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MBChB 3 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is overdrive suppression?

A

The phenomenon where a period of excitation at high frequency depresses automaticity of pacemaker cells. The firing of the SA node tends to suppress the automaticity in the other loci because the SA node has a greater intrinsic rhythmicity than the other latent pacemaking sites in the heart.

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2
Q

What is automaticity?

A

It is the ability of the heart to initiate its own beat.

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3
Q

First degree AV block

A

An abnormal prolongation of AV conduction time. This slowed conduction normally takes places in the N region.

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4
Q

AV block

A

As the repetition rate of atrial depolarisation is increased, conduction through the AV junction slows. First (slowed), second (only a fraction of impulses propagated) and third (none of the atrial impulses conducted).

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5
Q

Second degree AV block

A

Conduction pattern in which only a fraction of the atrial impulses are conducted to the ventricles. This type of block may protect the ventricles from excessive contraction frequencies.

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6
Q

Third degree (or complete) AV block

A

Conduction pattern in which none of the atrial impulses reach the ventricles over a substantial number of atrial depolarisations. Third degree block is often associated with syncope (Stokes-Adams attacks).

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7
Q

AV node

A

Atrioventricular node. Divided into 3 functional regions. 1) the AN region, the transitional zone. 2) N region-middle portion. 3) NH region- zone in which nodal fibres gradually merge with the bundle of His.

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8
Q

What is normal QRS axis?

A

-30 degrees to +90 degrees. Predominantly positive QRS in leads I and II.

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9
Q

What is an ECG?

A

Electrocardiograph. A recording of the electrical activity of the heart from the skin.

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10
Q

How do you determine heart rate from an ECG?

A

1) 300 divided by the no. of large squares between each QRS complex.
2) No. of QRS complexes across ECG (10 seconds) x 6.

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11
Q

What is the normal QRS interval?

A

<3 small squares or <120ms.

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12
Q

What is the normal PR interval?

A

<1 large square or <200ms.

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13
Q

What is the normal QT interval?

A

<11 small squares or <440ms.

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14
Q

What is the major therapeutic use of adenosine?

A

An antiarrhythmic drug for the rapid treatment of supraventricular tachycardias. Its supression of atrioventricular conduction makes it very useful in treating paroxysmal supraventricular tachycardia in which the AV node is part of the reentry pathway (as in Wolff-Parkinson-White Syndrome). For these indications, adenosine is administered either as bolus intravenous injection or as an intravenous infusion.

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15
Q

What is a clinical trial?

A

An evaluation of a new therapeutic intervention (drug, device, procedure, surgery) in human volunteers.

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16
Q

Put the heart valves in order of most common site of infective endocarditis.

A

1) Mitral valve-most common site of infection.
2) Aortic
3) Tricupsid (most common site in IVDU)
4) Pulmonary valve-least common site of infection.

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17
Q

What is infective endocarditis?

A

Infection of the endocardium which is the lining of the heart, and this results in damage to the valve cusps.

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18
Q

What is Quorum Sensing?

A

The ability to detect and to respond to cell population density by gene regulation.

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19
Q

What are the HACEK organisms?

A

H-Haemophilus species. A-Aggregatibacter species. C-Cardiobacterium hominis. E-Eikenella corrodens K-Kingella.

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20
Q

What organisms cause endocarditis?

A

Both bacterial and fungal causes. Bacterial causes more common.

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21
Q

What are the 3 classifications of endocarditis?

A

1) Native valve endocarditis
2) Endocarditis in IVDUs
3) Prosthetic valve endocarditis

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22
Q

What is the most common cause of native valve endocarditis?

A

Streptococci, S. Viridans first followed by enterococci.

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23
Q

What is the most common cause of endocarditis in IVDUs?

A

Staphylococcus aureus.

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24
Q

What is the most common cause of endocarditis in prosthetic valve endocarditis?

A

Staphylococcus but more CoNS than S. aureus.

