Cardiology Flashcards
How to work out rate in ECG
300/ Number of squares in R-R interval
how long should p wave be?
120-200ms
Prolonged PR interval indicates
AV block
Shortened PR interval indicates ? What other feature of this condition do you often see on ecg
atrial impulse to ventricles quicker i.e. accessory pathway
associated with delta wave (slurred QRS upstroke) in Wolff Parkinson White
QRS normal length ?
80-120ms
Where is the j point
where S waves meets ST segment
When is ST elevation significant?
> 1mm in 2 or more limb leads
or >2mm in 2 or more chest leads
What is the t wave?
ventricular repolarisation
When is a t wave “tall” what could this mean?
> 5mm in limb AND >10mm in chest
associated hyperacute STEMI and hyperkalaemia
Inverted T wave is normal where?
V1 and lead III
Inverted t waves association?
ischaemia, PE, BBB
What is sinus bradycardia
<60bpm
every P wave is followed by a QRS
Physiological causes of sinus bradycardia?
Pathological?
Physiological: athletes, young due to *high resting vagal tone (vagal activity is continuous)
Pathological: acute MI, drugs (BB, dig, amiodarone), hypothyroid, hypothermia, sick sinus, raised ICP
When do you treat bradycardia
<40bpm / symptomatic
Mx of symptomatic bradycardia
IV atropine - anticholinergic, i.e. muscarinic antagonist, reduces vagal tone
Temporary pacing wire
What is sick sinus syndrome? Causes ?
Result of dysfunction of SA node with impairment of ability to generate impulse
Normally idiopathic fibrosis of node
ischaemia
digoxin toxicity
Causes of AV block
MI/ischemia (inferior)
SLE
myocarditis
(lyme disease endocarditis, degeneration of HIS-PURKINJE, drugs (digoxin, BB, CCB))
1st degree heart block is?
PR > 0.2s, PR constant, every P followed by QRS
2nd degree heart block?
Intermittent failure of conduction from atria to ventricles. Some P are not followed by QRS
Mobitz type I (Wenckebach) failure at level of AV node.
PR interval progressively lengthens and is then blocked.
Mobitz type II intermittent failure of P wave conduction.
PR interval is constant + prolonged. Fixed PR interval, dropped QRS waves2:1 block or 3:1 block
What is 3rd degree heart block? Usual cause?
Complete failure conduction atria to ventricles
myocardial fibrosis
Name 3 causes of RBBB
Rheumatic heart disease
RVH
IHD, myocarditis, cardiomyopathy, degenerative disease conduction system
Name 2 changes on ECG of RBBB
MarroW
QRS > 0.12s
Secondary R wave in V1, V2 - RSR’ [Seconary R in RBBB]
Deep, wide slurred S wave in I, V5, V6
LBBB associated conditions. Name 2
Coronary artery disease, hypertensive heart disease, dilated cardiomyopathy, anterior infarction
Name 2 ECG changes in LBBB
WilliaM
Wide QRS > 0.12s
Absent Q in V5, V6
Broad R in I, V5, V6
Deep S in V1, V2 [Long S in LBBB]
Ix in brady?
12 lead ECG
electrolyte imbalance
UE, glucose, Ca, Mg, TFT, toxicology
Mx of brady
Treat cause - correct electrolytes / stop negative chronotropes
IV atropine 0.5mg (may repeat up to 3mg)
Poor response - transcutaneous pacing
\9May also try glycopyrrolate (antimuscarinic), glucagon (if due to BB or CCB))
Temporary or permanent pacing (esp @heart block, sick sinus)
What Sx do you get with sinus tachy and why?
In diastole coronary blood flow increases. As HR increases diastole shortens.
Decreased flow to heart with increased ventricular rate = angina type symptoms, chest pain, faintness, SOB
Definition and Some causes of sinus tachy
Every P followed by QRS, rate over 100
Physiological: exertion, anxiety, pain
Pathological: fever, anaemia, hypovolaemia
Endocrine: thyrotoxicosis, phaeo
Pharmacological: sympathomimetic, adrenaline, alcohol, caffeine, salbutamol
Ix in sinus tachy
12 lead ECG, cardiac enzymes, FBC (anaemia), TFT
Mx acute regular sinus tachy
Mx ongoing sinus tachy
Vagal manoeuvres: carotid massage (young pt due to stroke risk),
*vasalva manoeuvre (forceful exhalation against closed airway with nose pinched),
facial immersion in cold water
Ongoing:
BB
or non-dihydropyridine CCB (diltiazem, verapamil)
Eg of some SVTs
AF / fibrilation
Sinus tachy
AV re-entry tachy ….
