Disorders of Cardiac Function

1
Disorders of Cardiac Function
2
Introduction
3
The Heart as Two Pumps
4
The Heart as Two Pumps

• The heart is really two pumps in tandem
• The right heart sends blood to the lungs
• The left heart gets blood back from the lungs and
  sends the blood to the systemic circulation
• This is a bigger job because the systemic
  circulation is larger and has more gravity

5
(No Transcript)
6
Global Tissue Oxygenation
7
Global Tissue OxygenationMade Ridiculously Simple
100
Venous Oxygen Delivery
SvO2 75
25
Arterial Oxygen Delivery
Oxygen Consumption
8
Global Tissue OxygenationSimple Description
9
Global Tissue OxygenationSimple Description

• Each Hb molecule can carry four oxygen
  molecules
• The hemoglobin in the blood picks up oxygen in
  the lungs
• The hemoglobin sends the oxygen in the blood
  through the arteries to the tissues
• The tissues do not extract 100 of the oxygen
  from the hemoglobin
• 25 of oxygen is in the tissues, 75 in the veins
• The Hb then goes back to the loading station

10
Global Tissue OxygenationDetailed Description
11
Global Tissue OxygenationDetailed Description

• The lungs load each hemoglobin with 4 oxygen
  molecules.
• Oxygen content is 20 of total volume.
• At the tissue level, Oxygen extraction is a ratio
  of oxygen consumed (VO2 250 mL/min) to the
  amount delivered (DO2) 25
• Thus 75 of oxygen delivered is returned to the
  venous side, i.e. normal SvO2 75.
• Oxygen consumption (VO2) is a function of cardiac
  output and the difference between arterial (Hb x
  SaO2 x 13.4) and venous oxygen content (Hb x SvO2
  x 13.4).
• Given the same CO and Hb, VO2 is analogous to the
  difference between arterial and venous
  oxygenation.
• For example, 1 Hb will deliver 4 oxygen molecules
  to the tissue -gt 1 oxygen molecule is consumed
  (VO2) by the tissue 3 oxygen molecules are
  returned to the venous outflow.

12
Coronary CirculationDescription
13
Coronary CirculationDescription

• The arteries and veins in the heart perfuse the
  heart with oxygen
• The coronary arteries come off of the aorta at
  the place of the aortic valve
• Left and right coronary arteries
• Left almost immediately branches into the
  circumflex and the left anterior descending
  artery
• Nurses the left side of the heart
• Right
• Both nourish the septum
• Blood then goes into the capillaries and then the
  veins of the heart
• Large vein that delivers the blood back to the
  heart is the coronary sinus

14
Coronary Circulation
15
Cardiac Conduction System
16
Cardiac Conduction System

• Conduction system stimulates the myocardium to
  contract and pump blood
• Conduction system usually controls the rhythm of
  the heart (unless the person has a pacemaker)
• Heart has two conduction systems
• One controls atrial activity
• One that controls ventricular activity

17
Anatomy of the Conduction System
18
Anatomy of the Conduction System
SA Node AV Node Bundle of His Bundle
branches Purkinje fibers
Porth, 2007, Essentials of Pathophysiology, 2nd
ed., Lippincott, p. 331.
19
SA Node
20
SA Node

• Pacemaker of the heart
• Impulses originate here
• Located in posterior wall RA
• Fires at 60 -100 bpm
• Responsible for the heart rate in the normal
  person
• Impulse causes atrial contraction

21
AV Node
22
AV Node

• Connects the atria and ventricles, provides one
  way conduction
• Would beat independently
• Fires at 40 -60 bpm
• Can assume pacemaker function if SA fails to
  discharge
• There is a pause here
• The speed of conduction in the AV node is
  influenced by the SNS (beta-1)

23
Purkinjie Fibers
24
Purkinjie Fibers

• Supplies the ventricles
• Supplies the impulse to the cardiac muscle
• Large fibers, rapid conduction for swift and
  efficient ejection of blood from heart
• Large fibers fast conduction
• Small fibers slow conduction
• Fire 15-40 bpm
• Only occurs if there is no input from the other
  areas
• Assume pacemaker of ventricles if AV fails
• HR reflects intrinsic firing of these structures

25
Action Potentials (AP)
26
Action Potentials (AP)

• Stimulus
• The only intrinsic conduction in the heart is in
  the SA node
• Any other conduction comes from depolarization of
  the muscle
• ? excitable tissues (muscle and conduction
  system)
• ? evokes an AP characterized by a sudden change
  in voltage resulting from transient
  depolarization and then repolarization.
• APs are electrical currents involving the
  movement/flow of electrically charged ions at
  level of cell membrane.
• APs are conducted throughout the heart,
  responsible for initiating each cardiac
  contraction.

