Cardiology Flashcards
ECG Lead Position - Limb Leads
aVR - Right arm (wrist)
aVL - Left arm (wrist)
aVF - Left Leg
Neutral - Right leg
ECG Lead I
Information between (-) aVR and (+) aVL
ECG Lead II
Information between (-) aVR and (+) aVF
often used for the rhythm strip
ECG Lead III
Information between (-) aVL and (+) aVF
ECG Lead Position - Chest Leads
V1 4th ICS, right sternal edge. V2 4th ICS, left sternal edge. V3 midway between V2 and V4 V4 5th ICS, midclavicular line V5 5th ICS, anterior axillary line V6 5th ICS, mid-axillary line
ECG - Isoelectric Line
the imaginary line that forms the baseline of the ECG trace through the entire strip.
We measure the amplitude (height) of waves and deviation of segments from this reference point
ECG Square Sizes
Large Squares are 5mm x 5mm
Small Squares are 1mm x 1mm
ECG Calibration
Must be properly calibrated.
Normal calibration:
Amplitude (height) = 10mm/mV
=> 1 small square = 0.1mV
=> 1 large square = 0.5 mV
Duration (speed) - 25mm/s
=> 1 small square = 0.04 sec
=> 1 large square – 0.2 sec
What does the P-wave on an ECG represent and what are its normal parameters?
represents atrial depolarisation
Normal Parameters:
=> Duration – <0.12 secs (3 small squares)
=> Amplitude – <0.25 mV (2.5 small squares)
=> Direction – Upright in leads I, AvF, V3-V6
What does the PR segment on an ECG represent and what are its normal parameters?
= the distance between the P-wave and the QRS complex
represents the delay at the AV Node
Normal Parameters:
=> Amplitude – 0.0mV (i.e. isoelectric line)
What does the PR interval on an ECG represent and what are its normal parameters?
represents atrial depolarisation and delay at AV Node
Normal Parameters:
=> Duration – 0.12-0.20 secs (3-5 small squares)
What does the QRS complex on an ECG represent and what are its normal parameters?
represents ventricular depolarisation
Normal Parameters:
=> Duration – <0.12 secs (3 small squares)
=> Amplitude
>0.5 mV (in ≥1 limb lead)
>1mV (in ≥1 chest lead)
Upper Limit: 3.0mV (6 big squares)
=> Direction
Positive in I, II, V4-V6
Negative in aVR, V1 and V2
What does the QT interval on an ECG represent and what are its normal parameters?
represents the whole ventricular action potential
Normal Parameters:
=> Duration:
- Males: <0.40 secs (2 big squares)
- Females: <0.44 secs (11 small, or 2 big 1 small)
What does the ST segment on an ECG represent and what are its normal parameters?
represents the “Plateau Phase” of ventricular action potential
Normal Parameters:
=> Amplitude – Isoelectric, slanting up to the T-wave
=> Direction:
Elevation of up to 2mm normal in chest leads
Not normally depressed >0.5mm
What does the T-wave on an ECG represent and what are its normal parameters?
represents ventricular repolarisation
Normal Parameters:
=> Normally rounded and asymmetrical (gradual upslant)
=> Amplitude – >0.2 mV (2 small squares) in leads V3 and V4
=> Direction – Same as QRS in at least 5 of 6 limb leads.
What is an approach to interpreting ECGs?
Confirm patient demographics
Indication for test
Calibration
Rate
Rhythm
Axis
Abnormalities:
- P-wave
- PR interval
- QRS complexes
- ST segments
- T-waves
- QT interval
what is the normal cardiac axis?
-30° to 90°
what indicates normal cardiac axis on ECG?
QRS up in Lead I
QRS up in aVF
what indicates left axis deviation on an ECG?
what conditions are associated with this?
QRS up in Lead I
QRS down in aVF
essential hypertension or valvular heart disease
what indicates right axis deviation on an ECG?
QRS down in Lead I
QRS up in aVF
COPD and pulmonary hypertension
what indicates extreme axis deviation on an ECG?
QRS down in Lead I
QRS down in aVF
what would absence of P-waves indicate?
atrial fibrillation (alongside irregularly irregular rhythm)
What would cause prolongation or shortening of the PR interval?
