropy: Increased inotropy increases stroke volume and ejection fraction.

Oxygen Demand and Supply

• Myocardial oxygen consumption is the biggest determinant of coronary blood flow.
• Factors affecting oxygen supply and demand include heart rate, contractility, and wall stress.

Hemodynamic Equations

• CO = HR ims SV
• CI = CO / BSA
• SV = EDV - ESV
• MAP = CO ims SVR
• MAP = (2/3 ims diastolic pressure) + (1/3 ims systolic pressure)
• SVR = [(MAP - CVP) / CO] ims 80
• PVR = [(mean PAP - wedge) / CO] ims 80

Determining CO:

• Thermodilution
• Fick Method
• Echocardiography

Fick Method:

• CO = VO2 / (CaO2 - CvO_2)
• CO = 250 ml/min / (1.34 ims Hb ims SaO2) - (1.34 ims Hb ims SvO2)

Normal Hemodynamic Values

• Cardiac Index = 2.4 L per minute
• Cardiac Output = 5-7 L per minute
• Stroke Volume = 70-90 mL (1 mL/kg)
• MAP = 60-90 mm Hg
• CVP = 5-10 mm Hg
• SVR = 800-1,200 dyne/s/cm5
• PVR = <250 dyne/s/cm5
• PAOP = 6-12 mm Hg
• Mean PAP = 10-20 mm Hg

ECG Interpretation

Myocardial Infarction:

• Inferior MI: ST elevation in the inferior leads II, III, and aVF with reciprocal ST depression in the anterior leads.
• Old Inferior MI: Q wave in lead III wider than 1 mm, Q wave in lead aVF wider than 0.5 mm, and Q wave of any size in lead II.
• Acute Anterior MI: ST elevation in the anterior leads V1-6, I, and aVL with reciprocal ST depression in the inferior leads.
• Acute Posterior MI: Mirror image of acute injury in leads V1-3, tall R wave, and upright T wave in leads V1-3.

Arrhythmias:

• Atrial Fibrillation: Absence of P waves and irregularly irregular ventricular rhythm.
• Atrial Flutter with 2:1 AV Conduction: Sawtooth waveform in the inferior leads II, III, and aVF; suspect when the rate is about 150 bpm.
• Junctional Rhythm: Absent or retrograde P waves, narrow QRS complex, rate between 40-60 bpm.
• Paroxysmal Supraventricular Tachycardia (PSVT): Rate >150 bpm, regular rhythm, P waves are not easily seen.
• Ventricular Bigeminy: A ventricular premature beat follows each normal beat.
• Ventricular Tachycardia:
  • Monomorphic VT: Wide QRS complexes of similar appearance.
  • Polymorphic VT: Varied QRS complexes.
• Idioventricular Rhythm: Absent P waves, rate typically 20-40 bpm, regular rhythm.

Blocks:

• First Degree Block: PR interval >0.20 seconds.
• Second Degree Block:
  • Type I (Wenckebach): Progressive lengthening of the PR interval until a QRS is dropped.
  • Type II: Normal P waves with constant PR intervals but not all P waves are followed by a QRS complex.
• Third Degree Block (Complete): No relationship between P waves and QRS complexes; atrial and ventricular complexes are regular but dissociated.

Other ECG Findings:

• Hyperkalemia: Small or absent P waves, wide QRS, shortened or absent ST segment, wide, tall, and tented T waves.
• Hypokalemia: Small or absent T waves, prominent U waves, slight depression of the ST segment.
• Sinus Tachycardia: P wave rate greater than 100 bpm.
• Right Bundle Branch Block: Wide QRS, secondary R wave in lead V1, slurred S wave in lateral leads.
• Left Bundle Branch Block: Wide QRS complexes.
• Left Ventricular Hypertrophy (LVH): Sokolow + Lyon criteria, Cornell criteria, Framingham criteria, Romhilt + Estes point score system.
• Atrial Premature Beat (APB): An abnormal P wave occurs earlier than expected, followed by a non-compensatory pause.
• Atrial Bigeminy: Each normal beat is followed by an atrial premature beat.

Paced Rhythms:

• Ventricular Pacemaker: Pacing spikes are seen, and the paced QRS complexes are abnormally wide.
• Implantable Cardioverter Defibrillator (ICD): Defibrillator discharging in response to ventricular tachycardia.