Breathlessness- core conditions 2 Flashcards
Ventricular tachycardia
• Any broad complex tachycardia - consider VT until proven otherwise!
• Three or more consecutive broad ventricular complexes = VT
• VT can be sustained (lasting > 30 sec) or non-sustained (lasting < 30 seconds).
• This arrhythmia can impair cardiac output.
• Clinically: it may cause palpitations, chest pain, SOB, syncope and cardiac arrest (if it does not produce a pulse).
Monomorphic VT
Most common type of VT
• ECG: Broad QRS complex tachycardia.
• Features to suggest VT: Very broad complexes (>160ms) with AV dissociation (P and QRS complexes at different rates): Capture beats — occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.
• Fusion beats — occur when a sinus and ventricular beat coincide to produce a hybrid complex of intermediate morphology.
Polymorphic VT
• Multiple ventricular foci with the resultant QRS complexes varying in amplitude, axis and duration. The commonest cause of PVT is myocardial ischaemia.
• Management- IV magnesium
Polymorphic VT- Torsades de pointed (TdP)
• Torsades de pointes (TdP) is a specific form of polymorphic ventricular tachycardia occurring in the context of QT prolongation; the QRS complexes “twist” around the isoelectric line.
• TdP is often short lived and self terminating, however can be associated with hemodynamic instability and collapse, and may also degenerate into ventricular fibrillation (VF).
Ventricular fibrilation
The patient wont have a pulse
• The ventricles suddenly attempt to contract at rates of up to 500bpm, this rapid and irregular electrical activity renders the ventricles unable to contract in a synchronised manner, resulting in immediate loss of cardiac output
• Mechanism: Multiple re-entry circuits within the ventricle.
Ventricular fibrilation- causes and ECG
• Causes: myocardial ischaemia, cardiomyopathy, myocarditis, blunt trauma, drugs, drug induced QT prolongation, electrical shocks, hypothermia, sepsis.
• ECG: Chaotic irregular deflections of varying amplitude. No identifiable P waves, QRS complexes, or T waves. Rate 150 to 500 per minute. Amplitude decreases with duration (coarse VF -> fine VF)
Sinus bradycardia
Sinus rhythm with a resting hear rate of <60bpm in adults or below the normal range for age in children
1st degree AV block
- Clinically: Asymptomatic, has no haemodynamic consequences.
- Causes: Increased vagal tone, athletic training (normal variant). Can also be seen in pathology (inferior MI, post mitral valve surgery, Lyme disease, electrolyte disturbances e.g. hyperkalaemia) or after administration of AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin)
- ECG: PR interval > 200ms (five small squares)
2nd degree AV block Morbitz I
- Due to a reversible conduction block at the level of the AV node, they tend to progressively fatigue until they fail to conduct an impulse. This is different to cells of the His-Purkinje system which tend to fail suddenly and unexpectedly (Mobitz II block)
- Clinically: Asymptomatic
- Causes: Increased vagal tone, inferior MI, myocarditis, drugs that slow AV conduction (beta blockers, calcium-channel blockers, digoxin)
2nd degree AV block Morbitz I- ECG
Progressive prolongation of the PR interval culminating in a non-conducted P wave. The PR interval is longest immediately before the dropped beat. The PR interval is shortest immediately after the dropped beat. The P-P interval remains relatively constant
2nd degree AV block Mobitz II (4:1)
Difficult to see if its Mobitz I or Mobitz II, can be clarified after a period of observation (you could see an increasing PR interval- Mobitz I) or an increasing block 3:1 or 4:1 indicating Mobitz II
2nd degress AV block Mobitz II (4:1)- rate and causes
- Ventricular rate 33 bpm. Atrial rate 150 bpm (note P wave hidden in T wave). Intermittent non-conducted P waves without progressive prolongation of the PR interval
- Clinically: much more likely to be associated with haemodynamic compromise, severe bradycardia and progression to 3rd degree heart block. Onset of haemodynamic instability may be sudden and unexpected, causing syncope (Stokes-Adams attacks) or sudden cardiac death. The risk of asystole is around 35% per year
2nd degree AV block Mobitz II (4:1)- causes
1) Anterior MI (due to septal infarction with necrosis of the bundle branches)
2) Idiopathic fibrosis of the conducting system
3) Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair)
4) Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease, autoimmune - SLE, systemic sclerosis)
5) Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis)
6) Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone.
2nd degree AV block Mobitz II (4:1)- ECG
Intermittent non-conducted P waves without progressive prolongation of the PR interval, PR interval in the conducted beats remains constant, the P waves ‘march through’ at a constant rate, the RR interval surrounding the dropped beat(s) is an exact multiple of the preceding RR interval (e.g. double the preceding RR interval for a single dropped beat, treble for two dropped beats, etc).
3rd degree AV block
- In complete heart block, there is complete absence of AV conduction. None of the supraventricular impulses are conducted to the ventricles. To maintain organ perfusion, the heart contracts due to an escape rhythm, dictated by a junctional or ventricular focus. Without this, the patient may suffer ventricular standstill leading to syncope (if self-terminating) or sudden cardiac death (if prolonged).
- Clinically: syncope, chest pain, SOB.
3rd degree AV block: causes and ECG
- Causes: Inferior myocardial infarction, AV-nodal blocking drugs (e.g. calcium-channel blockers, beta-blockers, digoxin), idiopathic degeneration of the conducting system
- ECG: atrial rate is faster (approximately 100 bpm in this case) than the ventricular rate (approximately 40 bpm here) and the two rates are independent. There is no evidence that any of the atrial impulses are conducted to the ventricles.
Ventricular standstill with P waves
Atrial activity (P waves) with no ventricular activity (QRS complex)
Paced rhythm
- The insertion of a pacemaker with produce a paced rhythm
- Vertical spikes of short duration, usually 2ms
- Atrial pacing, with pacing spinked preceding the p wave
- Ventricular pacing, with pacing spikes preceding the QRS complex
Bradyarrhythmias- medication
If associated with adverse features, then give atropine and assess the risk of asystole. If not associated with adverse features, add interim measures as a bridge to pacing (final treatment for the patient).
Peak flow (PEFR)
- Measures how fast air can be blown out of the lungs
- Basic measure of large airway calibre
- Reduced in all conditions associated with airflow obstruction: asthma, COPD, tumour
- Characteristically variable (ideally >20%) in poorly controlled asthma/ more fixed in COPD
Spirometry: Pre and post bronchodilator
- Estimates the degree of reversibility
- 10-15 minutes after MDI SABA
- If FEV1 increases by 12% and increases by 200ml then it suggests responsiveness
What 3 conditions make up ACS
Unstable angina, NSTEMI, STEMI
ACS- clinical features
Chest pain lasting >20 minutes, not relieved by rest or GTN. May radiate to arm/neck/jaw, SOB, Nausea, Sweating.
ACS- investigations
- Bedside: Obs (including BP), ECG
- Bloods: FBC, U&E’s, CRP, glucose (HbA1c), lipid profile, troponin levels
- Imaging: Coronary angiography, may do CXR