PROLONGATION:
1st Degree Heart block
2nd Degree Mobitz Type I heart block
SHORTENING:
pre-excitation syndromes
what is counted as a narrow QRS complex? what does this represent?
<3mm
normal => represents fast, synchronised ventricular depolarisation
relies on the fast-conduction pathways
what is counted as a broad QRS complex? what does this represent?
> 3mm
caused by:
Abnormal depolarisation (e.g. bundle branch blocks, ventricular ectopic beats)
Pre-excitation (accessory pathways)
when is the ST segment elevated?
what does this indicate?
- 1mm in the limb leads (Leads I, II, III, aVR, aVL, aVF)
- 2mm in the chest leads (V1-V6).
must occur in 2+ adjacent leads
ST Elevation Myocardial Infarction (STEMI)
when is the ST segment depressed?
what does this indicate?
Any depression >0.5mm in 2+ leads is abnormal
Indicates ischaemia
what are “Tall and Tented” T-waves on an ECG?
what could this indicate?
Tall – at least ½ the amplitude of the preceding QRS complex)
Tented – look as if they’ve been pinched from above - i.e. a pointed peak, narrow base
Caused by hyperkalaemia.
Inverted T-waves
normal in Lead aVR (where everything should be negative)
can be a normal variant in Leads V1 and III
T-wave Inversion in other leads is a non-specific sign for Ischaemia, Bundle Branch Blocks, Pulmonary Embolism (PE), Hypertrophic Cardiomyopathy (HCM) etc.
Flattened T-waves
another non-specific sign, of ischaemia, or of electrolyte imbalance (e.g. Hypokalaemia)
Long QT Syndrome
carries a risk of life-threatening Arrhythmias
Some medications prolong the QT Interval, so should be carefully monitored, and avoided altogether in patients with Long QT Syndrome
1st degree heart block
a PR interval >200ms (5 small squares or 1 big square)
prolongation remains fixed in length, and P-waves remain associated with QRS complexes
2nd degree heart block, mobitz I
“Wenckebach”
PR-interval progressively elongates, eventually culminating in the non-conduction of one P-wave, before the cycle begins again with a minimally-prolonged/normal PR interval
2nd degree heart block, mobitz II
Intermittent conduction and non-conduction of P waves without PR-interval prolongation (can be no pattern, or fixed ratio)
3rd degree heart block
Total dissociation between atrial and ventricular activity
e.g. Atrial rate of 60bpm, and an overlying, but independent Ventricular rate of 27 bpm.
which heart blocks require a pacemaker?
2nd degree (Mobitz II) and 3rd degree heart blocks carry a high risk of asystole, and require pacemaker implantation
which heart blocks don’t normally require a pacemaker?
1st degree and 2nd degree (Mobitz I) heart blocks tend to be asymptomatic, and don’t tend to require pacing
Normal cardiac conduction pathway
Triggered at the SA node (right atrium)
AP spreads through the atria, causing atrial contraction.
AP reaches the AV node, delayed for a short time.
AV Node triggers the AP to travel rapidly down the septum via the bundle of His and the bundle branches.
At the apex of the heart, the AP spreads rapidly through the ventricles via the Purkinje Fibres, causing synchronised depolarisation
what is the purpose of the delay in conduction at the AV node?
to allow the ventricles to fill fully
What is the firing rate of the SA Node?
60 - 100 bpm
what is the firing rate of the ventricular cardiomyocytes?
10-40 bpm
what would indicate whether the arrhythmia is supra ventricular or ventricular?
SV - narrow QRS complex
V - broad QRS complex
Cardiac accessory pathways
AP is able to bypass the AV Node
triggers early depolarisation of part of the ventricle (seen as a Delta Wave on the ECG)
AP propagates slowly, as it spreads cell-to-cell through the heart muscle
Distribution of ST elevation in anterior MI?
Anterior zone supplied by left anterior descending (LAD) artery
elevated in Leads V1-V4
Distribution of ST elevation in lateral MI?
