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Year 3 - Diseases > Cardiology > Flashcards

Cardiology Flashcards

1
Q

List the 4 features of teratology of fallot

A
  • Pulmonary stenosis (main determinant of severity of symptoms)
  • Overriding aorta
  • Ventricular septal defect
  • Right ventricular hypertrophy
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2
Q

What type of disease is teratology of fallot?

A

Cyanotic congenital heart disease (most common)

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3
Q

Describe presentation of teratology of fallot.

A
  • Infancy or early childhood
  • Shortness of breath
  • Fatigue on exertion
  • Cyanotic episodes by ages 1-2. Relieved by squatting (increased systemic vascular resistance increasing LV pressure)
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4
Q

Describe diagnosis and management of teratology of fallot

A
  • Diagnosis confirmed by haematologic and radiologic studies

- Treatment varies from surgical intervention to pharmacotherapy

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5
Q

Describe the pain in peripheral vascular disease

A
  • Intermittent claudications (cramping)

- Pain upon exertion

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6
Q

What are cardiac abnormalities associated with in fetuses?

A

Poorly controlled gestational diabetes.

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7
Q

Describe treatment of septic shock

A
  • Intravenous fluid resuscitation
    to increase vascular preload
  • Vasopressor medications to increase systemic vascular resistance.
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8
Q

List common causes of ischaemic stroke

A
  • Embolic disease due to AF

- Atherosclerosis

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9
Q

Which type of murmur is heard in chronic rheumatic fever?

A
  • Mitral stenosis
  • Due to type II hypersensitivity reaction to M protein, which binds with factor H to decrease complement activation. This damages the heart and valves.
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10
Q

Describe characteristics of hypertrophic cardiomyopathy

A
  • Genetic disorder (autosomal dominant)
  • Crescendo- decreasenco systolic murmur
  • Jerky carotid pulse
  • Pulsus bisferiens (aortic waveform with 2 peaks per cardiac cycle) on physical examination
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11
Q

What is the leading cause of acute mortality following MI?

A
  • Ventricular tachycardia degenerating into ventricular fibrillation, pulseless electrical activity and asystole
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12
Q

Describe murmur in tricuspid valve stenosis

A
  • Diastolic murmur

- Heard at left lower sternal border, increases with inspiration

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13
Q

List main symptoms of rheumatic fever

A
  • Joint pain
  • Carditis
  • Erythema marginatum
  • Subcutaneous nodules
  • Chorea
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14
Q

What is dilated cardiomyopathy?

List its causes

A
  • Left ventricular dilation and systolic dysfunction
  • Commonly caused by ischaemia and long standing hypertension and:
Alcohol
Beriberi (B1 deficiency)
Coxsackie
Chagas
Cocaine
Doxorubicin
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15
Q

What is thromboangiitis abliterans?

A
  • Vasculitis affecting the hands and feet of smokers
  • Leads to claudication, ischaemic pain, gangrene and autoamputation of affected digits
  • Ischaemic pain secondary to inflammatory thrombi in the arteries and vessels
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16
Q

What is the main cause of sudden cardiac death/arrest?

A
  • Coronary heart disease

- Cessation of cardiac electrical activity with haemodynamic collapse

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17
Q

How do patients present upon examination with mitral valve regurgitation?

A
  • Pansystolic heart murmur over the mitral area
  • Louder on expiration
  • Commonly caused by mitral valve prolapse caused by posterior myocardial infarction
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18
Q

List major symptoms, signs and epidemiological factors of aortic valve stenosis

A
  • Shortness of breath on exertion
  • Syncope
  • Loud ejection systolic murmur on right sternal border with characteristic radiation to the carotids
  • Slow rising pulse and narrow pulse pressure
  • Presents 50-60 if bicuspid, 60-80 if not
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19
Q

What is myocardial infarction?

A
  • Necrosis of heart tissue as a result of ischemia.
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20
Q

What is the best thing to measure to identify an MI?

A

Troponin 1. Rises 2-3 hours post MI, peaks at 2 days and stays elevated for 7 days

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21
Q

Which virus causes kaposi sarcoma?

A
  • Human herpes virus 8

- Most often associated with HIV positive patients who are immunocompromised

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22
Q

Acute rheumatic fever

  • Who it affects
  • Cause
A
  • Common in children age 5-15 years old, 2-4 weeks after pharyngeal infection by group A streptococcus.
  • To meet criteria must be infection followed by 2 major or 1 major and 2 minor manifestations
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23
Q

List criteria for acute rheumatic fever (minor and major)

A

Major

  • Joints: migratory arthritis predominantly of large joints
  • Carditis
  • Nodules (subcutaneous)
  • Erythema marginatum
  • Sydenham chorea

Minor

  • Arthralgia
  • Fever
  • Elevated ESR and C-reactive protien
  • Prolongued PR interval
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24
Q

What causes rheumatic fever?

A
  • Cross reactivity between group A streptococcuses M protein and antigens in the myocardium, joints and CNS
  • Type II hypersensitivity reaction
  • Temporary or chronic
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25
Q

List consequences of rheumatic fever

A
  • Rheumatic heart disease
  • Left heart dilation
  • Left ventricular hypertrophy
  • Congestive heart failure
  • Arrythmia
  • Bacterial endocarditis
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26
Q

What is accelerated hypertension?

A
  • Blood pressure higher than 180/120
  • Hypertensive encephalopathy (papilledema)
  • Renal failure
  • Retinal haemorrhage or papilloedema
  • Also called malignant hypertension
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27
Q

Define aortic stenosis

A

Tightening of the aortic valve at the origin of the aorta

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28
Q

Describe aetiology of aortic stenosis

A
  • Calcification of the aortic valves: most common cause of AS in developed countries, typically occurring in elderly adults.
  • Congenital abnormality of the aortic valve: the aortic valve is normally composed of three cusps (known as a tricuspid valve), but in some cases, individuals have only two cusps (known as a bicuspid valve) which predisposes them to the development of AS as well as aortic regurgitation.
  • Rheumatic heart disease: a rare cause of AS in developed countries.
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29
Q

What are the signs and symptoms of aortic stenosis?

A
  • Syncope (exertional)
  • Angina
  • Dyspnoea (SOB)
  • On auscultation, crescendo decreascendo murmur heard loudest at right sternal edge in second intercostal space (ejection systolic), radiates to caroids
  • Louder on expiration
  • Narrow pulse pressure
  • Slow rising pulse
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30
Q

Describe findings upon examination in patent ductus arteriosus

A
  • Failure to thrive
  • Clubbing
  • Frequent respiratory infections
  • Wide pulse pressure
  • Continuous machine like murmur
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31
Q

List signs of mitral regurgitation

A
  • AF
  • Displaced, hyperdynamic apex beat
  • Pansystolic murmur at apex radiating to axilla
  • The more severe the largery the left ventricle
  • First heart sound followed by a high-pitched holosystolic murmur at the apex, that radiates to the clavicular area
  • Louder on expiration
  • Can cause pulmonary oedema due to increased pressure in lung capillaries
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32
Q

What is thrombophlebitis and how is it investigates?