What is the most common cause of paroxsysmal narrow complex tachy cardia (SVT) ? Usual onset?
AV nodal re entry tachy
late teens / 20s
ECG of SVT? Name 2 things
Regular rhythm, narrow QRS, rate 130-250
Retrograde atrial conduction: inverted P waves in II, III, AVF (inferior)
Atrial and ventricular depolarisation together - P waves buried in QRS
Mx of AVNRT (its an SVT)
1/2nd line?
prophylaxis?
curative?
First line: Vagal maneuvers may stop as transiently block AV node
Second line: *Adenosine (for junctional) can acutely stop as transiently blocks AV node. Feel like death.
Prophylaxis: one of the above or a BB
Curative: radiofrequency ablation
What is the delta wave seen in WPW ?
Slurred upstroke of the QRS
Mx of WPW
Acute?
Prophylaxis?
Currative?
Vagal maneuvres ± adenosine
Prophylaxis: drug for AV node and accessory: flecainide (1c) or sotalol (3)
Curative: radiofrequency ablation
Main complications of narrow complex SVT?
MI
HF
Mx of complications of Narrow SVT
(If BP<90, chest pain (MI), heart failure, heart rate >200 )
DC cardioversion with general anaesthetic
± IV amiodarone (150mg IV over 10 mins)
Rhythm in AF
Irregularly irregular ventricular rhythm
Paroxysmal = spontaneous termination within 7 days
Persistent = 7 days to one year
Permanent = over a year
Risk factors:
- old age
- family history
- male
- obesity
Causes:
- Ischaemia - MI
- infection - myocarditis, endocarditis
- structural - mitral stenosis or any valvular disorder
- hyperthyroid
- hyper K
Symtptoms:
- palpitations
- syncope
- dizziness
- chest pain
- fatigue
- SOB
Signs:
- hypotension
- irregularly irregular pulse
Main complications of AF
Rapid chaotic atrial firing causes stagnation of blood in atria leads to thrombus formation and risk of embolism leading to increased risk of stroke
Reduction of cardiac output (esp in ex) may lead to heart failure
Mx of AF
Rate control:
First line: standard BB or rate limiting CCB (diltiazem, verapamil)
Dual therapy add digoxin or two of above (**ONLY DILTIAZEM)
Rhythm control
Persist over 48 hours offer electrical cardioversion (DC) (transoesophageal)
Consider amiodarone for 4W before + 12M after
Anticoagulate
When can you not use fleicanide for AF?
Ischemic / structual cause
What to do if drug Mx fails in AF?
left atrial catheter ablation (if paroxysmal) or pace and ablate (if permanent) (AV node)
What is meant by pharmacological cardioversion
IV amiodarone
ECG of atrial flutter
Atrial rate 300 - no p waves *F waves
Undulating saw-tooth Flutter waves
Regular ventricular rhythm 150bpm (2:1 and 4:1 common)
Causes of Atrial flutter
Name 2
CAD, HTN, hyperthyroid, obesity, alcohol, COPD
Ix in atrial flutter
TFT, FBC (anaemia precipitates HF), UE (potassium), renal func, LFT/coag for warfarin
Imaging: echo for underlying cardiac function
Mx of atrial flutter
Rhythm control: cardioversion or medications
-DC cardioversion (if >48hours ensure adequate anticoag)
-Or IV amiodarone, sotalol, fleicanide
Mx of recurrence of atrilal flutter
radiofrequency catheter ablation
Management of broad complex tachy?
what to monitor?
If unstable?
Support ABC, O2 and venous access
Monitor ECG, BP, sats
Identify and treat reversible cause e.g. electrolyte abnormalities potassium
Unstable:
DC schock
Or AMIODARONE 300mg IV over 10-20 mins
What should you consider long term and why for VT
It is usually due to damage so requires maintenance anti-arrhythmics (BB/CCB)
or consider ICD implantable cardioversion defibrillator
What does torsades de points look like on ECG?
Like a sound wave
(In sinus:
Prolonged QT and prominent U wave
In tachycardia:
Varied axis and varied amplitude QRS)
What may happen to torsades if untreated?
Deteriorate to VF
Mx torsades?
IV magnesium sulphate
What does VF look like on ECG?
Chaotic (varying amplitudes)
No identifiable P, QRS, T
Rate 150-500
Mx of VF acute? long term?
Defibrillation
Long term:
BB and ICD (implantable cardioverter defibrillators)
Mx of brugada?
ICD implantable cardioverter defibrillator
What is the brugada sign?