Lateral zone is supplied by the Left Circumflex (LCx) Artery
elevated in Leads V5, V6, I and aVL
Distribution of ST elevation in inferior MI?
inferior zone is supplied by the Right Coronary Artery (RCA)
elevated in Leads II, III and aVF
Distribution of ST elevation in anterolateral MI?
when the Left Coronary Artery is occluded
affecting both the Anterior and Lateral zones as LAD and LCx branches affected
What might an ECG look like days/months after a STEMI?
may have a deep Q-wave (indicating tissue death)
Atrial flutter vs. Atrial fibrillation on an ECG
quivering baseline, no P-waves = atrial fibrillation
sawtooth pattern = atrial flutter
Causes of LVH
- Hypertension (most common cause)
- Aortic stenosis
- Aortic regurgitation
- Mitral regurgitation
- Coarctation of the aorta
- Hypertrophic cardiomyopathy
what are the two shockable cardiac arrhythmias?
Ventricular Tachycardia
Ventricular Fibrillation
What is cardiac failure?
a clinical syndrome, characterised by typical signs and symptoms
associated with abnormality of cardiac structure or function
leading to failure of the heart to deliver oxygen at a rate meeting the requirements of the metabolising tissues.
What are the types of heart failure?
- LV heart failure
- RV heart failure
- Biventricular failure
LV Heart failure
Poor output of the impaired LV leads to an increase in left atrial and pulmonary venous pressure
This causes pulmonary oedema, as the increased pulmonary venous pressure prevents the reuptake of fluid at the level of the capillaries.
RV Heart failure
RV output fails
Predominantly due to lung disease (cor pulmonale) and pulmonary valvular stenosis.
This typically leads to peripheral oedema
Biventricular Heart Failure
LVF and RVF may be present at the same time
Either:
i. Disease (e.g. IHD) has affected both sides of the heart
ii. LVF leads to pulmonary congestion which can then lead to RVF (termed “congestive heart failure”)
What are the most common causes of heart failure?
What are other causes?
IHD
Dilated cardiomyopathy
Hypertension
Other cardiomyopathies Valvular disease Congenital heart disease Cor pulmonale Alcohol/drugs AF/heart block Anaemia
what is ejection fraction ?
a measurement of how much blood the left ventricle pumps out with each contraction
expressed as a percentage
what is Stroke volume ?
the amount of blood pumped by the left ventricle of the heart in one contraction
expressed in mL
What is cardiac output?
How can it be worked out?
the amount of blood the heart pumps through the circulatory system in a minute
expressed in litres per minute
CO = Heart Rate (HR) × Stroke Volume (SV))
what is systolic dysfunction ?
insufficient pumping action or impaired contraction
what is diastolic dysfunction?
insufficient filling of the ventricle due to decreased compliance and impaired relaxation
Signs of LV failure
Fatigue
Exertional dyspnoea, Paroxysmal nocturnal dyspnoea, Orthopnoea
Pulmonary oedema/congestion
=> Inspiratory crepitations initially in lung bases, then throughout lungs if untreated.
=> Cough
“Gallop rhythm” – three distinct heart sounds.
Cardiomegaly, laterally displaced apex beat.
Signs of RV failure
Fatigue Breathlessness Anorexia/nausea (due to hepatomegaly) Raised peripheral venous pressure and JVP. Organomegaly – liver and spleen. Cardiomegaly Peripheral oedema Ascites
what are the maladaptive compensatory mechanisms in cardiac failure?
Reduced CO leads to activation of the SNS and RAAS.
RAAS activation leads to vasoconstriction (increasing afterload) and sodium/water retention (increasing preload) thus further increasing BP and cardiac work.
SNS activation initially maintains cardiac output but prolonged stimulation leads to myocyte apoptosis and necrosis
chronic heart failure => desensitisation of the myocytes to the SNS and the ventricles enlarge (however they contract less efficiently).
NYHA classification of heart failure
Class I – no limitation of physical activity.
Class II – slight limitation of activity (breathlessness/ fatigue with moderate exercise)
Class III – marked limitation of activity (breathlessness with minimal exercise)
Class IV – severe limitation of activity (dyspnoea at rest)
Cardiac Failure - Investigations
Bloods - FBC, U&Es, LFTs, thyroid function, (cardiac enzymes in acute failure).
BNP
CXR - any cardiomegaly? pulmonary oedema?
ECG - any ischaemia, HTN, or arrhythmias?
Echo - if ECG or BNP are abnormal, gold standard for diagnosis.
