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Phase 2A Tom > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Define atherosclerosis

A

Inflammatory process characterised by hardened atherosclerotic plaques in the intima of a vessel wall.

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2
Q

name 4 main constituents of an atheromatous plaque

A
  • Lipids
  • Cholesterol
  • Lymphocytes
  • Fibrous tissue
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3
Q

What is the primary cause of atherosclerosis?

A

Endothelial cell damage.

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4
Q

Outline the progression of athersclorosis.

A
  1. High levels of cholesterol damages endothelium.
  2. LDLs and inflammatory cells like monocytes and macrophages and T-cells begin to accumulate in arterial wall
  3. Macrophages try to break down, LDLs, turning into foam cells, which produce a LIPID CORE/FATTY STREAK
  4. This inflammatory reaction leads to tissue repair, so the smooth muscle proliferates forming a fibrous cap that encloses the lipid core.
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5
Q

does Tom have stinky feet?

A

yes

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6
Q

What are some risk factors for atherosclerosis?

A

age, gender, genetics, smoking, high blood pressure, high cholesterol, diabetes, and obesity.

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7
Q

Atherosclerosis - when the endothelium is damaged, what happens that leads to inflammation?

A

the accumulation of LDL-cholesterol in the artery wall, which leads to the activation of inflammatory cells

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8
Q

Atherosclerosis - Once the endothelium wall is inflamed, what will begin to accumulate? What does this lead to?

A

As the endothelial cells become damaged, they begin to accumulate fats, such as cholesterol, triglycerides, and phospholipids. These fats oxidize and cause the formation of fatty plaques in the artery wall.

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9
Q

What medications can help treat Atherosclerosis?

A

statins - Lower Cholesterol
blood pressure-lowering medications
Aspirin
Anticoagulants

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10
Q

How does Aspirin help reduce cardiovascular disease? What type of drug is it?

A

It is a NSAID, can be over the counter, in cardiology, can act As an antiplatelet
It irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation.

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11
Q

What type of Drugs are
a) Clopidogrel and
b) GPIIba antagonists? What is their effect on the CV system?

A

a) P2Y12 receptor blockers - Drugs like Clopidogrel block the P2Y12 receptor to Reduce platelet activation

b) These block glycoprotein IIb/IIIa receptors on their platelet’s plasma membrane and inhibiting fibrinogen binding - also reduce platelet activation.

*BOTH ANTIPLATELET

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12
Q

What do anticoagulants do? Give some examples

A

Anticoagulants work by preventing the formation of blood clots. They do this by *Inhibiting thrombin in the body that are involved in the clotting process

Eg Warfarin, Heparin

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13
Q

What is acute coronary syndrome (ACS)?

A

An umbrella term for a spectrum of disease caused by ischaemia

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14
Q

What are the 3 different diseases that fall under the term ACS?

A

STEMI- ST elevated myocardial infarction
NSTEMI- A non-ST elevated myocardial infarction can be shown by biochemical markers
Unstable angina- all the symptoms of ACS without biochemical or ECG markers

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15
Q

Describe the epidemiology of ACS

A
  • Coronary heart disease is the leading cause of death in the UK
  • 50% of deaths occur within the first 2 hours of symptom onset
  • 15% of MI’s are fatal
  • 300,000 cases per year
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16
Q

What are some risk factors for developing ACS?

A

Modifiable
- Age (strongest)
- Gender (male)
- Family history ]
Lifestyle
- Hypertension
- Diabetes
- Hyperlipidaemia
- Obesity
- Lack of exercise
- Smoking (damages endothelium)
- Alcohol

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17
Q

Describe how an atherosclerotic plaque forms

A
  1. Starts with damage to the endothelial cells of vessels, this can be by lipids, high BP. Changes in flow can cause. Aortic arch susceptible turbulent flow
  2. This results in accumulation of macrophages at tissue which when combined with lipids form foam cells
  3. This forms foam cells which secrete cytokines and result in immune activation and platelet aggregation
  4. This forms a fatty streak
  5. Over time this fatty streak will become a fibrous plaque as tissue and smooth muscle grows over it. This will narrow the lumen of the blood vessels
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18
Q

What two things usually occur that result in the symptoms of ACS?

A
  • The fibrous cap of the plaque itself gets a superficial injury, and a thrombus forms on it

-In more advanced, unstable plaques, the fibrous cap completely ruptures, and not only can some of the contents escape, but blood can also enter the plaques, forming a thrombus within the remaining cap of the plaque.

This can result in lack of blood flow (ischaemia) which will in turn lead to infarction of the cardiac muscle if it occurs in the coronary arteries

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19
Q

What do platelets secrete which can further worsen an MI?

A

Serotonin and thromboxane A2 and this causes vasoconstriction in the area resulting in reduced blood flow to the myocardium, and ischaemic injury.

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20
Q

What are the key presentations of ACS?

A
  • Chest pain (lasting longer than 20 mins) that can radiate to back, shoulder and arms
  • Dyspnoea (shortness of breath)
  • Pallor
  • Diaphoresis (sweating)
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21
Q

What percentage of patients have silent MI’s (without chest pain)

A

30%

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22
Q

In which groups of people are silent MI’s most common?

A
  • Women
  • Elderly
  • Diabetic patients
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23
Q

What are some signs of ACS?

A

Increase pulse rate, S4 heart sound - due to impaired left ventricle, hypotension, signs of heart failure e.g., oedema

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24
Q

What other symptoms can be experienced during ACS?

A

Nausea/vomiting, palpitations, dizziness

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25
Q

What would a STEMI look like on an ECG in the first few hours after symptoms present?

A
  • ST elevation
  • Tall t-waves
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26
Q

What would a STEMI look like on an ECG a few days after symptoms started?

A
  • Inversion of T-waves and presence of pathological q waves
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27
Q

What would a NSTEMI look like on an ECG?

A

○ ST depression; this indicates a worse prognosis
○ Transient ST elevation
○ T-wave changes.

  • Be aware that the ECG may be normal in more than 30% of patients.
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28
Q

How would you diagnose an NSTEMI with a normal ECG?

A

Perform a blood test. Troponin above the 99th percentile. Recommended to do 2 tests 2 hours apart and measure the difference

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29
Q

How would you diagnose unstable angina?

A

Symptoms of ACS without abnormal blood tests or ECG

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30
Q

What leads of an ECG represent the septal view of the heart?

A

V1 and V2

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31
Q

What leads of an ECG represent the anterior view of the heart?

A

V3
V4

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32
Q

What leads represent the lateral view of the heart?

A

V5
V6
Lead I
aVR
aVL

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33
Q

What leads represent the inferior view of the heart?

A

Lead II
Lead III
aVF

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34
Q

What are some differential diagnosis for ACS?

A

Aortic dissection
PE
Pneumothorax
Pneumonia
Pericarditis
Myocarditis
GORD

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35
Q

How would you manage ACS Pre-hospital?

A

Give oral aspirin and give opioid pain relief (as this will reduce sympathetic activation and lower blood pressure)

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36
Q

What would be first-line treatment for a patient with a STEMI?

A
  • Angioplasty would be first-line treatment, the best results are achieved within the first 120 minuets of symptom onset
  • Angioplasty involves either a balloon or coronary artery stenting (stenting associated with better outcomes)
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37
Q

How would you treat a STEMI if angioplasty was not an option?

A

If not available for STEMI use thrombolysis(Streptokinase, recteplacse or Tenecteplase) the sooner the better don’t give greater than 90 mins after the pain.

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38
Q

How would you treat a NSTEMI?

A

NSTEMI- refer to cardiology and angioplasty still often a good option (pci)

DON’T GIVE THROMBOLYSIS

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39
Q

What are some differntial for ACS?

