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Phase 4 Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

How do NICE define hypertension? (2)

A

> 140/90 in a clinical setting.

> 135/95 with ambulatory or home readings

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2
Q

Give 5 secondary causes of Hypertension

A

ROPED

Renal Disease (most common)
Obesity
Pregnancy/Pre-eclampsia
Endocrine
Drugs

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3
Q

If blood pressure is high and does not respond to treatment, what diagnosis should be considered? And what investigation confirms diagnosis?

A

Renal artery stenosis

Duplex ultrasound or MR or CT angiogram

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4
Q

Give 6 possible complications of hypertension

A

Ischaemic heart disease (angina and acute coronary syndrome).

Stroke/Intracranial haemorrhage

Vascular disease

Hypertensive retinopathy

Vascular dementia

Heart failure

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5
Q

Define stage 1 hypertension

A

Clinic reading >140/90

Ambulatory reading >135/85

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6
Q

Define stage 2 hypertension

A

Clinic reading >160/100

Ambulatory reading >150/95

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7
Q

Define stage 3 hypertension

A

Clinic reading >180/120

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8
Q

What investigations should be performed in new patients with hypertension to test for end organ damage? (4)

A

Urine albumin:creatinine ratio and dipstick (proteinuria/haematirua)

Bloods for HbA1c, renal function and lipids

Fundus examination (hypertensive retinopathy)

ECG (left ventricular hypertrophy)

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9
Q

What risk assessment is used to calculate the % risk that a patient will have a stroke or MI in the next 10 years?

A

QRISK

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10
Q

What does QRISK assess?

A

The % risk that a patient will have a stroke or MI in the next 10 years

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11
Q

When QRISK score is >10% what should be offered?

A

Statin - atorvastatin 20mg at night

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12
Q

What is the moa of statins?

A

Reduce cholesterol production in the liver by inhibiting HMG CoA reductase

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13
Q

What do NICE recommend with regards to starting patients on statins?

A

To check lipids after 3 months and at 12 months.

Increase the dose to aim for a >40% reduction in non-HDL cholesterol.

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14
Q

Other than statins, name 2 other cholesterol lowering drugs.

A

Ezetimibe - Inhibits absorption of cholesterol in the intestine

Evolocumab/Alirocumab (PCSK9 inhibitors - monoclonal antibodies)

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15
Q

Name 3 renal diseases that would cause hypertension

A

Glomerulonephritis

Chronic pyelonephritis

Polycystic kidneys

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16
Q

Name 3 endocrine diseases that may cause hypertension

A

Cushing’s disease

Conn’s disease (hyperaldosteronism)

Phaochromocytoma

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17
Q

Define malignant hypertension and give 3 symptoms

A

Describes acute/rapid rise in blood pressure leading to severe vascular damage.

Symptoms include;

Bilateral retinal haemorrhage and exudates
Headache
Visual disturbance (papilloedema)

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18
Q

Give 5 risk factors for hypertension

A

Age >65

Moderate/high alcohol intake + smoking

Physical inactivity, obesity and poor diet

Family history

Diabetes mellitus and hyperuricaemia

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19
Q

How is a diagnosis of hypertension confirmed?

A

Ambulatory/Home Blood Pressure Monitoring (ABPM/HBPM)

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20
Q

Describe the hypertension treatment ladder for patients <55 and NOT black African/Afro-Caribbean.

A
  1. ACEi/ARB
  2. ACE/ARB + CCB or Thiazide-like diuretic (indapamide)
  3. ACE/ARB + CCB + Thiazide-like diuretic (indapamide)
  4. Measure potassium levels.

If K+ is LESS than 4.5mmol/L give Spironolactone

If K+ is ABOVE 4.5mmol/L give alpha/beta blocker

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21
Q

Describe the treatment ladder for patients >55 and/or are of Black African/Afro-Caribbean origin

A
  1. CCB
  2. CCB + ACEi/ARB or Thiazide-like diuretic (indapamide)
  3. ACE/ARB + CCB + Thiazide-like diuretic (indapamide)
  4. Measure potassium levels.

