500 SBA's - Cardiology Flashcards
Histological changes wise, whats the difference between STEMI and NSTEMi
STEMI = infarction NSTEMI = ischaemia
What ECG changes do you expect to see with left circumflex artery occlusion?
ST elevation in V5 V6
Pt presents with HF and underlying cause of aortic stenosis. What signs do you expect to find OE?
And what signs should you not expect to find and why?
OE: bilateral basal crackles/crepitation
Because aortic stenosis will first cause left heart failure.
You wont expect to find: raised JVP and peodeal odema - these are right heart failure signs
You wont find pleural effusion YET - this is a late sign of HF, pulmonary oedema turns to effusion.
Whats the mechanism of aortic stenosis causing left heart failure?
Because the aorta is stenose the Left ventricle has to push against an increased pressure. This results in a backlog of blood and pressure into the pulmonary veins resulting in pulmonary oedema hence the first/early sign you would expect on LHF is bilateral basal crackles.
What are the signs you expect to find on CXR for HF?
A - Alveolar shadowing B - Kerley B lines C - Cardiomegaly D - Upper lobe diversion E - Effusion (oedema first)
Which stenosis is mainly associated with AF?
Mitral stenosis - because the enlarged atrium disrupts the normal electrical pathways
A murmur heard louder on inspiration points towards what?
A right sided valve lesion
Where would you hear the aortic valve/murmur?
right intercostal space and MCL
How would you hear a mitral regurgitation murmur best?
When the patient lies in the left lateral position
What main 3 signs do you expect to find on examination of aortic regurgitation?
- Early diastolic murmur S1 S2IIIII S1
- Wide pulse pressure
- Collapsing waterhammer pulse
What manoeuvre do you do to accentuate an aortic regurg murmur?
Sit patient front and make them hold their breath
What’s the chad2 score used for?
To predict the stroke risk in AF patients
Congestive HF Hypertension Age >75 Diabetes mellitus S2 Previous stroke or TIA
low risk - mx with aspirin
high risk - mx with warfarin
Acute coronary syndromes on ECG and troponin levels of each:
STEMI: elevated ST, elevated troponin
Aborted MI: elevated ST, normal troponin
NSTEMI: no st elevation, raised troponin
Unstable angina: no st elevation, normal troponin
What is the classic PC of PE?
MODERATE: SOB Pleuritic chest pain - on inspiration Haemoptysis Leg pain
MASSIVE: Severe central pleuritic chest pain Shock Collapse Acute right heart failure Sudden death
What are the signs OE of PE?
Pleural rub
Coarse crackles
Atrial FIbrillation
What are the signs OE of a massive PE?
Raised JVP
Raised RR
Raised HR
Hypotension
What are the causes of thrombus PE?
95% arise from DVT in the lower limbs
Rarely arises in the right atrium (in AF * patients)
What are embolic PE causes?
Amniotic fluid Air Fat Tumour Mycotic
What are the risk factors for PE?
Risk Factors: Surgical patients Immobility Obesity OCP Heart failure Malignancy
Identify appropriate investigations for pulmonary embolism
Bloods - ABG, thrombophilia screen
ECG -May be normal
May show tachycardia, right axis deviation or RBBB
May show S1Q3T3 pattern
CXR - often NORMAL but helps exclude other diagnoses
Spiral CT Pulmonary Angiogram (right)
FIRST LINE INVESTIGATION Poor sensitivity for small emboli
VERY sensitive for medium to large emboli
Ventilation-Perfusion (VQ) Scan
Identifies areas of ventilation and perfusion mismatch, which would indicate an area of infarcted lung
Pulmonary Angiography
Invasive
Rarely necessary
Doppler US of Lower Limb - allows assessment of venous thromboembolism
Echocardiography - may show right heart strain
What is the scoring system for PE? What is it used for exactly?
The Well's Score is used to determine the best investigation for PE Low Probability (Wells 4 or less) - use D-dimer High Probability (Wells > 4) - required imaging (CTPA)
Whats the mx for a primary prevention of PE?
Generate a management plan for pulmonary embolism Primary Prevention Compression stockings Heparin prophylaxis for those at risk Good mobilisation and adequate hydration
Whats the mx for PE if the pt is haemodynamically stable?
If haemodynamically stable O2 Anticoagulation with heparin or LMWH Switch over to oral warfarin for at least 3 months Maintain INR 2-3 Analgesia
What’s the mx for PE if the pt is haemodynamically UNSTABLE?
aka massive pe mx
If haemodynamically UNSTABLE (massive PE)
Resuscitate
O2
IV fluids
Thrombolysis with tPA may be considered if cardiac arrest is imminent
Surgical or radiological
Embolectomy
IVC filters - sometimes used for recurrent PEs despite adequate anticoagulation or when anticoagulation is contraindicated
Identify the possible complications of pulmonary embolism
Death
Pulmonary infarction
Pulmonary hypertension
Right heart failure
What does a mid systolic click and late systolic murmur indicate?
• Mitral Valve Prolapse
barlow syndrome/ click murmur syndrome
What is an Austin Flint murmur?
o Heard over the apex
o Caused by turbulent reflux hitting the anterior cusp of the mitral valve causing a physiological mitral stenosis
What would a patent ductus arteriosus sound like on auscultating?
Constant machinery murmur
Pt presents with severe tearing chest pain radiating towards the back/jaw
what is this
Classic aortic dissection
Will either radiate to back or jaw - it depends on where the aorta dissected exactly.
What is clopidogrel?
Clopidogrel, is an ANTIPLATELET medication used to reduce the risk of heart disease and stroke in those at high risk. It is also used together with aspirin in heart attacks and following the placement of a coronary artery stent. It is taken by mouth
When is clopidogrel used?
NSTEMI Unstable angina Secondary prevention of IHD Acute ischaemic stroke mx TIA
Define ventricular tachycardia
A regular broad-complex tachycardia originating from a ventricular ectopic focus. The rate is usually > 120 bpm.
What are the RF for ventricular tachycardia?
o Coronary heart disease
o Structural heart disease
o Electrolyte deficiencies (e.g. hypokalaemia, hypocalcaemia, hypomagnesaemia)
o Use of stimulant drugs (e.g. caffeine, cocaine)
Summarise the epidemiology of ventricular tachycardia
- Fairly common
- It is one of the shockable rhythms that is seen in cardiac arrest patients
- VT incidence peaks in the middle decades of life
Recognise the presenting symptoms of ventricular tachycardia
• Symptoms of ischaemic heart disease or haemodynamic compromise due to poor perfusion • Symptoms: o Chest pain o Palpitations o Dyspnoea o Syncope
Recognise the signs of ventricular tachycardia on physical examination
• Signs are dependent on the degree of haemodynamic instability o Respiratory distress o Bibasal crackles o Raised JVP o Hypotension o Anxiety o Agitation o Lethargy o Coma
What are the ECG features of ventricular tachycardia
- Rate > 100 bpm
- Broad QRS complexes *
- AV dissociation
• ECG
o It can sometimes be difficult to distinguish between VT and SVT with aberrant conduction
o If in doubt, treat as a VT
Generate a management plan for pulseless and unstable ventricular tachycardia
- ABC approach
- CHECK WHETHER THE PATIENT HAS A PULSE OR NOT
- Pulseless VT - follow advanced life support algorithm
- Unstable VT - reduced cardiac output
NOTE: VF and pulseless VT require defibrillation (unsynchronised), but other VTs can be treated with synchronised cardioversion
Correct electrolyte abnormalities
Amiodarone
What is the mx for stable VT?
o These patients DO NOT experience symptoms of haemodynamic compromise
o Correct electrolyte abnormalities
o Amiodarone *
o Synchronised DC shock (if steps above are unsuccessful)
What does the JVP provide information for?
Information regarding right atrial pressures and filling
What would you expect to find on JVP inspection in AF?
absent a waves - represents atrial systole
What is the normal PR interval?
0.12-0.20
What do you expect to see in a 1st degree HB?
Prolonged PR interval
>0.20s
What are canon a waves of the JVP?
Cannon A Waves: waves seen occasionally in the jugular vein of humans with certain cardiac arrhythmias. This occurs when the atria and ventricles contract simultaneously
Malar flush
Malar rash
Malar flush = mitral stenosis
Malar rash = SLE
What is the main SE of ACEi?
Dry cough that doesn’t seem to go away
How does a new aortic stenosis pt clasically present?