A

Aortic dissection
PE
Pneumothorax
Pneumonia
Pericarditis
Myocarditis
GORD
Renal failure

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40
Q

What drugs would you use to manage ACS?

A

Drugs for long term management of ACS (Secondary Prevention)
- C – Clopidogrel – antiplatelets
- O – Omacar – Omega 3
- B – Bisoprolol – β-blocker
- R – Ramipril – ACE use before beta blocker in under 55’s
- A – Aspirin
- A – Atorvastatin – very potent statin!

MONA - morphine, oxygen, NO, aspirin

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41
Q

What are some lifestyle managements for ACS?

A

Increase in exercise – encourage regular daily exercise, and at least 30 minutes, 3x/week strenuous exercise
* Sex – Should avoid for 1 month after MI
* Travel – avoid air travel for 2 months
Reduction in weight
Reduction in alcohol intake
Dietary modification (reduced fat intake) – diet should be:
* High in – oily fish, fibre, fresh fruit and veg
* Low in – saturated fat

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42
Q

What is pericarditis?

A

Inflammation of the pericardium. The acute form is defined as new onset that lasts from 4-6 weeks

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43
Q

Describe the epidemiology of pericarditis

A
  • Most common in young adults 20-50
  • More common in men than women
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44
Q

What is most common cause of pericarditis in developing countries?

A

TB

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45
Q

Name some causes of pericarditis?

A
  • Can be viral due to coxsackie B virus, Flu. adenovirus and echovirus V
  • Can be due to an autoimmune disorder e.g., rheumatoid arthritis, IBS
  • Can be Dressler’s syndrome
  • Can occur after an MI
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46
Q

What is Dressler’s syndrome?

A

Delayed pericarditis as a result of a previous MI. Usually occurs between 1-4 weeks after. But can occur years later

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47
Q

How does pericarditis cause disease?

A
  • Signs and symptoms as a result of inflamed pericardium. As it is highly innervated this is what results in the pain
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48
Q

How does pericarditis cause effusion?

A

When the pericardium is inflamed the chemical mediators result in an increased permeability of fluid thus resulting in effusion from the visceral pericardium

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49
Q

What are the key presentations of pericarditis?

A
  • Chest pain that can spread to shoulders and neck often worse when lying down symptoms can relieve when sitting up
  • Fever
  • Pericardial friction rub (high pitched superficial scratching heard during systole)

Pain is also aggregated by breathing

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50
Q

What would an ECG show of someone with pericarditis?

A
  • Saddle shaped ST elevation with PR depression
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51
Q

What tests other than an ECG would you perform on a patient with suspected pericarditis?

A

Serum troponin levels. Elevated in 50% of people. Correlates to extent of ECG change

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52
Q

How would you treat someone with suspected viral or idiopathic pericarditis?

A

NSAID, PPI and colchicine for 3 months

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53
Q

What is the benefit of giving colchicine?

A

Prevents the recurrence of pericarditis

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54
Q

What is cardiac tamponade?

A

Where fluid accumulates in the pericardial sac which puts pressure on the ventricles making it hard for them to expand and fill with blood

Can be fatal leading to a cardiac arrest

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55
Q

What can cause cardiac tamponade

A
  • Traumatic injury
  • Pericarditis
  • Cancer
  • Iatrogenic can occur after surgery
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56
Q

What are some symptoms of cardiac tamponade

A
  • Tachycardia
  • Shortness of breath
  • Chest pain
  • Pulsus paradoxes (systolic BP drops when breathing in)
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57
Q

What is Beck’s triad which is indicative of cardiac tamponade?

A

Hypotension
Muffled heart sounds
Raised JVP (jugular venous pressure)

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58
Q

What investigations would you perform for cardiac tamponade?

A

ECG, CXR, Echocardiogram

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59
Q

How would you treat cardiac tamponade?

A

Pericardiocentesis- can be performed in the emergency setting, this is using a long canula attached to a needle
Surgery- could make a pericardial window or pericardiectomy
Conservative- in a clinical setting closely monitored

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60
Q

What can acute pericarditis lead to?

A

Can become chronic pericarditis which over time will lead to constrictive pericarditis. This can lead to right sided heart failure

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61
Q

What is Infective endocarditis (IE)?

A

An infection involving the endocardial surface of the heart including the valves, chordae tendineae and sites of septal defects

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62
Q

Describe the epidemiology of IE

A

4-7 cases per 100,000 in general pop
15 cases per 100,000 in over 55s

50% occur in native valves, 50% in replacement ones. Becoming more common

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63
Q

What is the most common cause of IE in non-IV drug users?

A

Viridians Streptococci can be a result of poor oral hygiene

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64
Q

What is the most common cause of IE in IV drug users?

A

S.Aureus

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65
Q

What are the risk factors for developing IE?

A

Artificial heart valves, certain types of congenital heart disease, post heart transplant.
IV drug use

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66
Q

Describe the pathophysiology of IE?

A
  • It typically develops on the valvular surface of the heart which have sustained damage secondary to turbulent flow.
  • As a result, platelets and fibrin adhere to underlying collagen. Bacteraemia (bacteria in the blood stream) leads to colonisation of the thrombus which leads to further aggregation and a more mature vegetation
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67
Q

What are the key presentations of IE?

A
  • Fever
  • New heart murmur
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68
Q

What are some signs of IE?

A
  • Clubbing
  • Splinter haemorrhage
  • Janeway lesions
  • Splenomegaly
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69
Q

What are some symptoms of IE?

A
  • Night sweats
  • Shortness of breath
  • Headaches
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70
Q

What would the first line test for IE be?

A

Echocardiogram to work out diagnosis and shows complications

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71
Q

What is the gold-standard test for IE?

A

Blood culture for infective organisms need to take 3 samples within 24 hours

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72
Q

What other tests would you perform for IE?

A

ECG, full blood count may show anaemia

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73
Q

How would you manage an acute presentation of IE?

A

flucloxacillin, gentamycin

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74
Q

How would you treat a subacute presentation of IE?

A

benzylpenicillin, gentamycin

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75
Q

How else would you treat IE other than with medications?

A

Surgery between 25-50% of people will be treated surgically . This will involve valve replacement

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76
Q

What are some complications associated with IE?

A

Acute heart failure, AKI, valve vegetation/rupture/fistula
Splenic abscess

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77
Q

What is the prognosis for untreated IE?

A

Close to 100% mortality

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78
Q

What is the prognosis of treated IE?

A

30-40% mortality

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79
Q

What is mitral regurgitation (MR)?

A

Failure of the mitral valve (between the left atria and ventricle) to close.

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80
Q

What % of the population have MR?

A

2%

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81
Q

What are the two types of MR?

A

Primary- which is a valve disorder
Secondary-which is due to left ventricular dysfunction

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82
Q

What are some of the main causes of acute MR?

A

Infective endocarditis
Acute rheumatic fever
Ischaemic muscle dysfunction

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83
Q

What are some causes of chronic MR?

A

Degeneration of the mitral leaflets or chordae tendineae, mitral valve prolapse, and mitral annular enlargement

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84
Q

What connective tissue disorders can cause MR?

A

Marfan syndrome
Ehlers-Danlos syndrome

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85
Q

Describe the pathophysiology of MR?

A
  • Blood will not be efficiently pumped out of the heart due to backflow of blood
  • As a result the heart has to pump harder to produce the same stroke volume this will occur for 7-10 years and be asymptomatic
  • Eventually the LV will become hypertrophied and it will lead to LV dysfunction
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86
Q

What are the key presentations of MR?

A
  • Dyspnoea
  • Pansystolic murmur that radiates to the axilla
  • Hyperdynamic apex beat (misplaced)
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87
Q

What are some other signs of MR?