If K+ is LESS than 4.5mmol/L give Spironolactone

If K+ is ABOVE 4.5mmol/L give alpha/beta blocker

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22
Q

What’s the first drug you would prescribe to a 45 year old white male with hypertension?

A

ACEi/ARB

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23
Q

What’s the first drug you would prescribe to a 58 year old white male presenting with hypertension?

A

CCB

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24
Q

Name 4 calcium channel blockers

A

Verapamil

Diltiazem

Nifedipine

Amlodipine

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25
Q

What drug should NOT be given with verapamil (CCB)? And why?

A

Beta Blockers

Can cause a heart block

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26
Q

Give 4 side effects of verapamil (CCB)

A

Heart failure

Constipation

Hypotension/bradycardia

Flushing

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27
Q

Give 3 side effects of diltiazem

A

Hypotension/bradycardia

Heart failure

Ankle swelling

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28
Q

What is the moa of ACEi? (2)

A

Inhibits conversion of angiotensin I to angiotensin II.

Decreases in angiotensin II levels = vasodilation and reduced blood pressure + decrease in sodium and water retention in the kidney.

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29
Q

Describe 1 renoprotective mechanism of ACEi

A

Angiotensin II constricts the efferent glomerular arterioles.

ACEi therefore dilate the efferent arterioles which reduces glomerylar capillary pressure, reducing mechanical stress on the filtration barriers of the glomeruli.

This is important in preventing diabetic nephropathy

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30
Q

Give 4 side effects of ACEi

A

Cough (due to increased bradykinin levels)

Angioedema

Hyperkalaemia

First-dose hypotension

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31
Q

Give 4 contraindications for ACEi use

A

Pregnancy and breastfeeding

Renovascular disease (may result in renal impairment)

Aortic stenosis (may result in hypotension)

Hereditary of idiopathic angioedema

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32
Q

When using thiazide like diuretics, ACE inhibitors and spironolactone, what is it useful to monitor? and why?

A

U+Es

As Spironolactone and ACEi’s increase risk of hyperkalaemia

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33
Q

Name 4 drugs used in a hypertensive emergency (malignant hypertension)

A

Sodium nitroprusside

Labetalol

Glyceryl trinitrate

Nicardipine

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34
Q

Give 4 factors contributing to endothelial damage within blood vessels.

A

Bacterial infection (pneumonia)

Smoking

Inflammation

Low Density Lipoproteins (LDLs)

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35
Q

Describe the pathophysiology of atherosclerotic plaque formation (3)

A
  1. Initiation - Fatty streaks and Foam Cells
  2. Recruitment - Intermediate lesion formation (formed from smooth muscle cells, platelets and T lymphocytes)
  3. Advanced Lesions - Atheromatous plaque formation w/ Dense fibrous cap made from collagen, elastin and smooth muscle cells
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36
Q

Define angina

A

Describes chest pain caused by insufficient blood supply to heart muscle.

Here the myocardial oxygen demand transiently exceeds the supply, resulting in reversible myocardial ischaemia.

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37
Q

Name 4 types of angina

A

Stable angina (induced by effort, relieved by rest)

Unstable angina (occurs on minimal exertion or at rest)

Prinzmetal angina (occurs at rest due to coronary vasospasm)

Syndrome X (angina pain with NO evidence of atherosclerosis)

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38
Q

Give 4 causes of angina (which is the main?).

A

Atherosclerosis (main cause)

Anaemia

Aortic Stenosis

Arteritis/small vessel disease

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39
Q

Give 3 modifiable and 3 non-modifiable risk factors of angina

A

Modifiable; Hypertension, Smoking, Obesity

Non-modifiable; Age, Male, Family History

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40
Q

Describe the clinical presentation of Typical Angina (3)

A

Presents with all 3 of the following;
- Precipitated by physical exertion
- Constricting discomfort in the chest, neck, shoulders or jaw.
- Relieved by GTN spray or rest

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41
Q

Desribe the clinical presentation of atypical angina

A

Presents with 2 of the typical symptoms and atypical symptoms such as;

GI discomfort and/or breathlessness and/or nausea

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42
Q

What investigation confirms a diagnosis of angina?

