Disorders of Cardiac Function

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Introduction

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The Heart as Two Pumps

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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

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Global Tissue Oxygenation

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Global Tissue OxygenationMade Ridiculously Simple

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SvO2 = 75%

25%

Venous Oxygen Delivery

ArterialOxygenDelivery

Oxygen Consumption

100%

Global Tissue OxygenationSimple Description

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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

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Global Tissue OxygenationDetailed Description

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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 -> 1

oxygen molecule is consumed (VO2) by the tissue + 3 oxygen molecules are returned to the venous outflow.

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Coronary CirculationDescription

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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

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Coronary Coronary CirculationCirculation

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Cardiac Conduction System

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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

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Anatomy of the Conduction System

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Anatomy of the Conduction System

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SA NodeSA Node

AV NodeAV Node

Bundle of HisBundle of His

Bundle branchesBundle branches

Purkinje fibersPurkinje fibers

Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 331.

SA Node

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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

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AV Node

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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)

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Purkinjie Fibers

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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

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Action Potentials (AP)

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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.

• AP’s are electrical currents involving the movement/flow of electrically charged ions at level of cell membrane.

• AP’s are conducted throughout the heart, responsible for initiating each cardiac contraction.

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Types of Action Potentials

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SLOW SA & AV Nodes

FAST

Purkinje Fiber & Muscle

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Types of Membrane Ion Channels that Contribute to

Voltage Changes during the AP

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Types of Membrane Ion Channels that Contribute to Voltage Changes

during the AP

1. Fast Na+ channels• Rapid depolarization of muscles• Important in cardiac APs and Purkinje

fibers2. Slow Na+ channels

• Pacemaker activity (SA, AV)3. Potassium channels

• Speedy repolarization31

Three Phases of Action Potentials

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Three Phases of Action Potentials

• Resting

• Depolarization

• Repolarization

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Resting Phase

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Resting Phase

• Membrane is relatively permeable to K+, but much less so to Na+

• Inside is negative, outside is positive

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Cardiac Muscle Cell Firing

• Cells begin with a negative charge: resting membrane potential

• Calcium leak lets Ca2+ diffuse in, making the cell more positive

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Threshold potential

Resting membrane potential Calcium

leak

Depolarization Phase

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Depolarization Phase

• Cell membrane becomes permeable to Na+

• Na+ enters cell, inside the cell is more +

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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)

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Threshold potential

Resting membrane potential

Action potential

Calcium leak

Plateau Phase

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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

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Threshold potential

PLATEAU

Action potential

Calcium leak

Repolarization Phase

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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

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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

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Threshold potential

PLATEAUAction potential

Calcium leak

Cardiac Action Potentials

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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 46

Cardiac Muscle Action PotentialCardiac Muscle Action Potential 5 Phases5 Phases

Phase 0: Upstroke, rapid depolarization

Phase 1: Early, short repolarization

Seen only in ventricular musclePhase 2:

Plateau phase; membrane potential remains depolarized

Phase 3: Final rapid repolarization

Phase 4: Resting, diastolic repolarization

Unlike nerve cells, cardiac cells Unlike nerve cells, cardiac cells have 5 phases in their action have 5 phases in their action

potential.potential.

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Cardiac Muscle Cell Contraction

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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.

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Importance of Actions Potentials

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Lehne 5th ed Figure 47-2

Myocardium& His-Purkinje

System

SA Node &AV Node

Why are action potentials important?

• Source of dysrhythmias

• Targets of drug action

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Cardiac Conduction andRhythm Disorders

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ECGRelationship to Action Potential

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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)

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Electrical and Mechanical EventsDiagram

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57Lehne 5th ed Figure 47-3

Electrical event precedes mechanical event !!!

Location of Electrical Events in the Heart

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Porth 2007, Figure 16-12

P waveAtria

PR IntervalAV node

QRS complexventricles

T wave: Repolarization of the ventricles

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Disorders of Cardiac Rhythm and Conduction

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Disorders of Cardiac Rhythm and Conduction

1. Dysrhythmias (or arrhythmias)

– Term used to describe disorders of cardiac rhythm

– Occur in healthy and non-healthy people– Interfere with heart’s pumping ability

2. Disorders of impulse conduction– Impulses that originated in the SA node do not

get through or the SA node does not work well

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Causes of Dysrhythmias

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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

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Sinus Node Rhythms

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Sinus Node Rhythms

• Normal Sinus Rhythm

• Sinus Bradycardia

• Sinus Tachycardia

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Normal Sinus Rhythm

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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

