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ECG signs

  • Q-waves are associated with a previous myocardial infarction (Q waves are pathological if present in V2-V3, or >0.1mV for 0.03s or more in 2 contiguous leads)
  • Delta waves are associated with WPW Syndrome, alongside a short PR and prolonged qrs
  • Saddle ST elevation is associated with pericarditis
  • ‘J’ wave - small hump at the end of the QRS complex, assoc with hypothermia

PR 3-5, QRS 2-3


Signs of hypothermia on ECG


The following ECG changes may be seen in hypothermia
‘J’ wave - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias


What is AF?


Atrial fibrillation (AF) is a supraventricular tachyarrhythmia. It is characterised by uncoordinated atrial activity on the surface ECG can be due to ectopic foci or re-entry circuit.
Chaotic and irregular atrial arrhythmia, the prevalence of which increases progressively with age.
Causes significant morbidity and mortality including palpitations, dyspnoea, angina, dizziness or syncope, and features of congestive heart failure, tachycardia-induced cardiomyopathy, stroke, and death.
ECG shows absent P waves, presence of fibrillatory waves, and irregularly irregular QRS complexes. Also order electrolytes, cardiac enzymes (Myocardial ischaemia can be a cause or consequence of AF) and TFTs (thyroxtoxicosis can present with AF).
Mx: If haemodynamically unstable -> DC cardiovert (GA)
Most patients presenting with new-onset or ‘acute’ atrial fibrillation (AF) do not require immediate cardioversion

Most patients will require medical therapy to control ventricular rate using CCB/ b blocker. Check for RA thrombus using echo and anticoagulate with DOAC if needed. If CHADVASC is 2 or more add in heparin to antihypertensives.


When do use cardiac catheter ablation?


NICE recommends the use of catheter ablation for those with AF who have not responded to or wish to avoid, antiarrhythmic medication.

Technical aspects
the aim is to ablate the faulty electrical pathways that are resulting in atrial fibrillation. This is typically due to aberrant electrical activity between the pulmonary veins and left atrium. The procedure is performed percutaneously, typically via the groin both radiofrequency (uses heat generated from medium frequency alternating current) and cryotherapy can be used to ablate the tissue

should be used 4 wks before and during the procedure
it should be remember that catheter ablation controls the rhythm but does not reduce the stroke risk, even if patients remain in sinus rhythm. Therefore, patients still require anticoagulation as per there CHA2DS2-VASc score
if score = 0: 2 months anticoagulation recommended
if score > 1: longterm anticoagulation recommended

cardiac tamponade (fluid in the pericardium builds up, resulting in compression of the heart)
pulmonary valve stenosis
success rate around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously
longer term, after 3 years, around 55% of patients who’ve had a single procedure remain in sinus rhythm. Of patient who’ve undergone multiple procedures around 80% are in sinus rhythm


MI complications


Cardiac arrest

This most commonly occurs due to patients developing ventricular fibrillation and is the most common cause of death following a MI. Patients are managed as per the ALS protocol with defibrillation.

Cardiogenic shock

If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock. This is difficult to treat. Other causes of cardiogenic shock include the ‘mechanical’ complications such as left ventricular free wall rupture as listed below. Patients may require inotropic support and/or an intra-aortic balloon pump.

Chronic heart failure

As described above, if the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure. Loop diuretics such as furosemide will decrease fluid overload. Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure.


Ventricular fibrillation, as mentioned above, is the most common cause of death following a MI. Other common arrhythmias including ventricular tachycardia.


Atrioventricular block is more common following inferior myocardial infarctions.


Pericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients). The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.

Dressler’s syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

Left ventricular aneurysm

The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

Left ventricular free wall rupture

This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.

Ventricular septal defect

Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients. Features: acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgical correction is needed.

Acute mitral regurgitation

More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle. Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.


How to deal with choking?


Ask the pt “are you choking” if they answer verbally yes then it is mild. If they nod/don’t respond -> severe.
If mild airway obstruction
encourage the patient to cough

If severe airway obstruction and is conscious:
give up to 5 back-blows
if unsuccessful give up to 5 abdominal thrusts
if unsuccessful continue the above cycle

If unconscious
call for an ambulance
start cardiopulmonary resuscitation (CPR)


Causes of infective endocarditis


(historically Streptococcus viridans was the most common cause of infective endocarditis. This is no longer the case, except in developing countries.)
1 Staphy aureus is now the most common cause of infective endocarditis. Acute presentation & IVDUs
2.Staphylococcus epidermidis -commonly colonize indwelling lines, prosthetic valve surgery
3.Strep viridans ~20% of cases. found in the mouth ?poor dental hygiene/dental procedure
4. Streptococcus bovis - associated with colorectal ca

INFECTIVE, CULTURE -VE: Haemophilus, Coxiella eetc.