A

CT coronary angiography

Confirmed when coronary artery disease is found or when irreversible myocardial ischaemia is found.

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43
Q

What other investigations may be useful to perform when investigating angina? And why? (5)

A

ECG (may show signs of previous MI - Pathological Q waves, LBBB, ST elevation, flat/inverted T waves)

Troponin (should be unchanged in angina due to ischemia not infarction)

LFTs - required before starting statins

HbA1c - exclude diabetes

FBC - exclude anaemia

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44
Q

What are the 5 principles of angina management?

A

RAMPS;

Refer to cardiology

Advise about diagnosis, management and when to call an ambulance

Medical treatment

Procedural or surgical investigations

Secondary Prevention

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45
Q

What are the 3 aims of medical management of angina?

A

Immediate symptomatic relief (GTN spray)

Long term symptomatic relief (Beta blocker/CCB)

Secondary prevention (4As Aspirin, Atorvastatin, ACEi, Already on a beta blocker)

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46
Q

What is the 1st line treatment for angina?

A

GTN Spray + Beta blocker/Calcium Channel Blocker

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47
Q

Describe CCB use in the treatment of angina

A

If using CCB as a monotherapy, use RATE LIMITING CCB - Verapamil/Diltiazem

If using in conjunction with BB use SLOW RELEASE DIHYDROPYRIDINE - Nifedipine

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48
Q

What are the 2nd line treatments of angina? (4)

A

Isosorbide mononitrate (Long acting nitrate)

Ivabradine (inhibits funny channels)

Nicorandil (K channel inhibitor)

Ranolazine (inhibits late Na currents - prolongs ventricular action potential)

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49
Q

What is the moa of a beta blocker

A

Reduce force of contraction (negative inotrope) by acting on B1 receptors

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50
Q

What is the moa of CCB

A

Primary arterodilators - Dilate systemic arteries so reduces afterload (reducing blood pressure)

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51
Q

What drugs are used in the secondary prevention of angina?

A

4As

Aspirin 75mg OD
Atorvastatin 80mg OD
ACEi (If diabetes, hypertension, CKD or Heart failure are also present)
Already on a beta blocker

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52
Q

Name 2 surgical options for the treatment of angina.

A

Percutaneous coronary intervention (PCI)

Coronary artery bypass graft (CABG)

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53
Q

Name 3 potential graft vessels used for CABG

A

Saphenous vein (inner leg)

Internal thoracic artery (internal mammary artery)

Radial artery

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54
Q

Define acute coronary syndrome.

A

An umbrella term used to describe a range of conditions associated with a sudden reduction to blood flow to the heart.

(Acute presentations of ischaemic heart disease).

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55
Q

Name 3 types of Acute Coronary Syndrome

A

Unstable Angina

Non-ST elevation myocardial infarction (NSTEMI)

ST elevation myocardial infarction (STEMI)

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56
Q

Name 2 investigations (and their findings) used in diagnosis of STEMI

A

ECG - ST elevation (V2/V3), Pathological Q waves, LBBB)

Elevated Troponin

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57
Q

Give 5 clinical features of STEMI

A

Acute central chest pain lasting >20 mins

Nausea

Sweatiness

Palpitations

Dyspnoea

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58
Q
A
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59
Q

Describe the immediate management of a STEMI

A

MONA;

Morphine (if in severe pain)
O2 (only if sats <94%)
Nitrates
Aspirin 300mg (with ticagrelor unless there is a bleeding risk, otherwise offer clopidogrel)

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60
Q

What are the 2 types of coronary reperfusion therapy offered to STEMI patients? When are they offered?

A

Percutaneous coronary intervention (PCI) - Offered if presentation is within 12 hours of onset AND PCI can be delivered in 120 of time fibrinolysis could have been given

Fibrinolysis - Offered if presentation is within 12 hours of onset and PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given.

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61
Q

What medications are used in fibrinolysis? What is their moa?

A

Streptokinase/Alteplase

Act as thrombolytics by activating plasminogen to form plasmin, which degrades fibrin and breaks up thrombi.

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62
Q

Describe the secondary prevention of MI.