A
  • Inflammation and thrombus formation in lower superficial veins
  • Characterized by doppler ultrasound to rule out DVT
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33
Q

Define peripheral vascular disease

A

Narrowing and calcification of peripheral vessels

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34
Q

List risk factors of peripheral vascular disease

A
  • Smoking
  • Diabetes
  • Obesity
  • High BP
  • High cholesterol
  • Age
  • Family history
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35
Q

Define rheumatic fever

A

Systemic inflammatory disorder affecting children

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36
Q

List investigations performed in rheumatic fever

A
  • ECG (prolongued PR and tachycardia)
  • Vital signs (fever)
  • Throat swab for group A strep
  • Chest x ray
  • Doppler echocardiogram
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37
Q

Describe the symptoms of acute coronary syndrome and angina pectoris

A
  • History of sudden onset, central crushing chest pain radiating to both/ either arms, neck or jaw lasting a few minutes or half an hour
  • Angina pectoris pain occurs while exercising and stops at rest
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38
Q

Describe features of pulmonary embolism

A
  • Sudden onset shortness of breath, and/or haemoptysis and/or pleuritic chest pain in someone with an inflamed limb and/or risk factors for blood clots
  • Tachycardia
  • Signs of hypoxia (only if very large)
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39
Q

How are patients with acute coronary syndrome treated immediately (when in crisis)?

A
  • Morphine and metoclopramide
  • Oxygen (if required)
  • Nitrates (for vasodilation)
  • Aspirin 300mg
  • Clopidogrel or ticagrelor
    STEMI patients recieve coronary reperfusion by PCI if available within 2 hours or fibrinolysis under 12 hours (Cath lab, stent)
    NSTEMI angioplasty only (CABG, MABG), additionally fondaparinux (inhibits factor X) + LMWH. Grace score used to determine whether conservative management of PCI
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40
Q

What is variant angina?

A
  • Angina at rest that occurs in cycles
  • ECG captures diffuse ST elevations
  • Cardiac enzymes and markers are generally normal levels
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41
Q

How is AF treated?

A

If under 48hrs and haemodynamically stable

  • Rhythm control (DC cardioversion or chemical cardioversion (flecanide {contraindicated in CVD) or amiodarone)
  • Rate control (bisoprolol, verapamil, dilitazem, digoxin)
  • Chadvasc score for anticoagulation

If over 48 hours

  • Anticoagulation (LMWH + warfarin loading, 4-8 weeks later DC cadioversion)
  • Rate control (bisoprolol, verapamil, diliazem, digoxin)

If haemodynamically unstable
- DC cardioversion

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42
Q

How is atrial septal defect characterised?

A
  • Wide fixed splitting of S2 and a systolic murmur at the left third ICS
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43
Q

What does hypovolaemia cause?

A
  • Tachycardia
  • Hypotension
  • Sunken eyes
  • Dry mucous membranes
  • Perenal acute kidney injury due to increased renal perfusion (increased blood urea nitrogen to creatine and low sodium excretion)
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44
Q

Define infective endocarditis

A
  • Infection of the endocardial surfaces of the heart
  • Microorganism is introduced (eg. via surgery) and adheres to the heart. It then invades the valve (tricuspid) and surrounding areas.
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45
Q

List symptoms of infective endocarditis

A
  • Fever
  • Chills
  • Anorexia
  • Weight changes
  • Malaise
  • Headache
  • Myalgia
  • Night sweats
  • Shortness of breath
  • Cough
  • Arthralgia
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46
Q

List signs of heart failure due to left ventricular dysfunction

A
  • Pulmonary oedema
  • 3rd heart sound
  • Tachypnoea, tachycardia
  • Cardiomegaly (displaced apex beat) and prominent pulmonary vasculature on X ray
  • Pleural effusions
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47
Q

How is hypertension diagnosed?

A

2 or more seated blood pressure readings over outpatient meetings, ABPM HBPM

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48
Q

How is systolic hypertension treated?

A

Thiazide

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49
Q

What causes concentric hypertrophy?

A
  • Chronic hypertension

- Additonal sarcomere units are added in parallel to increase strength and overcome afterload

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50
Q

How do beta blockers work

A
  • Negative ionotrohic effect (reduce force of contraction)

- Negative chonotropic effect (reduce rate and rhythm by affecting conduction system)

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51
Q

List side effects of calcium channel blockers

A

Increased blood fluid due to vasodilation results in…

  • Ankle swelling
  • Headaches
  • Flushing
  • Palpatations
  • Constipation
  • Abdominal pain
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52
Q

Define first degree av block

A

Prolongation of PR interval to over 200msec

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53
Q

How is AV nodal reentrant tachycardia treated?

A
  • Short term with IV adenosine

- Long term with verapamil (non-dihydropyridine calcium channel blocker

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54
Q

Describe examination for DVT

A

Ultrasonography

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55
Q

List cardiovascular parameters that change during pregnancy

A
  • Decrease in systemic vascular resistance
  • Increase in cardiac output
  • Decrease in vascular resistance, leads to decreased afterload and increased stroke volume
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56
Q

How is unstable tachycardia treated?

A

Syncronised cardioversion

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57
Q

Describe ECG in second degree heart block

A
  • Type II block is characterized by intermittently conducted P-waves that are not preceded by progressive prolongations of the PR-interval. Ratio of p waves to QRS
    . In contrast, In type I block, there is progressive
    prolongation of the PR-interval before a QRS-complex is not conducted.
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58
Q

Describe second degree heart block (type 2)

A
  • Second degree atrioventricular block is usually due to failure of conduction at the level of the His-Purkinje system
  • There are 2 subtypes of second degree AV block.
  • Type I second degree AV block is more commonly due to a functional suppression of AV conduction (e.g. due to drugs, reversible ischemia). Progressive elongation of PR until QRS missed.
  • Type II block is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis). Randomly dropped QRS complexes, PR interval constant.
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59
Q

What is Behcets disease?

A
  • An immune complex small vessel vasculitis characterized by recurrent multiple aphthous ulcers, uveitis, and genital ulcers.
  • This condition has a high-incidence among Eastern-Mediterranean countries.
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60
Q

Describe signs and symptoms of a patient with a burst AAA

A
  • Abdominal, flank or back pain
  • Grey turners if retroperitoneal bleed
  • Syncope
  • Pulsatile mass on palpation
  • Tachycardia, hypotension
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61
Q

Define AAA

A
  • Dilation of the abdominal aorta over 50% of previous diameter. Usually asymptomatic until burst
  • Bursting is a medical emergency
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62
Q

List risk factors for AAA.