Non-infective: systemic lupus erythematosus (Libman-Sacks), malignancy: marantic endocarditis


Digoxin Toxicity ECG signs

ECG features
down-sloping ST depression ('reverse tick', 'scooped out')
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia

HF 3rd line treatment


Third-line treatment should be initiated by a specialist.
1. ivabradine
criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%
2. Sacubitril-valsartan
criteria: left ventricular fraction < 35%
is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
should be initiated following ACEi or ARB wash-out period
digoxin has also not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties
it is strongly indicated if there is coexistent atrial fibrillation
4. hydralazine in combination with nitrate
this may be particularly indicated in Afro-Caribbean patients
5.cardiac resynchronisation therapy
indications include a widened QRS (e.g. left bundle branch block) complex on ECG


How do we diagnose HTN?


If reading of >140/90 offer ABPM. If <135 monitor. If 135-150 that is stage 1 HTN. If >150 this is stage 2 HTN - treat immediately. If stage 1, treat if > 80 and they have a complication such as: end organ damage, q risk ~ 10% or more, diabetes, renal disease or established CVSD
If the blood pressure is >= 180/120 mmHg: you need to admit if they have chest pain or eye HTN signs. If not, urgently investigate.


How to assess prognosis most MI?


GRACE score
Creatinine (serum)
CHF (killip classes 1: No CHF, 2: Pulmonary rales/ jugular venous distension, 3: Pulmonary oedema 4: Cardiogenic Shock )
Other diagnostic factors: ST deviation, Cardiac arrest on presentation, Tropnins raised




PESI to see if they’re high risk. Or simplified PESI one point or more -> admit for anticoagulation: (one point). Score 0 - 1.1% mortality at 30days. Score above 1 - 30 day mortality is 9%.
Tachycardia (>110)
History of cancer
Eighty (age > 80)

Systolic hypotension (<110)
Oxygen sats below
Ninety percent




Apix/Rivaroxaban would be offered for haemodynamically stable PE, as DOACs are now increasingly used in PE.
PE that have led to RV dysfunction without haemodynamic collapse (i.e. BP<90 for 15 min despite resus)
RV dysfunction -> +ve troponin, ECG changes, Echo, raised BNP (signs of myocardial stretch), CTPA suggesting heart strain.
Tx: Admit, if you think they’re high risk give IV LMW and HDU monitor for at least 3d. Thrombolyse if deteriorate. Needs inpatient echo due to evidence of RH strain. Inpatient for 3-5days

Systolic <90 for over 15 min despite resus attempts or systollic drop > 40mmHg -> THROMBOLYSIS in ITU/RESUS/HDU
Periarrest/has arrested - 50mg stat atleplase (tPA) and then prolong resus (30-60 min CPR).
If no peri-arrest/arrest (hypotensive but no periarrest), give 10mg aleplase over 1-2min and then 90mg over 2 hours.
Complications: Haemorrhage, hypotension, anaphylaxis
Absolute CI: ICH, stroke in past 6 months, SAH, plts <30 (but absolute CI can become relative CI in life threatening cases, need 2 consultants involved)
Relative CI: TIA, already on oral anticoags, severe uncontrolled HTN, pregnancy, plts 30-60

Inferior vena cava filters may be offered in people who have recurrent PE despite anticoagulation.


Infective Endocarditis Diagnostic Criteria


Duke’s Criteria
• 2 major
• 1 major + 3 minor
• All 5 minor

1. +ve blood culture
• Typical organism in 2 separate cultures, or
• Persistently +ve cultures, e.g. 3, >12h apart
2. Endocardium involved
• +ve echo (vegetation, abscess, valve dehiscence) or
• New valvular regurgitation


  1. Predisposition: cardiac lesion, IVDU
  2. Fever >38
  3. Emboli: septic infarcts, splinters, Janeway lesions
  4. Immune phenomenon: GN (glom nephritis), Osler nodes, Roth spots, RF (rheumative fever)
  5. +ve blood culture not meeting major criteria

Other symptoms:
Splenomegaly, clubbing, splinter haemorrhages, janeway lesions, new/changing murmur, AV block, LVF


Post MI treatment

  • ACEi: start w/i 24hrs of MI (e.g. lisinopril 2.5mg)
  • β-blocker: e.g. bisoprolol 10mg OD (or, CCB)
  • Cardiac rehabilitation (group exercise and info)
  • DVT prophylaxis until fully mobile
  • Continue for 3mo if large anterior MI
  • Statin: regardless of basal lipids (e.g. atorv 80mg)
•	Stop smoking
•	Diet: oily fish, fruit, veg, ↓ sat fats
•	Exercise: 30min OD
•	Work: return in 2mo
•	Sex: avoid for 1mo
•	Driving :avoid for 1mo

NB. Continue clopidogrel for 1mo following STEMI Continue aspirin indefinitely.


