WK 3: Cardiac Flashcards
How are arrhythmias classified?
by site
- sinus rhythms
- atrial rhythms
- ventricular rhythms
Define sinus rhythm
= the normal rhythm set by the SA node aka pacemaker
- 60-100bpm (SA node fires 60-100)
Define and describe sinus bradycardia
= same rhythm as normal sinus but SA node fires <60bpm causing a HR of <60bpm.
- may be normal or clinical depending on the underlying cause.
Clinical significance
- symptomatic sinus brady refers to a HR that <60bpm and inadequate for the patient’s condition causing them to experience symptoms.
Causes
- May be normal during sleep, in those who are aerobic athletes.
- valsalva manoeuvre, carotid sinus manage, hypothermia, increased intraocular pressure, vagal stimulation and some meds (B-adrenegic blockers, some calcium channel blockers)
Is a common symptom of
- hypothyroidism
- increased intracranial pressure
- hypoglycemia
- inferior MI
Clinical manifestations
- chest pain
- syncope (faint/passout)
- pale
- cool skin
- hypotension
- weakness
- angina
- dizziness
- confusion or disorientation
- SOB
On ECG
- HR <60bpm
- regular rhythm
- P wave is present with normal shape and duration and proceeded QRS
- QRS is normal shape and duration
- PR interval is normal
Treatment
- atropine (anticholinergic med)
if atropine is ineffective
- transcutaneous pacing
- adrenaline
- dopamine
- isoprenaline
- permanent pacemaking is some instances
Define and describe sinus tachycardia
= normal sinus rhythm at a faster rate as SA node fires >100bpm causing a HR of >100bpm
Case:
- vagal (parasympathetic) inhibition
- physiological and psychological stressors
- exercise
- fever
- pain
- hypotension
- hypovolemia
- anemia
- hypoxia
- hypoglycemia
- myocardial ischemia
- heart failure
- hyperthyroidism
- anxiety
- fear
- meds (adrenaline, noadrenaline, atropine, caffeine, theophylline, nifedipine or hydralazine)
- over the counter cold anf lu meds e.g.pseudoephedrine
- may be normal or clinical depending on the underlying cause.
Clinical significance
- May be normal during exercise
- depends on the pt’s tolerance to increased HR
- causes increased myocardial oxygen consumption due to increased HR, anginal, increased infarction size when pt has as well as AMI or CAD.
ECG characteristics
- HR 101-200bpm
- regular rhythm
- P wave is present with normal shape and duration and proceeded QRS
- QRS is normal shape and duration
- PR interval is normal
Treatment
- based on underlying cause
- effective pain management where needed
- treat hypovolemia
- IV adenosine and B-adrenergic blockers (meyrprolol) may be used to reduce HR and decreased myocardial O2 consumption.
What are the always clinical atrial rhythms? and what are they forms of?
- Atrial flutter
- Atrial fribulation
- AV node re-entrant tachycardia
All forms of SVT
Describe atrial flutter and what it looks like on an ECG
= an atrial tachycardia that originates from an electrical impulse that travels around in a localised self-perpetuating loop that has a single ectopic focus in the right atrium or less commonly left atrium.
- for every one cycle around the loop, there is one contraction of the atria but not always one contraction of the ventricle. The number of F waves before a QRS complete indicated the number of loops before the AV nodes catches one and conducts it.
- called a re-enterant pathway
Cause
*rarely occurs in healthy hearts
Clinical significance
- high Ventricular rate/HR and loss of atria ‘kick’ are associated with decreased CO-> HF,
- increased risk of stroke due to risk of thrombus formation from atrialstatsis
Symptoms/associated w/
- CAD
- hypertension
- mitral valve disorders
- PE
- Chronic lung disease
- cor pulmonale, cardiomyopathy
- hyerthyrdoiism
- meds (such as digoxin, quinidine and adrenaline)
Management/treatment
- warfarin to prevent stroke from atrial blood stasis->thrombosis
- goal: slow ventricular response by increasing AV block
- meds to slow ventrciular rate (including: calcium-channel blockers, B-adrenergic blockers)
- meds (antiarrhythmias) amiodarone to convert to NSR or maintain NSR.
- Electrocardioversio to convert to NSR
- radio frequency catheter ablation is a potential treatment choice for AF. Low-voltage, high frequency electrical energy is used to ablate/destroy tissue in the R) atrium to terminate the point of arrhythmia source and restore NSR.
