Title: Disorders of Cardiac Function
1Disorders of Cardiac Function
2Introduction
3The Heart as Two Pumps
4The 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
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6Global Tissue Oxygenation
7Global Tissue OxygenationMade Ridiculously Simple
100
Venous Oxygen Delivery
SvO2 75
25
Arterial Oxygen Delivery
Oxygen Consumption
8Global Tissue OxygenationSimple Description
9Global 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
10Global Tissue OxygenationDetailed Description
11Global 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.
12Coronary CirculationDescription
13Coronary 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
14Coronary Circulation
15Cardiac Conduction System
16Cardiac 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
17Anatomy of the Conduction System
18Anatomy 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.
19SA Node
20SA 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
21AV Node
22AV 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)
23Purkinjie Fibers
24Purkinjie 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
25Action Potentials (AP)
26Action 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.
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28Types of Action Potentials
29SLOW SA AV Nodes FAST Purkinje Fiber
Muscle
30Types of Membrane Ion Channels that Contribute to
Voltage Changes during the AP
31Types 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
32Three Phases of Action Potentials
33Three Phases of Action Potentials
- Resting
- Depolarization
- Repolarization
34Resting Phase
35Resting Phase
- Membrane is relatively permeable to K, but much
less so to Na - Inside is negative, outside is positive
36Cardiac 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
37Depolarization Phase
38Depolarization Phase
- Cell membrane becomes permeable to Na
- Na enters cell, inside the cell is more
39Cardiac 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
40Plateau Phase
41Cardiac 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
42Repolarization Phase
43Repolarization 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
44Cardiac 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
45Cardiac Action Potentials
46Cardiac 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
47Cardiac 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
48Cardiac Muscle Cell Contraction
49Cardiac 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.
50Importance 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
52Cardiac Conduction andRhythm Disorders
53ECGRelationship to Action Potential
54ECGRelationship 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)
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56Electrical and Mechanical EventsDiagram
57Electrical event precedes mechanical event !!!
Lehne 5th ed Figure 47-3
58Location of Electrical Events in the Heart
59P wave Atria PR Interval AV node QRS
complex ventricles T wave Repolarization of
the ventricles
Porth 2007, Figure 16-12
60Disorders of Cardiac Rhythm and Conduction
61Disorders 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
62Causes of Dysrhythmias
63Causes 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
64Sinus Node Rhythms
65Sinus Node Rhythms
- Normal Sinus Rhythm
- Sinus Bradycardia
- Sinus Tachycardia
-
66Normal Sinus Rhythm
67Normal 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
68Sinus Bradycardia
69Sinus Bradycardia
- P before QRS
- RR regular
- Rate lt 60
- Slowing of conduction through AV node seen as a
lengthened PR interval (Vagal, PNS)
70Sinus Tachycardia
71Sinus Tachycardia
- P before QRS
- RR regular
- Rate gt 100
- Enhanced automaticity r/t SNS activation (fever,
exercise, stress)
72Class II Antidysrhythmics
73Class II Antidysrhythmic
Myocardium His-Purkinje System
SA Node and AV Node
Lehne 5th ed Figure 47-2
74Class II Antidysrhythmic Beta Blockers
75Class 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
76Class II Antidysrhythmic Mechanism of Action
77Class 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
78Class II Antidysrhythmic Therapeutic Uses
79Class 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
80Beta BlockersAdverse Effects
81Beta 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
82Beta Blocker Administration
83Beta 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
84Atrial Dysrhythmias
85Atrial 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
86A-Fib TreatmentDigoxin
87A-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
88DigoxinMechanism of Action
89DigoxinMechanism 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
90DigoxinTherapeutic Uses
91DigoxinTherapeutic Uses
- Heart failure
- Atrial flutter/fibrillation
92DigoxinMechanism of ActionDiagram
93Lehne 6th ed Figure 47-4
94DigoxinPharmacokinetics
95DigoxinPharmacokinetics
Absorption 60 80 (tabs) 70 85 (elixir) 90 100 (caps)
Metabolism Liver
Half Life 5-7 DAYS to eliminate T½ 1.5 days
96DigoxinAdministration Considerations
97DigoxinAdministration 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
98DigoxinAdverse Effects
99DigoxinAdverse 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
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101DigoxinContraindications
102DigoxinContraindications
- 2nd/3rd degree heart block
- V. Fib/V. Tach
- Sick Sinus Syndrome
- When the sinus node quits working
103Digoxin Precautions
104Digoxin Precautions
- Acute MI
- Renal insufficiency
- Hypokalemia
- Severe pulmonary disease
105DigoxinAdditional Considerations
106DigoxinAdditional 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
107DigoxinDrug?Drug Interactions
108DigoxinDrug?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)
109Drug?Drug InteractionsIncrease Risk of Digoxin
Toxicity
110Drug?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
111DigoxinNursing Implications
112DigoxinNursing Implications
Monitor ECG
Monitor potassium and digoxin levels
Apical pulse for 1 minute and document
113A-Fib, PSVT TreatmentClass IV Antidysrhythmic
Calcium Channel Blockers
114A-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
115Class IV AntidysrhythmicsDiagram
116Myocardium and His-Purkinje System
SA Node and AV Node
Lehne 5th ed Figure 47-2
117Class IV Antidysrhythmic Effects on the Heart
118Class 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
119Class IV Antidysrhythmic Therapeutic Uses
120Class 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
121Verapamil and DiltiazemAdverse Cardiac Effects
122Verapamil and DiltiazemAdverse Cardiac Effects
- Bradycardia
- AV block
- Decreased myocardial contractility ? decreased
cardiac output
123Verapamil and DiltiazemAdverse General Effects
124Verapamil and DiltiazemAdverse General Effects
- Dizziness due to increased vasodilation and less
perfusion to the brain - Facial Flushing
- Headache
- Peripheral edema
- Decreased GI motility
125Disorders of Atrioventricular Conduction
126Disorders of Atrioventricular Conduction
- First degree AV block
- Second degree AV block
- Third degree AV block (complete AV block)
127First Degree AV Block
128First Degree AV Block
- Slightly prolonged PR interval
- ALL atrial impulses are conducted to ventricles
- Asymptomatic.
- Everything is in the right order
129Second Degree AV Block
130Second Degree AV Block
- Not all atrial impulses are conducted to
ventricles - See some P waves not followed by QRS.
- Can be very symptomatic.
131Third Degree (Complete) AV Block
132Third 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
133Case Study Digoxin Toxicity
134Case Study Digoxin ToxicitySerum dig level
1.7 ng.ml (0.5-1.1 desired)
3rd degree AV Block
Temporary pacemaker inserted, SR ? 100 paced
135Complete A-V block with 100 atrio-ventricular
pacing
Atrial Pacing spike
Ventricular Pacing spike
QRS
P
136Ventricular Dysrhythmias More Serious!
137Ventricular Dysrhythmias More Serious!
- PVC premature ventricular contraction
- V-fib ventricular fibrillation
- V-tach ventricular tachycardia