Cardiovascular Physiology

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Cardiovascular Physiology

• Cardiovascular disease is 1 cause of death
• Major underlying cause is ischemia due to
• atherosclerosis (plaquing)
• white thrombus
• red thrombus
• artery spasm

2

• It ain't what you don't know that gets you into
  trouble. It's what you know for sure that just
  ain't so. Mark Twain

3
Connective Tissue

• Ordinary
• Loose connective tissue (areolar tissue)
• Dense ordinary connective tissue
• Regular vs. Irregular
• Special
• Adipose tissue (fat)
• Blood cells
• Blood cell forming tissue
• Myeloid or lymphatic tissue
• Cartilage
• Bone

4
Events in Hemostasis

• Hemostasis-prevention of blood loss
• Mechanisms
• vascular spasm
• formation of a platelet plug
• blood coagulation
• fibrous tissue growth to seal

5
Hemostasis

• Vascular Constriction-associated w/ trauma
• neural reflexes
• SNS induced constriction from pain
• local myogenic spasm
• responsible for most of the constriction
• local humoral factors
• thromboxane A2 from platelets
• Spasm ? trauma

6
Platelet Plug

• Platelets function as whole cells
• but cannot divide
• Platelets contain
• actin myosin
• enzymes calcium
• ADP ATP
• Thromboxane A2
• serotonin
• growth factor

7
Platelet Cell Membrane

• Contains
• Glycoproteins that avoid the normal
  endothelium but adhere to damaged area
• Phospholipids containing platelet factor 3
• a.k.a. thromboplastin-initiates clotting

8
Mechanism of Platelet Activation

• When platelets contact damaged area they 1)
  swell
• 2) irregular form w/ irradiating processes
  protruding from surface
• 3) contractile proteins contract causing
  granule release
• 4) secrete ADP, Thromboxane A2 serotonin

9
Thromboxane A2

• 1) Vasoconstrictor
• 2) Potentiates the release of granule
• contents
• (not essential for release to occur)

10
Platelets

• Important in minute ruptures
• lack of platelets associated with small
  hemorrhagic areas under skin and throughout
  internal tissues
• half-life of 8-12 days
• eliminated primarily by macrophage action
• (greater than 1/2 of all macrophages in spleen)
• 150,000-300,000 per ?l

11
Role of Endothelium

• Prevents platelet aggregation
• produces PGI2 (prostacyclin)-
• vasodilator
• stimulates platelet adenyl cyclase which
  suppresses release of granules
• limits platelet extension
• produces factor VIII (clotting)

12
Prostaglandin synthesis

• Phospholipid ?Arachidonic acid requires Lipase
• Arachidonic acid?PGG2-PGH2 requires fatty acid
  cyclooxygenase
• PGG2-PGH2?Thromb. A2 requires Thromb. synthetase
• PGG2-PGH2?PGI2 requires Prostacyclin synthetase
• Aspirin and Ibuprofen block Fatty acid
  cyclooxygenase

13
Anticoagulants vs Lysis of clots

• Anticoagulants
• prevents clots from forming
• chelators-tye up calcium (citrate, oxylate)
• heparin- complexes with Antithrobin III
• dicumarol-inhibition of Vit. K dependent factors
• factors II, VII, IX, X (synthesized by
  hepatocytes
• Aka cumadin, warfarin
• Lysis of Clots
• Plasmin (from plasminogen)

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Activators of Plasminogen

• Endogenous Activators
• tissues
• plasma
• urine
• Exogenous Activators
• streptokinase
• tPA (tissue plasminogen activator)

15
Aspirin Ibuprofen

• Block both thromboxane A2 prostacyclin
  production by blocking fatty acid cyclooxygenase
  which converts arachidonic acid to PGG2 PGH2
  (intermediates)
• Why take aspirin to prevent heart attacks?

