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Phase 2a > cardio > Flashcards

cardio Flashcards

1
Q

What is thrombosis?

A

Blood coagulation in a vessel

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2
Q

What is DVT?

deep vein thrombosis

A

The development of a blood clot within a vein deep to the muscular tissue planes

normally in a major deep vein in leg, thigh, pelvis, abdomen

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3
Q

Which factors does warfarin prevent synthesis of?

A

2
7
9
10

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4
Q

What scoring system is used in DVT?

A

Well’s diagnostic algorithm

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5
Q

What is an aneurysm?

A

a permanent and irreversible dilatation of a blood vessel by at least 50% of the normal expected diameter

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6
Q

What is the normal diameter of the abdominal aorta?

A

2cm
Increases with age

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7
Q

What is the threshold diameter of an AAA?

A

3cm

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8
Q

What are the different sizes of AAAs?

A

Normal: less than 3cm
Small aneurysm: 3 – 4.4cm
Medium aneurysm: 4.5 – 5.4cm
Large aneurysm: above 5.5cm

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9
Q

What is a pseudoaneurysm?

A

caused by blood leaking through the arterial wall but contained by the adventitia or surrounding perivascular tissue

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10
Q

What prophylaxis is offered to patients in hospital at higher risk of VTE?

A

Low molecular weight heparin
Compression stockings

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11
Q

What are contraindications to giving LMWH?

A

Active bleeding
Existing anticoagulation (warfarin, DOAC)

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12
Q

What is a contraindication to using compression stockings as prophylaxis for VTE?

A

Peripheral arterial disease

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13
Q

What is the epidemiology for VTE?

A

1 in 1000
2/3 of these are DVT, 1/3 PE

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14
Q

What is the aetiology of DVT and PE?

(and what model shows this?)

A

Virchow’s triad:
* Stasis: blood flows slowly or becomes turbulent, could be caused by immobility, long travel, varicose veins, obesity
* Hypercoagulability: blood coagulates quicker than normal, e.g. thrombophilia, oestrogen therapy, malignancy, infection and inflammation
* Endothelial injury: e.g. physical trauma, hypertension

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15
Q

What makes up Virchow’s triad?

A
  • Stasis: blood flows slowly or becomes turbulent
  • Hypercoagulability: blood coagulates quicker than normal
  • Endothelial injury
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16
Q

What are the risk factors for DVT and PE?

A

Immobility
Recent surgery
Pregnancy
Long haul travel
Hormone therapy with oestrogen, combined pill or HRT
Polycythaemia
Malignancy, cancer
SLE
Thrombophilia: e.g. antiphospholipid syndrome

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17
Q

Is the D-dimer test specific for VTE?

A

No
It’s sensitive so most patients with DVT will have a positive d-dimer
But not all positive d-dimers mean a DVT

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18
Q

What are 2 anticoagulants used in the treatment or prophylaxis of VTE?

A

apixaban
rivaroxaban

prophylaxis after some surgeries

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19
Q

What is a PE?

A

dislodged thrombi occluding the pulmonary vasculature

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20
Q

What are the key presentations for DVT/PE?

A

Calf or leg swelling and pain
Chest pain
Breathlessness

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21
Q

Differential diagnoses for PE

A

Angina
MI
COPD/asthma acute exacerbation
Pneumothorax
Congestive heart failure

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22
Q

Differential diagnoses for DVT

A

Cellulitis
Calf muscle tear/Achilles’ tendon tear
Calf muscle haematoma
Large or ruptured popliteal cyst (Baker’s cyst)
Pelvic/thigh mass/tumour compressing venous outflow from the leg

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23
Q

What investigations would you carry out for suspected DVT?

A

D-dimer
Doppler (venous) ultrasound

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24
Q

What investigation would you run for suspected PE?

apart from d-dimer

A

CTPA

CT pulmonary angiogram

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25
Q

How would you manage DVT/PE?

A

Initial resus for PE if needed
Run tests (D-dimer must be done before starting anticoags to avoid false negative)
Start anti-coagulants immediately, even before results: apixaban or rivaroxaban, if not suitable offer LMWH

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26
Q

How long after a case of DVT/PE would a patient stay on anticoagulants?

A

3 months at least

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27
Q

What are some complications of DVT?

A

PE
Bleeding during initial treatment
Heparin induced thrombocytopenia (HIT)

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28
Q

What are some complications of PE?

A

Pulmonary infarction
Cardiac arrest
Death

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29
Q

What are some signs of DVT?

A

tenderness, swelling, warmth, discolouration

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30
Q

What are some signs of PE?

A

tachycardia, tachypnoea, pleural rub, hypoxia, pyrexia, elevated JVP

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31
Q

What are the symptoms of DVT?

A

Limb pain and tenderness
Swelling of the calf or thigh (usually unilateral).
Pitting oedema.
Distension of superficial veins.
Increase in skin temperature.
Skin discoloration
A hard, thickened palpable vein

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32
Q

What are the symptoms of PE?

A

Dyspnoea
Pleuritic chest pain, retrosternal chest pain.
Cough and haemoptysis.
Any chest symptoms in a patient with symptoms suggesting a deep vein thrombosis (DVT).
In severe cases, RHF causes dizziness or syncope

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33
Q

Why do you use a d-dimer test for DVT?

A

Acute thrombus begins to be dissolved by the body’s fibrinolytic system as soon as a clot begins to form

elevated levels of breakdown products of cross-linked fibrin (D-dimer) appear in the blood soon after a clot begins to form

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34
Q

What is ischaemic heart disease?

A

an inability to provide adequate blood supply to the myocardium

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35
Q

When is IHD considered stable?

A

when symptoms, if any, are manageable and not rapidly progressive
no recent infarction, procedural intervention, or signs of significant ongoing cardiac necrosis

symptoms only come on with exertion and are always relieved by rest or glyceryl trinitrate

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36
Q

What are some modifiable risk factors for hypertension?

A

Excess weight.
Excess dietary salt intake.
Lack of physical activity.
Excessive alcohol intake.
Stress

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37
Q

What is the white coat effect?

A

blood pressure is raised due to the stress of being in clinic

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38
Q

What are some non-modifiable risk factors for hypertension?

A

Older age
Family history
Ethnicity
Gender

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39
Q

What is stage 1 hypertension?

A

clinic BP 140/90 mm Hg
135/85 on home or ambulatory readings

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40
Q

What is stage 2 hypertension?

A

Above 160/100 in clinic
Above 150/95 on home/ambulatory readings

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41
Q

What is stage 3 hypertension?

A

Above 180/120

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42
Q

What investigations would you do for someone with hypertension?

A

ECG
fasting metabolic panel with estimated GFR
lipid panel
urinalysis
Hb
thyroid-stimulating hormone

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43
Q

How would you monitor hypertension?

A

While adjusting medication dosage, blood pressure (BP) should be monitored every 2-4 weeks.
Once stabilised, BP should be checked and medications reviewed every 6-12 months

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44
Q

What are some secondary causes of hypertension?

A
  • Renal disease
  • Pregnancy and pre-eclampsia
  • Endocrine: Conn’s, thyroid disorders
  • Drugs: NSAIDs, steroids, oestrogen, liquorice, alcohol
  • Obesity
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45
Q

What is primary hypertension?

A

develops without secondary cause
90% of cases

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46
Q

What does hypertension increase the risk of?

A
  • IHD (angina and acute coronary syndrome)
  • Cerebrovascular accident (stroke or intracranial haemorrhage)
  • Vascular disease
  • Hypertensive retinopathy and nephropathy
  • Vascular dementia
  • Left ventricular hypertrophy
  • Heart failure
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47
Q

What are some differentials for hypertension?

A

Renal artery stenosis
Chronic kidney disease
Obstructive uropathy
Obstructive sleep apnoea/hypopnoea syndrome
Obesity hypoventilation syndrome

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48
Q

What is heart failure (HF)?

