Cardiology #2 Flashcards

1
Q

A 35yo female presents with a DVT in the third trimester of pregnancy. Whilst in the Emergency Department, she develops a left hemiparesis. What underlying cardiac abnormality is most likely to be responsible?

  • Primum ASD
  • Secundum ASD
  • Patent foramen Ovale
  • VSD
  • Patent ductus arterioles
A

Patent Foramen Ovale

Whilst Atrial Septal defects may allow emboli to pass from the right side of the heart to the left side, the most common cause in a Patent Foramen Ovale.

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2
Q

What is the relationship between Migraine and Patent Foramen Ovale (PFO)?

A

Some studies have reported improvement in migraine symptoms following closure of the Patent Foramen Ovale.

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3
Q

What is the management of patients with a Patent Foramen Ovale who’ve had a stroke?

A

The management of patients with PFO who’ve had a stroke remains controversial.
Options include anti platelet therapy, anticoagulant therapy, or PFO closure.

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4
Q

A 29yo man, with no Past Medical History, presents with a left middle cerebral artery (MCA) territory stroke. He reports trouble sleeping and lying flat at night that began after a flu-like illness 3 months ago. His Left Ventricular Ejection Fraction is 15% on a Cardiac Echocardiogram. Which of the following is the most likely factor which contributed to the cause of his stroke?

  • Epstein-Barr virus
  • Stenosed carotid arteries
  • Coxsackie virus
  • Influenza virus
  • Parvovirus B19
A

Parvovirus B19.

The underlying diagnosis is a Viral Myocarditis precipitating a Dilated Cardiomyopathy and causing a Cardioembolic stroke.

Previously, the enteroviruses (eg. Coxsackie virus) were the most common causes in the 1990’s.

More recently, Parvovirus B-19 and HHV-6 are considered the most common causes of viral myocarditis.

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5
Q

A 29yo had Viral Myocarditis, which has precipitated Dilated Cardiomyopathy and caused a Cardioembolic stroke. What might the echo show?

A
  • Reduced Left Ventricular Ejection fraction
  • Myocardial dysynchrony (myocardial segments contract at different points in time)
  • Thinning of the left ventricular wall
  • Dilated left ventricle.
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6
Q

Trouble sleeping and lying flat at night, in combination with exertional dyspnoea after a flu-like illness are key features suggestive of which cardiac disease?

A

Viral Myocarditis.

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7
Q

List 9 viral causes of Viral Myocarditis

A
  • Parvovirus B19
  • Human Herpes Virus 6 (HHV-6)
  • Coxsackie B virus
  • Adenovirus
  • Hepatitis C
  • Cytomegalovirus
  • Echovirus
  • Influenza virus
  • Epstein-Barr virus
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8
Q

Which is the most common cause of Cardiomyopathy?

A

Dilated Cardiomyopathy

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9
Q

What are the causes of Dilated Cardiomyopathy?

A
  • Idiopathic (most common cause)
  • Myocarditis: eg. Coxsackie B, HIV, Diphtheria, Chagas disease
  • Ischaemic heart disease
  • Peripartum
  • Hypertension
  • Iatrogenic: Doxorubicin
  • Substance abuse: alcohol, cocaine
  • Inherited
  • Infiltrative eg. haemochromatosis, sarcoidosis
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10
Q

Describe the inherited causes of Dilated Cardiomyopathy (DCM)

A
  • Familial genetic predisposition to DCM
  • Specific syndrome eg. Duchenne Muscular Dystrophy
  • around 1/3 of patients with DCM are thought to have a genetic predisposition
  • large number of heterogenous defects have been identified
  • the majority of defects are inherited in an AUTOSOMAL DOMINANT fashion, although other patterns of inheritance are seen.
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11
Q

Thiamine deficiency can lead to a restrictive cardiomyopathy. What is this called?

A

Wet beriberi

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12
Q

What is the pathophysiology of Dilated Cardiomyopathy?