A

ADBSA

ACEi (ramipril) (or ARB - candesartan)

Dual Antiplatelet Therapy (Clopidogrel + Aspirin)

Beta Blocker (Propranolol) (Use CCB - verapamil if bb contraindicated)

Statin (Atorvastatin)

Aldosterone antagonists (Spironolactone) (offered to patients who had an acute MI AND who have symptoms of heart failure)

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63
Q

How do NSTEMIs differ to STEMIs?

A

NSTEMI patients present with moderate myocardial necrosis (not as much as STEMI), typically due to partial occlusion of a coronary artery.

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64
Q

What may an NSTEMI ECG display? (3)

A

ST Depression

Deep T wave inversion

No pathological Q waves

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65
Q

Describe troponin levels in NSTEMI

A

Elevated (due to infarction)

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66
Q

Describe troponin levels in unstable angina

A

Unchanged (due to ischemia, not infarction)

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67
Q

What score is used in NSTEMI/Unstable angina? What does it predict?

A

GRACE score.

Used to predict 6 month mortality + risk of future cardiac events

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68
Q

Describe the immediate management of NSTEMI/Unstable angina (4)

A

Immediate coronary angiography

Aspirin (ASAP)

Fondaparinux (antithrombin) (unless high bleeding risk)

MONA - Morphine, Oxygen, Nitrates, Aspirin

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69
Q

Instead of fondaparinux, what should be given to patients where therapeutic levels of anticoagulation are required? (i.e mechanical prosthetic valves, AF, DVT ect)

A

Dalteparin or IV dose adjusted heparin

70
Q

Describe the management for patients who are deemed LOW risk via GRACE score (6 month mortality <3%)

A

Consider conservative management without angiotherapy

Offer ticagrelor with aspirin (unless bleeding risk)

71
Q

Describe the management for patients who are deemed intermediate/high risk risk via GRACE score (6 month mortality >3%)

A

Offer angiotherapy

Offer prasugrel or ticagrelor with aspirin (unless bleeding risk)

72
Q

Give 5 factors associated with an increased risk of death in NSTEMI/Unstable Angina

A

History of unstable angina

ST depression or widespread T wave inversion

Raised troponin

Age >70

General comorbidity - previous MI, poor LV function, DM

73
Q

Define afterload

A

The load the heart must push against during contraction.

Ventricular pressure (P) x ventricular radius (r)/ 2x wall thickness

74
Q

Define cardiac output

A

The volume of blood being pumped out of the left and right ventricle per unit time

CO = Heart rate x Stroke volume

75
Q

Define pre-load

A

The amount of ventricular myocyte stretch at the end of diastole (prior to contraction)

76
Q

Describe 3 heart sounds

A

S1 - tricuspid and mitral valves closing (atrioventricular) (occurs at start of systolic ventricular contraction)

S2 - Aortic and pulmonary valves (semi-lunar) (occurs once systolic contraction is complete)

S3 - Occurs due to rapid ventricular filling. (occurs in older HF patients as chordae tendinae and ventricles are stiff and weak, so reach their limit much quicker)

77
Q

Define stroke volume

A

The volume of blood ejected from the left ventricle during each systolic contraction

78
Q

Define end diastolic volume

A

The volume of blood in the ventricles at the end of diastole

79
Q

Describe the Frank-Starling mechanism (3)

A

Represents the relationship between stroke volume and end diastolic volume

States that, the stroke volume of the left ventricle will increase if there is an increase in end diastolic volume.

Occurs because increased volume of blood present induces stretching of cardiac myocytes. The greater the degree of stretching, the more forceful the contraction.

80
Q

What effect does a positive inotrope have on the frank starling curve?

A

Shifts curve to the left as there is an increase in stroke volume and end diastolic pressure.

81
Q

What effect does a negative inotrope have on the frank starling curve?

A

Shifts the curve to the right.

82
Q

Define heart failure

A

The efficiency of the heart as a pump is impaired.

Cardiac output is inadequate for the body’s requirements, due to impaired ventricular function.

The heart is unable to deliver oxygenated blood at a rate commensurate with the requirements of the metabolizing tissues, despite normal or increased filling pressures.