ECG
- recurring, regular, sawtooth-shaped flutter waves (in place of P waves)
- atrial flutter represents atrial depolarisation followed by repolarisation.
- Atrial rate: regular and rapid. Between 200-400bpm
- Ventricular rate (thus HR): varies based on conduction rate. Refractory properties of the AV node blocks part of atrial impulses from reaching the ventricles.
- thus the ventricle only contacts at a normal rate.
e.g. atrial flutter causing 3 localised impulse loops before one conducts with AV node to carry on the ventricular function. This is why HR usually appears regular within normal range. (this could be a 3:1 heart block)
- ventricular rhythm can be regular or irregular.
- PR interval is variable and not measurable
- QRS normal
- absence of normal P wave instead multiple flutter waves or ‘F’ waves are present
- looks like multiple un-uniform P waves (that are actually F) before the QRS and T.
Define and explain atrial fibrillation and also what it looks like on an ECG
= caused by multiple impulses that are disorganised and randomly occurring from mutliple ectopic sites in and around the atria.
- Commonly near the roots of the pulmonary veins.
= result in the atria quivering or fibrillation thus ineffective contraction.
Clinical significance
- most common in AUS/NZ
- results in decreased CO because of ineffective atrial contraction (loss of atrial kick) and/or rapid ventricular response.
Thrombi form in the atria because of blood stasis. Thrombis can move to brain cause stroke.
Risk factors
- increased age
- underlying heart disease including CAD, cardiomyopathy, hypertensive heart disease, HF, pericarditis.
- can be triggered by thyrotoxicosis, alch=ohol intoxication, caffeine use, electrolyte disturbances, stress or cardiac surgery.
ECG
- maybe paradoxical (spont beginning and ending) or persistent (lasting more than 7 days)
Atrial rate: extremely high 350-600bpm but most electrical impulses don’t pass through the AV node due to its refractory properties.
- p wave replaced by chaotic fibrillation waves.
Ventricular rate: irregular and can range from slow <60bpm to rapid >100bpm because the impulses that do make it through the AV node are irregular.
*when HR is between 60-100 it is atrial fibrillation with controlled ventricular response.
*A-fib with VR >100bpm= AF w/ rapid ventricular response.
- PR interval is not measurable
QRS complex usually has a normal shape and duration
- At times A-flutter and A-fib can co-exist
- characterised by the absence of P wave and irregular, narrow QRS complexes.
- flat or undulating baseline.
Treatment
- goal: decrease ventricular response
- prevent stroke
- conversion to NSR
- meds including calcium-channel blockers (diltiazem), B-adrenergic blockers (metoprolol) and dignsin.
- antiarrhythmic med such as amiodarone to convert and maintain in NSR.
- ECV
- anticoag therapy (warfarin) if in A-fib >48hrs and maybe long term if treatments don’t fix it.
- ablation may work for those with treatment resistant A-fib
- The Maze procedure may be used to stap AF. Incisions are made in both atria and cryoablation (cold therapy) is used to stop formation and conduction of signals to restore NSR.
Explain Ventricular tachycardia and how it looks on an ECG
*lethal
= defined by a run of three or more premature ventricular contractions
Commonly caused by a single strong firing site or circuit in the ventricles causing it to take over as pacemaker.
- impulses starting in the ventricles produce premature beats that are regular and fast ranging from 100-250bpm
- may progress into V fibrillation.
Sustained VT: longer than 30sec
- requires immediate treatment
Non-sustained VT: <30sec
Clinical associations/risk factors
- usually occurs in people with structural heart problems e.g. pHx heart attack or abnormalities of the heart muscle.
- MI
- CAD
- significant electrolyte imbalances
- cardiomyopathy
- mitral valve prolapse
- long QT syndrome
- medication toicity
- CNS disorders
Complications
- life threatening
- risk of decreased CO
- possible development of VF which is lethal
- Accepted atrioventricular rhythm (AIUR) can develop when the intrinsic pacemaker rate (SA or AV) becomes less that that of a ventricular ectopic pacemaker.
Clinical significance
- Stable VT causes sever decrease is CO because decreased ventricular diastolic filling time and loss of atrial contraction.
- thus causing hypotension, pulmonary oedema, decreased cerebral blood flow and cardiopulmonary arrest.