A
  • Pulmonary hypertension
  • AF
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88
Q

What are some symptoms of MR?

A
  • Any signs of heart failure e.g., pulmonary oedema
  • Fatigue
  • Palpitations
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89
Q

What tests would you perform on a patient with suspected MR?

A

ECG- p mitrale bifid (two peaks) due to hypertrophy
Trans-oesophageal echocardiogram- used to asses the level of valve damage

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90
Q

How would you treat MR?

A

Conservative- lifestyle advice

Medical- control the signs and symptoms e.g., diuretics, treat the AF

Surgical- patients may require surgery either prosthetic or metal (longer term but requires anticoagulants)

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91
Q

What are some complications associated with MR?

A

AF
Pulmonary hypertension
Stroke post op
Left ventricular dysfunction/heart failure

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92
Q

What is mitral stenosis?

A

Mitral stenosis is a narrowing of the mitral valve orifice, usually caused by rheumatic valvulitis producing fusion of the valve commissures and thickening of the valve leaflets.

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93
Q

Where is mitral stenosis more common?

A

Oceania, south Asia and sub-Saharan Africa as rheumatic fever is more common

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94
Q

What is the main cause of mitral stenosis?

A

Rheumatic fever (strep A infection usually)

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95
Q

What are some other causes of mitral stenosis?

A

Can also be caused by congenital deformity of the valve, carcinoid syndrome, amyloidosis and calcification

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96
Q

Describe how rheumatic fever can lead to mitral stenosis =?

A

There is a sharing of antigens between strep A and ones found on the heart.
This leads to an immune response causing the wall of the valve to thicken
This first leads to regurgitation which develops into stenosis

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97
Q

Describe how mitral stenosis causes disease?

A

The orifice is usually 4-6cm in diameter.

The disease begins when it is less than 2cm in diameter as this happens flow becomes progressively impeded and pressure in left atria remains higher than in left ventricle as blood is unable to move between them

This leads to pressure being referred to the lungs and due to small end diastolic volume in the ventricle cardiac output is reduced

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98
Q

What are the key presentations of mitral stenosis?

A

Pulmonary hypertension
Dyspnoea especially when lying down
Haemoptysis
Chronic bronchitis like picture, and can cause hoarseness

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99
Q

What are some signs of mitral stenosis?

A
  • Malar (blushing of cheeks)
  • AF
  • Mid diastolic murmur best heard on expiration
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100
Q

What is the gold standard test for diagnosing mitral stenosis?

A

Transthoracic echocardiogram

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101
Q

How would you treat mitral stenosis?

A
  • Diuretics
  • Balloon valvotomy
  • Maybe warfarin
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102
Q

What are some complications of mitral stenosis?

A

AF
Stroke
Infective endocarditis

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103
Q

Define aortic regurgitation (AR)

A

 Aortic regurgitation (AR) is the diastolic leakage of blood from the aorta into the left ventricle. It occurs due to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root.

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104
Q

what is the epidemiology of AR?

A

Not as common as aortic stenosis or mitral regurgitation. Prevalence greater with men and increases with age

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105
Q

What is the aetiology of AR?

A

Can be caused by primary disease of the aortic valve leaflets or dilation of the aortic root.

In developing countries rheumatic fever is the most common cause.

In developed countries congenital bicuspid aortic valve(when two leaflets fuse together) or aortic root dilation is the most common.

Causes of aortic root dilation include Marfan’s syndrome, related connective tissue diseases, and aortitis secondary to syphilis, Bechet’s, Takayasu’s, reactive arthritis,

Endocarditis can also cause rupture of leaflets. Also aortic root dissection can cause acute AR

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106
Q

What is the pathophysiology of AR?

A

Acute AR is a medical emergency with high mortality which results in acute rise in left atrial pressure, pulmonary oedema and cardiogenic shock.

Due to back flow of blood from the aorta left ventricular volume increases. This causes systolic hypertension and LV hypertrophy and chamber enlargement. This will remain asymptomatic for decades will eventually result in symptomatic congestive heart failure.

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107
Q

Key presentations of AR?

A

Presence of risk factors, with a diastolic murmur (best heard when expiring)

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108
Q

signs of AR?

A

Collapsing water hammer pulse (rapid rise and a quick collapse)

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109
Q

symptoms of AR?

A

Dyspnoea, fatigue, weakness, orthopneic, pallor, tachypnoea

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110
Q

1st line investigation for AR?

A

Echocardiogram

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111
Q

Gold standard investigation for AR?

A

colour flow doppler

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112
Q

Other investigations for AR?

A

ECG, chest x-ray

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113
Q

Management for AR?

A

Acute AR - inotropes + vasodilators + urgent aortic valve replacement/repair

Chronic AR - Aortic valve surgery

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114
Q

Monitoring of AR?

A

patients need to be serially monitored based on the severity of AR, left ventricular ejection fraction (LVEF), and left ventricular (LV) diameters.

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115
Q

complications of AR?

A

Heart failure
Arrythmias
IE
Sudden death
Ischaemia

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116
Q

prognosis of AR?

A

Normal LV function reported as 96% whereas that in patients with reduced LV function is 62%

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117
Q

what?

A

here have a freebie on me

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118
Q

define aortic stenosis (AS)

A

AS represents obstruction of blood flow across the aortic valve due to pathological narrowing. It is a progressive disease that presents after a decades-long subclinical period.

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119
Q

What is the epidemiology of AS ???

A

Largely a disease for older people preceded by aortic valve sclerosis (thickening without flow limitation)

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120
Q

what is the aetiology of AS?

A

Calcification and fibrosis of the normal trileaflet valves is the most common cause of AS and accounts for 80% of cases in UK. Smoking, hypertension, LDL and elevated c-reactive protein

Bicuspid valves account for most other cases.

Rheumatic heart disease is common in developing countries

bonus point if you even know what aetiology means

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121
Q

Risk factors for AS?

A

(tom you didnt have anything for this so I googled it)
high blood pressure
abnormal lipids
diabetes
CKD
Genetic predisposition

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122
Q

Pathophysiology of AS?

A

Aortic calcification is no longer thought to reflect age-related wear and tear, and is recognised to be an active process.

valvular endocardium is damaged –> inflammation a bit like atherosclerosis –> calcification and fibrosis happens and valvular leaflets mobility is reduced –> stenosis

Over time this puts pressure on the LV –> LV hypertrophy –> systolic heart failure

(toms notes a lot more detail than this ask him if youre confused)

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123
Q

key presentations for AS?

A

Angina

Exertional Syncope

Dyspnoea

Ejection systolic murmur

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124
Q

what are some signs for the condition known to us as aortic stenosis but known to french people as sténose aortique?

A

Ejection systolic murmur best heart in aortic arch (right second intercostal space)

Slow rising pulse, with narrow pulse pressure (difference between systolic and diastolic) this is a sign of severe

Signs of heart failure, lung bases, pink frothy septum and oedema

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125
Q

symptoms for AS?

A

Signs of valve defect fatigue and dyspnoea

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126
Q

First line investigation for AS?

A

ECG-

L- LBBB due to calcification
L- left axis deviation
L- LVH
P- poor R wave progression

MED SCHOOL exam paper says echocardiogram ///

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127
Q

Le standard d’or (gold) investigation for AS?

A

Doppler echo-This can assess the actual gradient across the valve as well as check for co-existing CAD

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128
Q

differential diagnosis for AS (found on google tom didnt have notes)

A

Hypertrophic obstructive cardiomyopathy.
Restrictive cardiomyopathy.
Constrictive cardiomyopathy.
Congestive heart failure with reduced ejection fraction

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129
Q

complications of AS?

