9-15th August Flashcards
How much does a large square represent on an ECG?
0.2 seconds
View of the heart from each lead?
- V1 and V2 septal view of the heart
- V3 and V4 anterior view of the heart
- V5 and V6 lateral view of the heart
- Lead I: lateral view
- Lead II and III: inferior views
- aVR and aVL lateral view
- aVF: inferior view
What is the normal HR?
Between 60-100bpm
How to calculate HR?
- 300/number of large squares R-R interval
- if irregular, count number QRS complexes x6 [as trace normally 10s long]
Cardiac axis
- lead II normally most positive
- lead I left axis deviation
- lead III right axis deviation
How long should PE interval be?
120-200ms [2-5 large squares]
What is a heart block?
Prolonged PR interval over 0.2s
Types of heart block?
- Prolonged PR interval over 0.2s suggests first-degree heart block [AV block]
o Second-degree heart block [type 1] also known as Mobitz type 1 AV block, or Wenckebach phenomenon: progressive prolongation PR interval until atrial impulse not conducted and QRS complex dropped
o Second-degree heart block [type 2]: Mobitz type 2 AV block. Consistent PR interval duration with intermittently dropped QRS complexes due to failure of conduction. Intermittent dropped QRS complexes typically follows a repeating cycle of every 3rd or 4th P wave
o Third-degree heart block: no electrical communication between the atria and ventricles due to a complete failure of conduction.
Cause of shortened PR interval?
o P-wave originate somewhere closer to the AV node and so conduction takes less time
o Atrial impulse getting to the ventricle by a faster shortcut instead of conducting slowly across the atrial wall. There is an accessory pathway and can be associated with a delta wave. Delta wave found in Wolff Parkinson White syndrome and includes a slurred upstroke of the QRS complex.
Classify a broad vs narrow QRS complex
- Width can be narrow [<0.12 seconds] or broad [>0.12]:
o Narrow: well-organised and syndronised ventricular depolarisation
o Broad: abnormal depolarisation for example if ventricular ectopic
Height in QRS complexes
- Height can be small or tall:
o Small: less than 5mm in limb leads, or 10mm in chest leads
o Tall: imply ventricular hypertrophy
Morphology of a QRS complex
-Morphology:
o Delta wave in WPW [though also needs tachyarrhythmias and Delta wave for Dx]
Summarise QRS findings on an ECG
Width can be narrow [<0.12 seconds] or broad [>0.12]:
o Narrow: well-organised and syndronised ventricular depolarisation
o Broad: abnormal depolarisation for example if ventricular ectopic
Height can be small or tall:
o Small: less than 5mm in limb leads, or 10mm in chest leads
o Tall: imply ventricular hypertrophy
Morphology:
o Delta wave in WPW [though also needs tachyarrhythmias and Delta wave for Dx]
Q-wave pathology
- Isolated Q waves can be normal
- Pathological Q wave is >25% the size of the R wave that follows it or >2mm in height and >40ms in width. Evidence of previous MI.
ST segment abnormalities
- Part of the ECG between the end of the S wave and the start of the T wave
- Healthy, it should be isoelectric line
- ST-elevation is significant when it is greater than 1mm [1 small square] in 2 or more contiguous limb leads or over 2mm in 2 or more chest leads -> commonly caused by acute MI
- ST depression of over 0.5mm in 2 or more contiguous leads indicated myocardial ischaemia
What are tall T waves associated with?
- Tall T waves is over 5mm in the limb leads AND over 10mm in the chest
- Associated with hyperkalaemia [“tall tented T waves”] and hyperacute STEMI
What would inverted T waves represent?
o Normally inverted in V1 and inversion in lead III is a normal variant
o Sign of variety of conditions including ischaemia, bundle branch bocks [V4-V6 in LBBB, V1-V3 in RBBB], PE, LVH [lateral leads], hypertrophic cardiomyopathy [widespread], general illness
o Around 50% ITU patients have some evidence of T wave inversion
Cause of biphasic and flattened T waves
- Biphasic T waves indicated ischaemia and hypokalaemia
- Flattened T waves -> may represent ischaemia or electrolyte imbalance-
What do U-waves represent?
U waves are not a common finding.
The U wave is a > 0.5mm deflection after the T wave best seen in V2 or V3.
These become larger the slower the bradycardia – classically U waves are seen in various electrolyte imbalances, hypothermia and secondary to antiarrhythmic therapy (such as digoxin, procainamide or amiodarone).