83
Q

Give 5 clinical signs/symptoms of heart failure

A

Breathlessness (dyspnoea)

Fatigue/tiredness

Fluid overload/peripheral oedema

Basal crepitations

Orthopnoea (breathless when lying flat)

84
Q

Describe paroxysmal nocturnal dyspnoea

A

Describes a symptom of heart failure characterised by suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.

85
Q

Define ejection fraction

A

The volume of blood ejected from the left ventricle during systole.

Usually 70% in healthy individuals.

86
Q

Name 2 types of heart failure

A

HF-REF (heart failure with reduced ejection fraction)

HF-PEF (heart failure with preserved ejection fraction)

87
Q

Define HF-REF

A

Describes an inability for the ventricles to contract (characterised by dilated LV) resulting in reduced cardiac output.

Defined by Left Ventricular Ejection Fraction of <40%

88
Q

Define HF-PEF

A

Describes an inability of the ventricles to relax and fill normally (usually due to thickening or stiffening of cardiac muscle), resulting in increased filling pressures.

Defined by a Left Ventricular Ejection Fraction of >50%

89
Q

Give 5 causes of chronic heart failure (state the most common)

A

Ischemic heart disease (most common)

Hypertension

Excessive smoking/alcohol intake

Valvular disease (aortic stenosis)

Cardiomyopathies

90
Q

Give 5 complications of heart failure

A

Atrial fibrillation (most common arrhythmia in HF patients)

Ventricular arrythmias

Depression

Cachexia (muscle wasting)

Chronic Kidney Disease

91
Q

Describe the New York Classification of Heart Failure (4)

A

Class I - No limitation to physical activity (asymptomatic)

Class II - Slight limitation - Comfortable at rest but ordinary physical exercise causes symptoms

Class III - Marked limitation - Comfortable at rest but less than ordinary physical exercise causes symptoms

Class IV - Inability to carry out physical exercise without discomfort.

92
Q

What blood test is used to aid heart failure diagnosis?

A

Anti NT-proBNP (N-terminal Pro Brain Natriuretic Peptide)

(released from heart in response to increased wall tension. Levels correlate with ventricular wall stress and severity of heart failure).

93
Q

What may a chest x-ray of a patient with heart failure show? (5)

A

ABCDE

A - Alveolar Oedema
B- Kerley B lines
C - Cardiomegaly
D - Dilated prominent upper lobe veins
E - Pleural Effusions

94
Q

List 4 investigations used in the diagnosis of heart failure

A

Blood Anti-NTproBNP

Chest x-ray (ABCDE)

Transthoracic Echocardiography (exclude valve disease and assess function of left ventricle)

ECG

95
Q

Describe the urgency for heart failure referral and assessment relative to NT-proBNP levels.

A

Levels from 400-2000ng/L should be seen and have an echocardiogram within 6 weeks.

Levels above 2000ng/L should be seen and have an echocardiogram within 2 weeks.

96
Q

Give 4 lifestyle changes required for those with chronic heart failure

A

Stop smoking and alcohol

Low salt diet

Avoid exacerbating factors (NSAIDs = fluid retention, Verapamil - negative inotrope)

Annual flu vaccine + one off pneumococcal vaccine

97
Q

What is the management of HF-PEF?

A

Low Dose Loop Diuretic (Furosemide)

98
Q

What is the management of HF-REF?

A

1st line - ACEi (ramipril) + Beta Blocker)

(Offer ARB in afro-caribbean)

(Offer hydralazine with nitrate if ACEi/ARB are not tolerated)

2nd line - Add Aldosterone antagonist (spironolactone)

Adjuncts;
- Diuretics (furosemide) to relive symptoms

99
Q

What medications should be avoided in patients with HF-REF?

A

Calcium channel blockers

100
Q

What blood test should be routinely performed in patients being managed for HF-REF? Why?