NYHA classification

  1. No limitation of activity
  2. Comfortable @ rest, dyspnoea on ordinary activity
  3. Marked limitation of ordinary activity
  4. Dyspnoea @ rest, all activity → discomfort

ECG electrolyte abnormalities signs


hypocalcemia is a prolonged QT interval, due to prolonged ST
hypermagnesemia prolonged PR interval is associated with.
hypercalcemia - shortened ST segment
hyperkalaemia - Tall, peaked T waves (earliest sign), flattened/ loss of p waves, broad complex bradycardia
Hypokalaemia - Tall and wide p waves, prolonged PR, flattening of t waves, ST depression


Constrictive Pericarditis - what is it


This is a complication of pericarditis whereby after the healing phase the pericardial cavity is replaced by granulation tissue. The tissue becomes fibrosed and then scarred and finally calcified. It is quite rare and commonly occurs 3-12 months after pericardial insult.
Western countries: idiopathic, post cardiac surgery and
post radiotherapy e.g. for lung cancer which scars the pericardium are top three causes.
Developing cause: TB is most common.
This is a diastolic form of heart failure due to the inelastic pericardium. Can cause RHF sx.


Constrictive pericarditis clinical features



  • RHF c¯ ↑JVP (prominent x and y descents)
  • Kussmaul’s sign: ↑JVP c¯ inspiration
  • Quiet heart sounds
  • S3
  • Hepatosplenomegaly
  • Ascites, oedema

Restrictive cardiomyopathy causes

miSS SHAPEN (*=main causes)
Systemic Sclerosis 
Primary: endocardial fibrosis
Eosinophilia - Lhoffler's eosinophilic endocarditis 
Neoplasia - tricuspid valve disease can  be caused by carcinoid tumour

Ix and Mx of constrictive pericarditis

- CXR: small heart + pericardial calcification
- Echo
- Cardiac Catheterisation 
M - NSAID, steroids, chemo HF management
S - Pericardiectomy

Dilated cardiomyopathy


Can present with LVF or RVF or arthymia
 Dystophy: muscular, myotonic, glycogen storage disease
 Infection: complication of myocarditis
 Late pregnancy: peri-, post-partum
 Autoimmune: SLE
 Toxins: EtOH, doxorubicin, cyclophosphamide, DXT
 Endocrine: thyrotoxicosis


Restrictive cardiomyopathy ix & management


Ix - catheter biopsy
Treatment of RCM includes treating the underlying cause (if identified) and heart failure management.
Underlying causes:
- Amyloid (AL - dexamethasone & melphalen chemo; AA - treat underlying cause of inflammation)
- Haemochromatosis - C: hepatitis vaccination and stop iron and vit c supplements; M: 1st line Venesection, 2ndline chelation therapy e.g Desferrioxamine + vit C
- Sarcoid - corticosteroids (acute- IV, chronic - oral)

Diuretics are the mainstay of treatment to reduce volume overload. Becareful- RCM pts rely on high filling pressures to maintain CO and excessive diuresis may result in tissue hypoperfusion.


Pericarditis Complications


Effusion ± tamponade

Constrictive pericarditis


Aortic Stenosis presentation + signs


Triad: angina, dyspnoea, syncope (esp. c¯ exercise)
 LVF: PND, orthopnoea, frothy sputum
 Arrhythmias
 Systemic emboli if endocarditis
 Sudden death
 Slow rising pulse c¯ narrow PP
 Aortic thrill
 Apex: Forceful, non-displaced (pressure overload)
 Heart Sounds
 Quiet A2
 Early syst. ejection click if pliable (young) valve
 S4 (forceful A contraction vs. hypertrophied V)


Aortic Stenosis presentation + signs


Triad: angina, dyspnoea, syncope (esp. c¯ exercise)
* LVF: PND, orthopnoea, frothy sputum
 Arrhythmias
 Systemic emboli if endocarditis
 Sudden death
 Slow rising pulse
* narrow PP
 Aortic thrill
 Apex: Forceful, non-displaced (pressure overload)
 Heart Sounds
* Quiet A2
 Early syst. ejection click if pliable (young) valve
* S4 (forceful A contraction vs. hypertrophied V)


Aortic stenosis echo findings


ACC criteria

1) Pressure gradient >40
2) Jet velocity >4m/s
3) valve area <1cm3


Which aetiologis are the different arrest rhythms associated with?