Pt syncopes for the firs time and comes to a&e
On further investigating pt reports SOB the past X months on exertion and chest pain sometimes (angina)
ECG/Echo reveal left ventricular hypertrophy
Acute Malignant Hypertension Management:
o IV betaMblocker (e.g. esmolol)
o Labetolol
o Hydralazine sodium nitroprusside *
o CAUTION: avoid rapid lowering of blood pressure because it can cause cerebral infarction
• This is because the autoregulatory mechanisms within the brain for regulating blood flow will cause vasoconstriction of the vessels in the brain when blood pressure is very high
• Lowering the blood pressure too rapidly would mean that the autoregulatory mechanisms do not adapt to the drop in blood pressure and so the vessels remain constricted
• A rapid drop in blood pressure with constricted vessels will cause an infarction
Intra arterial BP monitoring to make sure there are no drops in bp - can lead to acute cerebral, cardiac or optic hyperfusion.
What is coarctation of the aorta a RF for?
Hypertension
Usually in a young person with no other co-morbidities
52yo female pt who was been treated for HTN for years presents with loin pain, high blood pressure and haematuria.
What is this?
What is the first line investigation?
Classic Polycistic Kidney disease: HTN, haematuria, loin pain.
1st line Ix: US or CT will show multiple cysts bilaterally in enlarged kidneys.
If someone is having recurrent PE’s but dont have any RF such as: travel, pill, smoking what is the next Ix step?
Thrombophilia screen
49yo woman presents with increasing SOB on exertion over the past 3 months
Bilateral basal crackles
BP: 160/60mmh
Decrescendo diastolic murmur at the left sternal edge
What is the most likely diagnosis?
Aortic regurgitation
** PAY ATTENTION TO BP **
This is classic wide blood pressure for aortic regurg.
What are the RF for SVT?
• Risk Factors o Nicotine o Alcohol - "after a night out" o Caffeine o Previous MI o Digoxin toxicity
Recognise the presenting symptoms of SVT
- May have minimal symptoms or may present with syncope
- Symptoms vary depending on rate and duration of SVT
- Palpitations *
- Light-headedness
- Abrupt onset and termination of symptoms
- Other symptoms: fatigue, chest discomfort, dyspnoea, syncope
How does a SVT appear on ECG?
AVNRT AVRT?
AVNRT - normal
AVRT - delta waves
What is the mx for SVT if they are haemodynamically UNSTABLE?
o DC cardioversion
What is the mx for SVT if they are haemodynamically STABLE?
vagal monouevres + chemical cardioversion (+ IV adenosine)
o Vagal manoeuvres (e.g. Valsalva, carotid massage)
• Carotid massage could dislodge atherosclerotic plaques, so is only performed in young patients
If Vagal manoeuvres fail:
o Adenosine** 6 mg bolus (can increase to 12 mg)
• Contraindicated in ASTHMA as it can cause bronchospasm
What is the ix for phaeochromocytoma?
24 hr urine collection -
- check for catecholamine levels (and check for fractionated metanephrine levels)
o NOTE: metanephrines are metabolites of adrenaline
How does phaeochromocytoma?
EPISODAL/PAROXYSMAL
Headaches, anxiety, sweating, slow pulse rate
Other:
- palpitations, dyspnoea, chest pain
- nausea, constipation, epigastric pain
- weakness, tremor, anxiety
What does ST elevation in II III and AVF indiate
MI of the right coronary artery
Define constrictive pericarditis
Chronic inflammation of the pericardium with thickening and scarring. It limits the ability of the heart to function normally.
Recognise the presenting symptoms and signs of constrictive pericarditis
• Gradual-onset of symptoms
• EARLY - symptoms and signs may be very subtle
• ADVANCED - jaundice, cachexia, muscle wasting
• Right Heart Failure Signs
o Dyspnoea
o Peripheral oedema
o Raised JVP
o Kussmaul’s sign (paradoxical rise in JVP on inspiration) o Pulsatile hepatomegaly
What sign OE do you expect for constrictive pericarditis?
Kussmaul’s sign
paradoxical rise in JVP on inspiration
71yo man treated for congestive HF complains of anorexia and nausea
He sees yellow rings around lights
OE he has bradycardia and irregular pulse
What causes this?
DIGOXIN
classic.
Yellow-tinged vision = xanthopsia is specific to these drugs.
Bradycardia & irregular pulse = digoxin toxicity
29yo woman presents to GP with fatigue and palpitations
She notes weight loss
OE: 120bpm and irregularly irregular pulse, low BMI
What are you thinking?
What is the next step?
This is classic AF caused by thyrotoxicosis
AF in young people = thyrotoxicosis
(in the absence of valve disease)
Next step: TFT’s
What are Janeway lesions?