=> EF <45% is diagnostic of heart failure
B-type natriuretic peptide in heart failure
A normal level of BNP will exclude heart failure, so this a good screen for breathlessness
what is acute on chronic/decompensated part failure?
chronic heart failure with a sudden deterioration
Cardiac failure - goals of treatment
- Identify/treat any cause (valvular disease, IHD, etc.)
- Reduce cardiac workload
- Increased cardiac output
- Counteract maladaptation
- Relieve symptoms
- Prolong quality of life – reduce hospitalisation.
Acute heart failure - management
Sit the patient up!
High flow oxygen
IV diuretics at escalating doses.
Consider IV nitrates (caution in hypotension and heart failure secondary to severe aortic stenosis)
Consider non-invasive ventilation
Consider inotropic support
Consider device therapy (intra-aortic balloon pump, etc)
Consider referral for Left ventricular assist device or cardiac transplantation.
Chronic heart failure - management
Lifestyle advice
1st line therapy – ACEi and beta-blocker
Add diuretic if symptomatic oedema.
2nd line therapy – Aldosterone antagonists (e.g. spironolactone) / ATRA / hydralazine plus nitrate.
3rd line therapy – Cardiac resynchronisation therapy/ digoxin/ ivabradine
Consideration of cardiac transplant.
Cardiac Failure - Lifestyle advice
Obesity control,
dietary modification (salt and fluid restriction if severe heart failure).
Smoking cessation
Bed rest important following exacerbation, but generally low-level exercise is recommended.
=> Avoid strenuous exercise.
Vaccination – against pneumococcal disease and influenza.
Sex – avoid Viagra (can cause hypotension).
What role does an ACEi have in cardiac failure?
When would its use be avoided?
Works to reverse the neurohormonal adaptation
Should NOT be used with NSAIDs (risk of renal damage)
Avoided in patients with SBP <100 – risk of severe hypotension
What role does a beta-blocker have in cardiac failure?
What is important to note about initial effects?
When should beta-blockers be avoided?
Used to block the SNS activity causing maladaptation.
Also anti-arrhythmic effects
Symptoms initially become worse!!
Contraindicated in asthma, caution in COPD
What role do diuretics have in cardiac failure?
Mainly for symptomatic relief of pulmonary oedema (also venodilate)
Digoxin
Positive ionotrope and negative chronotrope
=> increases force of contraction but decreased heart rate
Impairs AVN conduction, increases vagal activity.
Contra-indicated in heart block and bradycardia.
Dose titrated to make sure HR does not go <60bpm.
Typical presentation of IHD
described as chest “discomfort” rather than pain.
Pain tends to be retrosternal
(can range from anywhere from umbilicus to the jaw)
Feels like a pressure or weight on the chest.
Pain normally lasts <10 minutes.
Exacerbating factors – inclines, cold weather, heavy meals.
Pain unrelated to respiration/position
characteristics of “Typical” angina
- Constricting discomfort in the front of the chest or in the neck, jaw, shoulder, or arm.
- Precipitated by physical exertion
- Relieved by rest or nitrates within 5 min.
How is angina graded?
According to its association with exertion.
I - only with strenuous exertion
II - with moderate exertion
III - with mild exertion
IV - at rest
What are some risk factors for IHD?
Hypertension Hypercholesterolaemia Diabetes Smoking Family History – presence of premature CAD
What investigations should be done for chest pain?
ECG
Bloods - FBC, U&Es, glucose, HbA1c, Lipids, TSH (cardiac enzymes)
CXR
Echo
what can be identified on an echocardiogram?
LV function
Regional wall motion abnormalities – IHD/previous MI
Valve disease
Cardiomyopathy
General management of IHD
Address modifiable risk and lifestyle factors
If patient has significant co-morbidities – consider treating medically
if patient is very high risk with symptoms despite treatment – proceed directly to invasive assessment
IHD - managing lifestyle factors
Smoking cessation,
Mediterranean diet, weight control (aim for BMI <25),
Sensible alcohol intake.
Diabetes control,
Hypertension control,
Dyslipidaemia control,
Physical exercise – 30-60 minutes per day.
Influenza vaccine
IHD - medical treatment
ANGINA SYMPTOMS:
- Short-acting GTN – used sublingually (can also use LA)
- Beta-blocker first line (HR 55-60bpm)
- Dihydropyridine CCB (e.g. amlodipine) – 2nd line if BB not tolerated.
