Acute Cardiac Disturbances Flashcards
Atrial Fibrillation
- Most common type of arrhythmia (abnormal heart beat)
- Extremely fast atrial contractions, and ineffective blood pumping
- ECG: absent wavy P waves, uneven QRS
Classification of AF
Paroxysmal: episode lasts less 7days, revert spontaneously or through cardioversion
Persistant: >7 days and do not self terminate without intervention
Long-standing: continuous for >1year despite intervention
Permanent: accepted AFib with no attemps to achieve SR
Pathophysiology
- Structural heart disease underlies most AF (hypertensive, valvar, ischaemic, congenital)
- Familial AF is rare but is a genetic cause
- In AF, rapidly firing ectopic triggers in the pulmonary veins cause disorganised electrical impulses which is maintained by abnormal cardiac tissue
S&S
- Can be asymptomatic
- Rapid heart rate, exercise intolerance, angina, fatigure, SOB
Treatment of AF
- Reduce thromboembolitic risk
- Rhythm control
- Rate control of ventricles
Most patients have minimal/no symptoms and only require rate control and anticoagulation
If symptoms are severe, reversion to SN is required (meds and cardioversion)
Forms of rate control
Beta blockers: slows down HR by blocking binding of A & NA on beta 2 adrenergic receptors
Digoxin: reduced HR - used for sedentary patients as it doesnt control exercise induced tachycardia, but it doesn’t lower BP (good for patients with HoTN and LVF)
Ablation or pacemaker
Accepting rhythm and focusing on rate control is more appropriate for elderly who have heart disease, permanent arrhythmia and tolerated syptoms
Pharmacological rhythm control (antiarrhythmic)
Amiodrone: most effective, works by prolonging the action potential and refractory period of cardiac tissue (acute and chronic use)
Sotalol: beta-blocker, most often used to maintain SR and prevent arrythmic activity (not so much reversion)
Flecainide: similar mechanism of action to amiodarone, used to revert/maintain SR in severe cases and where other drugs have failed
* Has significant side effects (proarrythmic) and is contraindicated in CAD and LVD
Non-pharm: Cardioversion, ablation, surgery
Rhythm treatment esp for young people with normal hearts or recent onset
Cardioversion in AF (electrical rhythm control)
Indicated for acute AF with rapid ventricular rate or symptoms of MI (<48H)
Stable symptomatic patients can attempt cardioversion after 4 weeks of anticoagulation
Not for patients with short SR periods between cardioversions
NB: the use of drugs to restore SN is a form of chemical cardioversion
Ablation and pacemaker
Ablation:use of heat or cold energy to create scars in tissue that is producing abnormal signalling
Pacemaker: implanted medical devide that generates rhythmic electrical impulses
Used for patients who don’t respond to pharmacological therapies or don’t tolerate hypotensive effects (but will require lifelong anticoagulation)
Ventricular Tachycardia
- very fast ventricular beats of 100-300 bpm but normal rhythm
- Often caused by diseases hearts that cause scarring (IHD, cardiomyopathy, MI)
- Other: electrolyte deficiencies, systemic diseases that affect the heart, drugs
- ECG: multiple regularly spaced but very wide QRS, absent P waves (dissociated)
Pathophysiology of VT
- Can quickly deteriorate into VFib and required defib
- Often the myocardium is stimulated by a ventricular premature complex (ectopic ventricular impulses)that propagate erratically and cause chaotic ventricular depolarisation = leads to VFib
- Scarring causes electrical reentrant circuits (similar to closed circuits that continuously loop)
Torsade de Pointes
- A form of VT
- The QRS complexes reflect above and below baseline (altitude changes)
- Usually reversible and is caused by drugs that lengthen QT interval (amiodarone, sotalol, MI, electrolyte disturbance)
VT manifestations and assessment
- May be short term stable or unstable with HoTN and no pulse
- Palpitation, light headedness, syncope, chest pain
- Patient will present with HoTN, tachypnea, decreased LOC, pallor, high jugular venous pressure, changed intensity of first heart sounds in aucultatoin
VT Treatment
Stable: amiodarone, sotalol infusion, synchronised electrical cardioversion
Unstable: = pulsless = CPR, unsynchronised cardioversion (defib) (if unresponsive, a cardioverter-defib is implanted)
* Implanted cardiovertor-defibrilator (ICD) similar to pacemaker but detects abnormal electrical activity and delivers shocks to correct
Monitor ECG, vitals signs, postsurgical care, medication education
VT Treatment
Conscious person: cardioversion or amiodarone with continuous monitoring
Unconscious: Defib, adrenaline, CPR
Ventricular fibrillation
- Rapid disorganised ventricular beating (quivering) caused by impulses firing from too many foci (no coordination with atrias)
- no rhythm = no cardiac output
- Caused by MI, untreated VT, electrolyte imbalances, hypothermia, hypoxia (results in Ca accumulation, free radicals and metabolic alterations)
- ECG: no identifiable markers, squiggled
VFib Treatment
- Immediate defib, CPR and adrenaline
- Will cause death if untreated
- Survival < 10% for every minute Vfib lasts
Heart block
Problem with the electrical conduction throughout the heart (complete or partial blockage) that slows down conduction or causes irregularities in heart beat
* A type of arrythmia
3rd Degree Heart Block
- Complete dissociation between atrial impulses and ventricular response (SA doesnt propogate), such that an accessory pacemaker in the V will start signalling contraction that is independent on A
- ECG: identifiable QRS but irregular and have no correlation with P wave, slow rate
- Caused by heart disease, MI, electrolyte imbalance, drugs (Av blocking drugs: BB, CCB, digoxin, amiodarone)
- Symptoms: dizziness, HoTN, syncope, signs of reduced CO
- Treated with an implantable cardioverting defibrillator that detects and terminates VTs, atropine
Pulseless electrical acitivity (PEA)
- Organised ECG activity with no detectable pulse or contractions (too weak to produce adequate CO)
- A major CV, resp or metabolic insult = inability to generate force
- This is often hypoxia secondary to resp failure
- Other causes: hypovolaemia, acidosis, hypoglycaemia, hypothermia, hypo/hyperkalaemia, pneumothorax, tamponade, toxins, heart or lung thrombus (4Ts and 4Hs)
PEA Treatment
- Non-shockable rhythm (defib wont work)
- Treat the underlying cause of the PEA
- CPR, IV line, intubation, O2
Asystole
- No CO and no ventricular repolarisation
- Non-shockable rhythm that requires immediate CPR and 1mg adrenaline
Adrenaline
- Catecholamine that binds adrenergic receptors (agonist)
- In cardiac arrest it causes peripheral vasocontriction via alpha to redirect blood flow to heart and brain and increase CO (beta)
- Also improves heart flow during CPR
- Use in VFib/VT after shocks have failed (2nd) then every second look
- Asystole/PEA, in initial loop then every second
- IV/IM, 1mg/10ml, HL 2-3min
Amiodarone
- Antiarrythmic that effects Na, K and Ca channels (prolonges duration of action potential and refractory period), as well as adrenergic properties
- Give 300mg bolus for VF/pulseless VT between third and fourth shock, or prophylactically for recurrent VF/VT
- HL 3-7h
- SE: HoTN, brady, heart block