A
  • Hypertension
  • Age
  • Connective tissue disorders (eg. Marfans)
  • Cigarette smoking
  • Hereditary/family history
  • Male sex (prevalence)
  • Female sex (rupture)
  • Hyperlipidaemia
  • COPD
  • Atherosclerosis (i.e., coronary artery disease [CAD], peripheral arterial occlusive disease)
  • Hypertension
  • Increased height
  • Central obesity
  • on-diabetic
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63
Q

Describe investigations for AAA

A
  • Ultrasonography is the definitive test (can also use radiography, CT scanning and MRI)
  • CT scan with contrast (angiogram) shows rupture, while ultrasound shows aneurysm but not whether it has ruptured
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64
Q

List risk factors for heart failure

A
  • Ischaemic heart disease (smoking, diabetes mellitus, hypercholesterolaemia, hypertension, south Asian descent, strong family history
  • Other atheroscleroticc disease
  • Hypertension
  • Valvular disease
  • Cardiomyopathy
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65
Q

Describe Stokes-Adams attacks and list their causes

A
  • Sudden transient loss of consciousness induced by a slow or absent pulse and subsequent loss of cardiac output
  • Underlying problem is either third-degree heart block or sinoatrial disease
  • Not associated with change in posture
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66
Q

How are Stokes-Adams attacks treated?

A

Implant a pacemaker

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67
Q

Define deep vein thrombosis

A

The formation of a blood clot within a deep vein, predominantly in the legs

  • Provoked is associated with a risk factor
  • Unprovoked in absence of a risk factor
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68
Q

List symptoms and signs of DVT

A
  • Pain in the leg (unilateral, occurs when walking or bearing weight)
  • Swelling of the calf
  • Redness
  • Warmness
  • Engorged superficial veins
  • Homans sign (pain on dorsiflexion)
  • Oedema, redness, warmth, venous distention
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69
Q

List risk factors for DVT

A
  • A history of DVT.
  • Cancer (known or undiagnosed).
  • Age over 60 years.
  • Being overweight or obese.
  • Male sex.
  • Heart failure.
  • Medical illness, for example acute infection.
  • Acquired or familial thrombophilia.
  • Inflammatory disorders (for example, vasculitis, inflammatory bowel disease).
  • Varicose veins.
  • Smoking.
  • Recent major surgery.
  • Recent hospitilisation.
  • Recent trauma.
  • Chemotherapy.
  • Significant immobility
  • Prolonged travel (for more than 4 hours).
  • Significant trauma or direct trauma to a vein (for example intravenous catheter).
  • Hormone treatment (for example oestrogen-containing contraception or hormone replacement therapy).
  • Pregnancy and the postpartum period.
  • Dehydration.
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70
Q

What is vasospastic angina?

A

Angina caused by coronary artery spasm

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71
Q

Which grafts are used to treat coronary artery disease?

A
  • LIMA (left interior mammary artery)

- CABG (uses saphenous vein, usually great)

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72
Q

Define myocarditis

A

Inflammation of heart muscle in the absence of acute or chronic ischaemia characteristic of coronary artery disease

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73
Q

List major causes of myocarditis

A

Infection

  • Adenovirus
  • Trypanosoma cruzi
  • Parvovirus B19
  • Coxsackie B - MOST COMMON IN EUROPE
  • HIV
  • CMV
  • Rubella
  • Polio
  • Enterovirus

Drugs

  • Cyclophosphamide, catecholamines (e.g. adrenaline, dopamine)
  • Amphetamines, ethanol, cocaine
  • Heavy metals (copper, iron, lead)

Hypersensitivity

  • Antibiotics (cephalosporins, penicillins, sulphonamides)
  • Clozapine
  • Diuretics
  • Lithium
  • Phenytoin

Inflammatory/immune disorders

  • Diabetes mellitus (type 1)
  • GPA (formerly known as Wegner’s)
  • IBD
  • Sarcoidosis
  • SLE
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74
Q

Describe symptoms of myocarditis

A
  • Flu like symptoms (eg. fatigue, fever, myalgia, URTI)
  • Chest pain (worse when laying down)
  • Dyspnoea
  • Orthopnoea
  • Fatigue
  • Palpatations
  • Syncope
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75
Q

List signs of myocarditis

A
  • Raised JVP
  • Tachycardia
  • Fever
  • Hypotension
  • Low oxygen sats
  • Pitting oedema
  • S3/4 gallops
  • Pericardial rub
  • Arythmia
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76
Q

Describe epidemiology of myocarditis

A
  • All age groups can be affected but it commonly affects those <50
  • Slightly higher incidence in men than women
  • 5% of patients with acute viral illness may have myocardial involvement
  • Approximately 10% of all sudden cardiac deaths in people under 35 can be attributable to myocarditis aetiology
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77
Q

Describe ECG appearance of left bundle branch block

What is it associated with?

A 
WiLLiaM
MoRRoW
- V1 W V6 M
- Widened QRS-interval, >120 ms, broad monomorphic R-waves in I and V6 with no Q-waves, and broad monomorphic S-waves in V1. 
- Negative complex in V1
- Associated with aortic stenosis
- 2 complexes at once
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78
Q

List the different types of hypertension

A
  • Primary hypertension (no identifiable cause, 90% of cases)
  • Secondary hypertension, usually in under 40s (10% cushings, hyperadrenalism, diabetic nephropathy, kidney disease, renal artery stenosis, phaeochromocytoma, connective tissue disorders, drugs eg. COCP)

Stage 1 135/85-149/94 HBPM, 140/90 - 159/199 clinic
Stage 2 over 150/95 HBPM, 160/100 clinic
Stage 3 over 180/120 in clinic

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79
Q

List risk factors for hypertension

A
  • Poor diet
  • Obesity
  • High cholesterol
  • Physical inactivity
  • Alcohol
  • Smoking
  • Family history
  • Age
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80
Q

What is done if a one of blood pressure reading of 140/90-180/120mmHg occurs?

A
  • Offer 24 hours blood pressure monitoring (ABPM)
  • Ask patients to measure blood pressure at home
  • Assess cardiovascular risk
  • Investigate for end organ damage
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81
Q

How is stage 1 hypertension treated?

A
  • If over 80 consider treatment
  • If under 80 with Q risk over 10% and target organ damage consider drug treatment
  • If under 60 and no end organ damage/ high CVD risk consider lifestyle management first
  • If under 40, investigate for underlying casue
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82
Q

How is target organ damage investigated in hypertension?