- Combination of BB and CCB
OTHER:
- Low-dose aspirin (or clopidogrel)
- Dual anti-platelet therapy
- potentially low-dose rivaroxaban in combination with aspirin
- Statin for lipid profile
- ACEi for those with diabetes, HTN or HF
What is important to remember with use of a long-acting nitrate?
a “nitrate free period” will be needed
this is to avoid down-regulation of nitrate receptors and reduced efficacy of the drug
what is dual anti-platelet therapy
A combination of two anti-platelet drugs
usually aspirin + clopidogrel
there are some newer anti-platelet therapies too
IHD - Revascularisation
Used for patients with increased mortality because a large area of myocardium is at risk (>10%) on functional testing.
Options are PCI or CABG
When is PCI favoured?
Tends to be favoured for a discrete narrowing/stenosis.
Favoured in advanced age/frailty/reduced life expectancy as it is less invasive than CABG
When is CABG favoured?
Favoured in diffuse CAD – 3 vessels affected.
Used for patients with re-stenosis of stents and patients that may need other cardiac pathologies treated at the same time (e.g. valvular disease, aortic aneurysm).
What does the “Lub” /S1 heart sound indicate?
Indicates the start of systole
Due to the increase in ventricular pressure and the closure of the mitral and tricuspid valves
will be heard WITH pulse.
when would you hear a “split” heart sound?
If there is pathology on one side of the heart and there is a delay in closure of one valve
What does the “dub” /S2 heart sound indicate?
Due to the closure of the aortic and pulmonary valves.
Occurs before diastole
Valve stenosis
narrowing of the valve that does not fully open, causes turbulent blood flow
Valve regurgitation/incompetence
valve does not shut properly and the blood regurgitates back through the valve
Aortic stenosis
Narrowing of the aortic valve, causing obstruction of blood flow across the valve
Aortic Stenosis - causes
- Congenital – bicuspid aortic valve (BAV).
- Rheumatic fever
- Age-related calcification.
Aortic Stenosis - common signs/symptoms
- Angina – SoB, chest pain
- Arrythmias (cardiac remodelling can lead to altered conduction)
- Exertional Syncope
- Left ventricular failure
Aortic Stenosis - On Examination
PALPATION
Pulse - small volume, slow rising, narrow pulse pressure.
Heaves - as left ventricle has to push hard to get blood out of stenosed valve
AUSCULTATION
Crescendo-decrescendo ejection systolic murmur
May have radiation to carotids (sitting forward on expiration)
Aortic Stenosis - investigations
- ECG – may show LVH
- CXR – any cardiomegaly?
- Echo – to see how thick the valves are and possible calcification
- Cardiac Catheterisation – to assess pressure gradient across the valve.
Aortic Stenosis - management
Acute – balloon valvuloplasty
Chronic – aortic valve replacement
Aortic Regurgitation
Leakage of blood from the aorta back into the left ventricle during diastole.
Due to imperfect closing of the aortic valve
Aortic Regurgitation - Causes
- Hypertension
- Aortic dissection
- Weak connective tissue – e.g. Marfan’s syndrome.
- Infection
Aortic Regurgitation - Common signs/symptoms
- Angina – SoB, chest pain
- Fatigue
- Palpitations
- Chest pains
- Fainting/syncopal episodes
Aortic Regurgitation - on examination
PALPATION
Pulse - wide volume, collapsing pulse
Displaced Apex beat
AUSCULTATION
Crescendo diastolic murmur at left sternal edge.
Aortic Regurgitation - investigations
- ECG – may show LVH
- CXR – any cardiomegaly?
- Echo – determine degree of regurgitation
- Cardiac Catheterisation – to assess pressure gradient across the valve.
Aortic Regurgitation - management
Acute – haemodynamic support
Chronic:
- Medical management – reduce BP, reduce cardiac contractility.
- Aortic valve replacement – if symptoms worsening.
Mitral Stenosis
Narrowing of mitral valve causing obstruction to blood flow
Mitral Stenosis - Causes
- > 95% of causes due to Rheumatic fever
- Congenital
- Old-age degenerative
- SLE
Mitral Stenosis - Causes
- > 95% of causes due to Rheumatic fever
- Congenital
- Old-age degenerative
- SLE
Mitral Stenosis - Common signs/symptoms
- SoB
- Fatigue
- Atrial fibrillation – due to left atrium dilation.