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25
Q

What are the risk factors for native valve endocarditis?

A

Underlying valve abnormalities in 55-75% of patients. Most common two: aortic stenosis and mitral valve prolapse.

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26
Q

What is rheumatic heart disease?

A

Rheumatic heart disease is cardiac inflammation and scarring triggered by an autoimmune reaction to infection with group A streptococci. In the acute stage, this condition consists of pancarditis, involving inflammation of the myocardium, endocardium, and epicardium. Chronic disease is manifested by valvular fibrosis, resulting in stenosis and/or insufficiency.

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27
Q

Early manifestations of IE

A

Fever and murmur=IE until proven otherwise.

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28
Q

What are the 2 hallmarks of embolic disease in IE?

A

Splinter haemorrhages and conjunctival petechiae.

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29
Q

How do you diagnose IE?

A

Blood culture and imaging. Blood culture-most important diagnostic, 3 bloods must be taken, must be done before giving antibiotics. Imaging is echocardiograph either transthoracic (non-invasive) or transopesophageal (invasive).

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30
Q

Define myocardial infarction

A

Any elevation of troponin in a clinical setting consistent with myocardial ischaemia. 5 different types.

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31
Q

CABG

A

A coronary artery bypass graft is a surgical procedure used to treat coronary heart disease. It diverts blood around narrowed or clogged parts of the major arteries to improve blood flow and oxygen supply to the heart.

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32
Q

Type 1 MI

A

Spontaneous MI due to primary coronary event (coronary artery plaque rupture and formation of thrombus).

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33
Q

Type 2 MI

A

Increased oxygen demand or decreased oxygen supply. Heart failure, sepsis, anaemia, arrhythmias, hypertension and hypotension.

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34
Q

Type 3 MI

A

Sudden cardiac death.

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35
Q

Type 4a MI

A

MI associated with percutaneous coronary intervention.

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36
Q

Type 4b MI

A

MI stent thrombosis documented by angiography or PM.

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37
Q

Type 5 MI

A

MI associated with CABG.

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38
Q

What are some chronic reasons for elevated troponin (not MI)?

A
  • renal failure
  • chronic heart failure
  • infiltrative cardiomyopathies eg. amyloidosis, sarcoidosis, haemochromatosis.
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39
Q

What is Glagov’s phenomenon?

A

Where arteries remodel to maintain constant flow despite increases in atherosclerotic mass. Eventually an expansion limit is reached and lumen narrows.

40
Q

On an ECG, what does ST elevation reflect?

A

Occlusion of a coronary artery.

41
Q

ST elevation in inferior=

A

Right coronary artery occlusion (mostly) or left circumflex artery.

42
Q

ST elevation in posterior=

A

Circumflex artery (mostly) or RCA.

43
Q

ST elevation in lateral=

A

Left circumflex artery.

44
Q

ST elevation in anteroseptal=

A

Left anterior descending artery

45
Q

LVSD

A

Left ventricular systolic dysfunction

46
Q

DC cardioversion

A

Direct Current Cardioversion is a procedure to convert an abnormal heart rhythm to a normal heart rhythm. Atrial Fibrillation (AF) is the most common cardiac arrhythmia (abnormal rhythm).

47
Q

Cardiac tamponade

A

Also known as pericardial tamponade, is when fluid in the pericardium builds up, resulting in compression of the heart.

48
Q

GRACE

A

Global Registry of Acute Coronary Events. Gives you a GRACE risk score, considers things like age, HR, SBP, creatinine levels, whether or not there is ST-segment deviation.

49
Q

DAPT

A

Dual anti-platelet therapy

50
Q

Systemic hypertension

A

Persistent elevation in arterial blood pressure >140/90mmHG.

51
Q

Non-modifiable hypertension risk factors

A
  • Age
  • Gender
  • Ethnicity
  • Genetic factors
52
Q

Modifiable hypertension risk factors

A
  • Diet
  • Physical activity
  • Obesity
  • Alcohol in excess
  • Stress
53
Q

Primary hypertension

A

90-95% of cases of hypertension. No identifiable cause. Both modifiable and non-modifiable risk factors.