A

a complex clinical syndrome resulting from the impaired ability of the heart to cope with the metabolic needs of the body

heart can’t meet perfusion needs

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49
Q

What is the LV ejection fraction in HF with reduced EF?

A

less than 40%

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50
Q

What is the LVEF in heart failure with mildly reduced EF?

A

41-49%

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51
Q

What is the LVEF in HF with preserved EF?

A

50% or more

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52
Q

What is HFrEF?

A

heart can’t pump with enough force to push enough blood into circulation
EF less than 40%

aka systolic HF

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53
Q

What is HFpEF?

A

heart can’t properly fill with blood during the resting period between each beat
EF 50% or more (stroke volume is low but so is EDV)

aka diastolic heart failure

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54
Q

What is the main cause of right sided HF?

A

Left sided HF

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55
Q

What is left sided heart failure?

A

the left side must work harder to pump the same amount of blood
HFrEF: left ventricle loses its ability to contract normally
HFpEF: Left ventricle loses its ability to relax normally because the muscle has become stiff

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56
Q

Equation for cardiac output

A

Heart rate (HR) x Stroke volume (SV)

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57
Q

What happens in right sided heart failure?

A

When the left ventricle fails and can’t pump enough blood out, increased fluid pressure is transferred back through the lungs.
This damages the heart’s right side. When the right side loses pumping power, blood backs up in the body’s veins

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58
Q

What are specific signs for heart failure?

A

Displaced apex beat
3rd heart sounds
Raised JVP

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59
Q

What are the NYHA classes of HF?

A

Class I: No limitation (Asymptomatic)
Class II: Slight limitation (mild HF)
Class III: Marked limitation (Symptomatically moderate HF)
Class IV: Inability to carry out any physical activity without discomfort (symptomatically severe HF)

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60
Q

Which NYHA class of HF is:
No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation or shortness of breath.

A

Class 1

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61
Q

Which NYHA HF class would this be:
Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, shortness of breath or chest pain.

A

Class 2

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62
Q

Which NYHA HF Class would this be:
Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, shortness of breath or chest pain

A

3

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63
Q

Which NYHA class of HF is this:
Symptoms of heart failure at rest. Any physical activity causes further discomfort

A

Class 4

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64
Q

How do you calculate ejection fraction?

A

stroke volume / end diastolic volume

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65
Q

Symptoms of L sided HF

A
  • Dyspnea on exertion
  • Orthopnea (shortness of breath when lying down flat)
  • Paroxysmal nocturnal dyspnea (wakes up short of breath at night)
  • persistent cough producing mucus
  • crackling on auscultation
  • fatigue (also present in R sided)

symptoms due to pulmonary oedema

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66
Q

Symptoms of R sided HF

A

Peripheral oedema
Raised JVP
Tachycardia
Hepatomegaly (backup of blood into IVC)
Ascites (from increased pressure in hepatic vessels)
Fatigue

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67
Q

What is shock?

A

a life-threatening, generalised form of acute circulatory failure with inadequate oxygen delivery to and utilisation by the cells

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68
Q

What is hypovolaemic shock?

A

volume of the circulatory system is too depleted to allow adequate circulation to the tissues of the body

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69
Q

What are the 4 types of shock?

A

Hypovolaemic
Cardiogenic
Obstructive
Distributive

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70
Q

What is cardiogenic shock?

A

Failure of the pump action of the heart, resulting in a decrease in cardiac output causing reduced end-organ perfusion

hypoperfusion and hypoxia despite adequate volume

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71
Q

What can cardiogenic shock be defined by?

A

Sustained hypotension
Tissue hypoperfusion

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72
Q

Risk factors for cardiogenic shock

A

Elderly
MI
Previous heart disease of infarction

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73
Q

What are the aetiologies of cardiogenic shock?

A

MI
Arrhythmias
Toxic substances
Acute mechanical causes: rupture, chest trauma, valvular incompetence
Infection
Non-adherence with meds
Excessive rise in BP
Cardiomyopathy

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74
Q

Signs and symptoms of shock

A

Tachycardia
Hypotension
Tachypnoea (increased RR and increased work)
Hypoxaemia
Oliguria
Skin changes: cool, clammy peripheries, cyanosis, sweating
Mental state changes

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75
Q

Signs and symptoms of cardiogenic shock

excluding general shock symptoms, e.g tachycardia, hypotension

A

Chest pain
Nausea and vomiting
Dyspnoea
Profuse sweating
Confusion/disorientation
Palpitations
Faintness/syncope
Bilateral basal pulmonary crackles or wheeze may occur
Quiet or extra heart sounds
Raised JVP/ distended neck veins

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76
Q

How would you manage shock?

A

ABCDE approach
Make sure airway is secure and breathing is maintained
Treat underlying cause ASAP

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77
Q

What are the vitals in hypovolaemic shock?

A

hypotensive
tachycardia
hypoxaemia

increased HR, decreased CO and BP

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78
Q

What are the reversible causes of cardiac arrest?

4Hs & 4Ts

A

Hypoxia
Hypokalaemia/hyperkalaemia
Hypothermia/hyperthermia
Hypovolaemia
Tension pneumothorax
Tamponade
Thrombosis
Toxin

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79
Q

What are the 2 types of hypovolaemic shock + their causes?

A

Haemorrhagic: bleeding
Non-haemorrhagic: burns, DKA, severe D&V, excessive use of diuretics, pancreatitis, severe dehydration

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80
Q

What are the symptoms of hypovolaemic shock?

A

Tachypnoea
Long CRT
Tachycardia
Hypotension
Cold peripheries
Hypoxaemia
Cool and clammy

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81
Q

What is afterload?

A

force or load against which the heart has to contract to eject the blood

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82
Q

What is preload?

A

the initial stretching of the cardiac myocytes prior to contraction

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83
Q

What is central venous pressure?

A

blood pressure in the vena cava as it enters the right atrium

reflects the volume of blood returning to the heart and therefore the volume of blood the heart pumps back into the arteries

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84
Q

What can cause obstructive shock?

A

PE
Cardiac tamponade
Tension pneumothorax

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85
Q

What happens in distributive shock?

A

Extreme vasodilation, lowers BP
Capillaries can become leaky

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86
Q

What are the different types of distributive shock?

A

Septic
Neurogenic
Anaphylactic

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87
Q

What can cause distributive shock?

A

Anaphylactic: severe allergic reaction
Septic: Severe infection
Neurogenic: spinal cord injury

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88
Q

Which types of shock have a reduced preload?

A

Hypovolaemic
Distributive
Obstructive: PE, tension PTX

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89
Q

Which types of shock have an increased preload?

A

Cardiogenic
Obstructive: cardiac tamponade

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90
Q

How do you treat hypovolaemic shock?

A

Fluid resus
Correct hypovolaemia and hypoperfusion before irreversible organ damage
Blood transfusion in haemorrhagic

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91
Q

What is the pathophysiology of haemorrhagic shock?

A
  • loss of blood volume from ruptured vessels
  • EDV + SV decrease
  • CO and BP decrease
  • Baroreceptors detect
  • Catecholamines, ADH and angiotensin II released to cause vasoconstriction, resistance and HR increased
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92
Q

What is obstructive shock?

A

Obstruction to the forward flow of blood in the great vessels or heart

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93
Q

What is the pathophysiology of distributive shock?

A

Septic shock: massive vasodilation in inflammatory reaction
Neurogenic: body can’t vasoconstrict so vasodilates
Anaphylaxis: IgE mediated type 1 hypersensitivity reaction, vasodilation

Vasodilation changes distribution of fluid in body

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94
Q

What investigations would you carry out in shock?

A

ABG (+ lactate)
Glucose
FBC + U&Es
ECG

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95
Q

How do you treat distributive shock?

A

Fluid resus
Septic: antibiotics
Neurogenic: vasopressors, corticosteroids
Endocrine: corticosteroids
Anaphylactic: adrenaline, antihistamines

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96
Q

Risk factors for an AAA

A

smoking
family history
increased age
hypertension
male sex (prevalence)
female sex (rupture)
aortic degeneration accelerated in marfans and pregnancy

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97
Q

What should you suspect in a patient with hypotension and atypical abdo pain?