- Haemoptysis – due to any back flow into the pulmonary circulation.
Mitral Stenosis - on examination
INSPECTION
Malar Flush
PALPATION
Pulse – small volume
Parasternal heave
AUSCULTATION
Mid-diastolic murmur – heard at apex (normally 5th ICS, mid-clavicular line).
Added sounds – due to blood flow turbulence and opening snap.
Can accentuate the murmur by asking the patient to lie in the left lateral position and listen as they breathe out.
Mitral Stenosis - investigations
- ECG – may show AF
- CXR
- Echo – determine the degree of stenosis
- Cardiac Catheterisation – to assess pressure gradient across the valve
Mitral Stenosis - management
Acute – haemodynamic support
Chronic
- Medical management – diuretics
- Percutaneous balloon valvotomy – widen stenosed valve.
Mitral regurgitation
Leakage of blood from the left ventricle to the left atrium during systole.
Due to imperfect closing of the mitral valve leaflets
Mitral regurgitation - causes
- Left ventricular dilatation
- Cardiomyopathy
- Old-age degenerative
- Infection – vegetations from infective endocarditis
- Autoimmune
Mitral regurgitation - common signs/symptoms
- SoB
- Fatigue
- Peripheral oedema – due to LVF
- Faint/dizziness
Mitral regurgitation - on examination
PALPATION
Pulse - possible AF
Parasternal Heave
AUSCULTATION
Pan-systolic murmur
Mitral regurgitation - investigations
- ECG – may show AF
- CXR
- Echo – determine degree of regurgitation
- Cardiac catheterisation – to assess pressure gradient across the valve.
Mitral regurgitation - management
Acute – haemodynamic support
Chronic:
- Medical management – ACEi, beta-blockers.
- Mitral valve replacement – if symptoms worsening.
Congenital causes of valvular heart disease
atria/ventricular septal defects,
Marfan’s syndrome,
abnormal valves – e.g. bicuspid aortic valve
Rheumatic causes of valvular heart disease
Rheumatic fever
Seronegative spondyloarthropathies
Degenerative causes of valvular heart disease
Small defects which slowly escalate to larger defects over time.
e.g. Plaque which gets progressively worse, leading to stenosis
Cardiac remodelling causes of valvular heart disease
Heart may change shape due to changes over time.
Disruption to anatomy, can lead to regurgitant valves
Infective endocarditis as a cause of valvular disease
Bacteria from the bloodstream can deposit on the valves.
Vegetations develop, leading to (permanent) valvular disruption.
In the acute infective phase, these patients deteriorate very rapidly
why does valvular disease ultimately lead to heart failure?
Stenosis – the heart has to work harder to force blood through the valve.
Regurgitation – the heart has to work harder to pump enough blood forward against blood that leaks back through the valve.
Tissue valve Vs. mechanical valve replacement
Mechanical valve is less likely to need to be replaced again
Mechanical valve has increased risk of blood clots - lifelong anticoagulation (warfarin) needed
(Tissue valve would only need life-long aspirin)
Mechanical valve has audible clicking noise.
When is the optimal timing for a valve replacement?
just as decompensation is starting to develop
Avoid replacing too early or too late
What is cardio-thoracic ratio?
On what CXR projection can this be officially assessed?
What should this be?
the ratio of the width of the heart versus the width of the chest at the same level
On a PA projection
should be <50% (>50% is cardiomegaly)
A systematic approach to interpreting CXRs
- Patient demographics
- Projection and technical adequacy.
- Tubes and lines
- A – airways
- B – Bones
- C – cardiac and mediastinal contours (cardio-thoracic ratio).
- D – diaphragm
- E – everything else: pleural spaces, lungs, etc.
- Review areas where pathology can be easily missed – lung apices, below the diaphragm, lung hila.
Causes of acute chest pain - lungs
Pleurisy (LRTI)
Pneumothorax
Tension PTX !
Causes of acute chest pain - cardiac
ACS !
Stable angina
Pericarditis
Aortic Dissection !
Coronary spasm
Causes of acute chest pain - MSK
Costochondritis
Varicella Zoster
Muscular Strain
Causes of acute chest pain - Other
Anxiety
Causes of acute chest pain - GI
GORD
Duodenitis/Gastritis
Boerhaave’s Oesophageal Perforation !