A

If untreated

Angina present- 2 years

Syncope present- 1 year

Dyspnoea present- 6 months

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130
Q

What is the definition of hypertension?

A

A blood pressure above 140/90

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131
Q

What % of the population suffer from hypertension?

A

30-40%

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132
Q

What groups of people are most at risk of hypertension?

A

Black Africans and men

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133
Q

What are the main causes of essential hypertension (type 1)

A
  • Idiopathic there is no one underlying cause
  • Thought to be 40-60% genetically linked
  • Other causes include environmental factors
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134
Q

management of AS?

A

Surgical aortic valve replacement

PLUS – long-term infective endocarditis antibiotic prophylaxis

CONSIDER – long-term anticoagulation if metal

CONSIDER – medical therapy

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135
Q

Name some environmental factors that can lead to hypertension?

A
  • Obesity
  • Sleep apnoea
  • Alcohol intake
  • Sodium intake
  • Stress
  • Insulin intake
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136
Q

What are some causes of secondary hypertension?

A
  • All renal disease
  • Endocrine diseases e.g., Cushing’s, Conn’s acromegaly
  • Congenital disease
  • Neurological diseases e.g., brainstem lesions and raised intercranial pressure
  • Pregnancy- pre-eclampsia
  • Drugs - Oral contraceptives
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137
Q

What is benign and what is malignant hypertension?

A

Benign- is the stable elevation of BP over many years (is still dangerous)
Malignant- is the acute and severe elevation of BP. If undiagnosed then it can lead to death within 2 years

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138
Q

What is classified as mild hypertension?

A

> 140 systolic or >90 diastolic

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139
Q

What is classified as moderate hypertension?

A

> 160 systolic or >100 diastolic

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140
Q

What is classified as severe hypertension?

A

> 180 systolic or >110 diastolic

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141
Q

What are the key presentations of hypertension?

A

Blood pressure above 140/90 and retinopathy

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142
Q

What are some key presentations secondary hypertension?

A
  • Papilledema, flame shaped haemorrhage and cotton wool spots on eyes
  • Also cardiac and renal symptoms e.g., chest pain
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143
Q

What are some other symptoms of hypertension?

A
  • Headache
  • Visual changes
  • Chest pain
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144
Q

How would you diagnose hypertension?

A

Clinical BP of 140/90 and ABPM or HBPM of above 135/90

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145
Q

What other tests might you perform on patients diagnosed with hypertension?

A
  • Bloods- HbA1c look for diabetes, creatinine and urea to asses renal function
  • ECG/echo to look for ventricular hypertrophy
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146
Q

At what BP would you start a patient immediately on mediations rather than advising lifestyle changes

A

160/100 in clinic/ 155/95 in home monitor readings

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147
Q

What would the first-line treatment be for a 50 year old white man diagnosed with hypertension?

A

ACE inhibitor (Ramipril and enalapril)

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148
Q

What would the first-line treatment be for a 50 year old black man diagnosed with hypertension?

A

Calcium channel blocker (amlodipine) or thiazide diuretic if not CCB not tolerated

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149
Q

What are the 3 types of medication usually used to treat hypertension?

A

ACE inhibitor (first line in under 55)
Calcium channel blocker (first-line in over 55)
Thiazide diuretic (first line in over 55 if CCB not tolerated)

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150
Q

What is the target BP of a patient with diabetes who has been diagnosed with hypertension?

A

Under 130/90

151
Q

What is the target BP for the general population diagnosed with hypertension?

A

Under 140/90

152
Q

What is the target BP of a patient who is over 80 and has been diagnosed with hypertension?

A

Under 150/90

153
Q

What are the 3 types of medication usually used to treat hypertension?

A

ACE inhibitor (first line in under 55)
Calcium channel blocker (first-line in over 55)
Thiazide diuretic (first line in over 55 if CCB not tolerated)

154
Q

What are some complications associated with hypertension?

A

Cardiovascular- Atherosclerosis, aortic aneurysm , cardiac failure, AF, stroke
Renal- renal failure
Eye effects- visual disturbances
Systemic hypertensive heart disease- changes that were initially adaptive to cope with the hypertension, lead to cardiac dilatation, congestive heart failure, and even sudden death

155
Q

Explain how hypertension can cause heart failure

A

The left ventricular wall hypertrophies (to increase the cardiac output in the face of increased peripheral resistance (afterload)

Initially, there is no reduction in left ventricular volume. Histologically there is enlargement of myocytes and their nuclei (hypertrophy).

However, in the long term, the myocytes will atrophy, and the ventricle will dilate, and have a reduction in muscle volume, causing the complications of left ventricular dilatation and congestive heart failure

156
Q

What is systolic heart failure?

A

It is the inability of the heart to contract efficiently and eject adequate volumes of blood to meet it’s metabolic demands. Ejection volume will be less than 40%

157
Q

What can cause systolic heart failure?

A

IHD, MI, Hypertension, Cardiomyopathies

158
Q

What is diastolic heart failure?

A

Reduction in the hearts compliance resulting in compromised ventricular filing. Therefore there is reduced ejection. Ejection fraction is normally greater than 50%

159
Q

What can cause diastolic heart failure?

A

Cardiac tamponade, Constrictive pericarditis, Hypertension

160
Q

What is left heart failure?

A

The inability of the left ventricle to pump adequate amount of blood leading to pulmonary circulation congestions and pulmonary oedema

It also usually results in RHF and will have a ejection fraction of less than 40%

161
Q

What is right heart failure?

A

inability of the right ventricle to pump adequate amounts of blood leading to systolic venous congestion and peripheral oedema and hepatic congestion and tenderness.

Most common causes are LHF and respiratory disease such as COPD

162
Q

What is congestive heart failure?

A

Failure of both the right and left ventricles

163
Q

What is low output heart failure?

A

Is heart failure that results in reduced cardiac output

164
Q

What is high output heart failure?

A

Heart failure when cardiac out remains normal but there is metabolic demand mismatch.
Occurs due to reduced oxygen carrying capacity (anaemia) or increased metabolic demand (hyperthyroidism)

Can also be referred to as preserved ejection fraction heart failure

165
Q

What is acute heart failure?

A

Acute onset of symptom presentation.

Not always due to an acute event but often due to MI, persistent arrhythmia or mechanical event, ruptured valve or ventricular aneurysm.

166
Q

What is chronic heart failure?

A

slow symptom presentation usually due to slow progressive underlying disease. CAD and hypertension

167
Q

What is acute-on-chronic heart failure?

A

Acute deterioration of a chronic condition usually following an acute event such as anaemia, infections or arrhythmias

168
Q

Define preload

A

The volume of blood in the ventricles just before contraction

169
Q

Define afterload?

A

The pressure at which the heart has to work to eject blood is systole

170
Q

What is definition of heart failure?

A

Heart failure is a condition in which the heart is unable to generate a cardiac output sufficient to meet the demands of the body without increasing diastolic pressure.

171
Q

What are the main causes of heart failure?

A

IHD
Hypertension
Valvular disease
Pericarditis
Arrhythmias
Cardiomyopathies
Pulmonary hypertension

172
Q

How does IHD cause heart failure?

A

It causes impaired ventricular function and therefore reduced contractility. Causes systolic heart failure

173
Q

How does hypertension cause heart failure?

A

It increases the strain on the heart since the heart has to pump against a high afterload leading to hypertrophy (this can lead to arrhythmias) and eventually the heart will become too big for the coronary arteries to perfuse leading to compromised function of the ventricles.

Will lead to systolic heart failure

174
Q

What is congestive cardiomyopathy and how can it cause heart failure?

