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Lecture Notes - Instructor Adelson > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Orientation of Heart in Body

A

Base of heart - is the point of attachment to the vessels, rest of heart is sitting on fluid and tissues which stabilize it where it belongs.

Apex - is at the bottom of the ventricles

Ligamentum arteriosum - ligament between Aorta and the pulmonary trunk; before birth it is responsible for providing nutrients by providing blood. Blunt force or trauma, can shear this stucture and tear Aorta

  • Base sits slightly L of midline/sternum
  • Apex points diagonally to the left
  • Heart is rotated on axis to Left, such that R Atrium and Ventricles are prominent, kind of faces left shoulder
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2
Q

Linings of the Heart

A
  • Pericardial Fluid between two serous membranes (parietal and visceral) normal volume si 15-50mL Pericarditis can be up to 200-300cc
  • Visceral Pericardium/Epicardium (kind of continuous) - lining that surrounds heart
  • Fibrous Pericardium - Pericardial sac
  • Parietal Paricardium Lining - Intermost lining of the fibrous pericardium

Pericarditis - is an inflamation of visceral and parietal pericardium

  • surfaces rub together causing friction and pain
  • associated with an increase in fluid which may progress to cardiac taponade which inhibits hearts ability to expand and contract
  • Caused by: rhumatic fever - strep throat left untreated, blunt trauma, cardiac trama, infection, radiation, etc
  • Histamines released due to irritation causing edema
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3
Q

Auricle

Cornary Sulcus

&

Anterior/Posterior Inerventricular Sulcus

A
  • Auricle - expandable portion of the atria R/L, when atria recieve blood, returns to floppy form when not in use
  • Cornary Sulcus - Deeper Groove between Artia and the ventricles - horizontal
  • Anterior/Posterior Inerventricular Sulcus - shallow grooves between ventricles, blood vessels run in these grooves along with fat tissues
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4
Q

Layers of the heart

A

Epicardium - Outermost lining of the heart, is essentially the same as Visceral pericardium

Myocardium - muscle layer - composed of cardiac muscle cells

  • sits below epicardium
  • in Atria - muscle sits in concentric circles of muscle
  • in Ventricles - muscle spirals towards the apex

Endocardium

  • composed of simple squamous epithelium that is continuous with vasculature
  • meaning that the inner layer is a single layer of flat cells that makes up inner lining of heart and blood vessels
  • there is no break between heart and vessels.
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5
Q

Cardiac Muscle Cell

A

Mitochondria - heavily populated in Cardiac muscle to aid in energy production, cannot fuction without oxygen

  • Glycolysis - Cytoplasm - anarobic metabolism that breaks down glucose
  • Krebs Cycle
  • Oxidative Phosphorlization - O2 required for production of ATP

Intercalated disks- physically/electrically join cells

Sarcoplasmic Reticulum - is like the endoplasmic reticulm for muscle cells

Sarcolemma - plasma membrane for muscle cells

T-Tubules - allow depolarization of the membrane to quickly penetrate to the interior of the cell.

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6
Q

Intercalated disk

A
  • composed of desmosomes - mechanical/physical conection between cells, anchoring cells together
  • gap junction- electrical connection between cells, allow action potential to pass very rapidly
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7
Q

Types of cardiac muscle cells

A
  • Pacemaker Cells - (SA/AV) Nodal Cells
  • Purkinje Cells - Conduction Cells
  • Contractile Cells - Working Cells
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8
Q

Interatrial Septum

Interventricular Septum

AV Valves

A

Inter artial/ventricular septum - muscular partitions in between each atrium and ventricles

AV Valves - valves that are one way doors that allow blood to pass from artia to ventrical without backflow

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9
Q

Right Atrium

A
  • All entrances are Posterior - blood is coming from systemic circulation
  • Superior Vena Cava (SVC) - blood arriving from Head, Neck, Chest, Upper limbs
  • Cornary Sinus - Return from Cardiac Veins
  • Inferior Vena Cava (IVC) - Trunk, Viscera, Lower Limbs
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10
Q

Right Ventricle

A
  • Pulmonary Semi-Lunar Valve one way valve leaving R Ventrical enroute to Pulmonary Trunk and Lungs
  • Tri-Cuspid Valve - Right AV Valve
    • Cusps - valve like structure
    • Chorde Tendonae - anchor muscle to valve
    • Papillary Muscles - operate AV Valves
  • AV Valves provide electrical insulation Between atria and ventricles
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11
Q