A

Ruptured AAA

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98
Q

Key presentations of an AAA

A

Pulsatile and expansile mass in abdomen
Pain in abdo, back, loin and groin

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99
Q

Signs of a ruptured AAA

A

Hypotension
Atypical abdo symptoms
Syncope, collapse
Shock

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100
Q

What investigation would you do for a suspected AAA?

A

aortic ultrasound

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101
Q

Differentials for AAA

A

GI haemorrhage
Mesenteric AA
IBS/IBD
Diverticulitis
Ureteric colic

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102
Q

How do you manage a AAA?

A

Ruptured or symptomatic: urgent surgical repair
Unruptured: surveillance and treatment of modifiable risk factors

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103
Q

How often would you do an aortic ultrasound for a known AAA?

A

Annually if the AAA measures 3.0 to 4.4 cm
Every 3 months if the AAA measures 4.5 to 5.4 cm

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104
Q

What are some possible complications of AAA repair?

A
  • Abdominal compartment syndrome
  • AKI
  • Colitis
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105
Q

What is the screening for AAA?

A

Routine screening for AAA for all men aged 65 years

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106
Q

What is pericarditis?

A

inflammation of the pericardium

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107
Q

What is the function of the pericardium?

A

Restrains volume of heart so it can’t overfill
Protects heart
Provides fluid layer in pericardial cavity to avoid friction

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108
Q

What is acute pericarditis?

A

new-onset inflammation of pericardium lasting <4 to 6 weeks

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109
Q

What 3 signs characterise pericarditis?

A

Chest pain
Pericardial friction rub
Serial ECG changes

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110
Q

How does a pericardial effusion occur from pericarditis?

A

Pericardium inflammation causes cytokines to be released. This causes blood vessels to become more permeable and fluid leaks into pericardial cavity.

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111
Q

Can pericarditis exist without pericardial effusion?

A

Yes
Majority of time some effusion, but not always

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112
Q

When does cardiac tamponade occur?

A

When pericardial effusion inhibits stretch of pericardium or happens rapidly

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113
Q

What can cause pericarditis?

A
  • Infectious: viral (EBV, CMV, SARS Cov2), bacterial (TB)
  • Autoimmune (Sjorgen, rheumatoid arthritis, SLE)
  • neoplastic (secondary metastatic tumours)
  • metabolic
  • trauma + iatrogenic
  • post MI, dressler’s syndrome
  • uraemia

viral causes or idiopathic are responsible for 90%

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114
Q

What is Dressler’s syndrome?

A

late-onset post-myocardial infarction pericarditis
Can occur anywhere up to 3 months after MI

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115
Q

What are the risk factors for pericarditis?

A

Male
Age 20-50
Transmural MI
Cardiac surgery
Infections
Uraemia or dialysis
Autoimmune disorders

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116
Q

What is chronic constrictive pericarditis?

A

chronically thickened pericardium

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116
Q

What is chronic pericarditis and its subtypes?

A

long-lasting, gradual inflammation of the pericardium
signs and symptoms lasting longer than 3 months
subtypes: effusive, constrictive

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117
Q

What is chronic effusive-constrictive pericarditis?

A

combination of tense effusion in the pericardial space and constriction by the thickened pericardium

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118
Q

What are the clinical criteria for diagnosing acute pericarditis?

At least 2 must be present

A
  • Characteristic chest pain; typically sharp, pleuritic, and relieved by sitting forwards
  • Pericardial friction rub
  • New widespread concave upwards ST elevation or PR depression on ECG
  • Pericardial effusion (new or worsening)
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119
Q

What are the symptoms of pericarditis?

A

Acute onset, sharp, pleuritic chest pain
Pericardial rub
Chest pain relieved on sitting forward
Fever
Signs of effusion

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120
Q

What investigations should be done for pericarditis?

A

ECG: saddle shape on ST segment, PR depression
FBC: increase in white cell count
CXR
Echocardiogram

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121
Q

What ECG changes are seen in pericarditis?

A

Saddle-shaped ST-elevation
PR depression

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122
Q

What are the differentials for pericarditis?

A

MI
Pneumonia
Pleurisy
PE
Aortic dissection
Pneumothorax
Myocarditis

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123
Q

How would you manage pericarditis?

A

Give NSAIDs and Colchicine
Check for tamponade

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124
Q

What are the possible complications of pericarditis?

A

Pericardial effusion
Cardiac tamponade
Chronic constrictive pericarditis

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125
Q

What is a pericardial effusion?

A

excess fluid collects within the pericardial sac

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126
Q

What can cause pericardial effusion?

A

Malignancy
Infections (from pericarditis)
Iatrogenic (post surgery)

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127
Q

What is cardiac tamponade?

A

the accumulation of pericardial fluid, blood, pus, or air within the pericardial space that creates an increase in intra-pericardial pressure, restricting cardiac filling and decreasing cardiac output

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128
Q

What normally happens during inspiration in the RV?

A

inhaling causes negative pressure, pulling blood into heart. RV expands into pericardial space so it doesn’t affect left heart volume

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129
Q

What happens in cardiac tamponade when the RV can’t expand into the pericardial space?

A

RV can’t move into pericardial space, so pushes into left instead.
Causes reduction in LV diastolic volume, lower SV and drop in systolic BP during inspiration.
Decrease in systolic BP of greater than 10mmHg is called pulsus paradoxus

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130
Q

What makes up Beck’s triad in diagnosing cardiac tamponade?

A

Hypotension
Elevated JVP
Muffled heart sounds

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131
Q

What are the signs of cardiac tamponade?

A

Becks triad
Fall in systolic BP (pulsus paradoxus)
Kaussmaul’s sign
ECG changes

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132
Q

What are the symptoms of cardiac tamponade?

A

Dyspnoea
Tachycardia
Hypotension
Cold and clammy peripheries
Elevated JVP
Signs of pericardial effusion

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133
Q

What are the differentials for cardiac tamponade?

A

Constrictive pericarditis
Restrictive cardiomyopathy
Cardiogenic shock

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134
Q

How do you treat cardiac tamponade?

A

Pericardiocentesis (not as great in smaller effusions or constrictive causes)
NSAIDS + Colchicine (pericarditis)

main point is drain the pericardium

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135
Q

What are the possible complications of cardiac tamponade?

A

Cardiac arrest
Organ hypoperfusion

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136
Q

What is the action of ACE inhibitors?

A

inhibit the conversion of angiotensin I to angiotensin II

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137
Q

What drugs can be used to treat hypertension?

A

ACE inhibitors
Angiotensin II receptor blockers (ARBs)
CCBs
Beta-adrenoreceptor blockers
Diuretics

others: Alpha-1 adrenoreceptor blockers
Centrally acting anti-hypertensives
Direct renin inhibitors

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138
Q

Examples of ACE inhibitors?

A

Ramipril
Perindopril
Enalapril

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139
Q

What are the indications for ACE inhibitors?

A

HF
Hypertension
Diabetic nephropathy

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140
Q

What are some possible adverse effects of ACE inhibitors cause by inhibting the breakdown of bradykinin?

A

Persistent dry cough
Rash
Anaphylactoid reactions

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141
Q

What are some adverse effects of ACE inhibitors?

A

Hypotension (related to AGT 2)
Acute renal failure (AGT 2)
Hyperkalaemia (AGT 2)
Teratogenic in pregnancy (AGT2)
Cough (related to kinins)
Rash (kinins)
Anaphylactoid reactions (kinins)

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142
Q

What are the contraindications of ACE inhibitors?

A

Pregnancy
History of angio-oedema
Diabetics on aliskiren with a eGFR below 60mL/minute

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143
Q

What are angiotensin II receptor antagonists (ARBs) used for?