54
Q

Secondary hypertension

A

5-10% of cases of hypertension. Causes include: endocrine, vascular, renal, drug and other eg. obstructive sleep apnoea.

55
Q

Out of office BP monitoring options

A

1) 24 hour ambulatory BP monitoring-portable device, BP taken every 20-30 mins, 2 hours over night
2) Home BP monitoring-2 readings, twice a day for 4-7 days

56
Q

DASH diet

A

Dietary Approaches to Stop Hypertension

57
Q

What is congenital heart disease?

A

Abnormality of fetal heart development. Encompasses a wide range of malformations, ranging in severity and treatment options.

58
Q

Where is the most common site for co-arctation of the aorta to occur?

A

After the left subclavian artery in a ‘juxta-ductal’ position.

59
Q

What is ‘rib notching’?

A

Rib notching refers to deformation of the superior or inferior surface of the rib. It can affect a single rib (from trauma or solitary masses e.g. schwannoma) or can affect multiple ribs.

60
Q

What are the 2 surgical options in transposition of the great arteries?

A

1) Atrial switch. Not as good, more traditional.

2) Arterial switch. Surgery of choice, less problems. However can sometimes effect coronary arteries- sudden MIs.

61
Q

What are the 4 components of the Tetralogy of Fallot?

A

1) Ventricular septal defect
2) Overriding aorta
3) Right ventricular outflow tract obstruction
4) RV hypertrophy

62
Q

What treatment is given to babies born with transposition of the great arteries?

A

IV prostaglandins to maintain patency of foramen ovale and ductus arteriosis until surgery can be done.

63
Q

What is Fontan circulation?

A

In a Fontan circulation the single functional ventricle is used to support the systemic circulation by disconnecting it from the pulmonary valve and artery. Then the IVC and SVC are redirected and plumbed straight into the pulmonary arteries ultimately bypassing the heart altogether. So now blue blood flows up the IVC directly into the pulmonary arteries without passing through any valves. The blue blood is oxygenated in the lungs and flows back to the left atrium as red blood, through the mitral valve into the single ventricle, through the aortic valve into the aorta and the remainder of the systemic circulation.

64
Q

What is the ductus arteriosis?

A

A vessel in the fetal circulation that joins the aorta to the pulmonary artery.

65
Q

Tricuspid valve

A

Between RA and RV

66
Q

Mitral valve

A

Between LA and LV. 2 leaflets-anterior (A1, A2, A3) and posterior (P1,P2,P3).

67
Q

Aortic valve

A

Between LV and aorta. 3 cusps- trileaflet. Right, left and non-coronary.

68
Q

Pulmonary vlave

A

Between RV and pulmonary artery

69
Q

What can go wrong with valve leaflets?

A

Calcification, thickening, degeneration, infection and prolapse.

70
Q

Stenosis

A

Pressure overload

71
Q

Regurgitation

A

Volume overload

72
Q

TAVI

A

Transcatheter aortic valve implantation. Non-surgical alternative to open heart surgery. Done in a cath lab.

73
Q

What is the definition of heart failure?

A

Pathophysiologic state in which the heart, via an abnormality of cardiac function (detectable or not) failed to pump blood at a rate commensurate with the requirements of the metabolising tissues or is able to do so only with an elevated diastolic filling pressure.

74
Q

What are the stages of congestive heart failure?

A

Stage 1- Redistribution in pulmonary vessels. PCWP 13-188mmHG.
Stage 2- Interstitial oedema. PCWP 18-25mmHg.

75
Q

What are Kerley B lines?

A

Seen in congestive heart failure on CXR. Septal lines- fluid leakage into interlobular septa. Seen at the bases perpendicular to pleural surface and measure 1-2cm. If transient or rapidly developing virtually diagnostic of interstitial pulmonary oedema.