16
Reperfusion injury

• Most of the frank tissue damage associated with
  infarction occurs upon reperfusion
• associated with the formation of highly reactive
  oxygen species with unpaired electrons. free
  radicals
• When pressure on tissues relieved again
  perfused with blood, free radicals are generated

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Collateralization

• The ability to open up alternate routes of blood
  flow to compensate for a blocked vessel
• Angiogenesis
• Vasodilatation
• Role of the SNS ??
• May impede
• May augment

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Blood Coagulation- Thrombosis

• Extrinsic mechanism-initiated by chemical factors
  released by damaged tissues
• Intrinsic mechanism-requires only components in
  blood trauma to blood or exposure to collagen
  (or foreign surface)

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Clotting factors

• I- fibrinogen
• II- Prothrombin
• III- Thromboplastin
• IV- Calcium
• V- Proaccelerin
• VII- Serum prothombin conversion acclerator
• VIII- antihemophilic factor (A)

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Clotting factors (cont.)

• IX- antihemophilic factor B christmas factor
• X- Stuart factor
• XI- antihemophilic factor C
• XII- Hageman factor
• XIII- Fibrin-stabilizing factor
• Prekallikrein- Fletcher factor
• High molecular weight kininogen
• Platelets

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Hepatocytes role in clotting

• Liver synthesizes 5 clotting factors
• I (fibrinogen)
• II (prothrombin)
• VII (SPCA)
• IX (AHF B)
• X (Stuart factor)
• Coumarin (warfarin or cumadin) depresses liver
  formation of II, VII, IX, X by blocking action of
  vitamin K

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Hemophilia

• Sex linked on X chromosome
• occurs almost exclusively in males
• 85 of cases- defect in factor VIII
• 15 of cases- defect in factor IX
• varying degree of severity from mild ? severe

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Blood Coagulation

• The key step is the conversion of fibrinogen to
  fibrin which requires thrombin
• thrombin
• fibrinogen---------------gtfibrin

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Intrinsic pathway

• Factor XII activated when blood contacts a
  negatively charged surface (collagen, glass)
• Activated XII Kalikrein Kinnogen will activate
  Factor XI
• Activated XI Ca will activate both Factors IX
  VIII
• Activated IX VIII Phospholipid Ca will
  activate Factors X V
• Activated X V Phospholipid Ca will
  convert Prothrombin to Thrombin

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Extrinsic Pathway

• Tissue thromboplastin Factor VII Ca will
  activate Factors X V
• Activated X V Phospholipid Ca will
  convert Prothrombin to Thrombin

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Final Common Steps

• Once Fibrinogen has been converted to Fibrin by
  Thrombin it is changed from the soluble monomer
  to the insoluble polymer by the activated Factor
  XIII
• Factor XIII is activated by Thrombin and Ca

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Lysis of Clots

• Clots may be liquefied by (fibrinolysis) by a
  proteolytic enzyme plasmin
• It circulates in the blood in an inactive form
  known as plasminogen
• Activators are found in tissues, plasma, and
  urine
• It can also be activated by exogenous activators
  such as tPA, or streptokinase

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Risk factors in Heart Disease

• Increasing age
• Male gender
• Heredity (including race)
• Tobacco Smoke
• High blood cholesterol
• High blood pressure
• Physical inactivity
• Obesity/overweight
• Diabetes Mellitus
• High blood homocysteine

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Homocysteine

• Amino acid in the blood that may irritate blood
  vessels promoting atherosclerosis
• Can also cause cholesterol to change into
  oxidized LDL
• Can make blood more likely to clot
• High levels in blood (gt 12 ?mol/L) can be reduced
  by increasing intake of folic acid, B6 and B12

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Heart muscle

• Atrial Ventricular
• striated enlongated grouped in irregular
  anatamosing columns
• 1-2 centrally located nuclei
• Specialized excitatory conductive muscle fibers
  (SA node, AV node, Purkinje fibers)
• contract weakly
• few fibrils

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Syncytial nature of cardiac muscle

• Syncytium many acting as one
• Due to presence of intercalated discs
• low resistance pathways connecting cardiac cells
  end to end
• presence of gap junctions

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Action potentials in cardiac muscle

• Duration of action potential is from .2-.3 sec
• Channels
• fast Na channels
• slow Ca/Na channels
• K channels
• Permeability changes
• Na sharp increase at onset of depolarization
• Ca increased during the plateau
• K increased during the resting polarized state

33
Membrane physiology

• In excitable tissue an action potential is a
  pulse like change in membrane permeability
• In cardiac muscle permeability changes for
• Na
• ? at onset of depolarization, ? during
  repolarization
• Ca
• ? at onset of depolarization, ? during
  repolarization
• K
• ? at onset of depolarization, ? during
  repolarization