A

Hypertension
HF when ACEi is contraindicated
Diabetic nephropathy

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144
Q

What are the contraindications of ARBs?

A

Pregnancy
History of angio-oedema
Diabetics on aliskiren with a eGFR below 60mL/minute
Breastfeeding women

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145
Q

What are some adverse effects of ARBs?

A

Hypotension (esp if volume depleted)
Rash
Potential for renal dysfunction
Hyperkalaemia
Angio-oedema

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146
Q

What is the action of ARBs?

A

Block angiotensin 2 by acting on AT-1 receptor

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147
Q

Examples of calcium channel blockers

A

Dihydropyridine:
- Amlodipine
- Felodipine
Benzothiazepines:
- Diltiazem
Phenylalkylamine:
- Verapamil

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148
Q

What are calcium channel blockers used for?

A

Hypertension
IHD – angina
Arrhythmia (tachycardia)

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149
Q

What are some contraindications of CCBs?

A

HF
Cardiac outflow obstruction
Cardiogenic shock
Avoid within 1 month of MI (amlodipine fine)

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150
Q

What are the actions of CCBs?

A

Act on L-type calcium channels
Dihydropyridines are arterial vasodilators and have little direct cardio effects
Verapamil mostly affects heart
Diltiazem has cardiac and peripheral effects

151
Q

What are the adverse effects of CCBs?

A

Flushing (related to vasodilation)
Headaches (vasodilation)
Oedema (vasodilation)
Palpitations (vasodilation)
Bradycardia
AV block
Worsening of cardiac failure
Verapamil causes constipation

152
Q

Examples of beta-adrenoceptor blockers

A

Propanolol
Bisoprolol
Atenolol

153
Q

What are the indications fo beta-adrenoceptor blockers?

A

IHD – angina
Heart failure
Hypertension
Arrhythmia

154
Q

What are the contraindications of beta-adrenoceptor blockers?

A

Asthma and COPD
2nd and 3rd degree AV block
Phaeochromcytoma

155
Q

What are the different classes of diuretics?

A

Thiazides
Loop diuretics
Potassium-sparing diuretics
Aldosterone antagonists

156
Q

Examples of thiazide diuretics

A
  • Bendroflumethiazide
  • Hydrochlorothiazide
157
Q

Examples of aldosterone antagonist diuretics

A

Spironolactone
Eplerenone

158
Q

What are thiazides used for?

A

used to relieve oedema due to chronic heart failure and, in lower doses, to reduce blood pressure

159
Q

What are loop diuretics used for?

A

used in pulmonary oedema due to left ventricular failure and in patients with chronic heart failure

160
Q

What are the main indications of diuretics?

A

HF
Hypertension

161
Q

What are some adverse effects of diuretics?

A

Hypovolaemia (loops)
Hypotension
Loss of electrolytes
Hyperuricaemia – gout
Impaired glucose tolerance
Erectile dysfunction

162
Q

What are the actions of nitrates?

A

Arterial and venous dilators
Reduction of preload and afterload
Lower BP

163
Q

What are the indications of nitrates?

A

IHD - angina
HF

164
Q

How much aspirin is used to treat an acute event? (e.g. TIA, MI)

165
Q

What effect does aspirin have on platelets?

A

Blocks synthesis of thromboxane A2
Low dose inhibits COX 1
High dose inhibits both COX 1 and 2

166
Q

Is aspirin used in primary or secondary prevention of CVD?

A

secondary
not recommended in primary prevention

167
Q

What is the dosage for aspirin in secondary prevention of cardiovascular disease?

A

75mg daily

168
Q

How does clopidogrel work?

A

inhibits the binding of ADP to its platelet receptor, blocking amplification of platelet aggregation

169
Q

What are some antiplatelet drugs?

A

Aspirin
Clopidogrel

170
Q

What is clopidogrel used for?

A

prevention of atherothrombotic events in patients with a history of symptomatic ischaemic disease

171
Q

When are clopidogrel and aspirin used in combo?

A

in patients with AF and at least 1 risk factor to prevent thromboembolic event when warfarin isn’t suitable

however does increase risk of bleeding

172
Q

What should be controlled before giving aspirirn?

A

Hypertension

173
Q

When could you prescribe 75mg aspirin?

A

Angina
AF with 75mg of clopidogrel for patients who don’t want anticoags
ACS
Patients undergoing CABG + tricagelor or prasugrel

174
Q

What is the preferred antiplatelet for secondary prevention of stroke/TIA?

A

Clopidogrel 75mg

175
Q

What is the main risk of antiplatelets?

A

Increase risk of bleeding

176
Q

What are the acute coronary syndromes?

A

Unstable angina
NSTEMI
STEMI

177
Q

What can cause acute coronary syndrome?

A

Rupture/erosion
thrombus from an atherosclerotic plaque blocking a coronary artery

178
Q

What’s atrial fibrillation?

A

a supraventricular tachyarrhythmia with uncoordinated atrial electrical activation and consequently ineffective atrial contraction

179
Q

What’s the pathophysiology of AFib?

A

Electrical activity is disorganised, causing atrial contraction to become uncoordinated, rapid and irregular.
It passes to ventricles, resulting in irregularly irregular ventricular contraction

Uncoordinated atrial activity means the blood can stagnate in the atria, forming a thrombus, which may lead to an ischaemic stroke

180
Q

What is an acute myocardial infarction?

A

myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand

181
Q

What does the RCA supply?

A

Right atrium
Right ventricle
Inferior aspect of the left ventricle
Posterior septal area

182
Q

What do the branches of the LCA supply?

A

Circumflex artery;
- L atrium
- Posterior L ventricle
Left anterior descending (LAD):
- Anterior L ventricle
- Anterior septum

183
Q

What are the risk factors for an MI?

A

smoking
HTN
diabetes
obesity
high cholesterol
physical inactivity
renal insufficiency
established coronary artery disease
family Hx of premature coronary artery disease
cocaine use
male sex
age >50 years
female after menopause

184
Q

What typically causes a STEMI?

A

complete atherothrombotic occlusion of a coronary artery due to atherosclerotic plaque rupture

185
Q

What’s the difference in aetiology for a STEMI and NSTEMI?

A

STEMI: complete occlusion
NSTEMI: transient/ near complete occulsion, e.g. plaque or thrombus

186
Q

What can cause an NSTEMI?

A
  • Plaque rupture with non-occlusive thrombus
  • Dynamic obstruction, such as in vasospasm
  • Progressive luminal narrowing
  • Inflammatory mechanisms (i.e., vasculitis)
  • Extrinsic factors leading to poor coronary perfusion (such as hypotension, hypovolaemia, or hypoxia)
187
Q

How is troponin related to an MI?

A

Troponin is a protein in cardiac muscle (myocardium) and skeletal muscle.
A rise in troponin is consistent with myocardial ischaemia, as they are released from the ischaemic muscle tissue
Non-specific marker for MI

used in diagnosis for NSTEMI

188
Q

How does an MI present?

A
  • central heavy chest pain
  • may radiate to the left arm, neck, or jaw
  • nausea, vomiting
  • dyspnoea
  • lightheadedness/ syncope
  • palpitations
189
Q

What are the ECG changes for an MI?

A

STEMI: ECG showing ST elevation or new LBBB
NSTEMI: ECG with no ST elevation, may show ST depression or T wave inversion

190
Q

What investigations should be done for a suspected MI?

A

Troponin: elevated
ECG

191
Q

What are some of the possible differentials for an MI?

A

Unstable angina
NSTEMI/STEMI (whichever it isn’t)
Ptx
PE
GORD
Aortic dissection

192
Q

What’s the initial management for an MI?

A
  • Aspirin 300mg immediately
  • IV morphine/ other pain relief
  • IV nitrate
193
Q

What’s the management of a STEMI?

after initial

A
  • Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting)
  • Thrombolysis if no PCI
194
Q

How is a NSTEMI managed?