A
  • Dilated heart leading to predominately systolic dysfunction
  • All 4 chambers are dilated, but the left ventricle more so than the right ventricle
  • Eccentric hypertrophy (sarcomeres added in series) is seen
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13
Q

List 4 features of Dilated Cardiomyopathy

A
  • Classic findings of heart failure
  • Systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
  • S3
  • ‘Balloon’ appearance of the heart on the CXR.
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14
Q

An 84yo female with a background of osteoporosis is given an infusion of Pamidronate. A week later she presents to her GP complaining of paraesthesia. On examination, she had hyperreflexxia and carpopedal spasm.
Given the electrolyte abnormality she is likely to have developed, what ECG abnormality is most associated with this?

A

Long QT.
Long QT is associated with hypocalcaemia.
Bisphosphonate infusions can lead to hypocalcaemia (although it is more common when using larger doses in malignancy induced hypercalcaemia, as opposed to the smaller dose used in osteoporosis).

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15
Q

A QT interval of greater than [?] is associated with the development of ventricular arrhythmia, syncope and sudden cardiac death.

A

QT interval of greater than O.44 seconds is associated with the development of ventricular arrhythmia, syncope and sudden cardiac death.

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16
Q

List some causes of Long QT.

A
  • Electrolyte abnormalities: hypokalaemia and hypocalcaemia
  • Drugs: Tricyclic antidepressants, Antihistamines, Erythromycin, Clarithromycin, Amiodarone, Haloperidol
  • Congenital Long QT syndromes
  • MI / significant active myocardial ischaemia
  • Cerebrovascular accident (subarachnoid haemorrhage)
  • Hypothermia
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17
Q

Which clinical signs are indicative of hypocalcaemia?

A
  • Hyperreflexia and carpopedal spasm indicate neuromuscular irritability (a feature of hypocalcaemia)
  • Chvostek’s sign: ipsilateral twitching of the muscles around the nose and lips when the facial nerve is tapped at the angle of the jaw.
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18
Q

Which one of the following clinical features would be LEAST consistent with a diagnosis of severe pre-eclampsia?

  • Headache
  • Epigastric pain
  • Reflexes difficult to elicit
  • Low platelet count
  • Papilloedema
A

Reflexes difficult to elicit

Severe pre-eclampsia is associated with hyperreflexia and clonus. A low platelet count may indicate the patient is developing HELLP syndrome.

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19
Q

What is ‘Pre-eclampsia’?

A

A condition seen after 20 weeks gestation characterised by pregnancy-induced hypertension in association with proteinuria (>0.3g/24hours).

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20
Q

List 5 problems that Pre-eclampsia predisposes to.

A
  • Fetal: prematurity, IUGR
  • Eclampsia
  • Haemorrhage: placental abruption, intra-abdominal, intracerebral
  • Cardiac failure
  • Multi-organ failure
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21
Q

List 5 ‘High risk’ factors for Pre-eclampsia.

A
  • Hypertensive disease in a previous pregnancy
  • Chronic kidney disease
  • Autoimmune disease (eg. SLE, Antiphospholipid syndrome)
  • Type 1 or Type 2 Diabetes
  • Chronic hypertension
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22
Q

List 6 ‘Moderate risk’ factors for Pre-eclampsia.

A
  • First pregnancy
  • Age 40+
  • Pregnancy interval of more than 10 years
  • BMI 35kg/m2 or more at first visit
  • Family history of pre-eclampsia
  • Multiple pregnancy
23
Q

List 8 features of severe pre-eclampsia.

A
  • Hypertension: typically >170/110mmHg and proteinuria (>0.3g/24hrs)
  • Proteinuria: dipstick ++/+++
  • Headache
  • Visual disturbance
  • Papilloedemia
  • RUQ / epigastric pain
  • Hyperreflexia
  • Platelet count < 100 x 10^6, abnormal liver enzymes or HELLP syndrome
24
Q

Describe the management of Pre-eclampsia

A
  • Treat BP > 160/110mmHg, although many clinicians have a lower threshold
  • Oral Labetalol is now first line. Nifedipine and Hydralazine may be used.
  • Delivery of the baby is the most important and definitive step. The timing depends on the individual clinical scenario.
25
Q
A 49yo female is admitted to A&amp;E with SOB.  
HR 114 
BP 106/66 
T 37.7
RR 30 
Peak expiratory flow rate 400l/min. 
ABG: 
pH 7.41
pCO2 4.0 kPa
pO2 7.2kPa 

Following O2 therapy, what is the next most important step in management?