A

It is the weakening and dilation of the ventricular walls leading overstretching and reduced contractility

175
Q

What is hypertrophic cardiomyopathy and how can it cause heart failure?

A

it is the thickening of the heart muscle wall. It increases the fibrous tissue of the heart leading to poor conduction and increased chance of arrhythmias.

Will also lead to reduced compliance and overstretching reducing CO

176
Q

What is restrictive cardiomyopathy and how can it cause heart failure?

A

It is reduced heart compliance without significant increases is muscle wall thickness leading to reduced muscle wall thickness. Reduces EDV and CO

Can be caused by sarcoidosis, amyloidosis, hemochromatosis, and endocardial fibrosis

177
Q

Describe how the heart compensates for heart failure?

A

HF causes a drop in MAP that initially stimulates baroreceptors

This decreases vagal tone increases sympathetic tone leading to increase an increase in heart rate and contractility

The sympathetic system also stimulates the contraction of arteries and veins and the release of adrenaline

The renin-angiotensin-system is also stimulated in heart failure due to reduced kidney perfusion.

Therefore, Angiotensin II is secreted ,which causes vasoconstriction, aldosterone release and ADH release causing sodium and water retention by the kidneys. These mechanisms are beneficial initially as they increase blood volume, maintaining a high CO

178
Q

How do the compensatory mechanisms in heart failure exacerbate the problem?

A

-Increase in TPR- increases the afterload and therefore workload of the heart
Increase in HR- means there is a higher workload and increased demand of oxygen for the heart
Fluid retention- Increases the stretching of the heart leading to the dilation of the ventricles therefore reducing contractility.

179
Q

What are the symptoms of LHF?

A

Exertional dyspnoea, fatigue, attacks of shortness of breath and coughing at night

180
Q

What are the symptoms of RHF?

A

Shortness of breath, nausea, anorexia

181
Q

What are the signs of LHF?

A

Cardiomegaly, displaced apex beat, pulmonary oedema (pink frothy sputum), reduced BP, heart murmur, tachycardia

182
Q

What are the signs of RHF?

A

Raised JVP (distension), hepatomegaly, pitting oedema, ascites and weight gain

183
Q

What blood test would you perform on a patient with suspected HF?

A

BNP test. Brain natriuretic peptide

> 2,000 – require urgent referral to cardiology for an echocardiogram (<2 weeks)
400 – 2,000 – require referral to cardiology for an echocardiogram (<6 weeks)
<400 – heart failure is unlikely and consider an alternative diagnosis

184
Q

What other tests might you perform on a patient with suspected HF?

A

ECG
CXR- may show fluid in the lungs or cardiomegaly

185
Q

What is the gold standard test for diagnosing HF?

A

Echocardiogram

186
Q

What are the main causes if LHF?

A

Main causes of Left-side heart failure are IHD, hypertension, cardiomyopathy, and aortic stenosis (in that order)

187
Q

What are the main causes of RHF?

A

LVF, hypertension, pulmonary stenosis, lung disease and shunt

188
Q

What is the management for chronic heart failure?

A

First line management would be a ACE inhibitor (Ramipril, enalapril), then a beta blocker (atenolol, bisoprolol), then a calcium channel blocker (amlodipine) and then a diuretic

ABCD

189
Q

How would you treat acute heart failure?

A

100% oxygen, nitrates, morphine and loop diuretic

190
Q

What is the prognosis for a patient with heart failure?

A

New York Heart Association [NYHA] Classification of Heart Failure. One year mortality in brackets
Grade I –(5%)
No limitation of function
Grade II – (10%)
Slight limitation. Moderate exertion causes symptoms, but no symptoms at rest
Grade III – (20%)
Marked limitation – mild exertion causes symptoms, but no symptoms at rest
Grave IV – (50%)
Severe limitation. Any exertion causes symptoms. May also have symptoms at rest – but not always the case

191
Q

What is a deep vein thrombosis?

A

DVT is the development of a blood clot in a major deep vein in the leg, thigh, pelvis, or abdomen. It may also occur in less common locations such as the arm veins; the portal, mesenteric, ovarian, or retinal veins; or the veins and venous sinuses of the brain

192
Q

What is the incidence of DVT’s?

A

1 in 1000

193
Q

What are the 3 factors that are most likely to cause a DVT?

A

Virchow’s triad
Vessel injury- surgery/ trauma, smoking
Venous stasis- caused by immobility
Activation of clotting system (changes in blood constituents)- Cancers, pregnancy, the pill

194
Q

What are some risk factors for developing DVT’s?

A

Bed ridden/long travelling
major surgery
Active cancer
Pregnancy
Smoking
Age
Medications (the pill)

195
Q

Where do most DVT’s form?

A

Most blood clots that develop in the venous system of the leg begin to from just above and behind valve.
They can also occur at the site of damage to a vessel wall.

196
Q

Where do clots most often form and where are they more dangerous?

A

They usually form in the lower part of the leg as this is where there is the worst venous drainage.
Most dangerous in the upper part of the leg as they are more likely to embolise from there.

197
Q

What are the key presentations of DVT’s?

A

Calf swelling and localised tenderness and swelling.. Can also be fever and pitting oedema. Dilated superficial veins. Positive well’s score makes more probable

198
Q

What is the well’s score?

A

A test to assess the probability that the symptoms presenting are a DVT

199
Q

What is a D-dimer test?

A

D-dimer- Is a breakdown product of fibrin. A negative test result will rule out DVT but a positive one does not mean patient has a DVT

200
Q

What is the gold standard test for DVT’s?

A

Venography. A radio-opaque dye is injected into the foot, and then you can see if it is blocked off as it travels up the leg

201
Q

What are 3 differential diagnosis of DVT’s?

A

Cellulitis
Ruptured baker’s cyst
Calf muscle haematoma

202
Q

How would you treat a DVT?

A

The initial management for a suspected or confirmed DVT or PE is with anticoagulation.

In most patients, apixaban or rivaroxaban. It should be started immediately in patients where DVT or PE is suspected, and there is a delay in getting the scan.

The NICE guidelines (2020) recommend considering catheter-directed thrombolysis in patients with a symptomatic iliofemoral DVT and symptoms lasting less than 14 days. This involves inserting a catheter under x-ray guidance through the venous system to apply thrombolysis directly into the clot.

203
Q

What are the risks associated with a DVT?

A

Pulmonary embolism
If hole in the heart can also cause stroke (very rare)

204
Q

What is the prognosis of a patient with a DVT?

A

0.4% will result in death

205
Q

What is a pulmonary embolism?

A

Pulmonary Embolism is most commonly a complication of venous thromboembolism (VTE) from another source – e.g. a clot in the legs or pelvis (a DVT) that becomes dislodged, flows via the bloodstream through the right side of the heart and gets lodged in the pulmonary circulation.

206
Q

Describe how a PE causes problems?

A

When a clot gets trapped in the pulmonary vasculature then it increases the resistance.
This causes the right ventricle to work harder to overcome this resistance leading to acute heart failure, this will then inhibit LV filling which will result in complete heart failure

207
Q

What are the key presentations of a PE?

A

Dyspnoea, chest pain, signs of DVT, low oxygen levels, no rule out PERC score, positive wells score

208
Q

What are some signs of a PE?

A

Tachypnoea
Tachycardia
Hypotension
Raised JVP
Raised respiratory rate

209
Q

What are some symptoms of PE?

A

Low grade fever
Cough without blood (haemoptysis)

210
Q

What would be first line tests for a PE if you were unsure?

A

D-dimer test- negative test would rule out
ECG- make sure not an MI instead
ABG- will have a respiratory alkalosis

211
Q

What is the gold standard test for diagnosing PE?