A
  • Unstable: angiography + revascularisation
  • Aspirin 300mg
  • Ticagrelor 180mg (clopidogrel if bleeding risk)
  • Morphine for pain relief
  • Heparin or fondaparinux
195
Q

What are some possible complications of an MI?

A

post-infarction pericarditis (Dressler’s syndrome)
congestive heart failure
ventricular arrhythmias
recurrent ischaemia and infarction

196
Q

What is peripheral arterial disease (PAD)?

A

the narrowing of the arteries supplying the limbs and periphery, reducing the blood supply to these areas

197
Q

What is intermittent claudication?

PAD

A
  • symptom of ischaemia in a limb, occurring during exertion and relieved by rest.
  • typically a crampy, achy pain in the calf, thigh or buttock muscles associated with muscle fatigue when walking beyond a certain intensity.
198
Q

What is critical limb ischaemia?

A
  • end-stage of peripheral arterial disease, where there is an inadequate supply of blood to a limb to allow it to function normally at rest.
  • There is a significant risk of losing the limb.
  • features are pain at rest, non-healing ulcers and gangrene.
  • Pain is worse at night when the leg is raised, as gravity no longer helps pull blood into the foot.
199
Q

What is acute limb ischaemia?

A
  • rapid onset of ischaemia in a limb.
  • Typically due to a thrombus (clot) blocking the arterial supply of a distal limb, similar to a thrombus blocking a coronary artery in myocardial infarction.
200
Q

What is gangrene?

A

refers to the death of the tissue, specifically due to an inadequate blood supply

201
Q

What are the features of acute limb ischaemia?

6 Ps

A

Pain
Pallor
Pulseless
Paralysis
Paraesthesia (abnormal sensation or “pins and needles”)
Perishing cold

202
Q

What is Leriche syndrome?

A

occlusion in the distal aorta or proximal common iliac artery. clinical triad of:
- Thigh/buttock claudication
- Absent femoral pulses
- Male impotence

203
Q

What is the main cause of PAD?

A

atherosclerosis

204
Q

What is the epidemiology of PAD?

A

Increases with age
Affects men and women equally

205
Q

What is the ankle-brachial index?

used to diagnose PAD

A

the ratio of systolic BP in the ankle compared with the systolic blood pressure in the arm

206
Q

What are the main features of PAD?

A

intermittent claudication
thigh or buttock pain with walking that is relieved with rest
diminished or absent pulses

most patients are asymptomatic

207
Q

What are the risk factors for PAD?

A

smoking
diabetes
HTN
hyperlipidaemia
age >40 years
hx of coronary artery disease/cerebrovascular disease
low levels of exercise

208
Q

What investigations should be done for PAD?

A

resting ankle-brachial index: ABI ≤0.90
Duplex ultrasound – ultrasound that shows the speed and volume of blood flow
Angiography (CT or MRI) – using contrast to highlight the arterial circulation

209
Q

What are the management options for PAD?

A

aggressive risk factor control
lifestyle limiting claudication: supervised 12-week exercise programme
anti-platelet therapy: aspirin or clopidogrel

statins: Atorvastatin
surgical:revascularisation

210
Q

What are the differentials of PAD?

A

Spinal stenosis
Arthritis
Venous claudication
Chronic compartment syndrome
Symptomatic Baker’s cyst
Nerve root compression

211
Q

What are the complications of PAD?

A

leg/foot ulcers
gangrene
permanent limb weakness/numbness
permanent limb pain

212
Q

What causes the first heart sound?

A

closing of the atrioventricular valves (mitral and tricuspid) at start of systolic contraction of ventricles

213
Q

What causes the second heart sound?

A

closing of the semilunar valves (the pulmonary and aortic valves) once the systolic contraction is complete

214
Q

What causes aortic stenosis?

and what does it often follow?

A

calcification and fibrosis of aortic valve
congenital bicuspid aortic valve

aortic sclerosis

215
Q

What is aortic stenosis?

A

obstruction of blood flow across the aortic valve due to aortic valve fibrosis and calcification

216
Q

What are the main symptoms in a patient presenting with aortic stenosis?

A

fatigue
decreased exercise capacity
exertional dyspnoea
exertional chest pain (angina)
syncope

decades long subclinical phase

217
Q

What is the murmur like in aortic stenosis?

A

ejection-systolic, high-pitched murmur with a crescendo-decrescendo pattern

218
Q

What would an ecg show for aortic stenosis?

A

left ventricular hypertrophy and absent Q waves, may have a bundle block

219
Q

What investigations should be done for aortic stenosis?

A

Doppler transthoracic echocardiography (TTE): elevated aortic pressure gradient
ECG: left ventricular hypertrophy and absent Q waves, may have a bundle block
CXR

220
Q

What are the differentials for aortic stenosis?

A

Aortic sclerosis
Ischaemic heart disease
Hypertrophic cardiomyopathy (HCM)

221
Q

How is aortic stenosis treated?

A

aortic valve replacement

222
Q

What is aortic regurgitation?

A

diastolic leakage of blood from the aorta into the left ventricle (LV)

223
Q

What causes aortic regurgitation?

A

inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root.

can be acute or chronic, acute is medical emergency

224
Q

How can acute AR present?

A

sudden onset of pulmonary oedema and hypotension or in cardiogenic shock

225
Q

What are some symptoms of chronic AR?

A

dyspnoea
fatigue
weakness
orthopnoea
paroxysmal nocturnal dyspnoea

often asymptomatic

226
Q

What investigations should be done for aortic regurgitation?

A

ECG: non-specific ST-T wave changes, left axis deviation, or conduction abnormalities
CXR
Echocardiogram

colour flow doppler can also be done

227
Q

What are the differentials for aortic regurgitation?

A

Mitral regurgitation (MR)
Mitral stenosis
Aortic stenosis
Pulmonary regurgitation

228
Q

What are the management options for aortic regurgitation?

A

Reassurance and monitoring for asymptomatic and good LV function
Symptomatic patients: aortic valve replacement (AVR) or repair

229
Q

What is mitral stenosis?

A

narrowing of the mitral valve orifice

230
Q

What can cause mitral stenosis?

A

Rheumatic fever leading to rheumatic heart disease (main cause)
congenital deformity of the valve
carcinoid syndrome

231
Q

What is the pathophysiology of mitral stenosis?

A

valve orifice reduced in mitral stenosis, flow between left atrium and left ventricle is progressively impeded
pressure in the left atrium remains higher than left ventricle.

  • Increased left atrial pressure is referred to the lungs, leading to congestion
  • Restricted orifice limits filling of the left ventricle, limiting cardiac output.
232
Q

What are the risk factors for mitral stenosis?

A

streptococcal infection (rheumatic fever)
female sex (3x more likely)

233
Q

What does the murmur for mitral stenosis sound like?

A

Diastolic low-pitched rumbling murmur with opening snap

234
Q

What are the symptoms of mitral stenosis?

A

Dyspnoea
Orthopnoea
paroxysmal nocturnal dyspnoea
peripheral oedema
neck vein distension

235
Q

What investigations would be done for mitral stenosis and what would they show?

A

Trans-thoracic echocardiography (TTE) showing typical valve deformities
ECG: AF, LA enlargement, RV hypertrophy
CXR: Kerley B lines

236
Q

What’s the management for mitral stenosis?

A

Furosemide diuretic
balloon valvotomy, valve replacement or repair

no therapy required for mild or asymptomatic, this is for severe

237
Q

What’s mitral regurgitation?

A

incompetent mitral valve, allowing blood to flow back from the left ventricle to the left atrium during systolic contraction of the left ventricle.

238
Q

What is going wrong in mitral regurgitation?

A

mitral valve dysfunction leads to backflow of blood into L atrium during contraction
reduced ejection fraction and a backlog of blood waiting to be pumped through the left side of the heart

resulting in congestive cardiac failure

239
Q

What are the main causes of secondary mitral regurgitation?

A

cardiomyopathy or coronary artery disease

primary MR caused be degeneration of mitral valve

240
Q

What are some possible presenting symptoms of MR?