A

Low Molecular Weight Heparin

Patient has a suspected PE.
Type 1 resp failure in a tachycardia, tachypnoeic female with an absence of chest signs points to a diagnosis of PE.
Low grade pyrexia is common in PE.

26
Q

Describe the anticoagulation regime for a patient with a PE.

A

LMWH / Fondaparinux should be given initially after a PE is diagnosed EXCEPT in patients with a massive PE where thrombolysis is being considered. In this situation, unfractionated Heparin should be used.

  • Warfarin (Vit K antagonist) should be given within 24 hours of the diagnosis.
  • LMWH / Fondaparinux: continue for at least 5 days, or until the INR is 2.0 or above for at least 24 hours.
  • Warfarin should be continued for at least 3 months.
  • Consider extending Warfarin beyond 3 months for patients with an unprovoked PE.
  • For patients with active cancer, use LMWH for 6 months.
27
Q

What is the first line treatment for Massive PE?

A

Thrombolysis: recommended as 1st line treatment for massive PE where there is circulatory failure (eg. hypotension).

28
Q

A patient has repeat Pulmonary Embolisms, despite adequate anticoagulation. What treatment might you consider?

A

Consider an Inferior Vena Cava (IVC) filter.
These work by stopping clots formed in the deep veins of the leg from moving to the pulmonary arteries.
IVC filter use is currently supported by NICE, but other studies suggest a weak evidence base.

29
Q

You review a 34yo woman who is 13 weeks pregnant. During her previous pregnancy, she developed pre-eclampsia and had to have a C-section at 36/40. Her BP both following the last pregnancy and today is normal. What should be offered to reduce the risk of developing pre-eclampsia again?

A

Low-dose Aspirin.

30
Q

Describe the normal pattern of changes in Blood Pressure during pregnancy.

A
  • BP usually falls in the 1st trimester (particularly the diastolic), and continues to fall until 20-24 weeks
  • After this time, BP usually increases to pre-pregnancy levels by term.
31
Q

Define ‘Hypertension in Pregnancy’.

A

Systolic > 140mmHg or Diastolic > 90mmHg

OR

An increase above booking readings of >30mmHg systolic or >15mmHg Diastolic.

32
Q

Describe ‘Pre-existing Hypertension’ with regards to Hypertension in pregnancy.

A
  • A history of HTN before pregnancy or an elevated BP > 140/90 before 20 weeks gestation
  • No proteinuria, no oedema
  • Occurs in 3-5% of pregnancies and is more common in older women
33
Q

Describe ‘Pregnancy-induced Hypertension’ / ‘Gestational Hypertension.

A

Hypertension >140/90 occurring in the 2nd half of pregnancy (after 20 weeks)

No proteinuria, no oedema

Occurs in around 5-7% of pregnancies

Resolves following birth (typically after 1 month).

Women with PIH are at increased risk of future pre-eclampsia or HTN in later life.

34
Q

Describe ‘Pre-eclampsia’.

A

Pregnancy-induced hypertension in association with proteinuria (>0.3g/24hours)

Oedema may occur but is now less commonly used as a criteria.

Occurs in around 5% of pregnancies.

35
Q

a 72yo man is started on Amlodipine 5mg OD for Hypertension. He has no other Past Medical History of note, and routine bloods (incl. fasting glucose) and ECG were normal. What should his target BP be once on treatment?

A

140 / 90 mmHg

Blood pressure target (clinic reading) for those over 80 is 140/90

36
Q

A 42yo Afro-Caribbean man is diagnosed with Hypertension. Secondary causes of hypertension have been excluded. What is the most appropriate initial drug therapy?

A

Calcium Channel Blocker eg. Amlodipine

ACEi have reduced efficacy in black patients and are therefore not used first line.