27
(No Transcript)
28
Types of Action Potentials
29
SLOW SA AV Nodes FAST Purkinje Fiber
Muscle
30
Types of Membrane Ion Channels that Contribute to
Voltage Changes during the AP
31
Types of Membrane Ion Channels that Contribute to
Voltage Changes during the AP

• Fast Na channels
• Rapid depolarization of muscles
• Important in cardiac APs and Purkinje fibers
• Slow Na channels
• Pacemaker activity (SA, AV)
• Potassium channels
• Speedy repolarization

32
Three Phases of Action Potentials
33
Three Phases of Action Potentials

• Resting
• Depolarization
• Repolarization

34
Resting Phase
35
Resting Phase

• Membrane is relatively permeable to K, but much
  less so to Na
• Inside is negative, outside is positive

36
Cardiac Muscle Cell Firing

• Cells begin with a negative charge resting
  membrane potential
• Calcium leak lets Ca2 diffuse in, making the
  cell more positive

Threshold potential
Resting membrane potential
Calcium leak
37
Depolarization Phase
38
Depolarization Phase

• Cell membrane becomes permeable to Na
• Na enters cell, inside the cell is more

39
Cardiac Muscle Cell Firing (cont.)

• At threshold potential, more Na channels open
• Na rushes in, making the cell very positive
  depolarization
• Action potential the cell responds (e.g. by
  contracting)

Action potential
Threshold potential
Resting membrane potential
Calcium leak
40
Plateau Phase
41
Cardiac Muscle Cell Firing (cont.)

• K channels open
• K diffuses out, making the cell negative again
  (starting to repolarize), but Ca2 channels are
  still allowing Ca2 to enter
• The cell remains positive plateau

Action potential
PLATEAU
Threshold potential
Calcium leak
42
Repolarization Phase
43
Repolarization Phase

• Outward flow of positive charges, mainly K
• Inside the cell is more negative
• Assisted by Na-K pump
• Relatively slow method of repolarization
• Potassium ions made a bigger, faster difference

44
Cardiac Muscle Cell Firing (cont.)

• During plateau, the muscle contracts strongly
• Then the Ca2 channels shut and it repolarizes
• The potassium channels opened a while ago so the
  potassium comes out, leading to repolarization

Action potential
PLATEAU
Threshold potential
Calcium leak
45
Cardiac Action Potentials
46
Cardiac Action Potentials

• Unlike nerve cells, cardiac cells have five
  phases in their action potential
• Phase 4 the resting membrane potential.
• Phase 0 there is rapid depolarization
• The QRS complex corresponds to this section
• Phase 1 there is a short repolarization (only
  observed in ventricular muscle)
• Occurs right in the end of depolarization
• Only observed in ventricular muscle
• Phase 2 the membrane potential remains
  depolarized in a plateau
• When calcium is entering the cell, so further
  repolarization is prevented (because cell is more
  positive)
• Phase 3 the membrane potential becomes
  repolarized.
• The T wave corresponds to the repolarization

47
Cardiac Muscle Action Potential 5 Phases
Unlike nerve cells, cardiac cells have 5 phases
in their action potential.
Phase 0 Upstroke, rapid depolarization Phase 1
Early, short repolarization Seen only in
ventricular muscle Phase 2 Plateau phase
membrane potential remains depolarized Phase 3
Final rapid repolarization Phase 4 Resting,
diastolic repolarization
48
Cardiac Muscle Cell Contraction
49
Cardiac Muscle Cell Contraction

• During Phase 2, the plateau, calcium ion enters
  the muscle cell, causing it to contract strongly.
• The strength of contraction is directly
  proportional to the number of calcium ions that
  enter the cell.
• Calcium channel opening is controlled by voltage
  (the calcium channels only open when the membrane
  is at a certain voltage) and by beta1 receptors
  in the ventricular myocardium.