A
  • Urine (haematuria and proteinurea using urine albumin:creatinine)
  • Bloods for U and Es
  • Fundoscopy for retinopathy (cotton wool spots, flame haemorrhage, blot haemorrhage, papilloedema)
  • ECG for left ventricular hypertrophy
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83
Q

Describe treatment of hypertension pharmacologically

A
  • If under 55 and not african carribbean, or if hypertension with type 2 diabetes first step is ACEi or ARB. Next step is to add CCB or thiazide like diuretic
  • If 55 or over or African Carribbean origin, CCB first line. Next add ACEi or ARB or thiazide like diuretic. CCB also first line for pregnant women
  • For both, stage 3 is to use ACEi or ARB and CCB and thiazide like diuretic
  • If this doesn’t work, spirinolactone or alpha blockers/beta blockers are used. Measure potassium first (lower potassium spironolactone, higher potassium alpha blocker)
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84
Q

List lifestyle advice in hypertension

A
  • Reduce sodium
  • Reduce caffeine
  • Smoking cessation
  • Reduce alcohol
  • Weight loss and exercise
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85
Q

Describe blood pressure targets in hypertensive patients

A
  • Under 80, aim for 140/90 clinic, ABPM/HBPM 135/85
  • If over 80, clinic BP less than 150/90, ABPM <145/85
  • If frail/multimorbidity use clinical judgement
  • If patient has postural hypotension, base target on standing BP
  • If Patient has t2dm target is the same without CKD, if evidence of CKD target is 130/80 in clinic and ABPM/HBPM 125/75
86
Q

What is done in hypertension annual review?

A
  • BP
  • Bloods and urine dipstick for renal function
  • Calculate Q risk and consider statins
87
Q

List symptoms of accelerated hypertension

A
  • Asymptomatic or signs of end organ damage (headache, fit, vomiting, visual disturbance, chest pain, neurological defect)
88
Q

How is accelerated hypertension maanged?

A
  • Same day reffereal
  • IV antihypertensives, aim to reduce over 24-48 hours (iabetalol, GTN, sodium nitroprusside)
  • Close monitoring (bloods, CXR, CT head)
  • Investigate underlying cause
89
Q

How is treatment of hyperlipidaemia determined?

A
  • Primary presention (guided by Q risk, risk of having CVD in next 10 years if over 10% consider statin)
  • Secondary prevention (all patients with established CVD advised to start statin)
  • If statin not tolerated PCSK9
90
Q

List factors considered in the QRISK3 assessment tool

A
  • Age
  • Sex
  • Diabetes
  • Smoking
  • CKD
  • AF
  • Hypertension
  • Arthritis
91
Q

Describe lifestyle advice for hyperlipidaemia

A
  • Healthy diet (increase fish, fruit and veg, reduce sugar saturated fat and salt)
  • Smoking cessation
  • Weight loss
  • Reduce alcohol
  • Encourage regular exercise
92
Q

Describe treatment of hyperlipidaemia

A
  • Atorvastatin 20mg daily primary prevention, then 80mg secondary prevention
  • Simvastatin or rosuvastatin
  • Ezetamibe
  • Bezadibrate
93
Q

List side effects of statins

A
  • Myopathy
  • GI disturbance
  • Headache
  • Sleep disturbance
  • Many drug interactions
94
Q

Describe diagnosis of hyperlipidaemia

A
  • Total cholesterol over 9mmol

- LDL over 7.5mmol

95
Q

How is lipid modification therapy monitored?

A
  • Repeat full lipid profile 3 months after starting statins
  • LFTs at baseline, 3 months and 1 months
  • Encourage self reporting side effects
96
Q

When is familial hypercholesterolaemia suspected?

A
  • Suspect if total cholesterol over 7.5mmol

- Personal or family history of premature coronary heart disease

97
Q

List signs on examination of high cholesterol

A
  • Xanthomata (skin)
  • Xanthelasma (eyelids)
  • Corneal arcus (white around edge of eye)
98
Q

How is aortic senosis diagnosed and treated?

A
  • Echocardiogram

- Valve repair or replacement (TAVI)

99
Q

If a persons blood pressure is over 180/120mmHg what is done?

A
  • Refer for same day specialist assessment if there are signs of retinal haemorrhage or papilloedema, or life threatening symptoms (confusion, chest pain, heart failure, acute kidney injury)
  • If not referring, carry out investigations for end organ damage as soon as possible
100
Q

List complications of blood pressure

A
  • Cardiovascular disease (heart attack, stroke, aneurysm)
  • Kidney failure
  • Retinopathy
101
Q

Compare the types of CRBs

A
  • Amlodipine is dihydropyradine, it is more selective for blood vessels
  • Diltiazem and verpamil are non-dihydropyradine, and is more selective for the heart
102
Q

Describe moa of thiazides

A
  • Act in late distal tubule

- Block the sodium chloride cotransport protein

103
Q

List common side effects of ACEi and ARB

A
  • Cough (increase of bradykinin)
  • Renal impairment
  • Allergic reaction
  • Rash
  • Hyperkalaemia (decreased sodium delivery and decreased aldosterone)
104
Q

List side effects of thiazides

A
  • Hypotension and renal impairment
  • Hypokalaemia (more sodium passing to later parts of the kidney resulting in reabsorption of sodium resulting in potassium loss)
  • Gout
  • Diabetes (thiazides interfere with insulin secretion by the pancreas)
  • Impotence
105
Q

How and why are patients with ACEi monitored?

A
  • Renal function due to renal artery stenosis (U+E within 2 weeks of starting)
  • ACEi reduces ability to constrict efferent arteriole resulting in blood entering the glomerulus at a lower rate than usual, with inability to constrict the efferent arteriole to increase blood flow.
  • In patients with renal artery stenosis this results in reduced renal function
106
Q

List pros and cons of DOACs and give some examples

A

Apixaban, rivaroxaban, edoxaban and dabigatran

Pros

  • Rapid onset/offset of action
  • Few drug interactions
  • Predictable pharmacokinetics, eliminating the requirement for regular coagulation monitoring

Cons

  • Lack of monitoring ability
  • Lack of antidote
  • Cost
107
Q

Compare oedema in left and right sided heart failure

A
  • Left sided pulmonary

- Right sided peripheral

108
Q

List what you look for in general inspection on cardiovascular exam

A
  • ECG leads
  • Anaemia, scars
  • Visible pulsations
  • Medical paraphernalia, syndrome features
109
Q

List what you look or in inspection of hands and arms in cardiovascular examination

A
  • Clubbing
  • Splinter haemorrhages
  • Oslers nodes
  • Janeway lesions
  • Peripheral cyanosis
  • Tendon xanthomas
  • Perfusion of hands, capillary refill
110
Q

List what you look for in inspection of the face in cardiovascular exam

A
  • Malar flush, xanthelasma, corneal arcus, anaemia (eyes)

- Central cyanosis, hydration, high arched palate (mouth)

111
Q

List what you look for in chest inspection in cardiovascular exam

A

Scars, including axilla

112
Q

Define angina pectoris and acute coronary syndrome

A

Chest, neck and jaw pain resulting from myocardial ischaemia

  • Stable is precipitated by exertion and relieved by rest. Lasts no longer than 10 minutes.
  • Unstable is new onset angina or abrupt deterioration in previously stable angina, often occurring at rest
  • ACS includes STEMI and NSTEMI
113
Q

List risk factors for angina and acute coronary syndrome

A
  • Atherosclerosis (high cholesterol)
  • Weight
  • Age
  • Family history
  • Male
  • Hypertension
  • Diabetes
  • Inativity, poor diet
114
Q