A

dyspnoea on exertion
orthopnoea
paroxysmal nocturnal dyspnoea
lower extremity oedema
palpitations
fatigue
sweating

241
Q

What can be heard in mitral regurgitation?

A

pan-systolic, high-pitched “whistling” murmur, radiates to the left axilla
diminished S1
S3 present (third heart sound)

242
Q

What investigations should be done for MR?

A

Transthoracic echo
ECG

243
Q

What are the surgical options for MR?

A

Mitral valve repair
Mechanical valve replacement + anticoags

244
Q

What are the complications of MR?

A

AF
Pulmonary HTN
LV dysfunction and CHF

245
Q

What are the common causes of AF?

SMITH pneumonic

A

S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension

246
Q

What are the typical symptoms of AF?

A

Palpitations
SOB
Fatigue
chest pain
dizziness

247
Q

What are the risk factors for atrial fibrillation?

A

increasing age
HTN
heart failure
diabetes mellitus
male
obstructive sleep apnoea
obesity + alcohol abuse
coronary artery disease
valve disease
other atrial arrhythmias
previous stroke/TIA
hyperthyroidism

248
Q

What would an ECG show for AF?

A

absent P wave
irregularly irregular QRS

249
Q

What is paroxysmal AF?

A

episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm.
These episodes can last between 30 seconds and 48 hours.

250
Q

What investigations should be done for atrial fibrillation?

A

ECG
Echocardiogram
electrolytes, urea, and creatinine
TFTs

251
Q

What are the differentials for atrial fibrillation?

A

Atrial flutter.
Supraventricular tachyarrhythmias.
AVNRT
Wolff-Parkinson-White syndrome.
Ventricular tachycardia.

252
Q

What are the management options for AF?

A

DOACs: rivaroxaban, apixaban for thrombi prevention
Beta-blockers: bisoprolol, metoprolol for rate control
Antiarrhythmics: amiodarone
Consider a DC cardioversion or ablation

253
Q

What are the complications of AF?

A

Stroke
MI
Congestive heart failure
Bradycardia

254
Q

What does the HAS-BLED score assess?

A

bleeding risk on an DOAC in AF

255
Q

What does the CHA2DS2-VASc score assess?

A

stroke risk for AF patients

256
Q

What is atrial flutter?

A

macro re-entrant atrial tachycardia with atrial rates usually above 250 bpm up to 320 bpm

257
Q

What is going wrong in atrial flutter?

A

Re-entrant rhythm starts in atrium, looping back and overriding SAN, causing atria to contract at fast rates (around 300bpm)
often results in two atrial contractions for every one ventricular contraction

258
Q

What are the risk factors for atrial flutter?

A

increasing age
valvular dysfunction
atrial septal defects
atrial dilation
recent cardiac or thoracic procedures
heart failure
hyperthyroidism
Resp: COPD, asthma, pneumonia

259
Q

What can cause atrial flutter?

A

structural or functional conduction abnormalities of the atria
- atrial dilation
- incisional scars
- toxins and metabolic: thyrotoxicosis, alcoholism, pericarditis
- antiarrhythmics converting AF to flutter, e.g. amiodarone

260
Q

What are some symptoms that could suggest atrial flutter?

A

Palpitations
Dypnoea
Fatigue
Light-headedness
Chest discomfort
Altered consciousness
Polyuria

261
Q

What would an ECG show for atrial flutter?

A

saw tooth pattern, regular
atria 300bpm
ventricles 150bpm

262
Q

What investigations should be done for atrial flutter?

A

ECG
transthoracic echocardiography (TTE)

fbc
tfts

263
Q

How is atrial flutter managed?

A

Beta-blocker for rate control
Electrical cardioversion for rhythm control

264
Q

What is the pathophysiology of WPW?

A

an extra electrical pathway connecting the atria and ventricles (bundle of Kent)
The additional pathway allows electrical activity to pass between the atria and ventricles, bypassing the AV node
Ventricles can then contract slightly early, pre-excitation

265
Q

What causes the issues in WPW?

A

presence of an accessory pathway between atria and ventricles

266
Q

How might WPW present?

A

Palpitations
Dizziness
SOB
chest pain
syncope (rare)
sudden cardiac death (rare)
arrthymias: atrioventricular re-entrant tachycardia (AVRT)

267
Q

What are the differences on an ECG for type A and B WPW?

A

type A (left-sided pathway): dominant R wave in V1, right axis deviation
type B (right-sided pathway): no dominant R wave in V1, left axis deviation

268
Q

What are the ECG findings for WPW?

A

ECG: Short PR interval, Wide QRS complex, Delta wave

269
Q

What are the management options for WPW?

A

radiofrequency ablation of the accessory pathway
amiodarone

270
Q

What is AV nodal re-entrant tachycardia?

A

supraventricular tachy where the re-entry point is back through the atrioventricular node

271
Q

What is aortic dissection?

A

a break or tear forms in the inner layer of the aorta, allowing blood to flow between the layers of the wall of the aorta

272
Q

What are type A and B aortic dissection?

A

Type A dissection involves the ascending aorta with or without involvement of the arch and descending aorta
Type B does not involve the ascending aorta, and predominantly involves only the descending thoracic and/or abdominal aorta

273
Q

What are the risk factors for aortic dissection?

A

HTN
male sex
smoking
atherosclerotic aneurysmal disease
Marfan syndrome
Ehlers-Danlos syndrome
bicuspid aortic valve

274
Q

What does aortic dissection result from?

A

results from an intimal tear that extends into the media of the aortic wall

275
Q

What is the pathophysiology of aortic dissection?

A

With aortic dissection, blood enters between the intima and media layers of the aorta.
A false lumen full of blood is formed within the wall of the aorta

276
Q

How does aortic dissection typically present?

A

abrupt onset chest, back, or abdominal pain that is severe in intensity or is described as ‘sharp’ or ‘stabbing’
blood pressure differential between the two arms
pulse differences

277
Q

What investigations should be done for aortic dissection?

A

CT angiogram
transthoracic echocardiography: intimal flap
ECG to rule out STEMI

278
Q

What are the differentials for aortic dissection?

A

Acute coronary syndrome
Pericarditis
Aortic aneurysm
MSK pain
PE
Mediastinal tumour

279
Q

How is an aortic dissection managed?

A

IV labetalol
Surgical repair urgently

280
Q

What are some complications of an aortic dissection?

A

MI
Cardiac tamponade
Aortic valve regurgitation
Aneurysmal degeneration
Stroke

281
Q

In cardiac arrest which rhythms are shockable?

A

V tachycardia
V fib

282
Q

What rhythms are not shockable in cardiac arrest?

A

Electrical activity that isn’t vfib or v tachycardia without a pulse
asystole

pulseless electrical activity

283
Q

What is long QT syndrome?

A

congenital or acquired condition that is characterised by a prolonged QT interval
associated with a high risk of sudden cardiac death due to ventricular tachyarrhythmias

mean age at diagnosis is 14

284
Q

How does LQTS typically present?

A

young people with cardiac arrest or unexplained syncope

285
Q

What does LQTS show on an ECG?

A

ECG showing prolonged QT and changes in T waves

286
Q

How does torsade present on an ecg?

A

appearance that the QRS complex is twisting around the baseline
heights get progressively larger then smaller etc

287
Q

What are ventricular ectopics?

A

premature ventricular beats caused by random electrical discharges outside the atria

288
Q

What does an ECG with ventricular ectopics show?

A

isolated, random, abnormal, broad QRS complexes
bigeminy is when every other beat is an ectopic

289
Q

What’s the management for ventricular arrthymias?

A

non-selective beta-blockers, e.g. nadolol

290
Q

What pathophysiologically causes angina?

A

atherosclerosis in coronary arteries, narrowing the lumen and reducing blood flow to the myocardium
During times of high demand, such as exercise, there is an insufficient supply of blood to meet the demand
Causes symptoms of angina

291
Q

When is angina unstable?