A

CPTA- computed tomographic pulmonary angiography

212
Q

How would you treat a PE?

A

If haemodynamically unstable- maintain BP as best as possible (fluids and oxygen) and give thrombolysis using alteplase or streptokinase
If haemodynamically stable- then give a DOAC apixaban or rivaroxaban

213
Q

How would you monitor a PE?

A

Evaluate patients 3 to 6 months after acute PE to assess the persistence (or new onset) and severity of dyspnoea or functional limitation, and to check for possible signs of venous thromboembolism (VTE) recurrence, cancer, or bleeding complications of anticoagulation.

Chronic thromboembolic pulmonary hypertension (CTEPH) should be ruled out in patients with persistent dyspnoea and poor physical performance. Consider transthoracic echocardiogram to assess for (chronic) pulmonary hypertension and consequently, possible CTEPH.

214
Q

What are the complications associated with a PE?

A

Pulmonary infarction
Cardiac arrest
Chronic thromboembolic pulmonary hypertension

215
Q

What is the prognosis of a PE?

A

<5% if no haemodynamic instability
30% if shock present
70% with cardiac arrest (in hospital)

216
Q

What is an atrial flutter?

A

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

217
Q

Is an atrial flutter more common in men or women?

A

Men

218
Q

What can cause an atrial flutter?

A

Results from either structural or conduction abnormalities.

Structural= atrial dilation, incisional scars and fibrosis of the atrium.
Can also occur as a result of taking drugs for atrial fibrillation

219
Q

What are some risk factors for developing an atrial flutter?

A

Age, valvular dysfunction, atrial septal defects, heart failure

220
Q

What are the key presentations of an atrial flutter?

A

Presence of the risk factors and worsening heart failure or pulmonary symptoms. Leads to a atrial HR of 300.

2:1 (most common)= 150 heart rate in ventricles

221
Q

What will an ECG show of a patient with an atrial flutter?

A

Sawtooth P waves with fast heart rate

222
Q

What are symptoms of an atrial flutter?

A

Palpitations and fatigue, racing pulse

223
Q

What tests would you run for an atrial flutter?

A

CXR, thyroid function tests, renal and serum electrolytes

224
Q

What are some differential for atrial flutter

A

AF
Atrial tachycardia

225
Q

How would you manage an atrial flutter?

A

If haemodynamically unstable then cardiovert either electrically or chemically
Use beta-blockers and CCB’s if not. Treat underlying cause

226
Q

What are complications associated with atrial flutter?

A

Acute stroke, myocardial ischaemia, then lots of medication related.

227
Q

What is AF?

A

Atrial fibrillation (AF) is a common tachycardia. It can be caused by many other underlying illness, especially in the acutely unwell patient (such as sepsis, pneumonia, hyperthyroidism or other illness). It may be reversible by treating the underlying cause.
Is also very common idiopathic

228
Q

What are the different types of AF?

A

Paroxysmal: episodes last >30 seconds but <7 days and are self-terminating but recurrent
* Persistent: episodes last less than or more than seven days but require electrical or chemical cardioversion
* Permanent: episodes fail to terminate with cardioversion OR a terminated episode that relapses within 24 hours OR long-standing AF (usually >1 year) in which cardioversion has not been indicated or attempted

229
Q

What is the prevalence of AF?

A

Most common sustained cardiac arrhythmia worldwide.
Prevalence 2-4%

230
Q

What can cause AF?

A

Sepsis
Mitral valve
Ischaemic heart disease
Thyrotoxicosis
Hypertension
COPD
Sleep apnoea

231
Q

What causes AF?

A

Disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node.

232
Q

What are the key presentations of AF?

A

Irregularly irregular pulse
Palpitations
Chest pain
Dyspnoea
Dizziness / syncope (particularly in paroxysmal)
ECG

233
Q

What are some signs of AF?

A

Heart failure, e.g., raised JVP, ankle swelling

234
Q

What would an AF ECG look like?

A

No p wave
Fluttering baseline

235
Q

How would you distungish what type of AF is present?

A

4-hour ECG monitor, a cardiac event recorder or a 7-day Holter monitor. To determine type

236
Q

What are some differentials of AF?

A

Atrial flutter
Wolf-Parkinson white
Atrial tachycardia

237
Q

What are the two principles for managing AF?

A

Two principles for treating AF:
Rate or rhythm control
Anticoagulation to prevent stroke

238
Q

What are some rate control medications for AF?

A

Beta blocker bisoprolol , CCB amlodipine

239
Q

How would you do rhythm control of AF?

A

Rhythm control can be achieved by either electrical or chemical cardioversion
Chemical cardioversion=
Flecainide
Amiodarone

240
Q

What would be the long term treatment for AF?

A

Left atrial ablation

241
Q

How would you determine anti-coagulant control?

A

Use CHAD-VASc score to determine anti-coagulant.

Used to be more warfarin now DOAC more commonly used e.g., apixaban/rivaroxaban

242
Q

Complications of AF?

A

Acute stroke (most common) due to blood pooling and coagulating in the atrium
MI
Congestive heart failure
Amiodarone related pulmonary toxicity/thyroid dysfunction
Hypotension

243
Q

What is the prognosis for AF?

A

30% higher risk of CV events. 15% of strokes caused by AF

244
Q

What is tachycardia?

A

Heart rate greater than 100

245
Q

What are the 2 shockable rhythms for a cardiac arrest?

A

Ventricular tachycardia
Ventricular fibrillation

246
Q

What are the two non-shockable rhythms?

A

Asystole- when there is no electrical activity
Pulseless electrical activity

247
Q

What are the different types of supraventricular tachycardia?

A

A sinus tachycardia

Focal atrial tachycardia

Atrioventricular re-entry tachycardia

AV nodal re-entry tachycardia

248
Q

What is sinus tachycardia?

A

Conduction happens correctly in the SAN but the impulses are initiated at too high a frequency.

This can be due to infection, pain, exercise, anxiety, dehydration, bleed, sepsis, drugs, anaemia

249
Q

What is focal atria tachycardia?

A

A group of cells in the atria act as the pacemaker going quicker than the SAN node often seen in patients with chronic lung disease. Normal P wave

250
Q

What is atrioventricular re-entry tachycardia (AVRT)?

A

Atrioventricular re-entry tachycardia- when there is an accessory pathway

ANTEGRADE (atria to ventricles) which is shown as pre-excitation on the resting ECG (the mythical DELTA wave) Wolf-Parkinson-White syndrome
RETROGRADE (ventricle to atria) which is not seen on a resting ECG

251
Q

What is a AV nodal re-entry tachycardia (AVNRT)?

A

This is where re-entry circuits form within the AV node, or anatomically adjacent similar tissue.

Most common type and more common in women. Can be caused by drugs and lifestyle. Usually sudden onset and can cause shortness of breath.

252
Q

What is a junctional tachycardia?

A

Where cells within the AVN become the pacemaker

253
Q

How would you manage a haemodynamically unstable patient with a supraventricular tachycardia?

A

Cardiovert them either chemically or electrically

254
Q

How would you manage a haemodynamically stable patient with a supraventricular tachycardia?

A

use vagal manoeuvres if that doesn’t work then can use adenosine which interrupts the AV node

255
Q

Do supraventricular tachycardias have wide or narrow QRS complexes?

A

Narrow unless present with bundle branch block

256
Q

What are the wide-complex QRS tachycardias?

A

Ventricular tachycardia,
Ventricular fibrillation
Torsades de pointes

257
Q

What is ventricular tachycardia?

A

Usually observed in the setting of ischaemic heart disease. IHD and CAD are the most common. Things such as Chagas disease can also cause.

Other forms of structural heart disease, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and anomalous coronary arteries are also associated with ventricular arrhythmias.