Describe epidemiology of angina pectoris and acute coronary syndrome

A
  • Cardiovascular disease (CVD) was responsible for 27% of all deaths in the UK in 2014.
  • Coronary heart disease (CHD), the most common cause of angina, and one of the main forms of CVD, accounted for 45% of CVD deaths.
  • CHD is the most common single cause of death in the UK.
  • In 2014, CHD caused 15% of male and 10% of female deaths — a total of around 69,000 deaths.
115
Q

List signs of ACS and angina pectoris

A
  • High cholesterol (corneal arcus/ xanthomata/ xanthelasma)
  • Signs of peripheral vascular disease (weak leg pulses, peripheral cyanosis, atrophic skin, ulcers, bruits in carotids)
  • Brady or tachyarrhythmia
116
Q

List investigations of ischaemic heart disease

A
  • Vital signs
  • ECG (STEMI vs NSTEMI, NSTEMI has ST depression or T wave inversion left bundle branch block)
  • Angiogram
  • Routine blood tests (LFT, U and E, FBC)
  • Troponin 1 (Raised in STEMI and NSTEMI and not in angina pectoris)
  • Exercise tolerance test for angina pectoris
117
Q

Describe long term management of patients with myocardial ischaemia

A
  • ACE inhibitor
  • Beta blocker
  • Cholesterol lowering agent
  • Duel antiplatelet therapy
  • Echo to assess heart function
  • Risk stratify NSTEMI with GRACE score. If high risk coronary angiography within 72 hours, if low risk conservative management and outpatient investigations (angiography, echo, ECG)
118
Q

List ECG leads affected by different infarctions

A
  • Inferior (right coronary artery) II, III avF
  • Anterior (left anterior descending) V1-V4, Anterioseptal V3-6
  • Lateral (left circumflex) I, aVL, V5/6
  • Posterior (posterior descending ) tall R wave, ST depression in V1-3
119
Q

List complications of ACS (ischaemic heart disease)

A
  • Sudden death
  • Pump failure
  • Rupture of papillary muscle or septum (ventricular septal defect)
  • Aneurysm and arrythmias
  • Embolism
  • Dresslers syndrome (pericarditis - chest pain a few weeks after heart attack)
  • Pulmonary oedema
  • Renal faiure
120
Q

List causes of midline sternotomy

A
  • Valve replacement
  • Valve repair
  • CABG
  • Repair of congenital defect
  • Heart transplant
121
Q

List rare types of angina

A
  • Decubitus lying dow
  • Prinzmetal coronary vasospasm
  • Coronary syndrome X symptoms with normal exercise and angiograms
122
Q

List causes of right heart failure

A
  • Left heart failure
  • Pulmonary hypertension
  • PE
  • Pulmonary valve disease
  • Chronic lung disease
  • Heart muscle
  • Heart valve (tricuspid regurg)
123
Q

List causes of left heart failure

A

Valvular

  • Aortic stenosis
  • Aortic regurgitation
  • Mitral regurgitation

Muscular

  • Ischaemia (IHD)
  • Cardiomyopathy
  • Myocarditis
  • Arrhythmias (AF)

Systemic

  • Hypertension
  • Amyloidosis
  • Drugs (e.g. cocaine, chemo)
124
Q

List symptoms of left sided heart failure

A
  • Dyspnoea (OE), orthopnoea
  • Feeling like youre drowning when laying down, restless
  • Poor exertional dyspnoea
  • Paroxysmal nocturnal dyspnoea
  • Cough with or without pink sputum (especially at night)
  • Wheeze
125
Q

List symptoms of right sided heart failure

A
  • Swelling ankles, abdomen, face
  • Weight gain
  • Fatigue
  • Decreased mobility
  • Cold peripheries
126
Q

List signs of right sided heart failure

A
  • Increased HR and RR
  • Murmur
  • Rasied JVP
  • Facial oedema
  • Abdominal distention, ascites/hepatomegaly
  • Pitting oedema
  • 3rd heart sound
  • Pulsus alternans (alternating between strong and weak beats)
127
Q

List investigations of heart failure

A
  • Bloods (FBC, U and E, LFT, BNP/ NT-proBNP, troponin raised in acute, HbA1c)
  • BNP under 100pg/ml /nt pro-BNP less than 400pg/ml normal
  • ECG
  • ABG
  • Chest x ray
  • Trans thoracic echocardiogram is diagnostic
128
Q

Describe management of acute heart failure

A
  • Sit patient up
  • High flow oxygen 15L/m via non-rebreath mask
  • IV diuretics (furosemide 40mg)
  • If systolic over 90 GTN, if systolic lower inotropes (nitrate infusion)
  • Analgesia if required
  • If patient worsens, can use CPAP (continuous positive airway pressure), further dose of furosemide, and consider alternative diagnosis
  • ICU if cardiogenic shock
129
Q

Describe management of chronic heart failure

A
  • Optomise CV risk (statin, HTN, DM, antiplatelet, stop smoking, exercise)
  • ACEi, beta blocker if REF
  • Add spironolactone if necessary for REF
  • Loop diuretic eg. furosemide for everyone, symptom relief but do not reduce mortality
  • Add digoxin if necessary (specialist treatment)
  • If none of this works cardiac resynchronisation therapy
  • Annual influenza vaccine and one off pneumococcal
130
Q

Define heart failure

A
  • Heart failure is a complex syndrome in which the ability of the heart to maintain the circulation of blood is impaired as a result of a structural or functional impairment of ventricular filling or ejection
  • Cardiac output inadequate to meet body demands
  • Acute heart failure occurs suddenly with more severe symptoms, while chronic occurs gradially
131
Q

Describe epidemiology of heart failure

A
  • Prevalence slowly increases with age until about 65 years of age, and then more rapidly.
  • In the UK, prevalence of 1 in 35 people 65–74 years of age. 1 in 15 people 75–84 years of age. Just over 1 in 7 people 85 years of age or older.
  • The average age at first diagnosis is 76
  • People with heart failure with preserved ejection fraction (HF-PEF - diastolic) are more likely to be older and female than those with heart failure with reduced ejection fraction (HF-REF - systolic)
  • Heart failure accounts for about: 2% of all NHS hospitalized bed-days and 5% of all NHS medical emergency admissions.
  • On average, a GP will look after 30 people with chronic heart failure and will suspect a new diagnosis in about 10 people annually
  • Nearly half of people with heart failure have HF-PEF.
  • 1 in 100 in UK
132
Q

Describe prognosis of heart failure

A
  • About 50% of people with heart failure die within 2 years of diagnosis
  • A UK population-based study found that the 6-month mortality rate for people with heart failure was 14%
  • A National UK Heart Failure audit found that hospital inpatient mortality was 11% in 2009
  • About 40% of people admitted to hospital with heart failure die or are re-admitted within 1 year
133
Q