50
Importance of Actions Potentials
51

• Why are action potentials important?
• Source of
• dysrhythmias
• Targets of
• drug action

Myocardium His-Purkinje System
SA Node AV Node
Lehne 5th ed Figure 47-2
52
Cardiac Conduction andRhythm Disorders
53
ECGRelationship to Action Potential
54
ECGRelationship to Action Potential

• Electrical events recorded on ECG
• Electrical events precede mechanical events know
  what they represent!
• P
• Represents the depolarization of the atria
• Then there is a delay from the AV node
• QRS
• Depolarization of the ventricle
• T
• Repolarization of the ventricle
• U wave
• Repolarization of the atria (at times may be
  masked by the QRS complex)

55
(No Transcript)
56
Electrical and Mechanical EventsDiagram
57
Electrical event precedes mechanical event !!!
Lehne 5th ed Figure 47-3
58
Location of Electrical Events in the Heart
59
P wave Atria PR Interval AV node QRS
complex ventricles T wave Repolarization of
the ventricles
Porth 2007, Figure 16-12
60
Disorders of Cardiac Rhythm and Conduction
61
Disorders of Cardiac Rhythm and Conduction

• Dysrhythmias (or arrhythmias)
• Term used to describe disorders of cardiac rhythm
• Occur in healthy and non-healthy people
• Interfere with hearts pumping ability
• Disorders of impulse conduction
• Impulses that originated in the SA node do not
  get through or the SA node does not work well

62
Causes of Dysrhythmias
63
Causes of Dysrhythmias

• Congenital defects in conduction system
• Degenerative changes
• As we get old, things do not work as well as it
  used to
• Ischemia and MI
• May lead to degenerative changes
• May be due to narrowing of the coronary arteries
  or a clot
• Fluid/electrolyte imbalances
• If the ions are not present in the proper
  concentration, it influences how they can rush
  into and out of the cell
• Drugs

64
Sinus Node Rhythms
65
Sinus Node Rhythms

• Normal Sinus Rhythm
• Sinus Bradycardia
• Sinus Tachycardia

66
Normal Sinus Rhythm
67
Normal Sinus Rhythm

• P wave precedes each QRS
• RR intervals (between each QRS complex) are
  regular
• Rate 60-100
• May vary slightly with breathing due to changing
  pressures within the heart chambers

68
Sinus Bradycardia
69
Sinus Bradycardia

• P before QRS
• RR regular
• Rate lt 60
• Slowing of conduction through AV node seen as a
  lengthened PR interval (Vagal, PNS)

70
Sinus Tachycardia
71
Sinus Tachycardia

• P before QRS
• RR regular
• Rate gt 100
• Enhanced automaticity r/t SNS activation (fever,
  exercise, stress)

72
Class II Antidysrhythmics
73
Class II Antidysrhythmic
Myocardium His-Purkinje System
SA Node and AV Node
Lehne 5th ed Figure 47-2
74
Class II Antidysrhythmic Beta Blockers
75
Class II Antidysrhythmic Beta Blockers

• Depress Phase 4 in depolarization
• Slow the heart rate
• Prolong PR interval and lead to bradycardia
  (because of chronotropic effects)
• Nonselective Carvedilol, Propranolol
• Block beta 1 and beta 2 receptors
• Blockage of beta-2 receptors may worsen asthma by
  blocking the bronchodilation of the receptors
• Cardioselective Metolprolol, Esmolol
• Block beta 1 only

76
Class II Antidysrhythmic Mechanism of Action
77
Class II Antidysrhythmic Mechanism of Action

• (-) Inotrope
• Refer to contractility of the heart
• Beta-1 receptors are in the ventricles and
  activation leads to contractility
• (-) Chronotrope SLOW the heart rate!
• Heart rate
• SA node
• (-) Dromotrope
• The speed of conduction, particularly in the AV
  node
• Beta-1 receptor stimulation speeds up the
  conduction of the AV node

78
Class II Antidysrhythmic Therapeutic Uses
79
Class II Antidysrhythmic Therapeutic Uses

• PSVT
• Paraxoysomal supra-ventricular tachycardia
• Comes and goes
• Above the ventricule (originates in the SA node
  or the AV node)
• Fast heart rate
• Common in young people
• Every once in a while, their heart starts racing
• May or may not be bothersome or disabling
• Beta-blockers prevent the rapid heart rate by
  slowing conduction in the AV node
• Angina
• The heart does not get enough oxygen
• The treatment is to decrease the oxygen demand of
  the heart
• The beta-blockers do this by slowing heart rate
  and reducing contractility
• AMI
• Beta-blockers prevent second MIs
• Hypertension (HTN) (not esmolol)
• Heart Failure (HF) (carvedilol, metoprolol)

See Lehne Table 18-2 and 18-3
80
Beta BlockersAdverse Effects
81
Beta BlockersAdverse Effects

• Hypotension
• May lead to fainting
• Syncope
• Precipitate heart failure
• This is because of their inotropic, chronotropic,
  and dromotropic factors
• Bradycardia
• AV block due to too much of a decrease in the AV
  node
• The ventricles (Purkinje fibers) take over at
  their slow speed
• The person may faint because the slow speed is
  not enough to get oxygen to the body
• Sinus arrest
• Problems in the SA node?
• Bronchospasm (non-selective beta blockers)
• Rebound cardiac excitation (if abruptly stopped)
• Need to taper the dose of the beta-blockers