Pulseless VT - high rate of electrical activity, leading to the heart being an ineffective pump, and not being able to support circulation
PEA - a rhythm that should produce a pulse but doesn’t- Tension Pneumothorax
Asystole - total cessation of the electrical activity of the heart, meaning an ECG will show no electrical activity. It is primarily a conducting system problem, not a problem with the heart as a pump.


Aortic Dissection Ix and Tx


Ix: CTA if too unstable, TOE
type A - ascending aorta - control BP (IV labetalol) + surgery. (Might have signs of AR)
type B - descending aorta - control BP(IV labetalol)


You are bleeped by the nurse in charge of a surgical ward to attend to a 52-year-old man with a background of hypertension. Upon review, the patient is unable to give a history, looks pale, and feels clammy.

On assessment you find the following results:
Blood pressure: 82/45mmHg,
Heart rate: 152 bpm,
Respiratory rate: 25/min,
Oxygen saturation: 98%,
Temperature: 36.6ºC.
An ECG shows an irregularly irregular rhythm with no clear P waves. You ask the nurse to place a medical emergency call.

What is the most appropriate immediate management?


Synchronised Shock!

The indications for synchronised cardioversion in a patient with an arrhythmia include shock (as in this case), myocardial ischaemia, heart failure, and syncope.


ECG changes requiring thrombolysis or PCI


ST elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) OR

ST elevation of greater than 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, avF, avL) OR

New Left bundle branch block (not RBB)


Complete heart block + syncope


Adverse sign requiring treatment
1st line Atropine (500mcg IV)

If there is an unsatisfactory response the following interventions may be used:
atropine, up to maximum of 3mg
Then: transcutaneous pacing
Then: IV Pacing: isoprenaline/adrenaline infusion titrated to response


ACE i monitoring


a rise in the creatinine and potassium may be expected after starting ACE inhibitors
acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.
significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis


BP goals


Age < 80 years 140/90 mmHg 135/85 mmHg
Age > 80 years 150/90 mmHg 145/85 mmHg
BP vs Ambulatory


Bradycardia tx


Bradycardia is defined as a heart rate of fewer than 60 beats per minute. Consider treating any potentially reversible causes of bradycardia once identified. It is important to identify the adverse signs of bradycardia and treat them promptly.

If adverse features are present, most patient’s initial management is Atropine (initially 500mcg then repeat every 5 min until total dose of 3mg). Pacing is typically considered in those unresponsive to pharmacological management or with a risk factor for asystole.

If a beta-blocker or calcium channel blocker is a likely cause of bradycardia, consider giving intravenous glucagon.
If the bradycardia due to digoxin toxicity, consider using digoxin-specific antibody fragments.
If bradycardia complicating acute inferior wall myocardial infarction, spinal cord injury or cardiac transplantation, consider using theophylline.

Transcutaneous pacing should be initiated immediately if there is no response to atropine or if atropine is contraindicated.




On a 12-lead ECG ST-elevation would not be noticeable and so only reciprocal changes are visible in leads V1-V3. The changes associated with these leads include:
ST depression
Tall, broad R-waves
Upright T-waves


Features of HOCM


results in predominantly diastolic dysfunction
left ventricle hypertrophy → decreased compliance → decreased cardiac output
O/E: jerky pulse, large ‘a’ waves, double apex beat
ejection systolic murmur
PC: Exertional dyspnoea, a/s, angina syncope
Associations: WPW and Friedrich’s Ataxia
- left ventricular hypertrophy, non-specific ST segment and T-wave abnormalities, progressive T wave inversion, deep Q waves, or atrial fibrillation.
Echo: MR, assymetrical hypertrophy




Wolff-Parkinson White is when someone has an accessory pathway in their heart’s electrical conduction. It presents on an ECG with a short PR interval (<120ms), wide QRS complex (>120ms), and an upsloping delta wave. I


Definition of angina and how to manage it


NICE define anginal pain as the following:
1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
2. precipitated by physical exertion
3. relieved by rest or GTN in about 5 minutes
patients with all 3 features have typical angina
patients with 2 of the above features have atypical angina
patients with 1 or none of the above features have non-anginal chest pain

For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes):
1st line: CT coronary angiography
2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)
3rd line: invasive coronary angiography


3rd line HF mx

  • ivabradine
    criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%
  • sacubitril-valsartan
    criteria: left ventricular fraction < 35%
    is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
    should be initiated following ACEi or ARB wash-out period
  • digoxin- has also not been proven to reduce mortality, may however improve symptoms, strongly indicated if there is coexistent AF
  • hydralazine in combination with nitrate. esp AC pts
  • cardiac resynchronisation therapy
    indications include a widened QRS (e.g. left bundle branch block) complex on ECG