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Slow vs Fast cardiac cell

• Relates to the channels that open during
  depolarization
• Typical cardiac muscle have both fast Na
  channels and slow Ca/Na channels that open
  during depolarization
• Specialized excitatory cells like the SA node
  only slow Ca/Na channels are operational
  during depolarization increasing depolarization
  time
• Tetradotoxin blocks fast Na channels selectively
  changing a fast response into a slow response

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Passive ion movement across cell

• Considerations
• Concentration gradient
• high to low
• Electrical gradient
• opposite charge attract, like charge repel
• Membrane permeability
• dependant on ion channels (open or closed)
• If ion channels are open, an ion will seek its
  Nerst equilibrium potential
• concentration gradient favoring ion movement in
  one direction is offset by electrical gradient

36
Resting membrane potential (Er)

• During the Er in cardiac muscle, fast Na and
  slow Ca/Na are closed, K channels are open.
• Therefore K ions are free to move, and when they
  reach their Nerst equilibrium potential, a stable
  Er is maintained

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Na/K ATPase (pump)

• The Na/K pump which is energy dependent
  operates to pump Na out K into the cardiac
  cell at a ratio of 32
• therefore as pumping occurs, there is net loss of
  one charge from the interior each cycle,
  helping the interior of the cell remain negative
• the protein pump utilizes energy from ATP
• Digitalis binds to inhibits this pump

38
Ca exchange protein

• In the cardiac cell membrane is a protein that
  exchanges Ca from the interior in return for
  Na that is allowed to enter the cell.
• The function of this exchange protein is tied to
  the Na/K pump
• if the Na/K pump is inhibited, function of this
  exchange protein is reduced more Ca is
  allowed to accumulate in the cardiac cell ?
  contractile strength.

39
Refractory Period

• Absolute
• unable to re-stimulate cardiac cell
• occurs during the plateau
• Relative
• requires a supra-normal stimulus
• occurs during repolarization
• In a Slow response cardiac muscle cell the
  relative refractory period is prolonged and the
  refractory period is about 25 longer
• in AV node bundle this serves to protect the
  ventricles from supra-ventricular arrhythmias

40
SA node

• Normal pacemaker of the heart
• Self excitatory nature
• less negative Er
• leaky membrane to Na/CA
• only slow Ca/Na channels operational
• spontaneously depolarizes at fastest rate
• overdrive suppression
• contracts feebly

41
Overdrive Suppression

• If you drive a self-excitatory cell at a rate
  faster than its own inherent rate, you will
  suppress the cells own automaticity
• Mechanism may be due to increased activity of
  Na/K pump creating more negative Er
• Cells of the AV node and purkinje system are
  under overdrive suppression by the SA node

42
AV node

• Delays the wave of depolarization from entering
  the ventricle
• allows the atria to contract slightly ahead of
  the ventricles (.1 sec delay)
• Slow conduction velocity due to smaller diameter
  fibers
• In absence of SA node, AV node may act as
  pacemaker but at a slower rate

43
Effect of HR on systole/diastole

• As heart rate (HR) ? cycle length (CL) ?
• At a resting heart rate systole (S) lt diastole
  (D)
• Both the duration of systole and diastole
  shorten, but diastole shortens to a greater
  extent
• At high HR the ventricle may not fill adequately
• HR of 75 BPM CL .8 sec. S .3 D .5
• HR of 150 BPM CL .4 sec. S .2 D .2
• During systole perfusion of the myocardium is
  restricted by the contracting cardiac muscle
  compressing blood vessels (especially in LV)

44
Cardiac Cycle

• Systole
• isovolumic contraction
• ejection
• Diastole
• isovolumic relaxation
• rapid inflow- 70-75
• diastasis
• atrial systole- 25-30

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Onset of Ventricular Contraction

• Isovolumic contraction
• Tricuspid Mitral valves close
• as ventricular pressure rises above atrial
  pressure
• Pulmonic Aortic valves open
• as ventricular pressure rises above pulmonic
  aortic artery pressure

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Ejection of blood from ventricles

• Most of blood ejected in first 1/2 of phase
• ventricular pressure peaks and starts to fall off
• ejection is terminated by closure of the
  semilunar valves (pulmonic aortic)