Pulmonary Trunk

A
  • Fed by Right Atrium via semi lunar valve
  • Feeds R. Pulmonary Arteries (3) and L. Pulmonary Arteries (2)
  • Carry deoxygenated blood to the lungs, which then return blood to L. Atrium via Pulmonary Veins
  • 2 pulmonary veins return from each set of lungs
  • Aorta tied to pulmonary trunk by Ligamentim Arteriorsum (may shear and rip aorta in blunt trauma)
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12
Q

Arteries carry blood _____ from the heart.

A

Away

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13
Q

Veins carry blood _____ the heart

A

to

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14
Q

Left Atrium

A
  • Pulmonary veins return oxygenated blood from the lungs.
  • Enter posteriorly
    • 2 from L Lung
    • 2 from R Lung
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15
Q

Left Ventricle

A
  • Bi-Cuspid Valve - Mitral Valve - Left AV Valve - Double flapped valve (mitral = 2 pointed cardinal hat) Controlled by Cusp, chortae tendonae, and papilary muscle.
  • Pumps oxygenated blood to Aorta via Aortic semi-lunar Valve
  • Mitral valve prolapse - if valve bukges in wrong direction, blood regurgetates into Artia; creating a heart Murmur. Mostly benign.
  • Blood exits L Ventrical via Aortic Semi-Lunar Valve enroute to Ascending Aorta
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16
Q

Aortic Arch

A
  • Aortic Semi-Lunar Valve - provides access during Diastole (when closed) to Aortic Sinus; unavaliable during Systole
  • Aortic Sinus turns into Cornary Artery which divide into 5 arteries which feed heart muscle
  • Ascending Aorta
    • Bracheocephalic Trunk (Right upper extremity Right side of head and neck)
    • Left Common Carotid (Left side of head and neck)
    • Left Subclavian (Left upper extremity)
  • descending Aorta ⇒ Abdominal Aorta
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17
Q

5 Main Coronary Arteries

A
  • Right Coronary Artery (RCA)
  • Left Main Coronary Artery (LCA)
  • Left Anterior Descending (LAD)
  • Left Circumflex (CX)
  • Posterior Descending Artery (PDA)
  • 90% - Right Dominant - RCA ⇒ PDA
  • 10% - Left Dominant - CX ⇒ PDA
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18
Q

Cornary Circulation

Anterior View

A
  • Heart is fed during Diastoyle via aortic sinus
    • Systole - Contraction
    • Diastyole - Resting
  • R Cornary Artery feeds
    • Right Atrium
    • Parts of both Ventricles
    • SA/AV Nodes
  • L Cornary Artery feeds
    • Left Ventricle
    • Left Atrium
    • Interventricular Septum
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19
Q

R Cornary Artery feeds

A
  • Right Atrium
  • Parts of both Ventricles
  • SA/AV Nodes
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20
Q

Left Cornary Artery feeds

A
  • Left Ventricle
  • Left Atrium
  • Interventricular Septum

Breaks into two other Coronary Arteries

  • Circumflex
  • Left Anterior Descending
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21
Q

Myocardial Infarction

A
  • Blockage of Coronary Artery

If blockage does not occur in Coronary Artery it is not a heart attack

* important to understand what coronary arteries feed which part of the heart so that can you can try to determine where blockage is occuring and what type of treatment to administer

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22
Q

90% of people are

A
  • Right Dominant
  • RCA gives rise to PDA

*

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23
Q

10% of people are

A
  • Left Dominant
  • CX gives rise to PDA
  • If you have Lateral and Inferior changes @ same time this PT may be left Dominant
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24
Q

Why it matters 90/10 when localizing a MI

A

If blockage occurs in Circumflex:

  • For right side dominant blood flow is only impacted distal to clot on CX
  • For L Dominant, circulation reduced for Distal CX and total PDA

For R Sided Blockage nitro is contraindicated because

  • Changes seen in 12 lead in II III & aVF, indicate RCA blockage (could be cutting out literally 50% of blood flow to heart
  • Providing nitro would dialate all vessels and reduce preload coming back into the heart, combined with broken pump function, BP would drop and further complicate patients condition
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25
Q