List possible complications of heart failure

A
  • Atrial fibrillation is the most common arrhythmia in people with heart failure.
  • The prevalence increases with the severity of heart failure, increasing from about 10% in people with mild to moderate heart failure (New York Heart Association [NYHA] classes II and III) to 50% in people with severe heart failure (NYHA class IV) .
  • Ventricular arrhythmias are common in people with heart failure, particularly people with a dilated left ventricle and reduced ejection fraction
  • Major depressive disorder is present in up to 20% of people with heart failure
  • Cachexia (wasting) 10-15% of people. It is associated with more severe symptoms, reduced functional capacity, more frequent hospitalization, and decreased survival rates
  • CKD
  • Sexual dysfunction is common in people with heart failure.
  • About half of the deaths in people with heart failure are related to sudden cardiac death
  • Resp failure
134
Q

Describe NYHA classification for staging of heart failure

A
  • Class I — no limitation of physical activity.
  • Class II — slight limitation of physical activity.
  • Class III — marked limitation of physical activity. Comfortable at rest but less than ordinary physical activity results in undue breathlessness, fatigue, or palpitations.
  • Class IV — unable to carry out any physical activity without discomfort. Symptoms at rest can be present. If any physical activity is undertaken discomfort is increased.
135
Q

List features of syncope

A
  • No aura (occurs in fits)
  • No tongue biting during
  • Afterwards no confusion, patient knows what has happened
136
Q

List differentials of collapse

A
  • Hypoglycaemia

Cardio

  • Vasovagal
  • Arrythmia (tachyarythmia, bradyarrythmia)
  • Outflow obstruction (left - aortic stenosis, hypertrophic obstructive cardiomyopathy right - PE)
  • Postural hypotension

Neuro
- Seizure

137
Q

Describe long QT syndrome

A
  • Abnormal ventricular repolarisation
  • Congenital (mutations in K+ channels)
  • FH of sudden death
  • Acquired - low K+/Mg2+, drugs
138
Q

List differentials of raised JVP (CARDIAC)

A
  • Right heart failure
  • Constrictive pericarditis (TB, inflammation, malignancy)
  • Tricuspid regurgitation (endocarditis, right ventricular dilatation, hepatomegaly)
139
Q

List differentials of systolic murmur

A
  • Aortic stenosis (radiates to neck, slow rising pulse)
  • Mitral regurgitation (hyperdynamic apex beat, loudest at apex, radiates to clavicle/axilla)
  • Tricuspid regurgitation (loudest at left sternal border, raised JVP)
  • Ventricular septal defect
140
Q

List causes of sinus tachycardia

A
  • Sepsis
  • Hypovolaemia
  • Endocrine (thyrotoxicosis, phaeochromocytoma)
141
Q

List causes of AF

A

Heart: Muscle, Valves, Pericardium

  • Congestive heart failre
  • Rheumatic disease
  • Hypertrophy
  • WPW
  • Sick sinus
  • Congenital heart disease
  • Pericarditis

Other

  • Lungs: pneumonia, PE, cancer
  • Infection
  • Neuronal dysfunction
  • Electrolyte depletion
  • Cancer
  • PE
  • DM
  • Pericarditis
  • Caffiene
  • Obesity
  • Alcohol
  • Smoking
  • Medication
  • Hyperthyroidism
142
Q

List causes of ventricular tachycardia

A
  • Ischaemia
  • Electrolyte abnormality
  • Long QT
143
Q

Describe management of supraventricular tachycardia

A
  • Vagal manoeuvres (neck massage, valsalva)
  • Adenosine with cardiac monitor. If this fails atenolol/amiodarone/ verapamil
  • DC cardioversion if haemodynamic compromise - Ablation
144
Q

Describe management of ventricular tachycardia

A
  • No haemodynamic compromise IV amiodarone
  • If unstable DC cardioversion
  • Look for underlying cause
  • ICD
  • Pulseless VT: defibrillate
145
Q

Describe voltage criteria of left ventricular hypertrophy

A
  • Deep S in V1/2
  • Tall R in V5/6
  • S in V1 + R in V5 or 6 >7 large squares
146
Q

List pathologies that can be suggested by ECG and what you look for

A
  • Ischaemia (ST, T, Q)
  • Arrythmia or conduction defects (rate, rhythm, PR, ARS, QT)
  • Ventricular strain or hypertrophy (axis, R, S)
147
Q

List causes of heart sounds S1-4

A
  • S1 mitral valve closing
  • S2 aortic valve closing
  • Atrial septal defect causes fixed spitting of S2
  • Ventricular filling S3 (congestive heart failure, venticular dilatation, kentucky)
  • Ventricular hypertrophy, hypertension with stiff ventricle S4 (before 1st heart sound - tennessee - S4 then S1 then S2 is the ‘see’)
  • End stage heart failure- summation)
148
Q

Determine axis deviation on ECG

A
  • Right towards each other, left away from each other
  • QRS positive in L1 and avF if normal axis
  • aVF more positive and lead 1 negative Right Axis Deviation, if aVF more negative and lead 1 more positive, left axis deviation
  • Left axis deviation due to left axis hypertrophy or right ventricle damage, right axis deviation due to the oposite
149
Q

Describe ECG appearance of right bundle branch block

A
  • MoRRoW
  • V1 M
  • V6 W
150
Q

Define pericarditis

A
  • Inflammation of the pericardium

- Viral infection or secondary to MI

151
Q

List symptoms of pericarditis

A
  • Sharp pain. Usually retrosternal, radiates to shoulders and neck
  • Aggravated by deep breathing, movement, change of position, exercise and swallowing
  • Relieved by leaning forwards, worse when lying flat
  • Dyspnoea , cough, arthralgia
152
Q

List risks for acute pericarditis

A
  • Infection (coxsackie, influenza, adenovirus)
  • Acute MI (massive ST elevation, anterior MI)
  • Dresslers syndrome (at least 2 weeks after MI)

Less commonly

  • Bacterial infection
  • Autoimmune
  • Trauma/ post-surgery
  • Neoplasm
  • TB
  • Rheumatic fever
  • HIV
153
Q

List signs of pericarditis

A
  • Fever
  • Pericardial friction rub (high pitched scratching sound produced by movement of pericardium). Heard best at left lower sternal edge at full expiration
154
Q

List investigations for pericarditis

A
  • Based on history
  • Repeated ECGs
  • Cardiac enzymes
  • Echo
  • CXR (cardiomegaly - may indicate pericardial effusion)
  • ECG shows widespread saddle shaped ST elevation (in all leads)
  • PR depression
  • T wave inversion
  • ST elevation in both inferior and anterior leads
  • PR elevation and ST depression in aVR
  • FBC - leukocytosis or lymphocytosis
  • Raised CRP/ESR
155
Q

Describe treatment of pericarditis

A
  • Colchicine
  • Steroids if colchincine doesnt help
  • Oral NSAIDs mainstay (ibuprofen or aspirin - regularly)
156
Q