First-degree heart-block pathology
Impulse that conducts from atria to the ventricles through the AVN is delayed and travels slower than normal
Common causes of AVN block
AV node disease Enahnced vagal tone [e.g. athletes] Myocarditis Acute MI Electrolyte disturbances Medications
Which medications can cause 1st degree heart block?
CCB Beta-blockers Cardiac glycosides Cholinesterase inhibitors Digitalis
When do tall T-waves typically present?
Typically in the hyper-acute period [3-30 minutes after onset]. In reality, rarely seen as ECG recordings typically later with ST elevation being more comonly noted.
Which leads have inverted T waves?
aVR and V1 T waves
Types of ECG rhythms
Sinus = regular rhythm
Regular irregular = ectopic
Irregularly irregular = AF
Rates of the nodes?
SAN has rate 70/80
AVN rate of 60s
Purkinje rate of 50s
Myocytes rate of 30
RBBB definition on ECG
- QRS duration > 120ms
- RSR’ pattern in V1-3 (“M-shaped” QRS complex)
- Wide, slurred S wave in lateral leads (I, aVL, V5-6)
LBBB definition
- QRS duration > 120ms
- Dominant S wave in V1
- Broad monophasic R wave in lateral leads (I, aVL, V5-6)
- Absence of Q waves in lateral leads
- Prolonged R wave peak time > 60ms in leads V5-6
Tx in ACS
Tx in ACS
- GTN spray -> reduce pre-load and afterload
- PCI referral [some CI to this, and thrombolysis]
- Problem in patients with arrhythmias cause deaths in patients [VT can lead to this], or cardiogenic shock
Monomorphic VT
Looks like scribbles
Polymorphic VT
Scirbbles with dip in middle
Tx with magnesium
Normal ranges on an ABG
pH: 7.35 – 7.45 PaCO2: 4.7 – 6.0 kPa || 35.2 – 45 mmHg PaO2: 11 – 13 kPa || 82.5 – 97.5 mmHg HCO3–: 22 – 26 mEq/L Base excess (BE): -2 to +2 mmol/L
Definition of hypoxia
<10kPa
Definition of severe hypoxia
<8kPa
Definition of type 1 respiratory failure
Hypoxaemia [<8kPa] with normocapnia [<6kPa]
Why does type 1 respiratory failure occur?
It occurs as a result of ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lung tissue. As a result of the VQ mismatch, PaO2 falls and PaCO2 rises. The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shape of the CO2 and O2 dissociation curves. The end result is hypoxaemia (PaO2 < 8 kPa /60mmHg) with normocapnia (PaCO2 < 6.0 kPa / 45mmHg).¹
Examples of VQ mismatch
- Reduced ventilation and normal perfusion (e.g. pulmonary oedema, bronchoconstriction)
- Reduced perfusion with normal ventilation (e.g. pulmonary embolism)
Define type 2 respiratory failure
Type 2 respiratory failure involves hypoxaemia (PaO2 is <8 kPa / 60mmHg) with hypercapnia (PaCO2 >6.0 kPa / 45mmHg). It occurs as a result of alveolar hypoventilation, which prevents the patient from being able to adequately oxygenate and eliminate CO2 from their blood.
When can hypoventilation occur?
Hypoventilation can occur for a number of reasons including:
• Increased resistance as a result of airway obstruction (e.g. COPD).
• Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures, obesity).
• Reduced strength of the respiratory muscles (e.g. Guillain-Barré, motor neurone disease).
• Drugs acting on the respiratory centre reducing overall ventilation (e.g. opiates)
What suggests acidosis is caused by respiratory, what suggests it’s caused by metabolic problems?
Caused by either CO2 [respiratory] or HCO3- [metabolic].
Go through pH, CO2 and HCO3- values in patient with: respriatory acidosis, respriatory alkalosis, and each of these with metaoblic compensation
see table
Underlying biochemistry with ABGs
CO2 + H20 <=> H2CO3 <=> HCO3- + H+
pH, HCO3- and CO2 in metaoblic acidosis, alkalosis, with and without respiratory compensation
see table
What do base excess levels represent?
correlates to high level of HCO3-
Rate of compensation in respiratory versus metabolic disorders
Respiratory
- quickyl due to increased/decreased alveolar ventilation
Metaoblic
- takes few days to occur, so can assume the respriatory derangement has been ongoing for a couple of days if not more