Coved ST segment elevation >2mm in >1 of V1-V3 followed by -ve T
ECG finding in PE
*Sinus tachycardia - main finding
S1Q3T3 - deep S, deep Q wave in 3, deep T wave in 3 - only 10%
ECG of hypothermia
brady
J wave
(Late delta wave, positive deflection at junction of QRS and ST segment)
What is amiodarone used for?
For tachyarrhythmias (AF, AFl, SVT) when other drugs or electrical cardioversion don’t work
Some adverse affects of amiodarone? name 2
Hypotension during IV infusion.
Chronic use
lungs (pneumonitis),
heart (AV block),
liver (hepatitis),
skin (grey discolouration),
thyroid (long half life - hypothyroidism / thyroid crisis)
Adenosine use?
First line diagnostic and therapeutic in SVT (inc junc)
What is important thing about adenosine
Pt feels like they gonna die for a bit
Blocks SA and AV node - causes bradycardia and asystole - doom feeling
May induce bronchospasm in asthma or COPD
What to do when giving adenosine
must always monitor with continuous ECG
Digoxin uses?
Reduce ventricular rate (AF, AFl) - after CCB or BB
Severe heart failure - 3rd line
Important to remeber with digoxin
low theraputic index
which drugs have bad interactions with digoxin
Loop + thiazide diuretics cause hypokalaemia - toxicity
Amiodarone, CCB, spironolactone all increase plasma digoxin - toxicity
SAC those drugs if you’re gonna use them with digoxin you must be LOOPY
How do you monitor for digoxin toxicity?
What target level in blood?
Monitor symptoms (or vent rate) + ECG + renal dysfunction + hypokalaemia
(Sx - Nausea, vomiting, diarrhoea, dyspnoea, confusion, dizziness, headache, blurred vision)
Target blood conc
Target 1.0-1.5nmol/l
Above 2.0nmol/l suggests toxicity
ST-segment depression - reverse tick sign
CCBs uses
Rate control in SVT inc AF +AFl
Why should you not give CCB with BB
both negatively inotropic and chronitropic so may cause HF, bradycardia + asystole
When ar BBS used 1st line?
IHD reduce angina
CHF improve prognosis
AF reduce rate and maintain sinus rhythm
SVT to restore sinus rhythm
SE of BBs
Fatigue, cold extremities, headache, impotence
When are BBs CI ? how to mitigate?
Asthma - B2 blockade causes bronchospasm, usually safe in COPD
Choose a B1 selective (ABM, atenolol, bisoprolol, metoprolol), rather than non-specific (propanolol)
Where to listen for heart valves
Mitral area - apex midclavicular, 5th IC
Tricuspid - inferior right sternal (4th IC)
Pulmonary - left 2nd IC next to sternum
Aortic - right 2nd IC next to sternum
What position are mitral murmurs best heard?
@apex + radiate to axilla, heard best in left lateral position
MR murmur
pansystolic
MS murmur?
Loud opening snap S1 and mid-diastolic murmur
How to differentiate between MR / TR
Both pansystolic but TR does not radiate to axilla
PS murmur ? Interesting fact?
Crescendo-decrescendo systolic (louder then softer).
disappear on inspiration
PR murmur
early diasolic
When are aortic murmurs best heard?
holding breath
AS murmur?
Crescendo-decrescendo systolic
Aortic regurge best heard?
Early diastolic best heard leaning forward on breath hold (pulmonary diappears)
Usual cause of AS
Senile calcification
triad of SX in AS
chest pain (predisposes to chest pain),
heart failure (obstruction -> LV hypertrophy -> LV failure),
syncope (insufficient blood)
o/e AS?
Slow rising pulse
Narrow pulse pressure (diff between syst and dia)
LV hypertrophy -> apex thrill
Crescendo-decrescendo early systolic murmur heard at R2IS transmitted to carotids
What Ix confirms Dx of AS? other Ixs?
Echo
ECG
CXR
Mx of AS ? what if not fit for sugery?
Avoid heavy exertion, modify RF for CAD
If symptomatic - prompt valve replacement - first line
If not fit for surgery
Second line - balloon valvuloplasty - risk of re-stenosis
TAVI - transcatheter aortic valve replacement
Complications of mechanical heart valves
Predisposition to infective endocarditis
Small emboli
Decompensation - increased pressure in pulmonary - CHF
How to prevent IE with new heart vlaves
ABX prophylaxis
Target INR in valve replacement
Anticoagulate mechanical heart valves
Target INR 2.5-3.5 for aortic
Causes of AR
Bicuspid
rheumatic fever
IE
collagen
Marfans / ehler danlos / turners