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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.