37
Q

An 82yo man is referred to Cardiology by his GP with increasing dyspnoea on exertion and a systolic murmur. BP is 100/80mmHg and he has a slow rising pulse. What is the most likely cause of his condition?

A

Calcification of the Aortic Valve -> leading to Aortic stenosis

The most common cause of Aortic Stenosis in patients over 65y is Calcification.

The most common cause of Aortic Stenosis in the under 65s is a Bicuspid Aortic valve.

38
Q

A 71yo male with a history of ischaemic heart disease is brought to A&E following a ‘collapse’. He now feels back to normal. ECG shows Sinus rhythm, HR 94, with LBBB.
Given the ECG findings, what is likely to be heard on auscultation of the heart?

A

Reversed split S2 -> associated with LBBB.

Causes of a Reversed (paradoxical) split S2 (P2 occurs before A2):

  • LBBB
  • Severe aortic stenosis
  • Right ventricular pacing
  • Woolf-Parkinson-White Type B (causes early P2)
  • Patent ductus arteriosus
39
Q

List the causes of a loud S2.

A
  • Hypertension: systemic (loud A2) or pulmonary (loud P2)
  • Hyperdynamic states
  • Atrial septal defect without pulmonary hypertension
40
Q

List a cause of a Soft S2

A

Aortic Stenosis.

41
Q

What causes fixed split S2?

A

Atrial septal defect

42
Q

What causes a widely split S2?

A
  • Deep inspiration
  • RBBB
  • Pulmonary stenosis
  • Severe mitral regurgitation
43
Q

Causes of reversed (paradoxical) split S2 (P2 occurs before A2).

A
  • LBBB
  • Severe aortic stenosis
  • Right ventricular pacing
  • WPW Type B (causes early P2)
  • Patent ductus arteriosus
44
Q

A 25yo female patient with known Bartter’s disease presents to A+E with severe muscle weakness. While awaiting a Potassium result from the laboratory, which ECG findings would be suggestive of severe hypokalaemia?

A

U waves

ST depression

T- wave inversion

  • In hypokalaemia, the quoted figure is that ECG abnormalities begin to appear when Potassium falls below 2.7mmol/l
45
Q

List 5 features of Hypokalaemia present on an ECG.

A
  • U waves
  • Small or absent T waves (occasionally inversion)
  • Prolonged PR interval
  • ST depression
  • Long QT
46
Q

What is the PassMed suggested rhyme to remember the ECG features of hypokalaemia?

A

In hypokalaemia:

U have no Pot and no T, but a long PR and a long QT.

47
Q

An 83yo male presents with ischaemic sounding chest pain that has persisted for the past hour. A 12-lead ECG is performed and shows deep T wave inversion in leads V1 and V2. Which is the most likely implicated coronary artery?

A

Proximal Left Anterior Descending Artery

-> Ischaemic changes in leads V1-V4 = Left Anterior Descending.

48
Q

What is Wellens’ syndrome?

A

Wellens’ syndrome is an ECG manifestation of critical proximal LAD coronary artery stenosis in patients with unstable angina.

It is characterised by symmetrical, often deep (>2mm) T wave inversions in the anterior precordial leads.

49
Q

ECG changes are seen in V1 - V4. Which coronary artery is affected?
Which coronary territory does this supply?

A

Left Anterior Descending

-> Supplies Anteroseptal territory

50
Q

ECG changes are seen in II, III and aVF. Which coronary artery is affected?
Which coronary territory does this supply?

A

Right coronary

-> Supplies the Inferior territory

51
Q

ECG changes are seen in V4 - V6, I, aVL. Which coronary artery is affected?
Which coronary territory does this supply?

A

Left anterior descending OR Left Circumflex

-> Supplies Anterolateral coronary territory

52
Q

ECG changes are seen in I, aVL +/- V5 - V6. Which coronary artery is affected?
Which coronary territory does this supply?

A

Left circumflex

-> Supplies the Lateral coronary territory

53
Q

Which coronary artery is affected if ‘Tall R waves coupled with changes in V1-V2’ are seen on an ECG?
Which coronary territory does this supply?

A

Usually Left Circumflex, also Right Coronary artery

-> Supplies posterior aspect of the heart