A

U&Es

As diuretics, ACEi’s and aldosterone antagonists can cause electrolyte imbalances, such as hyperkalaemia

101
Q

Name 4 specialist treatments for patients with heart failure

A

SGLT2 inhibitors (dapagliflozin)
Ivabradine
Hydralazine with a nitrate
Digoxin

102
Q

Name 3 drugs used in the secondary prevention of heart failure

A

Aspirin (anti-platelets)

Statins (lower LDL levels)

Anticoagulants (ticagrelor, prasugrel, clopidogrel)

103
Q

Name 1 procedural/surgical intervention used in the treatment of HF-REF and state when it is offered?

A

Cardiac resynchronisation therapy (CRT).

Used in severe failure with an ejection fraction of <35%.

Involves biventricular pacemakers with leads in the right atrium and ventricle and left ventricle.

Aim is to synchronise the contractions in these chambers to optimise heart function

104
Q

Describe acute heart failure

A

Describes a life-threatening emergency characterised by sudden onset or worsening of HF symptoms.

More commonly occurs due to decompensated chronic heart failure (in patients with a Hx of HF)

105
Q

Give 4 potential triggers for decompensated chronic heart failure

A

Iatrogenic (aggressive IV fluids in a frail elderly patient with impaired left ventricular function)

Myocardial infarction

Sepsis

Hypertensive emergency (acute, severe increase in blood pressure)

106
Q

Give 3 symptoms of acute heart failure

A

Acute shortness of breath (exacerbated by lying flat and improves on sitting up)

Cough with a frothy white/pink sputum

Orthopnoea

107
Q

Give 5 clinical signs of acute heart failure

A

Raised respiratory rate

Reduced O2 sats

Tachycardia

Bilateral basal crackles

Raised JVP + peripheral oedema (if HF is right sided)

108
Q

What type of respiratory failure is caused by acute heart failure?

A

Type 1 respiratory failure (low oxygen with normal Co2)

109
Q

Give 6 assessments for a patient presenting with ? acute heart failure

A

Clinical assessment (Hx, examination, ABCDE)

ECG

Bloods (FBC, U&E, LFTs, BNP, Troponin)

ABG

CXR (May show cardiomegaly, ABCDE)

Echocardiogram (assessing ventricular function)

110
Q

Describe the MOA of BNP (4)

A

Relaxes smooth muscle in blood vessels, promoting vasodilation.

Reduces systemic vascular resistance.

Acts on kidneys to promote water excretion in the urine.

Overall reduces circulating volume in someone that is fluid overloaded.

111
Q

Describe the management of acute heart failure

A

SODIUM;

Sit Up (helps oxygenate the lungs)

Oxygen (if sats are <95%)

Diuretics (furosemide)

IV fluids should be STOPPED

Underlying causes (need to be identified and treated)

Monitor fluid balance

112
Q

Decompensated heart failure can lead to pulmonary oedema. What is the treatment of this?

A

IV loop diuretic (furosemide)

113
Q

Rate control should be offered to all patients with AF, except those with what? What is offered instead (4)

A

Offer rhythm control instead.

A reversible cause of AF

New onset AF (within the last 48 hours)

Heart failure caused by AF

Symptoms despite being effectively rate controlled

114
Q

Give 3 medications used for rate control of AF

A

Bisoprolol (Beta blocker)

Verapamil/Diltiazem (Calcium channel blocker)

Digoxin

115
Q

What is used for rhythm control in AF? (2)

A

Cardioversion

Long term rhythm control

116
Q

Name 2 types of cardioversion used in rhythm control of AF

A

Immediate cardioversion

Delayed cardioversion

117
Q

When is immediate cardioversion offered in AF?

A

If AF is;

Present for <48 hours

Causing life threatening haemodynamic instability

118
Q

Name 2 types of immediate cardioversion

A

Pharmacological - Flecainide/Amiodarone

Electrical - Using a cardiac defib to shock heart into sinus rhythm

119
Q

When is delayed cardioversion offered? What form is offered?

A

If AF present for >48 hours and are stable

Transoesophageal echocardiography- guided cardioversion.

Amiodarone considered before/after electrical to prevent AF from recurring

120
Q

What is the anticoagulation process for treating AF with delayed cardioversion?