258
Q

What causes ventricular tachycardia?

A

Areas previously scarred are the substrate for re-entry causing rapid ventricular depolarisation

259
Q

What are the symptoms of VF?

A

Hypotension and syncope. Along with racing pulse and dyspnoea

260
Q

How would you treat a patient with VF?

A

Treatment if they are haemodynamically unstable with a pulse- do a cardioversion and look for underlying cause try and solve.

Consider using antiarrhythmic medication amiodarone

If stable then use adenosine/amiodarone then cardiovert if not successful

261
Q

What is Torsades de pointes?

A

Looks like normal ventricular tachycardia on an ECG however there is an appearance that the QRS complex is twisting around the baseline.

The height of the QRS complexes progressively get smaller, then larger then smaller and so on. It occurs in patients with a prolonged QT interval.

262
Q

What causes Torsades de Pointes?

A

A prolonged QT interval means that there is a longer peroid before ventriuclar repolarisation

263
Q

What causes Torsades de Pointes?

A

A prolonged QT interval means that there is a longer period before ventricular repolarisation. This leads to repolarisation of myocytes.

These abnormal spontaneous depolarisations prior to repolarisation are known as “afterdepolarisations”.

These depolarisations spread throughout the ventricle, leading to a ventricular contraction prior to proper repolarisation occurring. When this occurs and the ventricles continue to stimulate recurrent contractions without normal repolarisation it is called Torsades de pointes.

264
Q

What causes prolonged QT?

A

Long QT syndrome (inherited)
Medications (antipsychotics, flecainide, sotalol, amiodarone, macrolide antibiotics)
Electrolyte disturbances- hypokalaemia, hypomagnesaemia, hypocalcaemia)

265
Q

How would you treat Torsades de Pointes?

A

Correct the disturbance
Magnesium sulphate
cardioversion if the problem does not resolve

266
Q

What is the long term management of prolonged QT syndrome?

A
  • Avoid medications that prolong the QT interval
    • Correct electrolyte disturbances
    • Beta blockers (not sotalol)
      Pacemaker or implantable defibrillator
267
Q

What are ventricular ectopic?

A

They are caused by pre-mature ectopic beats caused by random electrical discharges from outside the atria. Patients often present complaining of random, brief palpitations.

268
Q

What is ventricular bigeminy?

A

When ventricular ectopics are occurring so frequently that they happen after every sinus beat.

269
Q

What is the management of ventricular ectopic?

A

Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities

Reassurance and no treatment in otherwise healthy people

Seek expert advice in patients with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, family history of sudden death)

270
Q

How would you manage heart blocks?

A

First line would be using beta agonist e.g., Atropine

No improvement would use other inotropes e.g., isoprenaline

271
Q

What heart blocks are the most likely to cause asystole?

A

2nd degree type II
3rd degree

Would require a pacemaker

272
Q

What is Wolf-Parkinson-White syndrome?

A

Is a supraventricular tachycardia due to an accessory pathway in the heart (bundle of Kent). Occurs in 1-3 per 1000

273
Q

What causes WPW?

A

The accessory pathway leads to the stimulation of the ventricles.

It causes the signal to bypass the AV node and stimulate the ventricles prematurely, this along with excitation by the AV node leads to a double excitation.

Can be left or right sided.

274
Q

Is WPW more common in men or women?

A

Most common in men in 30-40s

275
Q

What are the symptoms of WPW?

A

Can be asymptomatic
Palpitations
Feeling light-headed
Presyncope
Syncope
Cardiac arrest

276
Q

What are the signs of WPW?

A

Short PR interval, delta wave-slurred upstroke of QRS.

277
Q

What is type A WPW?

A

Type A (left-sided): positive delta wave in the precordial leads (I, II, III, aVL, aVR, aVF), R>S in V1

278
Q

What is type B WPW?

A

Type B (right-sided): negative delta wave in leads I and II

279
Q

How would you manage WPW?

A

Often, episodes of pre-excitation are short, self-terminating and do not cause problems. In people who only experience occasional symptoms, no treatment is needed, and they are followed up regularly by a cardiologist.

However if persistent then treat with vagal manoeuvres, then adenosine and then cardioversion.

Can have an ablation long term

280
Q

How would you manage WPW?

A

Often, episodes of pre-excitation are short, self-terminating and do not cause problems. In people who only experience occasional symptoms, no treatment is needed, and they are followed up regularly by a cardiologist.

However if persistent then treat with vagal manoeuvres, then adenosine and then cardioversion.

Can have an ablation long term

281
Q

What drugs would you use to treat WPW

A

amiodarone, flecainide or sotalol

NOT DIGOXIN

282
Q

What is aortic dissection?

A

Is where a separation has occurred in the aortic wall intima, causing blood flow into a new false channel composed of the inner and outer layers of the media.

283
Q

Describe the epidemiology of aortic dissection

A

Men are predominantly affected, typically older than 50 years of age.

0.5-2.95 cases per 100,000 annually

284
Q

What can cause an aortic dissection

A

Abrupt, transient, severe increase in blood pressure

Bicuspid aortic valve or coarctation of the aorta

Aortic instrumentation or surgery including percutaneous stenting or catheter insertion

285
Q

What are the risk factors for aortic dissection?

A

Male
Age 50-70
Hypertension (most common)
Connective tissue disorders (Marfans or Ehlers-Danlos syndrome)
Smoking

286
Q

What happens when an aortic dissection occurs?

A

There is a tear in the wall of the intima of the aorta. This causes blood to flow into the channel in the media of the aorta.

This channel is called the false lumen

287
Q

What are the key presentations of aortic dissection?

A

A severe sudden onset chest or inter-scapular back pain. Classically described as sharp ripping or tearing.

pain can often settle creating impression there is nothing wrong

288
Q

What are the signs of aortic dissection?

A

Pulse deficit- a difference of >20mmHg in blood pressure between limbs/a weaker/absent pulse compared to contralateral side.

Hypertension

Hypotension

Tachycardia

Diastolic murmur

289
Q

What investigations might you initially run on a patient with a suspected aortic dissection?

A

ECG to assess for any MI, do blood tests (d-dimer could rule out), chest x-ray/CT, echo

290
Q

What is the gold standard test for aortic dissection?

A

CT angiogram (CTA) whole aorta is the investigation of choice as it can confirm the diagnosis and classify the dissection)

291
Q

What are the two Stanford classifications of aortic dissection and which is more common?

A

Type A: is when the dissection involves the ascending aorta. Accounts for 60-70% of cases

Type B: involves only the descending aorta (distal to subclavian) accounts for 30-40% of cases

292
Q

What are the differentials for aortic dissection?

A

ACS
Cardiac tamponade
Pericarditis
Pneumothorax
PE

293
Q

How would you manage a type A aortic dissection?

A

ABCDE

Give a beta-blocker/CCB and then perform endovascular repair

294
Q

How would you manage type B aortic repair?

A

Give beta-blocker or CCB (labetalol, verapamil)

Consider surgery if serious if not monitor.

295
Q

What are the complications associated with aortic dissection?

A

Acute aortic regurgitation
MI
Cardiac tamponade
Acute limb ischaemia
Renal failure
Bowel ischaemia

296
Q

What is the prognosis for aortic dissection?

A

Overall aortic dissection carries a high mortality of 10-35%.

The highest mortality period is within the first 10 days, and 20% of patients die before reaching hospital.

297
Q

What percentage of people with an aortic dissection will be asymptomatic?

A

10%

298
Q

What is an abdominal aortic aneurysm?

A

Abdominal aortic aneurysm (AAA) is a permanent pathological dilation of the aorta with a diameter >1.5 times the expected .The most commonly adopted threshold is a diameter of 3 cm or more.