List complications of pericarditis

A
  • Chronic pericarditis
  • Pericardium thickens, resulting in restricted ventricular filling (restrictive pericarditis)
  • Pericardial effusion (leading to backflow, raised JVP, hepatomegaly, peripheral oedema)
157
Q

Describe epidemiology of pericarditis

A
  • Most common disease of pericardium in clinical practice

- 01-0.2% hospitalised patients, 5% of ED patients with non-ischaemic chest pain

158
Q

Describe prognosis of pericarditis

A
  • Cardiac tamponade rarely occurs

- Good long-term prognosis

159
Q

Describe epidemiology of infective endocarditis

A
  • 50% cases occur on normal valves
  • 50% abnormal tissue
  • 4-7 per 100000 UK
  • Rare before age 55 in UK. 15 per 100000 in over 55s
160
Q

List risk factors for infective endocarditis

A
  • Now strep aureus most common, used to be strep viridans
  • Mitral valve most commonly affected in non IVDU
  • Previous rheumatic heart disease
  • Age related valvular degeneration
  • Prosthetic valve
  • IV drug use (usually affects right side, tricuspid valve causes strep aureus most commonly)
  • Pneumonia
  • Colonic malignancy (streptococcus bovis)
  • Chronic cholecystitis
  • Miscarriage
  • Dental work (strepotococcus viridans)
161
Q

List signs of infective endocarditis

A
  • New murmur (tricuspid regurg commonly)
  • Petichiae
  • Splinter haemorrhages
  • Fever
  • Purpura
  • Oslers nodes (palm and sole, painful)
  • Janeway lesions (palm or sole, not painful)
  • Splenomegaly
  • Roth spots (boat shaped retinal heamorrhage with pale centre)
162
Q

Describe diagnosis of infective endocarditis

A

Duke classification
Diagnosis is made on 2 major, 1 major/3 minor or >5 minor criteria

MAJOR CRITERIA

  • Positive blood vulture on 2 tests 12 hours apart or 3 tests more than 1 hour apart
  • Echocardiogram showing strictures, abscesess, unusual blood flow (vegetation or abscess)
  • New valve regurg

MINOR

  • Fever
  • Predisposition (eg. cardiac lesion or IV drug use)
  • Unusual echo
  • Immunological factors present (oslers nodes, rheumatoid factor)
  • Culture postive
  • Vascular abnormalities (janeway lesions)
163
Q

List investigations used in

infective endocarditis

A
  • FBC
  • U and E
  • LFT
  • Inflammatory markers
  • Immunoglobulins and compliment
  • Urine (proteinurea, haematuria)
  • PCR
  • Echocardiogram
  • Blood culutre (at least 3 samples in 24 hours)
  • ECG (new block)
  • MSU
  • Ultrasound abdomen
  • CXR sepsis and pulmonary infiltrates suggests right sided
164
Q

Describe treatment of infective endocarditis

A
  • Antibiotics 4-8 weeks

- Surgery, ususally valve replacement or partial repair

165
Q

List complications of infective endocarditis

A
  • MI
  • Pericarditis
  • Arrythmia
  • Cardiac valvular insufficiency
  • Heart failure, complete heart block
  • Aneurysm
  • Emboli (TIA)
  • Arthritis, myositis
  • Glomerulonephritis, renal failure (AKI)
  • Stroke
  • Mesenteric or splenic abscess or infarct
166
Q

Describe prognosis of infective endocarditis

A
  • 50% survival after 10 years
  • Survival more likely if early surgical treatment, age under 55, lack of congestive heart failure, and initial presence of more symptoms of endocarditis
  • 100% mortality if untreated
167
Q

Define atrial fibrillation

A
  • A supraventricular tachyarrhythmia resulting from irregular, disorganized electrical activity and ineffective contraction of the atria.
  • Paroxysmal lasts 30 secs to 7 days
  • Persistant lasts longer than 7 days
  • Permanent fails to terminate using cardioversion
168
Q

Describe epidemiology of AF

A
  • 2.5% prevalence in England
  • 1.4 mill
  • Higher in men than women
  • Lifetime risk 16%
169
Q

List symptoms of AF

A
  • Breathlessness.
  • Palpitations.
  • Chest discomfort.
  • Syncope or dizziness.
  • Reduced exercise tolerance, malaise/listlessnes, decrease in mentation, or polyuria.
170
Q

List signs of AF

A

Irregularly irregular radial pulse

171
Q

Describe investigations of AF

A
  • ECG
  • No p-waves
  • Irregular ventricular rate
  • Tachycardia
  • Complexes look normal
  • 24 hours ambulatory ECG if asymptomatic paroxysmal AF
172
Q

Describe ECG of atrial flutter

A
  • Saw tooth pattern
  • Regular atrial activation on ECG
  • Due to large re-entry circuit in RA
  • May be regular with a ratio of P waves to QRS
173
Q

Describe management of AF

A
  • Onset less than 48 hours with haemodynamic instability, immediate cardioversion
  • Determine underlying cause
  • CHAD VASC risk
  • Anticoagulant treatment if over 48 hours (rivaroxaban, apixaban, vitamin K antagonist eg. warfarin) + HAS BLED
  • Digoxin to convert fast AF to slow AF
  • Rate control treatment (B blocker or CCB)
  • Cardioversion if symptoms persist after heart rate controlled
174
Q

List complications of AF

A
  • Stroke
  • Thromboembolism
  • Heart failure
  • Cardiomyopathy
  • CKD
  • Sudden cardiac death
175
Q

Describe prognosis of AF

A
  • High risk of stroke and thromboembolism
  • 46% increase in all cause mortality
  • Poorer quality of life
176
Q

Define supraventricular tachycardia

A

A fast heart rate arising from above the bAVN

177
Q

Describe epidemiology of supraventricular tachycardia

A
  • Most common cause is AVNRT
  • More common in women (2:1)
  • May occur at any age
178
Q

List risk factors for supraventricular tachycardia

A
  • Caffeine
  • Alcohol
  • Exercise
  • Drugs
  • Beta agonists
  • Sympathomimetics
179
Q

List symptoms and signs of supraventricular tachycardia

A
  • Sudden onset sensation of regular palpitations
  • If CHD, may be chest pain
  • SOB
  • Dizziness/ syncope with drop of BP
  • Relieved by vagal manouvres (hyperventillation, carotid sinus massage, valsalva, dipping face in cold water, pressure on eyeballs)
180
Q

List investigations for supraventricular tachycardia and the results

A
  • Tachycardia, regular, no p-waves
  • Re-entry circuit
  • AVNRT (AV node re-entrant, SVT with no P waves, no delta wave)
  • AVRT (accessory ‘kent’ pathway, shows delta wave ie. slurred upstroke, short PR interval, Wolff Parkinson White)
  • Bloods
181
Q

List complications of supraventricular tachycardia

A
  • Heart failure
  • Unconsciousness
  • Cardiac arrest
  • DVT
  • MI
  • Cardiomyopathy
182
Q