Janeway lesions are non-tender, small erythematous or haemorrhagic macular or nodular lesions on the palms or soles only a few millimeters in diameter that are indicative of infective endocarditis.
What organisms commonly cause infective endocarditis?
o Streptococci (40%) - mainly a-haemolytic S. viridans and S. bovis o Staphylococci (35%) - S. aureus and S. epidermidis o Enterococci (20%) - usually E. faecalis
o Other organisms: • Haemophilus • Actinobacillus • Cardiobacterium • Coxiella burnetii • Histoplasma (fungal)
What is the pathophysiology of infective endocarditis?
Pathophysiology
o Vegetations form when organisms deposit on the heart valves during a period of bacteraemia
o The vegetations are made up of platelets, fibrin and infective organisms
o They destroy valve leaflets, invade the myocardium or aortic wall leading to abscess cavities
o Activation of the immune system can lead to the formation of immune complexes –> vasculitis, glomerulonephritis, arthritis
What are the RF for infective endocardatis?
o Abnormal valves (e.g. congenital, calcification, rheumatic heart disease)
o Prosthetic heart valves
o Turbulent blood flow (e.g. patent ductus arteriosus)
o Recent dental work**/poor dental hygiene (source of S. viridans)
Recognise the presenting symptoms of infective endocarditis
• Fever with sweats/chills/rigors o NOTE: this might be relapsing and remitting • Malaise • Arthralgia • Myalgia • Confusion • Skin lesions • Ask about recent dental surgery**** or IV drug use
Recognise the signs of infective endocarditis on physical examination
• Pyrexia • Tachycardia • Signs of anaemia • Clubbing • New regurgitant murmur or muffled heart sounds • Frequency of heart murmurs: o Mitral > Aortic > Tricuspid > Pulmonary • Splenomegaly
• Vasculitic Lesions
o Roth spots on retina
o Petechiae on pharyngeal and conjunctival mucosa
o Janeway lesions (painless macules on the palms which blanch on pressure)
o Osler’s nodes (tender nodules on finger/toe pads)
o Splinter haemorrhages
Identify appropriate investigations for infective endocarditis
• Bloods
o FBC - high neutrophils, normocytic anaemia
o High ESR/CRP
o U&Es
o NOTE: a lot of patients with infective endocarditis tend to be rheumatoid factor positive
• Urinalysis
o Microscopic haematuria
o Proteinuria
• Blood Culture **
o Do microscopy and sensitivities as well
• Echocardiography **
o Transthoracic or transoesophageal (produces better image)
• Duke’s Classification - a method of diagnosing infective endocarditis based on the findings of the investigations and the symptoms/signs
Generate a management plan for infective endocarditis
• Antibiotics for 4-6 weeks
• On clinical suspicion = EMPIRICAL TREATMENT
o Benzylpenicillin
o Gentamicin
• Streptococci - continue the same as above
• Staphylococci
o Flucloxacillin/vancomycin
o Gentamicin
• Enterococci
o Ampicillin
o Gentamicin
• Culture Negative
o Vancomycin
o Gentamicin
• SURGERY - urgent valve replacement may be needed if there is a poor response to
antibiotics
Identify the possible complications of infective endocarditis
- Valve incompetence
- Intracardiac fistulae or abscesses
- Aneurysm
- Heart failure
- Renal failure
- Glomerulonephritis
- Arterial emboli from the vegetations shooting to the brain, kidneys, lungs and spleen
Summarise the prognosis for patients with infective endocarditis
- FATAL if untreated
* 15-30% mortality even WITH treatment
What is the rhythm mx of AF?
RHYTHM control:
o If > 48 hrs since onset of AF
• Anticoagulate for 3-4 weeks before attempting cardioversion
o If < 48 hrs since onset of AF
• DC cardioversion (2 x 100 J, 1 x 200 J)
• Chemical cardioversion: flecainide or amiodarone
- NOTE: flecainide is contraindicated if there is a history of ischaemic heart disease
o Prophylaxis against AF • Sotalol • Amiodarone • Flecainide • Consider pill-in-the-pocket (single dose of cardioverting drug (e.g. flecainide) for patients with paroxysmal AF) strategy for suitable patients
What is the rate mx of AF?
o Chronic (Permanent) AF • Control ventricular rate with: ! Digoxin ! Verapamil ! BetaMblockers • Aim for ventricular rate ~ 90 bpm