12 Lead EKG Intrepretation

A
  • Primary focus is on L Ventricle because if it fails, it is the biggest problem
  • Walls of the heart that may be impacted
    • Inferior II, III, aVF
    • Anterior V3, V4
    • Posterior
    • Lateral V5, V6, I, aVL
  • Impact to any one Coronary Artery could impact in some way the L Ventricle
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26
Q

Inferior Wall is read in ECG in

A

II

III

aVF

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27
Q

Anterior wall in ECG is read in

A

V3

V4

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28
Q

Lateral Wall is read in ECG in

A

V5

V6

I

aVR

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29
Q

Great Cardiac Vein

A
  • begins at the apex of the heart and ascends along the anterior longitudinal sulcus to the base of the ventricles.
  • It then curves to the left in the coronary sulcus, and reaching the back of the heart and returns the blood to the atrium
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30
Q

Blood Flow through Body

A
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31
Q

Conduction System

A
  • Three types of cells: Nodal Cells, Conducting Cells, Contracting Cells
  • SA Node - Sino Atrial & AV Node - Atrio Ventricular Node are made of nodal/pacemaking cells
  • Purkinje Cells - Conducting cells
    • Internodal Pathways
    • Underneath AV Node are purkinje fibers
    • Bundle of HIS splits into
    • Parallel structures called L/R Bundle Branches
    • Bundle Branches are the terminal fillaments of purkinje fibers
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32
Q

Automaticity

A
  • cardiac muscle contracts in absence of neural or hormonal stimulation
  • Does not require body or brain to tell it what to do, because of the SA & AV cells
  • Will beat without the influence of SA/AV nodes
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33
Q

Conducting Cells

A

Initiate & distribute electrical impulses which lead to cardiac muscle contraction

SA node sends message to conduction system which is relayed to contaction system, which tells heart to squeeze.

There is critical relationship between conduction and contraction; when one of the parts fails ⇒ the heart fails.

34
Q

SA Node

A
  • Found in the walls of the R Atrium
  • considered to be official pacemaker of the hear
  • generates action potential at inherrent pacing rate of 80-100 min
35
Q

Internodal Pathways

A
  • distribute contractile stimulus to atria and send impulse to AV Node
  • inherrent pacing rate of 60-80 bpm
36
Q

AV Node

A
  • Located in the floor of R Atrium
  • Slows the conduction rate to allow blood to flow into Ventricle
37
Q

Bundle of HIS

A
  • Considered the AV Junction
  • Inherent pacing rate is 40-60 bpm
38
Q

Bundle Branches

&

Terminal Purkinje Fibers

A
  • Job is to distribute stimulus/AP to the ventricles
  • inherrent pacing rate 20-40 bpm
39
Q

Conduction leads to Contraction

A

Electrical Function leads to Mechanical function

40
Q

Control of Respiration

A

Local - isolated local event ie shunting from fluid in lungs

Neural - Brain exerting control over body systems

Endocrine - to be discussed at later date

41
Q

Local Control of Respiration

A
  1. Increase in metabolic demand; increase in O2 uptake into cells = increase in pressure gradient
    • exercise creates an increase in demand for O2 to do work = heaver breathing = increased pressure gradient
  2. Increase in CO2 capillaries near peripherial tissues; arterial smooth muscle relaxation ⇒ increased blood flow
    • vasodialation ⇒ allows for more blood to pass through to pick up CO2 to be expelled
  3. Shunting - relating to lungs/alveoli
    • ie Congestion/fluid in alveoli
    • shunted toward the alveoli with high PO2
    • air entering lungs is shunted toward capillaries with high PCO2
42
Q

Neural control of respiration

A
  1. Pons & Medulla:
    • increase in CNS stimulation
    • ie. increase in body temp ⇒ increase in rate of breathing because of impact on pons & medula and their dictated response
  2. Reflexes
    • baroreceptors -
      • free nerve endings in walls of distensible organs
      • Stretching causes distortion of dendrites (nerve endings) ⇒ changes route of AP formation
    • Hering-Breuer Reflexes
      • inflation/deflation reflex - prevents overexpansion/total collapse of lung
      • Increase in BP ⇒ decrease in Respiratory rate and vice versa
    • chemoreceptors - located in carotid and aortic bodies - monitor PCO2 & PO2 concentrations
      • Primary respiratory drive - increased PCO2 = increased respiration rate
      • Secondary (Hypoxic) respiratory drive - decreased PO2 = increased respiratory rate; seen in pt’s with COPD
  3. Higher Centers or cerebral cortex ⇒ concious control of breathing; physical manipulation of breathing needs; reverts to automatic when not being thought about.
43
Q

Normal Plasma pH

A

acidosis - 7.35 < WNL < 7.45 alkalosis

44
Q

Acid Base Balance

Problems caused by:

A

Changes in pH ⇒

  • disruption in stability of cell membranes
  • decrease in pH (increase in [H+] = denaturation of proteins (non-functional)
  • inactivation of critical enzymes
  • Problems or changes with pH/[H+] concentration are fixed with Buffers
45
Q

Buffers

A

composed of Salt + Weak Acid

stabilize pH by removing or replacing H+ ions

either

Take H+ out of solution so that they are bound to something else and not contributing to acidosis

or

rearranges chemical compounds so that the H+’s are occupied

* does not have to have anything to do with a base or H+

46
Q

3 most important/pertinent buffer systems in human body

A
  1. Protein buffer sustem - ie Hb; amino acids/proteins in blood may function as buffers by binding H+ and removing them from solution
  2. Carbonic Acid Buffer system
  3. Phosphate Buffer System - Reversible reation between H+ + HPO4 ⇔ H2PO42-, stabilizes pH of Urine by removing H+ from solution.
47
Q

H+ + HCO3 ⇔ H2CO3 ⇔ H2O + CO2

A
48
Q

Arterial Blood Gas (ABG)

A

Samples of blood values directly from artery vs veins provides more accurate representation of how sick patient is

  • pH = 7.35-7.45
  • PCO2 = 35-45
  • PO2 = 70-100
  • HCO3 = 22-26
  • SaO2 > 90%
49
Q

Respiratory Acidosis

A

Primary Respiratory Problem

  • hypoventilation
  • increased CO2
  • not breathing
  • Narcotic OD

H+ + HCO-3 ⇔ H2CO3 ⇔ H2O + CO2

increase in CO2<strong><em> </em></strong>by default results in decrease in pH (increase in H+)<strong><em> </em></strong>& Increase in HCO-3

**patients who are not breathing sufficently will have disturbance in pH associated with not breathing

  • CO2 increases ⇒ body then converts CO2 into carbonic acid ⇒ which makes more H+ and bicarbonate
50
Q

Respiratory Alkalosis

A

Hyperventalation Syndrome

H+ + HCO-3 ⇔ H2CO3 ⇔ H2O + CO2

**pt who is hyperventilating is depleting CO2 , causing reaction to move left to right

results in decrease in CO2, causing Increase in pH (decrease in H+) & decrease in HCO-3 to H2O and CO2

51
Q

Metabolic Acidosis

A
  • DKA
  • Sepsis - Lactic acidocis
  • ASA OD
  • TCD OD
  • Chronic Renal Failure

H+ + HCO-3 ⇔ H2CO3 ⇔ H2O + CO2

decrease in pH (increase in H+ in blood) as a result of the different disease processes; ie if blood becomes acidic proteins denature and critical enzymes become inactive

Body compensates by driving reaction to right and increasing production of CO2 by default Respiratory rate increases

decrease in HCO-3

*Most important because pt is breathing fast (tachypnea) for any number of reasons, but provider fails to recognize that the patient is critically ill

52
Q

Metabolic Alkalosis

A
  • Tums OD
  • Vommiting

H+ + HCO-3 ⇔ H2CO3 ⇔ H2O + CO2

Increase in pH (decrease in H+), HCO-3

(decrease in CO2)

Vommiting reduces your stomach acid which is Hydrogen Ions, increases HCO-3, and decreases available CO2

53
Q

Tachypnea in absence of respiratory distress usually indicates

A

Metabolic Acidosis

Tachypnea in presence of clear lung sounds or no obvious respiratory distress usually indicates

DKA

Sepsis - Lactic Acid

ASA OD

TCA OD

Chronic Renal failure

54
Q

Purpose of Buffer Systems in Body

A
  • maintain/stabilize pH all the time
  • dynamic effort by body constant shifting to:
    • if there is a decrease in avaliable H+ available ⇒ then released from appropriate buffer system
    • if there is an increase in avaliable H+ then more will be taken up
55
Q

Sources of Buffer compensation

A
  • Respiratory - Fast Compensation
  • Renal - Slow Compensation

Buffers are compensation effort by body, when they fail/resources used up ⇒ disease

56
Q

Respiratory vs Metabolic

A

Problems with CO2 = Respiratory

Problems with BiCarb (HCO-3) = Metabolic

57
Q

SA/AV Node and action potentials

A
  • The SA/AV nodes do not have a steady state/ resting potentials
  • Pacemakers drift between depolarized to repolarized in fashion similar to sine wave
  • Leak channels are responsible for changing of ions that are present; once one cell depolarizes primarily due to gap junctions cells near by depolarize and influences other cells ie the Atria
  • SA’s depolarization sends wave of depolarization down internodal pathways to AV where it slows and sends wave on to Purkinje Fibers which then spreads across to the ventricles
58
Q

Atria and Ventricle AP flow

A

depolarization ⇒ repolarization ⇒ plateau ⇒ depolarization ⇒ rest

Resting Potential for Atria is 80mV

Resting Potential for Ventricles is 90mV

59
Q

Ventricular AP : Phase 4

A
  • Resting Phase/Potential
  • -90mV
  • Threshold is -75mV
  • Resting portential maintained by NA+/K+ Pump
  • Resting phase is associated with Diastole
60
Q

Ventricular AP: Phase 0

A
  • Rapid depolarization Phase (3-5ms)
  • prepotential activated by SA/AV Node
  • leading to rapid entry of Na+ ions causing a change in membrane potential to +30mV
61
Q

Ventricular AP: Phase 1

A
  • Repolarization Phase (175ms)
  • Na+ reaches approximate equilibrium and Na channels close and are inactivated until return to relative refractory period (approx -60mV)
  • K+ channels open and repolarization
62
Q

Ventricular AP: Phase 2

A
  • Plateau Phase (75ms)
  • Ca2+ exchanged for Na+ maintains membrane potential at 0mV
  • Major difference between what Ca2+ is used for in Neurons and what it is used for in cardiac/muscle cells
  • Ca2+ arrives for sarcoplasmic reticulum and T-Tubules because it is in higher concentration in ECF and stored in sarcoplasmic reticulum
  • Entry of Ca2+ makes muscle contraction possible, ie:troponin⇒topomyosin⇒actin/myosin b
  • Ca2+arrival is critical to linking conduction and contraction
63
Q

Ventricular AP: Phase 3

A
  • Rapid/Main Repolarization phase (50ms)
  • Ca2+ channels close
  • K+ Channels exit enabling rapid repolarization
  • Cell returns to resting phase/potential (-90mV) where Na/K pump works to maintain membrane potential
64
Q

Absolute vs Relative

Refractory Periods in Cardiac Cell

A
  • Absolute - Period of time from when Na+ channels are inactivated until they are just closed and can be opened again which is around -60 mV
  • generally long absolute period in cardiac vs skeletal isn’t as possible for tetany (sustained contraction), allows heart muscle to relax befor contracting again
  • Relative - from -60 to -90mV during relative refractory where Na+ is closed but is able to be opened again
65
Q

Components of muscle contraction

A
  • Topomyosin - microfiliment located on actin filament
  • Troponin - Binding site for Ca2+ on Tropomyosin which unlocks binding site for Myosin to cause crossbridge-powerstroke-muscle contraction
  • Actin - Thin micro filaments containing toponin and tropomyosin
  • Myosin - Thick micro filament, has head that binds to Actin to produce muscle contraction; has both ADP and Pi
  • ADP and Pi - located on Myosin, Pi released when myosin forms Crossbridge (links with Actin) ADP expended during Powerstroke
  • ATP links with Myosin to release Actin which causes ATP to break down into ADP + Pi and heads return to resting
66
Q

Resting Muscle cell

A
  • Consists of Actin and Myosin not touching
  • Myosin has ADP + Pi attached to binding head
  • Actin’s Myosin Binding sites are blocked by Tropomyosin which has troponin (Ca2+) binding sites on them
67
Q

When we decide to move

what happen to actin and myocin, how does it relate to cardiac action potential?

