Cardiology IV Flashcards

1
Q
A
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2
Q

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]

A

peri-partum cardiomyopathy:
- last month of pregnancy and 5 months post-partum
- usually older; greater parity and multiple gestations

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3
Q

Name two infective organisms that can cause cardiomyopathy [2]

A

Coxsackie B virus
Chagas diesease

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4
Q

State an autoimmune disorders that dispose patients to cardiomyopathy [1]

A

SLE

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5
Q

Explain the clinical consequences of HOCM [5]

A

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.

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6
Q

Describe the typical signs seen in HOCM patient [7]

A

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.

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7
Q

Increased left ventricular wall thickness ≥[] mm in the absence of any other identifiable cause is consistent with HCM

A

Increased left ventricular wall thickness ≥15 mm in the absence of any other identifiable cause is consistent with HCM

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8
Q

Describe the medical managment plan for a patient with HOCM used to reduce symptoms and LVOT obstruction [5]

A

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.

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9
Q

Which drug classes should be avoided in HOCM patients? [3]

A

nitrates
ACE-inhibitors
inotropes

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10
Q

How do you manage arrhythmogenic right ventricular cardiomyopathy? [3]

A

Management
* drugs: sotalol is the most widely used antiarrhythmic
* catheter ablation to prevent ventricular tachycardia
* implantable cardioverter-defibrillator

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11
Q

Describe the different classifications of Necrotising soft tissue infections (NSTIs) with regards to their infective organisms

A

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).

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12
Q

NSTI:Type 2 is caused by []

PassMed

A

type 2 is caused by Streptococcus pyogenes

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13
Q

Treatment of gangrene varies depending on location and cause but is centred around radical surgical debridement +/- amputation. Surgical procedures may also include what? [4]

A
  • Removal of embolus or thrombus
  • Balloon catheterisation or stent
  • Arterial or venous bypass surgery
  • Hyperbaric oxygen treatment.
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14
Q

Which of the following is usually caused by trauma, such as a bite?

Type 1
Type 2
Type 3
Type 4

A

Which of the following is usually caused by trauma, such as a bite?

Type 1
Type 2
Type 3
Type 4

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15
Q

You investigate a patient who is demonstrating signs of CLI.

How do you determine from the vessel affected if this patient needs open surgery or endovascular revascularization? [2]

A

Open surgery: lesions of common femoral artery and infrapopliteal disease
Endovascular: short segments: aortic iliac disease

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16
Q

What ECG changes would indicate myocarditis [3]

A
  • tachycardia
  • Prolonged QRS
  • QT prolongation
  • Diffuse T wave inversion

Can trigger arrhythmias

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17
Q

What are the potential complications of myocarditis? [2]

A

Complications
* heart failure
* arrhythmia; frequent premature ventricular complexes, irregular and polymorphic VT, or ventricular fibrillation possibly leading to sudden death
* dilated cardiomyopathy: usually a late complication

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18
Q

What treatment is given to patients with suspected giant cell myocarditis? [1]

A

In patients with suspected giant cell myocarditis, steroids are recommended and have been shown to improve survival

E.g. methylprednisolone

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19
Q

Define pericardial effusion [1]

Define pericardial tamponade [3]

A

Pericardial effusion is when the potential space of the pericardial cavity fills with fluid. This creates an inward pressure on the heart, making it more difficult to expand during diastole (filling of the heart).

Pericardial tamponade
* Pericardial effusion is large enough to raise the intra-pericardial pressure.
* This increased pressure squeezes the heart and affects its ability to function: it reduces heart filling during diastole, decreasing cardiac output during systole.
* This is an emergency and requires prompt drainage of the pericardial effusion to relieve the pressure.

20
Q

What are the triad (Beck’s) assocaited with cardiac tamponade? [3]

A

Classical features - Beck’s triad:
* Hypotension
* Raised JVP
* Muffled heart sounds

Other features:
* Dyspnoea
* Tachycardia
* An absent Y descent on the JVP - this is due to the limited right ventricular filling
* Pulsus paradoxus - an abnormally large drop in BP during inspiration
* Kussmaul’s sign - much debate about this
* ECG: electrical alternans

21
Q

What are key differences between constrictive pericarditis and cardiac tamponade with regards to: [4]

  • JVP
  • Pulsus paradoxus
  • Kussmauls sign
  • Features on CXR
A
22
Q

What sign is thought to be is considered to be specific for pericarditis? [1]

A
  • Pain that has radiation to the trapezius ridge
23
Q

The main consequence of chronic pericarditis is development of [].

A

The main consequence of chronic inflammation of the pericardium is development of constrictive pericarditis.

24
Q

Patients with constrictive pericarditis typically present with symptoms related to what? [1]

A

Patients characteristically present with features of right heart failure.

Symptoms
* Shortness of breath
* Leg swelling
* Abdominal swelling
* Exercise intolerance

Signs
* Raised jugular venous pressure
* Peripheral oedema
* Ascites
* Hepatomegaly

25
Q

Which heart sound is likely heard in constrictive pericarditis

S1
S2
S3
S4

A

Which heart sound is likely heard in constrictive pericarditis

S1
S2
S3
S4

26
Q

What is the most common mechanism resulting in heart failure in patients with constrictive pericarditis?