A

appear randomly whilst at rest
this is a form of ACS and requires urgent management

292
Q

How does stable IHD (angina) typically present?

A

chest pressure or squeezing lasting several minutes
provoked by exercise or emotional stress
relieved by rest or glyceryl trinitrate

may radiate to jaw or arm

293
Q

What are the risk factors for developing angina?

A

advancing age
smoking
HTN
elevated LDL or low HDL cholesterol
diabetes
inactivity
obesity
illicit drug use
male sex

294
Q

What are the two diagnostic tests for angina?

A

Cardiac stress testing: assessing the patient’s heart function during exertion, e.g. walking on a treadmill or giving dobutamine
Coronary computed tomography angiography (CCTA): injecting contrast in CT to find narrowing

295
Q

Apart from stress testing and CCTA, what other investigations should be done for angina?

A

resting ECG: can be normal or abnormal
haemoglobin: possible anaemia
lipid profile: elevated LDL is risk, HDL is protective
fasting blood glucose or HbA1c: diabetes important risk factor

296
Q

What are some differentials for angina?

A

MI - unstable angina
Pleuritis - unstable angina
PE
GORD
Ptx
Aortic dissection
Pericarditis
Biliary disease

297
Q

What medications are used for secondary prevention of stable angina?

A

A – Aspirin 75mg once daily
A – Atorvastatin 80mg once daily
A – ACE inhibitor (if diabetes, hypertension, CKD or heart failure are also present)
A – Already on a beta blocker for symptomatic relief

298
Q

How is stable angina managed?

A

Immediate symptomatic relief:
- sublingual glyceryl trinitrate (GTN) spray or tablets. GTN causes vasodilation
Long-term symptomatic relief:
- Beta blocker (e.g., bisoprolol)
- Calcium-channel blocker (e.g. amlodipine)
Lifestyle management

299
Q

Complications of angina

A

MI
Stroke
PAD
HF

300
Q

What is unstable angina?

A

myocardial ischaemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury/necrosis

301
Q

What characterises unstable angina?

A

prolonged (>20 minutes) angina at rest
new onset of severe angina
angina that is increasing in frequency, longer in duration, or lower in threshold
angina that occurs after a recent MI

302
Q

What’s the most common cause of unstable angina?

A

coronary artery narrowing caused by a thrombus that develops on a disrupted atherosclerotic plaque and is usually non-occlusive

303
Q

What investigations should be done for unstable angina?

A

ECG: no evidence of STEMI, may be normal or show ST-segment depression, transient ST-segment elevation, or T-wave inversion
Troponin: no dynamic elevation
FBC, U&Es, LFTs, BM, CRP

304
Q

How should unstable angina be managed?

A

Acute management includes antiplatelet and anticoagulant therapy
- Aspirin
- Fondaparinux
- Morphine/ GTN
Ongoing management
- Beta blockers, e.g. bisoprolol
- GTN

305
Q

What is prinzmetal’s angina?

A

intense vasospasm of a coronary artery

306
Q

What is paroxysmal nocturnal dyspnoea?

A

suddenly waking at night with a severe attack of shortness of breath, cough and wheeze

307
Q

What can be used in the management of HFrEF?

A

ACE inhibitor + Beta-blockers first line
Second line Aldosterone antagonists, e.g. spironolactone
SGLT2 inhibitor, e.g. dapagliflozin

308
Q

What investigations are done for heart failure?

A

Clinical assessment (history and examination)
N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test: elevated
ECG: evidence of underlying disease
Transthoracic echocardiogram: accurate determination of biventricular systolic and diastolic function
Bloods
CXR: abnormal

309
Q

What are the differential diagnoses for heart failure?

A

Ageing/ inactivity
COPD
PE
Pneumonia
Post-partum cardiomyopathy
Nephrotic syndrome

310
Q

What can cause chronic heart failure?

A

Ischaemic heart disease
Valvular heart disease (commonly aortic stenosis)
HTN
Arrhythmias (commonly atrial fibrillation)
Cardiomyopathy

311
Q

How is HFpEF treated?

A

SGLT2 inhibitors (e.g., dapagliflozin)
Lifestyle changes and treatments

focused on reducing congestion, identification and treatment of underlying causes and comorbidities, implementing lifestyle

312
Q

What are the complications of heart failure?

A

pleural effusion
chronic kidney disease
anaemia
acute decompensation of chronic heart failure
AKI
sudden cardiac death
hyperkalaemia

313
Q

What are the CXR findings for heart failure?

A

A: alveolar oedema (perihilar/bat-wing opacification)
B: Kerley B lines (interstitial oedema)
C: cardiomegaly
D: dilated upper lobe vessels
E: effusions

314
Q

What is cor pulmonale?

A

right-sided heart failure caused by respiratory disease

315
Q

What happens in cor pulmonale?

A

increased pressure and resistance in the pulmonary arteries (pulmonary HTN) limits RV pumping blood into the pulmonary arteries.
This causes back-pressure into the RA, VC and systemic venous system

316
Q

What are the symptoms of cor pulmonale?

A

Shortness of breath
Peripheral oedema
Breathlessness of exertion
Syncope (dizziness and fainting)
Chest pain

317
Q

What can cause AV blocks?

A

fibrosis and calcification of the conduction system
coronary artery disease
medication: beta-blockers, CCB, digitalis, antiarrhythmics
cardiomyopathy

318
Q

How does a first degree heart block present on an ecg?

A

Fixed prolongation of the PR interval >0.2 seconds (5 small squares) with no failure of AV conduction.

319
Q

What are second degree heart blocks?

A

some atrial impulses do not make it through the AV node to the ventricles, some P waves not followed by QRS

Mobitz type 1 and 2

320
Q

How does a second degree mobitz type 1 heart block show on an ECG?

A

increasing PR interval until a P wave is not followed by a QRS complex.
PR interval then returns to normal, and the cycle repeats itself

321
Q

What is a second degree mobitz type 2 heart block?

A

intermittent failure of conduction through AV node, with an absence of QRS complexes following P waves.
There is usually a set ratio of P waves to QRS complexes, e.g. three P waves for each QRS complex (3:1 block).
The PR interval remains normal.
risk of asystole with Mobitz type 2

322
Q

How does a 2nd degree Mobitz type 2 block present on an ECG?

A

occasional loss of AV conduction for 1 beat preceded and followed by fixed
unchanging PR intervals
2:1 block = two P waves for each QRS complex

323
Q

What is a 3rd degree (complete) heart block?

A

also called complete heart block.
There is no observable relationship between the P waves and QRS complexes.
There is a significant risk of asystole

324
Q

What’s a bundle branch block?

A

electrical signal gets completely blocked or held up along one of the bundle branches

caused by fibrosis, or scarring

325
Q

How do bundle branch blocks appear on an ecg?

A

LBBB there is a ‘W’ in V1 and a ‘M’ in V6
RBBB there is a ‘M’ in V1 and a ‘W’ in V6

WiLLiaM MaRRoW

326
Q

What happens in a RBBB?

A

The sino-atrial node acts as the initial pacemaker
Depolarisation reaches the atrioventricular node
Depolarisation through the bundle of His occurs only via the left bundle branch. The left branch still depolarises the septum as normal.
The left ventricular wall depolarises as normal.
The right ventricular walls are eventually depolarised by the left bundle branch, this occurs by a slower, less efficient pathway

327
Q

What does a LBBB look like on an ECG?

A

Broad QRS complex: >120 ms (3 small squares)
Dominant S wave in V1
Broad, monophasic R wave in lateral leads: I, aVL, V5-V6
Absence of Q waves in lateral leads
Prolonged R wave >60ms in leads V5-V6

WiLLiaM

328
Q

What does a RBBB look like on an ECG?

A

Broad QRS complex: >120 ms (3 small squares)
RSR’ pattern in V1-V3: small upward deflection (R wave), a larger downward deflection (S wave), then another large upward deflection (a second R wave, which is indicated as R’)
Wide, slurred S wave in lateral leads: I, aVL, V5-V6

MaRRoW

329
Q

What happens in a LBBB?