A
  • Calcium is delivered from sarcoplasmic reticulum and from ECF via the T-Tubules
  • Ca2+ binds to troponin causing tropomyosin to reveal myosin binding sites
  • Corresponds to plateau phase of Ventricular action potential; as Ca2+ arrives to cause muscle contraction
68
Q

Cross Bridge Formation

&

Powerstroke

&

Reset/Rest

A
  • Once Myosin binding sites are revealed on Actin; Myosin heads release Pi molecule as they bind to Actin toform cross bridge formation.
  • ADP is expended as Myosin head pulls themselves along Actin causing muscle to contract (shortening muscle)
  • Affinity to the arrival of a new ATP molecule causes Myosin to release and return to it’s resting phase, which breaks ATP down into ADP + Pi
  • If calcium is still present, cycle will repeat; increased calcium causes prolonged muscle contraction
  • When ATP runs out it is not possible to seperate the Actin and Myosin, Hence rigamortis a couple hours after death due to lack of O2, runs out of glucose, runs out of ATP.
69
Q

Cardiac Enzymes

A
  • When heart muscle has block in coronary artery
  • Muscle not recieving nutrients it becomes
    • irritable
    • ischemia not enough O2
    • injury
    • infarc - tissue death
  • With no ATP = No Na/K Pump = wrong membrane potential ⇒ shifting of fluids ⇒ cells to lyse ⇒ contents released into bloodstream ⇒ changes what you see on EKG ⇒ perhaps ST elevation = MI
  • even if there is no ST elevation, pt may still be having MI, revealed via analysis of cardiac enzymes (Troponin, myoglobin, CK(MB))
70
Q

Cardiac Cycle

Ventricular / Atrial Diastole

A
  • Heart is relaxed both A & V are resting
  • Pulmonary circulation returns from lungs & Systemic circulation returns from body and begin to passively fill ventricles as much as it can before atrial systole
71
Q

Atrial Systole

Ventricle Diastole

A
  • phase following atrial depolarization the atrium will contract
  • 70% of returning blood has passively filled ventricle, remaining 30% will be pushed into ventricles during contraction.
  • Approximatley 130mL remain in Atria following contraction
72
Q

Atrial Diastole

Ventricular Systole

A
  • AV Valves close⇒ increasing pressure (bp rises) ⇒ when BP is > Aorta/Pulmonary Trunk Pressure ⇒ Blood is expelled into circulation
  • Then returns to Atrial/Ventricular diastole, blood passively fills from circulation
73
Q

Mechanical Function of the heart is guided by

A

electrical function

74
Q

End Diastolic Volume

vs

End Systolic Volume

A

EDV - Amount of blood in Ventricles after Atrial contraction last moment of ventricular diastole ie the maximum amount of blood they will recieve (130mL)

ESV - Amount of blood remaining in ventricles after Ventricular contraction (50mL)

75
Q

Stroke Volume

A

Amount of blood actually pumped out of heart in single beat

70-80mL for healthy adult

76
Q

Ejection Friction

A

SV divided by EDV

% of blood ejected from single heart beat

Normal ejection fraction runs between 60 and 70%

77
Q

Cardiac Output

A

SV x HR

amount of blood pumped out of heart each minute

  • changes to EDV or ESV ⇒ change in SV ⇒ CO
  • neural or hormonal stimulation ⇒ changes in HR ⇒ changes in CO
78
Q

A-Fib

A
  • Atrials are incompetent
  • Atrias quiver rather than push blood from Atria to Ventricles
  • 30% of blood that doesn’t get pushed into ventricles is called Atrial Kick
  • Blood pools in Atria and doesn’t circulate,
  • Pooling blood can clot ⇒ when shocked, clot can begin to circulate causing clots in pulmonary circulation or systemic circulation
79
Q

Results of NE binding to A1, B1 or B2 receptors

A
  • Increase in the opening or likelihood of opening of Na+ and Ca2+ channels ⇒ increase in the influx of positive ions ⇒ results in muscle contraction
  • Increase in rate at which depolarization occurs = an increase in heart rate
  • Example of SA node involvement
80
Q

Results of binding ACh to B1, A1, A2 receptors

A
  • Muscarinic - ACh Receptor linked to K+ channels
  • Binding ACh ⇒ Opens K+ channels ⇒ exit of K+ from cell ⇒ hyperpolarization ⇒ slows the rate of spontaneous depolarization
  • example of effect on AV node

Lecture Notes - Instructor Adelson (8 decks)

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