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Sinus Bradycardia

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Sinus Bradycardia

• P before QRS

• RR regular

• Rate < 60– Slowing of conduction through AV node seen as

a lengthened PR interval (Vagal, PNS)

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Sinus Tachycardia

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Sinus Tachycardia

• P before QRS

• RR regular

• Rate > 100

• Enhanced automaticity r/t SNS activation (fever, exercise, stress)

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Class II Antidysrhythmics

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Lehne 5th ed Figure 47-2

Myocardium& His-Purkinje

System

SA Node andAV Node

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Class II Antidysrhythmic

Class II Antidysrhythmic Beta Blockers

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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

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Class II Antidysrhythmic Mechanism of Action

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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

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Class II Antidysrhythmic Therapeutic Uses

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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)

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See Lehne Table 18-2 and 18-3

Beta BlockersAdverse Effects

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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

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Beta Blocker Administration

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Beta Blocker Administration

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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

Atrial Dysrhythmias

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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

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A-Fib TreatmentDigoxin

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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

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DigoxinMechanism of Action

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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 impulses89

DigoxinTherapeutic Uses

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DigoxinTherapeutic Uses

• Heart failure

• Atrial flutter/fibrillation

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DigoxinMechanism of Action

Diagram

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Lehne 6th ed Figure 47-4

DigoxinPharmacokinetics

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DigoxinPharmacokinetics

Absorption 60 – 80% (tabs)

70 – 85% (elixir)

90 – 100% (caps)

Metabolism Liver

Half Life 5-7 DAYS to eliminate

& T½ 1.5 days

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DigoxinAdministration Considerations

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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 ( > 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

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DigoxinAdverse Effects

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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) halos99

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DigoxinContraindications

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DigoxinContraindications

•2nd/3rd degree heart block

•V. Fib/V. Tach

•Sick Sinus Syndrome–When the sinus node quits working

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Digoxin Precautions

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Digoxin Precautions

•Acute MI

•Renal insufficiency

•Hypokalemia

•Severe pulmonary disease

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DigoxinAdditional Considerations

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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

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DigoxinDrugDrug Interactions

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DigoxinDrugDrug 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)

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DrugDrug InteractionsIncrease Risk of Digoxin Toxicity

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DrugDrug 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

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DigoxinNursing Implications

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DigoxinNursing Implications

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Apical pulse for 1 minute and document

Monitor ECG

Monitor potassium and digoxin levels

A-Fib, PSVT TreatmentClass IV Antidysrhythmic Calcium Channel Blockers

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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

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Class IV AntidysrhythmicsDiagram

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Lehne 5th ed Figure 47-2

Myocardiumand His-Purkinje

System

SA Node andAV Node

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Class IV Antidysrhythmic Effects on the Heart

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Class IV Antidysrhythmic Effects on the Heart

Three effects on the heart1. Slow SA node automaticity slow HR

2. 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

3. 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 blockers118

Class IV Antidysrhythmic Therapeutic Uses

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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

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Verapamil and DiltiazemAdverse Cardiac Effects

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Verapamil and DiltiazemAdverse Cardiac Effects

• Bradycardia

• AV block

• Decreased myocardial contractility decreased cardiac output

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Verapamil and DiltiazemAdverse General Effects

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Verapamil and DiltiazemAdverse General Effects

• Dizziness due to increased vasodilation and less perfusion to the brain

• Facial Flushing• Headache• Peripheral edema• Decreased GI motility

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Disorders of Atrioventricular Conduction

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Disorders of Atrioventricular Conduction

• First degree AV block

• Second degree AV block

• Third degree AV block (complete AV block)

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First Degree AV Block

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First Degree AV Block

• Slightly prolonged PR interval

• ALL atrial impulses are conducted to ventricles

• Asymptomatic.

• Everything is in the right order

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Second Degree AV Block

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Second Degree AV Block

• Not all atrial impulses are conducted to ventricles– See some P waves not followed by QRS.

• Can be very symptomatic.

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Third Degree (Complete) AV Block

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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

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Case Study: Digoxin Toxicity

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Case Study: Digoxin ToxicitySerum dig level = 1.7 ng.ml (0.5-1.1 desired)

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33rdrd degree AV degree AV BlockBlock

Temporary pacemaker inserted, SR Temporary pacemaker inserted, SR 100% 100% pacedpaced

Complete A-V block with 100% atrio-ventricular pacing

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Atrial Pacingspike

Ventricular Pacingspike

P QRS

Ventricular Dysrhythmias: More Serious!

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Ventricular Dysrhythmias: More Serious!

• PVC – premature ventricular contraction

• V-fib – ventricular fibrillation

• V-tach – ventricular tachycardia

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