A

Depolarisation down the bundle of His occurs only via the right bundle branch. The septum is abnormally depolarised from right to left.
The right ventricular wall is depolarised as normal.
The left ventricular walls are eventually depolarised by the right bundle branch, this occurs by a slower, less efficient pathway

330
Q

What can cause a LBBB?

A

conduction system degeneration or myocardial pathologies such as ischaemic heart disease, cardiomyopathy and valvular heart disease.

LBBB may also occur after cardiac procedures

ALWAYS PATHOLOGICAL

331
Q

What should you consider in an ecg with broad complexes?

332
Q

What is infective endocarditis?

A

infection of the endothelium (the inner surface) of the heart.
Most commonly, it affects the heart valves.
acute, subacute or chronic

333
Q

What are the risk factors for infective endocarditis?

A

Hx of infectious endocarditis
IV drug use
Structural heart pathology: valvular or congenital, hypertrophic cardiomyopathy, implantable cardiac devices
CKD (particularly on dialysis)
Immunocompromised

334
Q

What causes infective endocarditis?

A
  • Staphylococcus aureus.
  • Streptococcus (notably the viridans group of streptococci): biggest cause of native IE
  • Enterococcus (e.g., Enterococcus faecalis)
335
Q

What are the symptoms of infective endocarditis?

A

Fever
Fatigue
Night sweats
Muscle aches
Anorexia
SOB

336
Q

What are the signs of infective endocarditis?

A

New or “changing” heart murmur
Splinter haemorrhages (thin red-brown lines along the fingernails)
Petechiae
Janeway lesions
Osler’s nodes
Roth spots

337
Q

What is the Duke Criteria for diagnosing endocarditis?

A

Major:
- persistently positive blood cultures
- Single positive blood culture for Coxiella burnetii or phase I IgG antibody titre >1:800
- Evidence of endocardial involvement (abscess, vegetation, valvular)
Minor:
- Predisposition
- Fever above 38°C
- Vascular phenomena
- Immunological phenomena
- Microbiological phenomena

2 major or 1 major and 3 minor or 5 minor

338
Q

What investigations should be done for infective endocarditis?

A

3 sets of blood cultures from different venepuncture sites taken at 30-minute intervals
Echocardiography
FBC and CRP

339
Q

What’s the management for infective endocarditis?

A

IV broad-spectrum Abx
Abx for staph: beta-lactams: flucloxacillin
Abx for strep: benzylpenicillin or amoxicillin + gentamicin
Surgery: to remove infected tissue completely and repair/replace the affected valves

340
Q

What are some of the complications of infective endocarditis?

A

acute HF
systemic embolization (including stroke)
AKI
anterior mitral valve vegetation
splenic abscess
mycotic aneurysms

341
Q

What is cardiomyopathy?

A

disorders of the heart muscle

342
Q

What is hypertrophic cardiomyopathy?

A

development of a hypertrophied, non-dilated left ventricle in the absence of another predisposing condition

characteristically age-related

343
Q

What are common features of hypertrophic cardiomyopathy?

A

atrial arrthymias
diastolic dysfunction
higher risk of thromboembolism

344
Q

What investigations are done for cardiomyopathy?

A

ECG and Echo

345
Q

What tends to cause hypertrophic CM?

A

autosomal dominant defect in the genes for sarcomere proteins

346
Q

How can patients with hypertrophic CM present?

A

SOB
Fatigue
Dizziness
Syncope
Chest pain
Palpitations

mostly asymptomatic

347
Q

What might be found on examination for hypertrophic CM?

A

Ejection systolic murmur at the lower left sternal border
Fourth heart sound
Thrill at the lower left sternal border

348
Q

What is dilated cardiomyopathy?

A

presence of left ventricular dilatation and systolic dysfunction in the absence of abnormal loading conditions or significant coronary artery disease

RV dilation often present too

genetic cause

349
Q

What is restrictive cardiomyopathy?

A

presence of a restrictive ventricular filling pattern

heart becomes rigid and stiff, causing impaired V filling in diastole

350
Q

How is hypertrophic cardiomyopathy treated?

A

Beta-blockers
CCBs
avoid strenous exercise (risk of sudden cardiac death)

351
Q

What are some complications of hypertrophic cardiomyopathy?

A

Sudden cardiac death
Arrhythmias: supraventricular (especially atrial fibrillation) and ventricular in origin
Heart failure
Infective endocarditis

352
Q

What is rheumatic fever?

A

autoimmune condition triggered by streptococcus bacteria
a multi-system disorder that affects the joints, heart, skin and nervous system

353
Q

Why is rheumatic fever rare in the UK?

A

early treatment of streptococcus with Abx

354
Q

What are the main manifestations of rheumatic fever?

A

carditis
arthritis
chorea
erythema marginatum
subcutaneous nodules

355
Q

What causes rheumatic fever?

A

group A beta-haemolytic streptococcal, typically strep pyogenes causing tonsillitis
antibodies created that also match and attack body cells, e.g. myocardium

356
Q

What type of hypersensitivity reaction is rheumatic fever?

357
Q

What investigations are done for rheumatic fever?

A

Throat swab for bacterial culture
ASO antibody titres
Echocardiogram, ECG and chest xray

358
Q

What criteria is used to diagnose rheumatic fever?

359
Q

What are the symptoms (not signs) of rheumatic fever?

A

Fever
Joint pain
Recent sore throat
Rash

360
Q

How is rheumatic fever treated?

A

single injection of benzathine benzylpenicillin
NSAIDs
Aspirin and steroids are used to treat carditis

361
Q

What are the complications of rheumatic fever?

A

Recurrence of rheumatic fever
Valvular heart disease, most notably mitral stenosis
Chronic heart failure

362
Q

What are L to R shunts?

A
  • Lesions that allow blood to shunt from the left side to the right side of the heart
  • Increased pulmonary blood flow and are typically acyanotic
  • Cyanosis occurs only if the lesions are large and not repaired in childhood
363
Q

What are some examples of L-R shunts?

A

atrial septal defect
patent ductus arteriosus

364
Q

What is the recommended imaging and primary intervention for left to right shunts?

A

Echocardiography
cardiac catheterisation primary intervention

365
Q

What are R to L shunts?

A

Lesions that result in de-oxygenated blood reaching the aorta
associated with an increased or decreased pulmonary blood flow

366
Q

What is tetralogy of fallot?

A

a congenital condition where there are four coexisting pathologies:
- Ventricular septal defect (VSD)
- Overriding aorta
- Pulmonary valve stenosis
- Right ventricular hypertrophy

right to left shunt

367
Q

What are the symptoms of TOF?

A
  • Cyanosis (blue discolouration of the skin due to low oxygen saturations)
  • Clubbing
  • Poor feeding
  • Poor weight gain
  • Ejection systolic murmur heard loudest in the pulmonary area
  • “Tet spells” (cyanotic episodes due to shunt worsening)
368
Q

What is ventricular septal defect?

A
  • 20% of congenital heart diseases
  • a congenital hole in the septum between the two ventricles, can be big enough to form one ventricle
369
Q

What can happen in a left to right shunt?

A

A left to right shunt leads to right sided overload, right heart failure and increased flow into the pulmonary vessels.

370
Q

What can cause a pan-systolic murmur?

A

ventricular septal defect
mitral regurgitation
tricuspid regurgitation

371
Q

What is coarctation of the aorta?

A

a congenital condition where there is narrowing of the aortic arch, usually around the ductus arteriosus

weak femoral pulses in neonates

372
Q

What is seen on an ECG for cardiac tamponade?

A

low QRS voltage
electrical alternans

373
Q

What can cause cor pulmonale?

A

COPD (the most common cause)
Pulmonary embolism
Interstitial lung disease
Cystic fibrosis
Primary pulmonary hypertension

Phase 2a (14 decks)

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