- the arrthymia must be treated quickly even if it occurs only briefly and stops abruptly. Episodes may recur if prophylactic treatment is not started.
- VF may develop
ECG:
- V rate/HR: fast, 100-250bpm
- rhythm may be regular or irregular
- AV dissociation may be present with P waves occurring independently of the QRS complex.
- atria may be depolarised by the ventricles in a retrograde fashion
- P wave is usually buried in QRS complex
- PR interval is not measured.
- QRS is distorted and wide
- T wave is in opposite direction of QRS
- wide and bizarre-looking QRS complexes.
- P wave is absent.
Treatment
- treat cause
- IV amiodarone
- B-adrenergic blockers
- lignocaine
- sotalol
- cardioversion IV magnesium
- isoprenaline
- phenytoin
- lignocaine
- antitachycaria pacing
- CPR and rapid defib
- adrenaline if defib is unsuccessful
*VT without a pulse is life threatening
Explain Ventricular fibrillation and how it appears on an ECG
= caused by multiple weak ectopic sites in the ventricles.
- unsynchronised chaotic electrical signals cause the ventricles to quiver or fibrillate rather than contract.
- heart pumps little to no blood due to no effective contraction and thus no CO.
Clinical significance
*lethal rhythm
- can quickly lead to cardiac arrest
ECG: irregular random wave forms of varying amplitude with no identifiable P wave, QRS complex or T wave.
- amplitude decreases with time from initial coarse V-fib to fine V-fib and ultimately to flat line.
Treatment
- immediate CPR and ALS with further use of defib
What is an ECG measuring?
= electrical activity generated from the movement of ions across the membranes of myocardial cells.
What is the value of each of the squares on an ECG?
Horizontally
Large square: 0.20 sec
- 1 large contains 25 smaller
- thus 300 large= 1minute
Small square: 0.04sec
Vertically
Small square: (1mm)= 0.1 millivolt (mV)
Large square: 0.5 mV
How do you calculate HR from an ECG?
- count the QRS complex in 1 minutes (300 large squares)
- Count the number of R-R intervals in 6 secs (so two of the marked 3sec) and multiply by 10.
- count the number of large squares between R-R intervals and divide this number into 300.
Describe a normal P wave, the normal duration and sources of possible variation
= represents passage of impulse though atrium causing depolarisations/contraction.
- should be upright
Duration: 0.06-0.12sec
Possible source of variation:
disturbance in conduction within atria.
Describe a normal PR interval, the normal duration and sources of possible variation
= from the beginning of P wave to the beginning of QRS complex.
- Represents time taken for impulse to spread through the stria, AV node and bundle of His, the bundle branches and Purkinje fibres to a point of immediately preceding ventricular contraction.
Duration: 0.12-0.20sec
Possible source of variation:
- disturbance in conduction usually in AV node, bundle of His or bundle branches but can be in atria also.
Describe a normal Q wave of QRS, the normal duration and sources of possible variation
= first negative deflection after p wave, short, narrow, not present in several leads.
Duration: <0.03sec
Possible source of variation:
- MI may result in development of pathological Q wave that is wide (>0.3sec) and deep (>25% of hight of R wave)
Describe a normal R wave of QRS, the normal duration and sources of possible variation
= first positive deflection in the QRS complex
Duration: not usually measured
Possible source of variation:
- nil noted
Describe a normal S wave of QRS, the normal duration and sources of possible variation
= first negative deflection after R wve
Duration: not usually measured
Possible source of variation:
- nil noted
Describe a normal QRS complex, the normal duration and sources of possible variation
= Represents time taken for depolarisation/contraction of both ventricles (systole)
- measured from the beginning of QRS
Duration: not usually measured
Possible source of variation:
- nil noted
Describe a normal ST segment, the normal duration and sources of possible variation
= time between ventricular depolarisation and repolarisation/diastole.
- should be isoelectric (flat)
- measurement from S wave to beginning of T wave.
Duration: 0.12sec
Possible source of variation:
- ischemia
- injury
- infarction
(may be elevation of depression)
Describe a normal T wave, the normal duration and sources of possible variation
= Represents time taken for ventricular repolarisation
- should be upright
Duration: 0.16sec
Possible source of variation:
- electrolyte imbalances
- ischemia
- infarction
(tall, peaked or inverted)
Describe a normal OT interval, the normal duration and sources of possible variation
= Represents time taken for entier electrical depolarisation/contraction and repolarisation of the ventricles
- measured from the beginning of QRS complex to end of T wave
Duration: 0.34-0.43
Possible source of variation:
- medication
- electrolyte imbalances
- changes in HR
(usually affect depolarisation more than repolarisation)
What is the relationship between HR nd the duration of the normal ECG intervals?