82
Beta Blocker Administration
83
Beta Blocker Administration
Drug Route ½ Life (hrs) Indication
Esmolol IV ONLY! 0.15 Dysrh, angina
Metoprolol IV, PO 3-7 Dysrh, angina, AMI, HF, HTN
Atenolol IV, PO 6-9 Dysrh, angina, AMI

Carvedilol PO 5-11 Angina, AMI, HF, HTN
Propanolol IV, PO 3-5 Dysrh, angina, AMI, HTN
84
Atrial Dysrhythmias
85
Atrial Dysrhythmias

• Atrial Fibrillation
• The impulse arises in the atrium, but not in the
  SA node
• Chaotic and disorganized impulse generation in
  the atria
• There is no organized contraction of the atria
• Atria are depolarizing without contracting (just
  quivering).
• Occasional ones will be conducted and cause AV
  contraction
• Ventricular rhythm irregular because not all of
  the contractions are conducted to the AV node
• Only irregularly irregular rhythm.
• There is no pattern to it
• No discernable P waves.
• Because there is no organized depolarization of
  the atria

86
A-Fib TreatmentDigoxin
87
A-Fib TreatmentDigoxin

• First want to use an anti-coagulant in order to
  prevent the formation of a blood clot
• A cardiac glycoside that is used for atrial
  fibrillation or atrial flutter.
• Slows conduction in the AV node and thereby slows
  ventricular rate.
• Allows fewer of the atrial fibrillations or
  impulses to get to the AV node and the ventricles
• Does not treat the dysrhythmia, just slows the
  heart rate

88
DigoxinMechanism of Action
89
DigoxinMechanism of Action

• Mechanism of Action
• Inhibits Na-K ATPase pump
• More intracellular calcium available inside the
  cell
• ? inotrope
• Increases the force of contraction
• Enhance vagal influence (SA and AV node effect)
• ? - chronotrope, - dromotrope
• Negative dromotrope helps control the response of
  chaotic impulses

90
DigoxinTherapeutic Uses
91
DigoxinTherapeutic Uses

• Heart failure
• Atrial flutter/fibrillation

92
DigoxinMechanism of ActionDiagram
93
Lehne 6th ed Figure 47-4
94
DigoxinPharmacokinetics
95
DigoxinPharmacokinetics
Absorption 60 80 (tabs) 70 85 (elixir) 90 100 (caps)
Metabolism Liver
Half Life 5-7 DAYS to eliminate T½ 1.5 days
96
DigoxinAdministration Considerations
97
DigoxinAdministration Considerations

• PO or IV (mcg NOT mg)
• Digitalization
• Can give an IV loading dose
• Digoxin levels (0.5 - 1.1 ng/ml)
• VERY narrow therapeutic range
• Digoxin immune FAB (antidote) for toxic levels (
  gt 2.0 ng/ml)
• The antibody binds up all of the digoxin in the
  bloodstream
• D/C drug until toxicity resolves
• Toxicity can be fatal

98
DigoxinAdverse Effects
99
DigoxinAdverse Effects

• Digoxin induced dysrhythmias
• All types!
• Bradycardia
• AV block most common
• Ventricular flutter/fibrillation is the most
  dangerous effect
• This is how most people die
• GI Anorexia, N/V
• CNS Drowsiness/weakness,
• Blurred vision/colored (yellow) halos

100
(No Transcript)
101
DigoxinContraindications
102
DigoxinContraindications

• 2nd/3rd degree heart block
• V. Fib/V. Tach
• Sick Sinus Syndrome
• When the sinus node quits working

103
Digoxin Precautions
104
Digoxin Precautions

• Acute MI
• Renal insufficiency
• Hypokalemia
• Severe pulmonary disease

105
DigoxinAdditional Considerations
106
DigoxinAdditional Considerations

• Potassium levels
• Keep in 3.5 5.0 mEq/L range
• Digoxin competes with K at binding sites
• If potassium is low, there may be more binding
  sites for toxicity
• Hyperkalemia ? decreases digoxin effect
• Diuretics may cause hypokalemia
• ? digoxin toxicity

107
DigoxinDrug?Drug Interactions
108
DigoxinDrug?Drug Interactions

• Reduce digoxin therapeutic effect
• ACE-I and ARBs
• Increase potassium
• Additive digoxin effect
• Sympathomimetics
• work in conjunction with digoxin to increase
  contractility and HR
• Increase risk of tachydysrhythmias
• Numerous interactions (Lehne Table 47-2)