47
Ventricular Relaxation

• Isovolumetric (isometric) relaxation-As the
  ventricular wall relaxes, ventricular pressure
  (P) falls the aortic and pulmonic valves close
  as the ventricular P falls below aortic and
  pulmonic artery P
• Rapid inflow-When ventricular P falls below
  atrial pressure, the mitral and tricuspid valves
  will open and ventricles fill

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Ventricular Relaxation (cont)

• Diastasis-inflow to ventricles is reduced.
• Atrial systole-atrial contraction actively pumps
  about 25-30 of the inflow volume and marks the
  last phase of ventricular relaxation (diastole)

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Ventricular Volumes

• End Diastolic Volume-(EDV)
• volume in ventricles at the end of filling
• End Systolic Volume- (ESV)
• volume in ventricles at the end of ejection
• Stroke volume (EDV-ESV)
• volume ejected by ventricles
• Ejection fraction
• of EDV ejected (SV/EDV X 100)
• normal 50-60

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Terms

• Preload-stretch on the wall prior to contraction
  (proportional to the EDV)
• Afterload-the changing resistance (impedance)
  that the heart has to pump against as blood is
  ejected. i.e. Changing aortic BP during
  ejection of blood from the left ventricle

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Atrial Pressure Waves

• A wave
• associated with atrial contraction
• C wave
• associated with ventricular contraction
• bulging of AV valves and tugging on atrial muscle
• V wave
• associated with atrial filling

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Function of Valves

• Open with a forward pressure gradient
• e.g. when LV pressure gt the aortic pressure the
  aortic valve is open
• Close with a backward pressure gradient
• e.g. when aortic pressure gt LV pressure the
  aortic valve is closed

54
Heart Valves

• AV valves
• Mitral Tricupid
• Thin filmy
• Chorda tendineae act as check lines to prevent
  prolapse
• papillary muscles-increase tension on chorda t.
• Semilunar valves
• Aortic Pulmonic
• stronger construction

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Valvular dysfunction

• Valve not opening fully
• stenotic
• Valve not closing fully
• insufficient/regurgitant/leaky
• Creates vibrational noise
• aka murmurs

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Heart Murmur Considerations

• Timing
• Systolic
• aortic pulmonary stenosis
• mitral tricuspid insufficiency
• Diastolic
• aortic pulmonary insufficiency
• mitral tricuspid stenosis
• Both
• patent ductus arteriosis
• combined valvular defect

57
Law of Laplace

• Wall tension (pressure)(radius)/2
• At a given operating pressure as ventricular
  radius ? , developed wall tension ?.
• ? tension ? ? force of ventricular contraction
• two ventricles operating at the same pressure but
  with different chamber radii
• the larger chamber will have to generate more
  wall tension, consuming more energy oxygen
• Batista resection
• How does this law explain how capillaries can
  withstand high intravascular pressure?

58
Terminology

• Chronotropic ( increases) (- decreases)
• Anything that affects heart rate
• Dromotropic
• Anything that affects conduction velocity
• Inotropic
• Anything that affects strength of contraction
• eg. Caffeine would be a chronotropic agent
  (increases heart rate)

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Control of Heart Pumping

• Intrinsic properties of cardiac muscle cells
• Frank-Starling Law of the Heart
• Within physiologic limits the heart will pump all
  the blood that returns to it without allowing
  excessive damming of blood in veins
• heterometric homeometric autoregulation
• direct stretch on the SA node

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Mechanism of Frank-Starling

• Increased venous return causes increased stretch
  of cardiac muscle fibers. (Intrinsic effects)
• increased cross-bridge formation
• increased calcium influx
• both increases force of contraction
• increased stretch on SA node
• increases heart rate

61
Heterometric autoregulation

• Within limits as cardiac fibers are stretched the
  force of contraction is increased
• more cross bridge formation as actin overlap is
  removed
• more Ca influx into cell associated with the
  increased stretch

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Homeometric autoregulation

• Ability to increase strength of contraction
  independent of a length change
• Flow induced
• increased stroke volume maintained as EDV
  decreases
• Pressure induced
• increase in aortic BP (afterload) will force of
  contraction
• Rate induced
• increased heart rate will force treppe

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Direct Stretch on SA node

• Stretch on the SA node will increase Ca and/or
  Na permeability which will increase heart rate

64
Extrinsic Influences

• Autonomic nervous system
• Hormonal influences
• Ionic influences
• Temperature influences

65
Control of Heart by ANS

• Sympathetic innervation-
• heart rate
• strength of contraction
• conduction velocity
• Parasympathetic innervation
• - heart rate
• - strength of contraction
• - conduction velocity

66
Interaction of ANS

• SNS effects on the heart blocked using
  propranolol (beta blocker) which blocks beta
  receptors
• Para effects blocked using atropine which blocks
  muscarinic receptors
• HR will increase
• Strength of contraction decreases
• What can be concluded?