A

Anticoagulate with DOAC for 3 weeks before delayed cardioversion

121
Q

How is paroxysmal atrial fibrillation managed? (3)

A

Pill in the pocket approach - Take a pill to terminate AF when symptoms begin.

Flecainide

Anticoagulate according to CHADSVASc score

122
Q

What is the MOA of Dabigatran?

A

Direct thrombin inhibitor

123
Q

What is the MOA of Apixaban, Edoxaban and rivaroxaban?

A

Direct factor Xa inhibitor

124
Q

How often are apixaban and dabigatran taken?

A

Twice daily

125
Q

How often are edoxaban and rivaroxaban taken?

A

once daily

126
Q

What medication reverses the effects of apixaban and rivaroxaban?

A

Andexanet alfa

127
Q

What medication is used to reverse the effects of dabigatran?

A

Idarucizumab

128
Q

What score is used to assess whether a patient with AF requires anticoagulation? What factors does it use?

A

CHADSVCAc

C - Congestive heart failure
H - Hypertension
A2 - Age above 75 (scores 2)
D - Diabetes
S2 - Stroke or TIA previously (Scores 2)
V - Vascular disease
A - Age 65-74
S - Sex (female)

129
Q

How does the score of CHADSVASc determine treatment?

A

0 = No anticoagulation

1 = Consider anticoagulation in men

2 or more = Offer anticoagulation

130
Q

What score is used to assess the risk of major bleeding in patients with AF taking anticoagulation? What factors does it use?

A

ORBIT

O - Older age (Age >75)
R - Renal impairment (GFR <60)
B - Bleeding previously (Hx GI or Intracranial bleed)
I - Iron (low Hb or haematocit)
T - Taking antiplatelet medication

131
Q

What treatment is offered to patients with contraindications to anticoagulation and who have a high stroke risk?

A

Left Atrial Appendage Occlusion

132
Q

What causes an ejection systolic murmur that is louder on expiration? (2)

A

Aortic stenosis or Hypertrophic obstructive cardiomyopathy

133
Q

What causes an ejection systolic murmur loudest on inspiration? (2)

A

Pulmonary stenosis or atrial septal defect

134
Q

What causes a pansystolic murmur?(2)

A

Mitral/tricuspid regurgitation or ventricular septal defect

(Tricuspid regurgitation is heard loudest during inspiration)

135
Q

What causes a late systolic murmur?

A

Mitral valve prolapse or coarctation of the aorta (2)

136
Q

What causes an early diastolic murmur?

A

Aortic regurgitation

137
Q

What causes a mid-late diastolic murmur?

A

Mitral stenosis

138
Q

What causes a continuous machine-like murmur?

A

Patent ductus arteriosus

139
Q

Name 3 patterns of presentation in patients with peripheral artery disease

A

Intermittent claudication

Critical Limb Ischaemia

Acute limb-threatening ischaemia

140
Q

Name 2 ways of assessing for peripheral artery disease by the bedside

A

Check the femoral, popliteal, posterior tibialis and dorsalis pedis pulses

Check ankle brachial pressure index (ABPI)

141
Q

What is the 1st line is used to diagnose peripheral artery disease?

A

Duplex ultrasound

142
Q

When investigating PAD, what should be performed prior to any intervention?

A

Magnetic resonance angiography (MRA)

143
Q

What ABPI result would indicate claudication?

A

1 = Normal

0.6-0.9 = Claudication

0.3-0.6 = Rest pain

<0.3 = Impending

144
Q

How is PAD managed? (4)

A

Quit smoking

Treat comorbidities (Hypertension, diabetes, obesity)

Start statin (80mg Atorvastatin)

Exercise training

145
Q

Name 2 treatments for severe PAD/critical limb ischaemia

A

Endovascular revascularisation (Used for short segment stenosis <10cm)

Surgical revascularisation (Used for long segment lesions >10cm)

146
Q

An ABPI of what would indicate critical limb ischaemia?

A

<0.5

147
Q

What features are seen in critical limb ischaemia? (3)

A

1 or more of;

Rest pain in foot for more than 2 weeks

Ulceration

Gangrene

148
Q

What features are seen in acute limb threatening ischaemia?

