Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of disease is teratology of fallot?

A

Cyanotic congenital heart disease (most common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the pain in peripheral vascular disease

A
  • Intermittent claudications (cramping)

- Pain upon exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are cardiac abnormalities associated with in fetuses?

A

Poorly controlled gestational diabetes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe treatment of septic shock

A
  • Intravenous fluid resuscitation
    to increase vascular preload
  • Vasopressor medications to increase systemic vascular resistance.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

List common causes of ischaemic stroke

A
  • Embolic disease due to AF

- Atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the leading cause of acute mortality following MI?

A
  • Ventricular tachycardia degenerating into ventricular fibrillation, pulseless electrical activity and asystole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe murmur in tricuspid valve stenosis

A
  • Diastolic murmur

- Heard at left lower sternal border, increases with inspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List main symptoms of rheumatic fever

A
  • Joint pain
  • Carditis
  • Erythema marginatum
  • Subcutaneous nodules
  • Chorea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A
  • Coronary heart disease

- Cessation of cardiac electrical activity with haemodynamic collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is myocardial infarction?

A
  • Necrosis of heart tissue as a result of ischemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which virus causes kaposi sarcoma?

A
  • Human herpes virus 8

- Most often associated with HIV positive patients who are immunocompromised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

List consequences of rheumatic fever

A
  • Rheumatic heart disease
  • Left heart dilation
  • Left ventricular hypertrophy
  • Congestive heart failure
  • Arrythmia
  • Bacterial endocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Define aortic stenosis

A

Tightening of the aortic valve at the origin of the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Define peripheral vascular disease

A

Narrowing and calcification of peripheral vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

List risk factors of peripheral vascular disease

A
  • Smoking
  • Diabetes
  • Obesity
  • High BP
  • High cholesterol
  • Age
  • Family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Define rheumatic fever

A

Systemic inflammatory disorder affecting children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How is atrial septal defect characterised?

A
  • Wide fixed splitting of S2 and a systolic murmur at the left third ICS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

List symptoms of infective endocarditis

A
  • Fever
  • Chills
  • Anorexia
  • Weight changes
  • Malaise
  • Headache
  • Myalgia
  • Night sweats
  • Shortness of breath
  • Cough
  • Arthralgia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How is hypertension diagnosed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How is systolic hypertension treated?

A

Thiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What causes concentric hypertrophy?

A
  • Chronic hypertension

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Define first degree av block

A

Prolongation of PR interval to over 200msec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How is AV nodal reentrant tachycardia treated?

A
  • Short term with IV adenosine

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Describe examination for DVT

A

Ultrasonography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How is unstable tachycardia treated?

A

Syncronised cardioversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Define AAA

A
  • Dilation of the abdominal aorta over 50% of previous diameter. Usually asymptomatic until burst
  • Bursting is a medical emergency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How are Stokes-Adams attacks treated?

A

Implant a pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is vasospastic angina?

A

Angina caused by coronary artery spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Which grafts are used to treat coronary artery disease?

A
  • LIMA (left interior mammary artery)

- CABG (uses saphenous vein, usually great)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Define myocarditis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

List signs of myocarditis

A
  • Raised JVP
  • Tachycardia
  • Fever
  • Hypotension
  • Low oxygen sats
  • Pitting oedema
  • S3/4 gallops
  • Pericardial rub
  • Arythmia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

List risk factors for hypertension

A
  • Poor diet
  • Obesity
  • High cholesterol
  • Physical inactivity
  • Alcohol
  • Smoking
  • Family history
  • Age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

List lifestyle advice in hypertension

A
  • Reduce sodium
  • Reduce caffeine
  • Smoking cessation
  • Reduce alcohol
  • Weight loss and exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

A

60%

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions