Cardiology V Flashcards
Which drug can you use to treat PAD pain? [1]
Naftidrofuryl oxalate
State 4 classical causes of dialted cardiomyopathy [4]
Alcohol
Coxsackie B virus
Wet beri beri (thiamine deficiency)
Doxorubicin
At which stage of pregnancy does peri-partum cardiomyopathy usually occur [1] and go on till? [1]
Which subpopulations of pregnant women usually suffer from peripartum cardiomyopathy? [2]
peri-partum cardiomyopathy:
- last month of pregnancy and 5 months post-partum
- usually older; greater parity and multiple gestations
Name two infective organisms that can cause cardiomyopathy [2]
Coxsackie B virus
Chagas diesease
State an autoimmune disorders that dispose patients to cardiomyopathy [1]
SLE
Define HOCM [1]
Describe the pathophysiology of HOCM
HOCM: is defined as increased ventricular wall thickness or mass not caused by pathologic loading conditions.
Pathophysiology:
- mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C
- This results in predominantly diastolic dysfunction:
- left ventricle hypertrophy → decreased compliance → decreased cardiac output
Explain the clinical consequences of HOCM [5]
Myocardial hypertrophy:
- predominantly in the interventricular septum
- asymmetric septal hypertrophy narrows the left ventricular outflow tract (LVOT).
Diastolic dysfunction:
- Reduced compliance and elevated filling pressures ddue to hypertrophy
LVOT obstruction:
- The interventricular septal hypertrophy, combined with systolic anterior motion (SAM) of the mitral valve, causes dynamic obstruction of the LVOT during systole.
- This increases the pressure gradient across the LVOT, reducing cardiac output and provoking symptoms.
Mitral regurgitation:
- The SAM of the mitral valve contributes to mitral regurgitation by displacing the valve leaflets, exacerbating the hemodynamic abnormalities and worsening heart failure symptoms
Arrhythmogenesis:
- Myocardial disarray, fibrosis, and ischemia increase the risk of ventricular and atrial arrhythmias
- can lead to sudden cardiac death.
Describe the typical signs seen in HOCM patient [7]
Ejection systolic murmur (left ventricular outflow obstruction):
- harsh crescendo-decrescendo shortly after S1 and loudest at the apex and lower left sternal edge
Mid-late systolic murmur (mitral regurgitation):
- occurs at the apex. Depending on the extent of mitral regurgitation and the direction of the jet regurgitating through the mitral valve it may be pansystolic
S4 gallop:
- This can be heard in patients with impaired diastolic function, reflecting atrial contraction against a noncompliant left ventricle.
Heave (visible or palpation pulsation)
Thrill (palpable murmur)
Features of heart failure:
- raised JVP, crackles on lung auscultation, peripheral oedema
Bifid carotid pulse:
- A rapid upstroke followed by a mid-systolic dip may be observed, known as the ‘spike and dome’ pulse.
Increased left ventricular wall thickness ≥[] mm in the absence of any other identifiable cause is consistent with HCM
Increased left ventricular wall thickness ≥15 mm in the absence of any other identifiable cause is consistent with HCM
How would an ECG indicate HOCM? [3]
Left ventricular hypertrophy (LVH)
T-wave inversions:
- Deep, symmetric T-wave inversions in the precordial leads are suggestive of HOCM.
Arrhythmias:
- Atrial fibrillation or ventricular tachycardia may be detected.
Which imaging modality can be usefull to differentiate HOCM from other causes of LVH? [1]
Cardiac Magnetic Resonance Imaging (CMR): provides detailed assessment of myocardial hypertrophy, fibrosis (using late gadolinium enhancement), and ventricular function.
Describe the medical managment plan for a patient with HOCM used to reduce symptoms and LVOT obstruction [5]
A. Beta blockers
- 1st line: atenolol or propranolol
B. CCBs:
- Verapamil
C. antiarrhythmic agents:
- Disopyramide
D. Diuretics:
- furosemide
- Caution is warranted due to the potential for hypovolemia and exacerbation of LVOT obstruction.
E. Anticoagulation:
- Indicated in patients with atrial fibrillation or a history of thromboembolic events.