High-output heart failure
Low-output heart failure
Systolic dysfunction
Diastolic dysfunction

A

What is the most common mechanism resulting in heart failure in patients with constrictive pericarditis?

High-output heart failure
Low-output heart failure
Systolic dysfunction
Diastolic dysfunction

27
Q

Explain the effect of cardiac tamponade on chamber pressures [2]

A
  • Because the pericardial sac isn’t very compliant, when it becomes full of liquid it doesn’t expand much
  • Therefore the pressures inside the heart chambers equalise as the ventricles have less room to fill during diastole
  • Therefore EDV, SV & BP decrease
28
Q

What is Kussmaul’s sign? [1]

A

Increased jugular venous pressure with inspiration

29
Q

What is the difference between Kussmaul’s sign and pulsus paradoxus? [2]

Which pathologies do they relate to? [2]

A

Kussmaul’s sign is typical of constrictive pericarditis, and is a raised JVP with inspiration

Pulsus paradoxus, which is an abnormally large drop in blood pressure (and stroke volume) caused by inspiration, and is typical of cardiac tamponade.

30
Q

Describe the management for a STEMI

A

Immediately assess eligibility for coronary reperfusion therapy. There are two types:

Primary coronary intervention:
- Offered if the presentation is within 12 hours of onset of symptoms AND PCI can be delivered within 120 minutes of the time when thrombolysis could have been given
- Prior to PCI: ‘dual antiplatelet therapy’, i.e. aspirin + another drug.
if the patient is not taking an oral anticoagulant: aspirin & prasugrel;
if taking an oral anticoagulant: aspirin & clopidogrel
- During PCI: patients with radial access:
unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)
- During PCI: patients with femoral access:: bivalirudin with bailout GPI

Thrombolysis:
- should be offered within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when thrombolysis could have been given
- streptokinase, alteplase and tenecteplase.

31
Q

How do you determine which drugs to give if prior to PCI based on their current medication? [2]

A

Prior to PCI: ‘dual antiplatelet therapy’, i.e. aspirin + another drug.:

If the patient is not taking an oral anticoagulant:
- prasugrel

If taking an oral anticoagulant:
- clopidogrel

32
Q

How do you determine which drugs to give if during to PCI based on their access? [2]

A

patients with radial access:
- unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)

Patients with femoral access:
- bivalirudin with bailout GPI

33
Q

What is the medication used following NSTEMI as seconary prevention? [6]

A

6 As AAAAAA

  • Aspirin 75mg once daily indefinitely
  • Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months
  • Atorvastatin 80mg once daily
  • ACE inhibitors (e.g. ramipril) titrated as high as tolerated
  • Atenolol (or another beta blocker – usually bisoprolol) titrated as high as tolerated
  • Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
34
Q

State the different risk stratifications based of GRACE scores [5]

A
35
Q

How do you determine if an NSTEMI patient needs coronary angiography (with follow-on PCI if necessary):

Immediately [1]
Within 72 hours [1]

A

immediate:
- patient who are clinically unstable (e.g. hypotensive)

within 72 hours:
- patients with a GRACE score > 3% i.e. those at immediate, high or highest risk

coronary angiography should also be considered for patients is ischaemia is subsequently experienced after admission

36
Q

What drug therapy should be given to patients with NSTEMI undergoing PCI? [2]

A

unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not

further antiplatelet (‘dual antiplatelet therapy’, i.e. aspirin + another drug) prior to PCI:

If the patient is not taking an oral anticoagulant:
- prasugrel or ticagrelor

if taking an oral anticoagulant:
- clopidogrel

37
Q

How do you decide which PY12 inhibitor should give for conservative managament of unstable angina / NSTEMI based off their risk of bleeding? [2]

A

if the patient is low-risk of bleeding:
- ticagrelor

if the patient is at a high-risk of bleeding
- clopidogrel

38
Q

Describe the 4 types of MI [4]

A

Type 1: Traditional MI due to an acute coronary event

Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)

Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event

Type 4: MI associated with procedures such as PCI, coronary stenting and CABG

NB: Type 1 MI have better prognosis than Type 2 MIs

39
Q

Describe what causes T ype 2 MI [1]

Give two examples of Type 2 MI [2]

A

Troponin leak due to ischaemia due to oxygen supply and demand imbalance.

E.g. Severe HTN & sustained tachy arythmias

40
Q

Describe what causes Type 3 MI [2]

Give 2 examples [2]

A

Troponin rise without acute ischaemia due to acute myocardial inury

E.g. Acute heart failure or myocarditis

41
Q
A
42
Q

MI complications:

What would cause persistent ST elevation without chest pain? [1]

A

Ventricular aneurysm

43
Q
A

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.

44
Q

How do you differentiate between a posterior and anterior MI on an ECG?

A

Anterior MI
- ST-segment elevation in the precordial leads V1-V4

Posterior MI
- tall R waves V1-3 PosteRioR contains 2 tall Rs
- Horizontal ST depression in V1-3

Posterior MI
45
Q

Posterior MI is usually by an occlussion to which which arteries? [2]

A

Left circumflex;
RCA

46
Q

How do you confirm a posterior MI? [1]

A

Posterior infarction is confirmed by ST elevation and Q waves in posterior leads (V7-9)