Dysrhythmias Flashcards
Dysrhythmias matter bc
Impacts on CO
Pts will compensate
Phases of heart beat
1 Atrial depolarization/contraction
2 Isovlumetric contraction
3 Rapid ejection
4 Reduced ejection
5 Isovolumetric relaxation
6 Ventricular filling
Atrial Kick
The contraction at the end of passive ventircle filing
30% of CO
Two types of myocardial tissue
Contractile
Conductive
Conduction system of heart
SA, AV, Bundle of His, and Perkinje fibers
Are able to spontaneously discharge electrical impulses WITHOUT stimulation causing a contraction
All dysrthmias originate with a defect in the conduction system
Which nerve is responsible for PSNS of heart
Vagus nerve
What is automaticity
The way that the heartt repeatedly beats using it;’s conducitve system (SA Node) without any stimulation
What nerves control sympathetic NS of heart?
Fibers of SNS
SA node fires in what range
60-100 BPM
AV node
Has an automaticity associated with it, but lesser than SA
40-60 BPM
Automatic intrinsic rate of purkinje fibers and Bundle of his
20-40 BPM
Primary pace maker in the heart
SA Node
3 distinct waves in cardiac cycle
P wave
QRS complex
T wave
Dysrhythmias
Alterations in normal impulses or conduction of normal myocardial beating
Ectopic Pacemakers/Focci
Origination of eletrical impulse is occuring somewhere other than SA (Competing with SA)
Two primary causes of dys
Ectopic focci
Lack of blood flow to normal conduction systems of heart
Classifaction of dysrhythmias
Location: Atrial or ventricular
Type: Flutter (Regular),
fibrillation. (Disorganized), \block (Delay or block of electrical flow through part of heart)
Afib
Passive entering of blood into ventricles, no atrial kick
- Blood sits in atrium, often resulting in clot
SS of Dysrhythmias
Syncope
SOB
Weakness
Fatigue
Tingling periphres
Decreased exercise tolerance
Palpitation
Risk factors for dysrhythmias
High cholesterol
Metabolic syndroe
HTN
CAD
Hyper/hypoK
MI
DM
HF
Anyone without a healthy heart
Asymptomatic dysrhythmias tx
Little or no benefit to treatment with medications
Acute dysrhythmias tx
In life-threatening cases, medications warranted
Prophylaxis of dysrhythmias tx
Generally onluy for high risk pts
Avoid drug combinations that increase QT interval
Antidysr drugs
Prevent impulse conduction problems
Can also CAUSE dysrythmias
- High risk with them
Non pharm tx
Cardioversion or Defibrillation
- Serious
Cardiac ablation
- Laser therapy of ectopic cells
Cardiac Pacemakers
Implantable Cardioverter Defibb (ICDs)
- Keeps pt alive
Common reasons for Bradydysrhthmias
HR Less than 60 BPM
Common in older adults
Medication can cause
Common types:
Sinus bradycardia
Sinoatrial node dysfunction (sick sinus syndrome)
Atrioventricular (AV) conduction block
Normal sinus rhythm
Heart beat originate in sinoatrial node
Tachydysrythmias
HR 100
Incidence increases in older adults and those with preexisting cardiac disease
Common tachydysrhythmias
Atrial tachycardia
Paroxysmal supraventricular (Intermittent) tachycardia (PSVT)
Atrial flutter
Atrial fibrillation
Ventricular tachycardia
Torsades de pointes
Ventricular fibrillation
AFib
CHronic or intermittent
Totally disorganized atrial electrical activity
Loss of CO
Tx:
- sychronized cardioversion
- Anticoagulant
- Rate control (Beta blocker, Ca channel blocker)
- Long term anticoagulation (CHADS score)
CHADS score
Way in which MDs compare risk-benefit for coagulation therapy in Afib
COntraindicaitons include:
High bleed risk
High fall risk
Antidysrythmic drugs act in two ways
Blocking ion flow through ion channels
Altering Autonomic activity
Therapeutic goals are?
Terminate or tx existing dysrythmia
Prevent reccurance of abnormal rhythm
Dysrthymic drugs Therapeutic range
Have a narrow therapeutic margin between therapeutic and toxic effects and can actually worsen or create further dysthymias.
Antidysrhythmia Agent Categories
Sodium Channel Blockers (Class 1)
Beta-adrenergic Blockers (Class 2)
Potassium Channel Blockers (Class 3)
Calcium Channel Blockers (Class 4)
Miscellaneous antidysrhythmic drugs
Sodium Channel Blockers (Class 1)
Largest group of antidysrhythmics
Similar in structure and function to local anesthetics
- Prevents depolarization (conduciton of nerve impulses)
Lidocaine, procainamide
Beta-Adrenergic Antagonists: Class II
Treat HTN, MI, HF, and dysrhythmias
Block calcium channels in SA and AV nodes
Slow HR ( NEGATIVE Chronotropic effect)
Decrease conduction velocity
Prototype Drug – Propranolol (Inderal)
Non selective (B1 and B2)
For pts as PRN for intermittent PSVT (spontaneous HR racing)
Asthmatics should NOT take (Acute asthma attack
AE: HTN Bcardia, fatigue, bronchoconstriction
Potassium Channel Blockers: Class III
Block potassium ion channels in myocardial cells
Delay repolarization (Restoring electrical balance)
Prolong refractory period
Limited use due to serious adverse effects
Prototype Drug – Amiodarone (Cordarone)
K+ Channel blockers
Therapeutic effects and uses
Atrial and ventricular dysrhythmias
Resistant ventricular tachycardia
Recurrent fibrillation
Mechanism of action
Exact mechanism unknown
Blocks potassium channels but also blocks sodium ion channels and inhibits sympathetic activity
AE Slow to resolve
Nausea
Vomiting
Anorexia
Fatigue
Dizziness
Hypotension
Visual disturbances
Rashes
Photosensitivity
Pneumonia like syn
Calcium Channel Blockers: Class IV (1 of 2)
Limited number approved as antidysrhythmics: Diltiazem, Verapamil
Effects similar to those of beta adreneric antagonists
Safe
Nursing Considerations for Patients Receiving Antidysrhythmic Therapies
VS. and ECG
Educate on self monitoring for dizziness, ortho HOTN
Monitoring electrolytes
Dysrhythmias associated w/ Acute Coronary Syndrome (ACS)
Typical ECG Changes seen in myocardial ischemia
ST segment depression
T Wave inversion
Syncope
Brief lapse in consciousness accompanied by a loss in postural tone (fainting)
Cardiovascular vs noncardiovascular
CV causes of syncope
Vasovagal syncope
Primary cardiac dysrhythmias
Prosthetic valve malfunction
Pulmonary emboli
Aortic dissection