As HR increases the duration of intervals shorten.
- especially those of the PR, QT intervals
What are some common causes of arrhythmias?
Cardiac conditions including;
- accessory pathways
- cardiomyopathy
- conduction defects
- heart failure
- myocardial ischemia, infarction
- valve disease
Others
- acid-base imbalances
- alcohol
- caffeine, tobacco
- connective issue disorders
- medications or toxicity
- B-adrenergic blockers
- electrical shock
- electrolyte imbalances (hyperkalemia, hypocalcemia)
- emotional crisis
- hypoxia
- metabolic conditions (thyroid dysfunction)
- near drowning
- sepsis, shock
- toxins
Explain your approach to assessing a heart rhythm
- P wave
- ?present
- ?upright or inverted
- ?one with every QRS complex or more?
- ?are atrial flutters or fibrillations present? - Evaluate Atrial rhythm
- ?regular or irregular
- recall this related to the presence of P wave and regular QRS complex - calculate atrial rate
- PR interval
- measure duration ?normal ?prolonged - Ventricular rhythm
- ?regular or ?irregular - Calculate ventricular rate
- QRS complex
- ?measure duration ?prolonged ?normal - ST segment
-?isoelectric (flat, elevated or depressed) - Measure Qt interval
- ?normal ?prolonged duration - P wave
- ?upright or inverted
Additional questions to consider
- what is the dominant or underlying rhythm, and/or arrhythmias?
- what is the clinical significance of your findings?
- what is the treatment for the particular rhythm?
What are some typical assessment findings of arrhythmias?
- irregular rate and rhythm; tachy or brady
- hypo or hyper tension
- decreased O2 sats
- chest, neck, shoulder, back, jaw or arm pain
- dizziness, syncope
- dyspnoea
- extreme restlessness, anxiety
- decreased level of consciousness, confusion
- feeling of impending doom
- numbness, tingling of arms
- weakness and fatigue
- cold, clammy skin
- diminished peripheral pulses
- diaphroesis
- pallor
- palpitations
- N + V
What are some initial interventions you would carry out on a pt with an arrhythmia?
- ensure ABCs
- obtain baseline vitals (including o2 sats)
- administer O2 via NC or non-rebreather
- obtain 12lead ECG
- initiate continuous ECG monitoring
- identify underlying rate and rhythm
- identify arrhythmia
- establish IV access
- obtain baseline labs (FBC or electrolytes)
How does ischemia appear on an ECG?
- ST segment depression (significant if at least 1 small box below the isoelectric line in at least 2 continuous and neighbouring leads)
- T wave inversion
Both occur when in response to inadequate supply of blood and oxygen which causes electrical disturbances in the myocardial cells.
- once adequate blood flow restores post treatment the ECG changes resolve and ECG returns to pts baseline.
What are some ongoing interventions you would carry out on a pt with an arrhythmia?
- monitoring vitals signs, level of consciousness, 2 sats and cardiac rhythm
- anticipate need for administration of antiarrhythmic meds and analgesics
- prepare to initiate advanced life support
Define asystole and describe its on an ECG
= represents the total absence of ventricular electrical activity. Occasionally, P waves are seen.
- no ventricular contraction occurs because depolarisation does not occur.
- pt are unresponsive, pulseless and anoeic.
- asystole is a lethal arrthymia that requires immediate treatment.
- VF may masquerade as asystole.
Treatment: CRO and ALS
Normal sinus rhythm
State the;
- Rate
- P wave
- PR interval
- QRS complex
Rate: 60-100 bpm, regular
P wave: normal
PR interval: normal
QRS complex: normal
Sinus bradycardia
State the;
- Rate
- P wave
- PR interval
- QRS complex
Rate: <60bpm regular
P wave: Normal
PR interval: Normal
QRS complex: Normal
Sinus tachycardia
State the;
- Rate
- P wave
- PR interval
- QRS complex
Rate: 101-200bpm regular
P wave: Normal
PR interval: Normal
QRS complex: Normal