Cholecystitis
Peptic Ulcer Disease
Oesophageal Spasm
What conditions are considered acute coronary syndromes (ACS)?
STEMI
NSTEMI
Unstable angina
what is atheroma and what does it lead to?
= an abnormal accumulation of material within the walls of the coronary arteries
reduces the size of the lumen and thereby reduces blood flow to the myocardium => ischaemic damage
predisposes to thrombus and aneurysm formation
Percutaneous coronary intervention (PCI)
involves the use of a balloon to inflate the vessel, and sometimes addition of a stent.
pharmacotherapy for coronary interventions
the patient will need to have dual anti-platelet therapy (aspirin and clopidogrel) before undergoing PCI
to prevent peri-procedural thrombosis (due to the plastic catheters in the arteries temporarily) unfractionated heparin is normally given
What is infective endocarditis?
an infection of the endocardial surface of the heart, or mainly an infectious vegetation on a heart valve
described as “pyrexia, with a new/changing murmur”
Causes of infective endocarditis
Damaged Endothelium
=> Damaged valves
=> Prosthetic valves
=> Congenital heart disease
High levels of sustained bacteria
=> IV drug users
=> Infected intravascular devices
=> Untreated abscess/collection elsewhere
Most common infective organism - native valves
~80% are caused by various staphylococci or streptococci
e.g. Strep. viridans, Strep. mitis, Staph. aureus
Most common infective organism - prosthetic valves
Coagulase negative staphylococcus (such as Staph. epidermidis).
Usually <2 months after surgery.
After 2 months – tend to revert to the normal causative organisms
Most common infective organism - IV drug users
Staph. aureus is especially common
tends to be right-sided heart disease, as this is the side that the bacteria reach first from the periphery
Other infective organisms/causes of endocarditis
Strep. bovis – found in association with bowel malignancy.
Enterococcus – has there been manipulation of GU/GI tract?
Difficult to grow organisms / “Culture negative endocarditis”
Non-infectious endocarditis – SLE
Signs/Symptoms of endocarditis
Fever + new/changing murmur
Microscopic haematuria
Splenomegaly
Osler’s Nodes – tender red nodules in fingers due to immune complex deposition.
Clubbing
Splinter haemorrhages
Roth’s Spots – pale areas with surrounding haemorrhage on retina.
Janeway lesions – painless palmar/plantar macules.
Petechial rash
Digital infarcts
Investigations for infective endocarditis
Bloods – FBC, CRP/ESR, U&E
Blood cultures – ideally take 3 sets, 1 hour apart, different sites, before antibiotics.
Urinalysis – proteinuria and microscopic haematuria.
ECG – at regular intervals (?MI)
CXR – any evidence of heart failure/abscesses/emboli
Transthoracic Echocardiography – in all patients, but negative echo does not rule out endocarditis.
Duke’s Criteria - Major
Positive culture (typical organism in two cultures).
Endocardial involvement on echo (vegetations, abscess, new regurgitation
Duke’s Criteria - Minor
Predisposition – e.g. heart condition, IVDU
Fever >38C
Vascular phenomena
Immunologic phenomena
Positive blood culture/echo but not sufficient for “major” criteria.
What criteria are required for a diagnosis of infective endocarditis?
2 major and 1 minor criteria or 1 major and 3 minor criteria or 5 minor criteria
Management of infective endocarditis
MEDICAL
Antibiotics – correct choice, strength, frequency, and duration.
SURGICAL
Excision of infected or damaged valve and replacement with prosthetic (ideally after no longer bacteraemic)
Draining of metastatic abscesses
SOCIAL
Manage pre-disposing factors (e.g. IV drug use)
Is prophylaxis used for infective endocarditis?
Not routinely anymore
Sometimes for high-risk patients undergoing dental procedures.
Cardiovascular exam - inspection of hands (and arms)
HANDS
Temperature – cool could mean poor cardiac output/hypovolaemia
Clubbing
Peripheral cyanosis
Janeway Lesions, Osler’s Nodes.
Xanthomata – deposition of yellowish cholesterol-rich material, indicating hyperlipidaemia
Capillary refill time – hypovolaemia
Tar staining
ARMS
Track marks (IV drugs?)