Name and describe the results seen in th 1st investigations to order for suspected HOCM? [3]
BMJ BP
ECG:
- Deep, narrow (“dagger-like”) Q waves in lateral (I, aVL, V5-6) +/- inferior (II, III, aVF) leads
- LVH (present with QRS complexes that are tallest in the midprecordial leads): deep T wave inversion in I, II, VL & V3-6
- ST-T wave abnormalities;
- normal
CXR:
- cardiomegaly
- normal
echocardiography
- cardinal feature is left ventricular hypertrophy (LVH)
- asymmetric septal hypertrophy
Describe the surgical managment that can be given for severe, symptomatic LVOT obstruction refractory to medical therapy? [2]
Septal myectomy:
- Surgical removal of a portion of the hypertrophied septum, with a low operative mortality rate and durable long-term symptomatic relief.
Alcohol septal ablation
- A percutaneous approach, involving injection of ethanol into a septal coronary artery to induce localized myocardial infarction and septal thinning.
- Outcomes are comparable to septal myectomy but may be less effective in patients with extreme septal thickness.
Which differentials should you think of when investigating TCM? [3]
Requires the exclusion of other potential causes, such as acute coronary syndrome (ACS), myocarditis, and pheochromocytoma
Which specific type of cardiomyopathy is the most well characterised arrhythmogenic cardiomyopathy caused by a genetic mutation? [1]
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is the most well characterised ACM caused by a genetic mutation.
What is a good pneumonic for learning causes of restrictive CM? [5]
What is the management for HOCM? [5]
Management:
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*
Which drug classes should be avoided in HOCM patients? [3]
nitrates
ACE-inhibitors
inotropes
Describe what is meant by Arrhythmogenic right ventricular cardiomyopathy
Form of inherited cardiovascular disease which may present with syncope or sudden cardiac death:
* inherited in an autosomal dominant pattern with variable expression
* the right ventricular myocardium is replaced by fatty and fibrofatty tissue
* around 50% of patients have a mutation of one of the several genes which encode components of desmosome
[] is generally regarded as the second most common cause of sudden cardiac death in the young after hypertrophic cardiomyopathy.
Arrhythmogenic right ventricular cardiomyopathy
How would you investigate arrhythmogenic right ventricular cardiomyopathy? [3]
- ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex
- echo changes are often subtle in the early stages but may show an enlarged, hypokinetic right ventricle with a thin free wall
- magnetic resonance imaging is useful to show fibrofatty tissue
How do you manage arrhythmogenic right ventricular cardiomyopathy? [3]
Management
* drugs: sotalol is the most widely used antiarrhythmic
* catheter ablation to prevent ventricular tachycardia
* implantable cardioverter-defibrillator
Describe the different classifications of Necrotising soft tissue infections (NSTIs) with regards to their infective organisms
Type I:
- polymicrobial: typically mixed anaerobes & aerobes, on average four or more organisms
Type II:
- group A streptococcus (Strep. pyogenes +/- Staph. aureus)
Type III:
- Gram-negative monomicrobial infection.
- Typically associated with Vibrio species infection
Type IV:
- Fungal infection (typically Candida species, zygomycetes).
Describe the pathophysiology of NSTI [3]
Microbial invasion and enzyme release
- Initially there is microbial invasion within the superficial fascia (e.g. from minor trauma).
- The release of enzymes and endo/exotoxins results in rapid spread through the fascial planes.
Disruption to microcirculation
- Thrombosis of the small veins and arteries which pass up through the fascia results in ischaemia to the overlying skin.
- Early on, these skin changes are NOT obvious, despite extensive infection below.
Haemorrhagic bullae, ulceration & necrosis
- As the infection progresses skin necrosis becomes more evident. In the later stages, signs of profound sepsis and multi-organ failure may appear.
Describe a key clinical feature of NSTI [1v]
Disproportionate pain compared with physical findings is typical.
Pain often PRECEDES skin changes by 24-48hrs.
Venous ulcers typically occur in which areas of the body? [1]
Occur in the gaiter area (between the top of the foot and bottom of the calf muscle)
What are key differences between constrictive pericarditis and cardiac tamponade with regards to: [4]
- JVP
- Pulsus paradoxus
- Kussmauls sign
- Features on CXR
What sign is thought to be is considered to be specific for pericarditis? [1]
- Pain that has radiation to the trapezius ridge
When is pericardiocentesis indicated in pericarditis? [2]
Pericardiocentesis is only indicated where there is suspicion of a bacterial or neoplastic aetiology.
It may also be done as a therapeutic intervention for a large pericardial effusion.
What is Kussmaul’s sign? [1]
Increased jugular venous pressure with inspiration
Name the ECG alteration shown [1]
What pathology is it pathognomic for? [1]
Electrical alternans
- Alternating loud and soft QRS complexes during to variation in fluid around the heart in each beat
- is suggestive of cardiac tamponade