76
Q

What is pleural effusions?

A

Fluid within potential space between parietal and visceral pleura. Transudates and exudates. Protein levels >30g/l, LDH>200IU consistent with exudate. pH<7.1 also suggests exudate.

77
Q

What are the common causes of exudate pleural effusions?

A

Pulmonary embolism, bacterial infection, bronchial carcinoma.

78
Q

What are the common causes of transudate pleural effusions?

A

Left ventricular failure, cirrhosis, nephrotic syndrome.

79
Q

What is a subpulmonic effusion?

A

Fluid can accumulate in a subpulmonic location, can be difficult to detect as upper edge of fluid mimics contour of diaphrgam. Principal sign is elevation of hemidiaphragm.

80
Q

What is acute heart failure?

A

AHF often used to mean new onset acute or characterised by signs of pulmonary +/ or peripheral oedema.

81
Q

What are the causes of acute arterial occlusion?

A

Thrombosis or embolism.

82
Q

Thrombosis causing acute arterial occlusion

A

Thrombosis may occur at the site of a pre-existing atheromatous plaque in a patient with peripheral vascular disease, following plaque rupture. A history of intermittent claudication makes this likely.

83
Q

Embolism causing acute arterial occlusion

A

Embolus from another source, such as the left atrium in a patient with AF. Embolism would be the more likely diagnosis in the absence of a previous history of PVD.

84
Q

Atheroma in coronary arteries can lead to

A

Myocardial ischaemia, angina and infarction.

85
Q

Atheroma in carotid artery disease

A

Transient ischaemic attacks, stroke.

86
Q

Atheroma in mesenteric arteries

A

Abdominal angina, infarction.

87
Q

Atheroma in renal arteries can lead to

A

Hypertension, renal failure (ONLY if bilateral renal artery stenosis).

88
Q

Why don’t we use beta blockers in peripheral vascular disease?

A

They drop peripheral pressures really low- this exacerbates the symptoms as less oxygen then goes to the peripheries.

89
Q

Metabolic syndrome

A

‘Prediabetic’ group of obese individuals with abnormal lipid profiles who are at risk of vascular disease.

90
Q

What is intermittent claudication?

A

Pain in the leg brought on by walking and relieved by rest. Most common in the calf muscles but can affect thigh or buttocks IC is an indicator of widespread vascular disease, and patients with PVD are at risk of cardiac, renal and cerebrovascular events.

91
Q

Critically ischaemic limb

A

Six P’s:

  • Pale
  • Painful
  • Pulseless
  • Paretic
  • Perinshingly cold
  • Paraesthetic
92
Q

What clinical evidence might suggest muscle necrosis?

A

Loss of sensation and muscle tenderness.

93
Q

How do you treat PVD?

A

Treat hypertension, avoid beta blockers, stop smoking, reduce weight, introducing regular, sensible exercise.

94
Q

Heparin MOA

A

Activates antithrombin III. Antithrombin III inhibits thrombin, which converts fibrinogen to fibrin. Hence it is an anticoagulant. It’s activity can be monitored by use of APTT.

95
Q

What is Eisenmenger’s syndrome?

A

Process in which a long-standing left-to-right cardiac shunt caused by a congenital heart defect (typically by a ventricular septal defect, atrial septal defect, or less commonly, patent ductus arteriosus) causes pulmonary hypertension. and eventual reversal of the shunt into a cyanotic right-to-left shunt. Because of the advent of fetal screening with echocardiography early in life, the incidence of heart defects progressing to Eisenmenger’s has decreased.

96
Q

How is claudication diagnosed?

A

Ankle-brachial index is a quick, noninvasive way to check for peripheral artery disease. ABI test compares the blood pressure measured at your ankle with the blood pressure measured at your arm. A low ankle-brachial index number can indicate narrowing or blockage of the arteries in your legs.

MBChB 3 (13 decks)

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