Scars (e.g. CABG)
Cardiovascular exam - inspection of face and neck
EYES
conjunctival pallor, xanthelasma, corneal arcus
MOUTH
central cyanosis, anaemia, dental hygiene
NECK
Palpate carotid pulse
Assess JVP
Where would you auscultate the aortic valve?
Right 2nd ICS, near the sternal edge
Where would you auscultate the pulmonary valve?
Left 2nd ICS, near the sternal edge
Where would you auscultate the mitral valve?
Left 5th ICS at the mid-clavicular line
Where would you auscultate the tricuspid valve?
Left 4th/5th ICS, near the sternal edge
How do you feel for ventricular heave?
What would this indicate?
Palpate over left sternal edge with heel of hand and fingers to look for chest wall moving with each heartbeat
volume or pressure overload (hypertrophy)
How do you feel for thrills?
what would this indicate?
feel gently with fingertips in 2nd and 3rd ICS
turbulence of blood over the valves - palpable murmurs
Where would you palpate the apex beat?
Left 5th ICS at the mid-clavicular line; palpate with flat hand.
How would you “complete” a cardiovascular examination?
Peripheral vascular exam
Peripheral pulses
ECG
Measure BP
What are causes of ankle swelling?
Heart failure (worse later in the day) Drugs (especially amlodipine) Venous diseases Renal causes Hypoalbuminaemia
What is useful to ask about a patient’s palpitations?
Get them to tap out the rhythm!
Ask about any triggers? (e.g. caffeine, exercise, anxiety, etc.)
Frequency and duration
Associated features?
Any history of thyroid disease?
What are some relevant PMH conditions to ask about in a history about a cardiovascular complaint?
MI, HTN, CVA, Diabetes
Previous surgery and details of procedures
Rheumatic fever
Recent dental work
What are some relevant aspects of family history to ask about in a history about a cardiovascular complaint?
Any ischaemic heart disease?
Any sudden cardiac death? (particularly < 40 years)
unstable angina
atheromatous plaque is ruptured and thrombus forms, causing partial occlusion of the vessel and supply ischaemia
Pain occurs at rest or progresses rapidly over a short period of time.
In what acute coronary syndromes will cardiac enzymes be elevated?
STEMI
NSTEMI
What is the difference between a STEMI and NSTEMI?
STEMI
- complete occlusion of vessel
- transmural ischaemia
- ST-elevation/hyperacute T waves
NSTEMI
- partial occlusion of vessel
- subendocardial ischaemia
- normal/inverted T waves/ ST depression
At what time after an MI would microscopic changes be visible?
at 12-24 hours
At what time after an MI does the acute inflammatory reaction to dead muscle occur?
What does this look like?
at 24-72 hours
The area becomes soft and pale.
Early complications of MI
Sudden death due to cardiac dysrhythmia
Sudden death due to acute left ventricular failure
Rupture of myocardium -> haemopericardium
Rupture of papillary muscle -> acute valve failure ->LVF
Mural thrombus on infarct -> embolism -> stroke & others
Fibrinous Pericarditis & extension of MI
Late complications of MI
Chronic LVF
Ventricular Aneurysm
what is aortic dissection?
A tear in the intima of the aorta, causing a false lumen in the tunica media into which blood can enter.
How does aortic dissection present?
Sudden “tearing” chest pain
Radiation to the back
There can be occlusion of aortic branches, with symptoms depending on which branch is affected.
Risk factors for aortic dissection
Hypertension Connective tissue disorders Vascular inflammation Trauma Surgery Smoking/drugs
Long-term management of MI
Beta-blocker
ACEi- Ramipril
Dual Antiplatelet – Aspirin and Ticagralor
Increase statin dose
Smoking cessation
Cardiac rehabilitation
Return to exercise, driving & work advice
Immediate Management of MI
Analgesia (morphine?)
Oxygen, if required
GTN
Aspirin/anti-platelets
PCI?
Possible causes of loss of consciousness
ACS – STEMI, NSTEMI or Unstable Angina Tachy/bradycardia Aortic dissection Postural hypotension Simple faint – vaso-vagal Pulmonary Embolism (PE) Hypoglycaemia Intracranial haemorrhage
When does blood flow to the coronary arteries occur?
During diastole