67
Interaction of ANS

• From the previous results it can be concluded
  that under resting conditions
• Parasympathetic NS exerts a dominate inhibitory
  influence on heart rate
• Sympathetic NS exerts a dominate stimulatory
  influence on strength of contraction

68
Interaction of the SNS PSNS
Cardiac cell

• SNS
• PARA

?
NE
?
-
ACh
Gs
?
Ad. Cycl.
cAMP
Gi
?
NPY NE
-
ACh
M
69
Direct vs. Indirect SNS influence

• Direct innervation of Cardiac cells accounts for
  most of the SNS effect.
• Norepinephrine acting on ?-1 receptors. (85)
• Indirect effects would be due to circulating
  catacholamines (epinephrine norepinephrine)
  released primarily from the adrenal medulla
  (blood borne) which would find their way to the
  cardiac ?-1 receptors. (15)

70
Cardioacclerator reflex

• Stretch on right atrial wall stretch receptors
  which in turn send signals to medulla oblongata
  SNS outflow to heart
• AKA Bainbridge reflex
• Helps prevents damning of blood in the heart
  central veins

71
Neurocardiogenic syncope

• Benzold-Jarisch reflex (Baroreceptors in
  ventricles)
• Stimulation of sensory endings mainly in the
  ventricles (some in the atria) that reflex via
  the X CN to the CNS
• Inferoposterior wall of LV which is supplied by
  the circumflex artery is site of majority of
  receptors
• Reflex effects results in hypotension
  bradycardia
• Reflex stimulated by
• Occlusion of circumflex artery (inferior wall
  infarct)
• ? in LVP LV volume (eg. Aortic stenosis)

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Major Hormonal Influences

• Thyroid hormones
• inotropic
• chronotropic
• also causes an increase in CO by ? BMR

73
Ionic influences

• Effect of elevated KECF
• dilation and flaccidity of cardiac muscle at
  concentrations 2-3 X normal (8-12 meq/l)
• decreases resting membrane potential
• Effect of elevated Ca ECF
• spastic contraction

74
Effect of body temperature

• Elevated body temperature
• HR increases about 10 beats for every degree F
  elevation in body temperature
• Contractile strength will increase temporarily
  but prolonged fever can decrease contractile
  strength due to exhaustion of metabolic systems
• Decreased body temperature
• decreased HR and strength

75
Energy substrate for cardiac cells

• Heart is versatile can use many different
  energy substrates
• Fatty acids-70 preferred
• Glucose
• Glycerol
• Lactate
• Pyruvate
• Amino acids

76
Relationship of energy to work

• 75 of energy the heart utilizes is converted to
  heat
• The remaining 25 is utilized as work which is
  broken down into
• Pressurization of blood (gt99)
• Acceleration of blood (lt1)

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Work output of the heart

• Pressurization of the blood (potential energy)
• Moving blood from low pressure to high pressure
  (volume pressure work or external work)
• The majority of the work (gt99)
• Acceleration of blood to its ejection velocity
  (kinetic energy)
• Out the aortic pulmonic valves normally
  accounts for less than 1 of the work component
• Can increase to 50 with valvular stenosis

78
EKG

• Measures potential difference across the surface
  of the myocardium with respect to time
• lead-pair of electrodes
• axis of lead-line connecting leads
• transition line-line perpendicular to axis of lead

79
Rate

• Paper speed- 25 mm/sec 1 mm .04 sec.
• Normal rate ranges usually between 60-80 bps
• Greater than 100 tachycardia
• Less than 50 bradycardia

80
Intervals

• PR interval (includes AV nodal delay)
• should be about .16 sec
• greater than .20 sec. 1st degree AV block
• less than .10 sec. inadequate delay-possible
  accessory conduction pathway from atria to
  ventricle