109
Drug?Drug InteractionsIncrease Risk of Digoxin
Toxicity
110
Drug?Drug InteractionsIncrease Risk of Digoxin
Toxicity

• Calcium channel blockers (verapamil)
• Increase serum digoxin level
• Decrease HR
• Bradydysrhythmias or complete heart block
• Diuretics may reduce potassium levels
• Increase risk of dig-induced dysrhythmias
• Herbal interactions increase metabolism
• It is too complicated with metabolism to use
  herbal medications

111
DigoxinNursing Implications
112
DigoxinNursing Implications
Monitor ECG
Monitor potassium and digoxin levels
Apical pulse for 1 minute and document
113
A-Fib, PSVT TreatmentClass IV Antidysrhythmic
Calcium Channel Blockers
114
A-Fib, PSVT TreatmentClass IV Antidysrhythmic
Calcium Channel Blockers

• Verapamil, diltazem
• Nondihydropyridines
• Mechanism of Action
• Inhibits calcium influx during depolarization
• Depresses phase 4 of depolarization
• Prolongs phases 1 and 2 of depolarization

115
Class IV AntidysrhythmicsDiagram
116
Myocardium and His-Purkinje System
SA Node and AV Node
Lehne 5th ed Figure 47-2
117
Class IV Antidysrhythmic Effects on the Heart
118
Class IV Antidysrhythmic Effects on the Heart

• Three effects on the heart
• Slow SA node automaticity ? slow HR
• Delay AV node conduction ? prolong PR
• The pause is greater at the AV node
• The PR interval is what is going on in the AV
  node
• ? myocardial contractility ? ? CO
• Note same effects as Beta Blockers!!!!!
• Need to be mindful of the effects because they
  may be increased
• Blood pressures decrease when on calcium channel
  blockers

119
Class IV Antidysrhythmic Therapeutic Uses
120
Class IV Antidysrhythmic Therapeutic Uses

• PSVT
• Atrial Fib/Flutter (slow ventricular rate)
• Angina
• Angina is caused by ischemia, which is caused by
  lack of bloodflow to the heart (which means lack
  of oxygen)
• Calcium channel blocker is used to treat angina
  because it slows heart rate and decreases
  contractility, so the myocardium will not use as
  much oxygen
• It is also helpful because it makes diastole
  longer, so there is more time to have oxygen
  perfusion
• Hypertension
• Note not effective for ventricular dysrhythmias
  !!
• Only affects the SA and AV nodes

121
Verapamil and DiltiazemAdverse Cardiac Effects
122
Verapamil and DiltiazemAdverse Cardiac Effects

• Bradycardia
• AV block
• Decreased myocardial contractility ? decreased
  cardiac output

123
Verapamil and DiltiazemAdverse General Effects
124
Verapamil and DiltiazemAdverse General Effects

• Dizziness due to increased vasodilation and less
  perfusion to the brain
• Facial Flushing
• Headache
• Peripheral edema
• Decreased GI motility

125
Disorders of Atrioventricular Conduction
126
Disorders of Atrioventricular Conduction

• First degree AV block
• Second degree AV block
• Third degree AV block (complete AV block)

127
First Degree AV Block
128
First Degree AV Block

• Slightly prolonged PR interval
• ALL atrial impulses are conducted to ventricles
• Asymptomatic.
• Everything is in the right order

129
Second Degree AV Block
130
Second Degree AV Block

• Not all atrial impulses are conducted to
  ventricles
• See some P waves not followed by QRS.
• Can be very symptomatic.

131
Third Degree (Complete) AV Block
132
Third Degree (Complete) AV Block

• Conduction link between atria and ventricles lost
• Each controlled by independent pacemakers
• Atria continue at their rate, ventricles contract
  at their rate (30-40 bpm)
• The P wave and the QRS wave occur at regular
  intervals but they do not coincide

133
Case Study Digoxin Toxicity
134
Case Study Digoxin ToxicitySerum dig level
1.7 ng.ml (0.5-1.1 desired)
3rd degree AV Block
Temporary pacemaker inserted, SR ? 100 paced
135
Complete A-V block with 100 atrio-ventricular
pacing
Atrial Pacing spike
Ventricular Pacing spike
QRS
P
136
Ventricular Dysrhythmias More Serious!
137
Ventricular Dysrhythmias More Serious!

• PVC premature ventricular contraction
• V-fib ventricular fibrillation
• V-tach ventricular tachycardia