A

1 or more of the 6 P’s;

Pale
Pulseless
Painful
Paralysed
Paraesthetic
Perishing with cold

149
Q

How is acute limb threatening ischaemia initially investigated by the bedside? (2)

A

Handheld arterial Doppler

Ankle-brachial pressure index (ABPI)

150
Q

Name 3 factors that would suggest acute limb threatening ischemia has been caused by a thrombus (as opposed to an embolus)

A

Pre-existing claudication with sudden deterioration

Reduced or absent pulses in contralateral limb

Evidence of widespread vascular disease (MI, stroke,TIA)

151
Q

Name 4 factors that would suggest acute limb threatening ischemia has been caused by an embolus (as opposed to a thrombus)

A

Sudden onset of painful leg (<24 hours)

No history of claudication

Clinically obvious source of embolus (AF, recent MI)

No evidence of PAD (normal pulses in contralateral limb)

152
Q

How is acute life threatening limb ischaemia initially managed? (4)

A

ABC approach

IV opioids

IV Unfractioned Heparin

Vascular review

153
Q

Name 5 definitive managements of acute life threatening limb ischaemia

A

Intra-arterial thrombolysis

Surgical embolectomy

Angioplasty

Bypass surgery

Amputation (for patients with irreversible ischaemia)

154
Q

Define Wolff-Parkinson White Syndrome

A

Describes presence of a congenital accessory conducting pathway between the atria and ventricles.

Leads to atrioventricular re-entrant tachycardia (AVRT).

155
Q

What is one harmful complication of WPW?

A

Accessory pathway does not slow conduction so AF can rapidly degenerate to VF

156
Q

What will an ECG likely show for WPW? (5)

A

Short PR interval (<120ms)

Delta Waves - Wide QRS complexes with slurred upstroke

QRS prolongation (>110ms)

Left axis deviation (if right sided accessory pathway)

Right axis deviation (if left sided accessory pathway)

157
Q

Name 3 associations with WPW

A

Hypertrophic Obstructive Cardiomyopathy

Ebsteins anomaly

Mitral valve prolapse

Thyrotoxicosis

158
Q

What ECG findings are seen in Hypertrophic Obstructive Cardiomyopathy? (3)

A

Left ventricular hypertrophy (Left axis deviation)

T wave inversion

Deep Q waves

159
Q

What ECG leads monitor the Right Coronary Artery?

A

Inferior Leads (II, III, aVF)

160
Q

What ECG leads monitor the left anterior descending artery?

A

Anteroseptal leads - V1-V4

161
Q

What ECG leads monitor the Left circumflex artery?

A

Lateral Leads (V5-6, I and aVL)

162
Q

What is the correct width for a PR interval?

A

120-200ms (3-5 little squares)

163
Q

What is the correct width for the QRS complex?

A

Should not exceed 110ms (<3 little squaes)

164
Q

Describe 1st degree heart block

A

Describes patients experiencing slow conduction velocity, resulting in prolonged PR interval (>200ms)

165
Q

What will an ECG show in a patient with a 1st degree heart block?

A

Prolonged PR interval (>200ms = >5 small squares)

166
Q

Describe Mobitz I heart block (Second degree)

A

Progressive prolongation of PR interval followed by blocked/non-conductive P wave

167
Q

Give 2 causes of Mobitz I heart block

A

Hyperkalaemia

AV nodal blocking dugs (BB, CCB, Digoxin)

168
Q

Describe Mobitz II heart block. What is seen on ECG?

A

Occurs due to failure of conduction through His-Purkinje system.

ECG shows;
Constant PR interval
Dropped QRS complexes (all that remains is P wave)

169
Q

Do mobitz I heart blocks require a pacemaker?

A

No

170
Q

Do mobitz 2 heart blocks require a pacemaker?

A

Yes. Due to high risk of sudden complete AV block

171
Q

Describe third degree heart block

A

Complete absence of AV node conduction, resulting in no association between P waves and QRS complexes.

172
Q

What may be seen on ECG for 3rd degree heart block?

A

Bradycardia (due to ventricular escape rhythm)

Independent P waves and QRS complexes

Phase 4 Medicine (15 decks)

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