81
Electrocardiography

• P wave-atrial depolarization
• QRS complex-ventricular depolarization
• T wave-ventricular repolarization
• Atrial repolarization is buried in the QRS complex

82
Leads

• A pair of recording electrodes
• electrode is active
• - electrode is reference
• The direction of the deflection ( or -) is based
  on what the active electrode sees relative to the
  reference electrode
• Routine EKG consists of 12 leads
• 6 frontal plane leads
• 6 chest leads (horizontal)

83
Type of Deflection
84
Frontal Plane Leads

• Bipolar limb leads
• Lead I ( LA -RA)
• Lead II ( LL - RA)
• Lead III ( LL - LA)
• Unipolar limb leads (Augmented )
• AvR (RA -LA LL)
• AvL (LA -RA LL)
• AvF (LL -RA LA)

85
Chest Leads (V leads)

• The positive electrodes are on the chest wall
• VI-4th intercostal space- right sternal border
• V2-4th intercostal space-left sternal border
• V3-equidistant between V2 V4
• V4-5th intercostal space-mid clavicular line
• V6 left mid axillary line
• The negative (reference) electrode is all limb
  electrodes hooked together

86
Analysis of EKG

• Rate
• Rhythm Intervals
• Axis
• Hypertrophy
• Infarction

87
Rate

• Tachycardia
• heart rate greater than 105 B/min
• Bradycardia
• heart rate less then 60 B/min
• 300-150-100-75-60-50

88
Rhythm Intervals

• PR interval
• time from SA node to entering the ventricle
• includes the AV nodal delay
• 1st degree AV block
• PR interval greater than .2 sec.
• Prolonged QT interval
• increased incidence of sudden cardiac death
• Sinus arrhythmia
• longest shortest RR vary by gt .16 sec
• heart rate variability

89
AV Block

• 1st degree AV block
• Depolarization wave from atria to ventricle is
  delayed excessively
• PR interval gt .2 sec
• 2nd degree AV block
• Some depolarization waves pass, others blocked
• dropped beat-P wave with no associated QRS
  complex
• 3rd degree AV block
• All depolarization waves from atria to ventricles
  are blocked
• No relationship between P waves and QRS complexes

90
Rhythm Intervals (cont.)

• QRS complex
• duration .06-.08 sec.
• Prolonged gt .12 sec.
• Associated with ventricular hypertrophy or
  conduction block in purkinje system

91
Axis

• Mean electrical axis (MEA)
• average direction of ventricular depolarization
• the ventricle depolarizes from base to apex
  from endocardium to epicardium (A.D.I.O.)
• vector analysis using 2 frontal plane leads
• if QRS of lead I AvF is positive MEA is normal.
• normal axis between -30 105 degrees
• axis deviation
• conduction block hypertrophy shift axis to the
  side of the problem. i.e. Left bundle branch
  block creating a left axis deviation

92
Hypertrophy

• Hypertrophy of one ventricle relative to the
  other can be associated with anything that
  creates an abnormally high work load on that
  chamber.
• e.g. Systemic hypertension increasing work load
  on the left ventricle
• prolonged QRS complex (gt .12 sec)
• axis deviation to the side of problem
• increased voltage of QRS in V leads

93
Blood flow to myocardium

• The myocardium is supplied by the coronary
  arteries their branches.
• Cells near the endocardium may be able to receive
  some O2 from chamber blood
• The heart muscle at a resting heart rate takes
  the maximum oxygen out of the perfusing coronary
  flow (70 extraction)
• Any ? demand must be met by ? coronary flow

94
Ischemia

• Normally the first cells to depolarize are the
  last to repolarize.
• Depolarization repolarization waves are in
  opposite directions
• QRS and T wave point in the same direction
• Ischemia prolongs depolarization therefore
  delays repolarization
• Depolarization repolarization waves are now in
  the same direction
• This will cause an inversion in T wave (opposite
  deflection compared to QRS)

95
Infarction

• Damaged cells lose ability to repolarize
• Most of the frank damage occurs upon reperfusion
  is associated with free radical damage.
• Damaged area is in an abnormal state of
  depolarization
• When normal myocardium is in a resting polarized
  state, there is a current of injury between
  damaged normal myocardium
• creates a depressed baseline which appears as an
  elevated ST segment