Define ventricular tachycardia

A
  • Fast heart rate

- Caused by ventricles

183
Q

Describe epidemiology of ventricular tachycardia

A
  • 16% in men with coronary artery disease
  • 15% in women with coronary artery disease
  • 9% in men and 8% in women with hypertension, valvular disease or cardiomyopathy
  • 3% in men and 2% in women with no cardiovascular disease
184
Q

Describe prognosis of supraventricular tachycardia

A
  • Small risk of sudden death if no WPW
  • Dependent on underlying structural heart disease
  • Excellent prognosis if normal heart
185
Q

List risks for ventricular tachycardia

A
  • Age
  • Cardiomyopathy, heart failure, CHD, sarcoidosis
  • Previous MI
  • Abnormal heart valves
  • Family history of ventricular tachycardia (long QT)
  • Illicit drugs
  • Electrolyte imbalances
186
Q

List symptoms and signs of ventricular tachycardia

A
  • Lightheadedness
  • Dizziness
  • Palpitations
  • Fatigue
  • Chest pain
  • SOB
  • Syncope
187
Q

Describe investigations of ventricular tachycardia

A
  • ECG (regular, wide complex tachycardia with no/integrated P waves)
  • Widened QRS complex
  • Absence of left or right bundle branch block morphology
  • Extreme axis dissociation
188
Q

List complications of ventricular tachycardia

A
  • Sudden death
  • Heart failure
  • Frequent fainting
189
Q

Describe prognosis of ventricular tachycardia

A
  • Varies with ventricular function
  • Sudden death mortality 30% in 2 years if ischaemic cardiomyopathy
  • If idiopathic, prognosis is excellent
190
Q

List causes and symptoms of digoxin toxicity

A
  • Digoxin toxicity development is associated with patients who have hypokalemia, hypercalcemia, and some drugs that elevate plasma digoxin levels.
  • Toxicity is characterized by CNS symptoms, visual aberrations, and the development of hyperkalemia
191
Q

Describe investigations and management of DVT

A

Wells score over 2

  • Proximal leg ultrasound scan (with results in 4 hours)
  • Interim therapeutic anticoagulation (apixaban, rivaroxaban first line then LMWH followed by dabigatran or edocaban, or LMWH with vitamin K antagonists)
  • d-dimer

Wells score less than 2

  • D dimer
  • Interim therapeutic anticoagulation if takes more then 4 hours
  • If D dimer positive, ultrasound

Aim for INR of 2-3 if warfarin used

192
Q

Describe epidemiology of DVT

A
  • VTE 1-2 per 1000 per year. 2/3 of these DVT and 1/3 PE
  • During pregnancy, 1 in 1000 live births
  • In critically ill patients, incidence of 37.2%
193
Q

List complications of DVT

A
  • PE
  • Post thrombotic syndrome (chronic venous hypertension, causing pain swelling hyperpigmentation, dermatitis and ulcers. 50% of patients within 2 years)
  • Bleeding due to anticoagulation treatment
  • Heparin induced throbocytopenia
194
Q

Describe prognosis of DVT

A
  • Without treatment, 3% risk of fatal PE
  • Most patients recover within weeks
  • Post phlebotic syndrome can result in long term leg ulcers
195
Q

When is aspirin used?

A
  • When patients have atheroma in the arterial system
  • 75mg coronary artery disease
  • 150mg stroke
  • Prevents platelet aggregation
196
Q

When are NOACs /warfarin used?

A
  • Clots are not involving platelets
  • Used when blood is pooling or clots are in the venous system
  • Prevents clotting cascade
197
Q

Compare fast and slow AF

A
  • Fast AF is where the ventricle is responding often to the atrial contraction, leading to a faster ventricular rate. You can block the AV node to slow the ventricular response using digoxin when patient is healthy otherwise. BB used when patients exercise a lot eg. running and need increased cardioversion.
  • Slow AF is where the ventricle reacts slowly, so overall heart rate is not fast
198
Q

Which risk scores are used for AF?

A
  • CHADS-VASc
  • HAS-BLED (when I go on warfarin am I at risk of bleeding?)
  • EHRA
199
Q

Why is the complex narrow in AF?

A

The wave of depolarisation goes down the left and right bundle at the same time, leading to one very sharp R wave

200
Q

Describe epidemiology of AAA

A
  • Highest prevalence in white male smokers
  • 4 to 6 times more common in men
  • 1.34% among 65 yo men UK
  • Increased with age
  • Reduction in mortality and hospital admissions over time (attributed to lower smoking)
201
Q

Compare HF PEF vs HR REF

A
  • PEF is diastolic, failure of filling

- REF is systolic, failure of contraction

202
Q

What is the normal ejection fraction?

203
Q

What is BNP?

A

A hormone secreted by cardiomyocytes in response to stress

204
Q

List signs of heart failure on CXR

A

ABCDE

  • Alveolar shadowing
  • Kerley B lines (pulmonary oedema)
  • Cardiomegaly (cardiothoracic ratio over 0.5 on PA - cannot comment on AP)
  • Upper lobe diversion (dilated upper lobe vessels)
  • Pleural effusions
205
Q

Describe MOA of furosemide.

A

Acts on ascending limb of loop of henle, inhibiting Na+/K+/2Cl- co-transporter

206
Q

Describe MOA of thiazides

A

Inhibits Na/Cl in DCT

207
Q

What is a common side effect of ACEi?

What is the alternative where side effects occur?

A
  • ACEi can cause dry cough cough

- ARB

208
Q

List causes of high cardiac output

A
  • Nutritional (B1/thiamine deficiency)
  • Anaemia
  • Pregnancy
  • Malignancy
  • Endocrine
  • AV malformations
  • Liver cirrhosis
  • Sepsis
209
Q

Describe the framington criteria

A

Clinical diagnosis of HF. 2 majors or 1 major 1 minor

Major

  • Paroxysmal nocturnal dyspnoea
  • Bibasal crepitations
  • S3 gallop
  • Cardiomegaly
  • Increased central venous Pressure
  • Weight loss
  • Neck vein distension
  • Acute pulmonary oedema
  • Hepatojugular reflux

Minor

  • Bilateral ankle oedema
  • Dyspnoea on ordinary exertion
  • Tachycardia
  • Decrease in vital capacity by 1/3
  • Nocturnal cough
  • Hepatomegaly
  • Pleural effusion
210
Q

List ECG changes in hyperkalaemia

A
  • Loss of P waves
  • Tall tented T waves (FIRST SIGN)
  • Widened QRS complex
211
Q

Describe ECG appearance of junctional tachycardia

A
  • Inverted p waves
  • Tachycardia
  • Type of SVT
212
Q

Describe management of hyperkalaemia

A
  • First calcium gluconate if there are ECG changes, for cardiac stabilisation
  • Then insulin/salbutamol

Year 3 - Diseases (27 decks)

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