More than 90% of aneurysms originate below the renal arteries

299
Q

Who is invited for screening for an AAA?

A

Men over 65

300
Q

What are the tow casues of AAA?

A

Congenital- there is natural degeneration with age, made worse by certain conditions are lifestyle
Infectious- Infection is a rare cause

301
Q

What infections can cause an AAA?

A

Staphylococcus
Salmonella
Chlamydia
Syphillis

302
Q

What are the risk factors associated with AAA?

A

Smoking
Family history
Increased age
Male sex
Congenital tissue disorders

DIABETES IS NOT ONE ACTUALLY REDUCES RISK

303
Q

Describe the pathophysiology of an AAA?

A

There is degradation of the aortic wall connective tissue. Proteolytic enzyme activity in the aortic wall promotes the deterioration of proteins in the cell wall.

Inflammation and immune responses cause cascade of cytokines which activate these proteases

Also biochemical wall stress: elastin decreases down the aorta so more likely further down

304
Q

What are the key presentations of AAA?

A

Abdominal, flank or back pain and palpable pulsatile abdominal mass

305
Q

What are the 3 key presentations of an inflammatory AAA?

A

Weight loss, abdominal pain and elevated erythrocyte sedimentation

306
Q

What are some other symptoms of an AAA?

A

Abdominal distension, fever, hypotension, pallor

307
Q

What is the first line investigation for an AAA?

A

Aortic ultrasound

308
Q

What are some differential diagnosis of an AAA?

A

Diverticulitis
Ureteric colic
IBS

309
Q

How would you treat an AAA?

A

If ruptured/or symptomatic needs urgent surgical repair.
If less than 5.5cm than monitor, make sure it’s not rapidly growing. May choose elective surgical repair

310
Q

How often would you have a scan if you had an 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.

311
Q

What is the prognosis for an AAA?

A

The natural course involves slow and steady growth with ultimate progression to rupture.

Most patients with rupture will not survive to reach the operating theatre. Given the morbidity and mortality associated with surgical intervention, repair is typically deferred until the theoretical risk of rupture exceeds the estimated risk of operative mortality.

Five year survival rate for a repair is 60-75%

312
Q

Is rupture of an AAA more common in men or women?

A

Women

313
Q

What is peripheral vascular/arterial disease?

A

PAD includes a range of arterial syndromes that are caused by atherosclerotic obstruction of the lower-extremity arteries.

314
Q

What causes PAD?

A

Atherosclerosis

Can also be acute due to a thrombus

315
Q

What are the risk factors for PAD?

A

Smoking
Alcohol
High BMI
Age
Gender

316
Q

What are the four different classifications of PAAD?

A

Stage 1: asymptomatic
Stage 2: Mild claudication/severe
Stage 3: Ischaemia rest pain
Stage 4: Ulceration or gangrene

317
Q

What is intermittent claudication?

A

Is a symptom of ischaemia in a limb during exertion and relieved by rest. It is typically a crampy achy pain in the calf, thigh or buttock muscles associated with muscle fatigue

318
Q

What is critical limb ischaemia?

A

The end-stage of peripheral vascular disease where there is an inadequate supply of blood to a limb to allow it to function properly at rest.

Features are pain, non-healing ulcers and gangrene

319
Q

What are the 6 P’s of critical limb ischaemia?

A
  • Pain
  • Pallor
  • Pulseless
  • Paralysis
  • Paraesthesia (abnormal sensation or “pins and needles”)
  • Perishing cold
320
Q

What are the signs of PAD?

A
  • Weak pulse
  • Cold distal limbs
  • Postural colour change (Bureger’s test)
321
Q

What are the symptoms of PAD?

A
  • Cyanosis
  • Dependant redor
  • Muscle wasting
  • Hair loss
  • Ulcers
  • Poor wound healing
  • Gangrene
322
Q

How would you investigate PAD?

A
  • Duplex ultrasound – ultrasound that shows the speed and volume of blood flow
  • Angiography (CT or MRI) – using contrast to highlight the arterial circulation
323
Q

What is the ankle-brachial index?

A

Used to determine extent of PAD.

Measures the difference between systolic blood pressure of arm to ankle. Done using a Doppler probe

324
Q

What do the different ratios on ABI indicate?

A

0.9-1.3 is normal
0.6-0.9 indicates mild
0.3-0.6 indicates moderate to severe
<0.3 indicates critical ischaemia

325
Q

What are some differential diagnosis of PAD?

A

Spinal stenosis
Arthritis
Venous claudication

326
Q

How would you treat PAD with mild claudication?

A

Statin, clopidogrel (anti-platelet) and Naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a peripheral vasodilator). Cilostazol for symptom relief

327
Q

How would you treat critical limb ischaemia?

A

Urgent revascularisation can be achieved by:

Endovascular angioplasty and stenting
Endarterectomy
Bypass surgery
Amputation of the limb if it is not possible to restore the blood supply

328
Q

How would you monitor PAD?

A

Annual visits recommended for those with claudication ABI taken and Duplex ultrasound

329
Q

What are the complications associated with PAD?

A

Permanent limb weakness
Leg/foot ulcers
Amputation
Gangrene

330
Q

What is the prognosis for PAD?

A

Mild claudication normally remains stable (risk factors diabetes and low ABI make prognosis worse)

Critical limb ischaemia 1 year 25% dead and 30% amputation and 5 years 60% dead

331
Q

What is Buerger’s test?

A

The first part involves the patient lying on their back (supine). Lift the patient’s legs to an angle of 45 degrees at the hip. Hold them there for 1-2 minutes, looking for pallor. Pallor indicates the arterial supply is not adequate to overcome gravity, suggesting peripheral arterial disease. Buerger’s angle refers to the angle at which the leg is pale due to inadequate blood supply. For example, a Buerger’s angle of 30 degrees means that the legs go pale when lifted to 30 degrees.

The second part involves sitting the patient up with their legs hanging over the side of the bed. Blood will flow back into the legs assisted by gravity. In a healthy patient, the legs will remain a normal pink colour. In a patient with peripheral arterial disease, they will go:

Blue initially, as the ischaemic tissue deoxygenates the blood
Dark red after a short time, due to vasodilation in response to the waste products of anaerobic respiration

332
Q

What is shock?

A

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

333
Q

Describe the epidemiology of shock?

A

Septic shock is the most common form of shock in ICU. The annual incidence of septic shock is 0.3 to 0.7 per 1000.

Cardiogenic occurs in 7-9% of MI.

Hypovolaemic is the most common in children worldwide due to diarrhoea and trauma.

334
Q

What are the different causes of shock?

A

Septic- infection with any organism it causes acute vasodilation from inflammatory cytokines

Anaphylactic- IgE mediated histamine release which causes vasodilation and results in hypotension and no airway

Neurogenic- spinal cord injury, epidural or spinal anaesthesia results in hypotension and bradycardia

Hypovolaemic- loss of >20% of the body’s fluid or blood supply makes it impossible for the heart to pump sufficient amounts of blood around the body. Non-haemorrhagic causes include burns and diabetic ketoacidosis.

Cardiogenic (pump dysfunction): most commonly occurs after myocardial infarction but other causes include tachyarrhythmias (e.g., atrial fibrillation or ventricular tachycardia), bradyarrhythmia’s, toxic substances

335
Q

Describe what happens when patient goes into shock?

A
  • Hypoperfusion is a lack of adequate oxygen delivery at a cellular level.
  • This triggers a systemic stress response, including tachycardia and peripheral vasoconstriction.
  • Once these mechanisms are overwhelmed it leads to organ dysfunction and failure and death.

In septic shock vasodilation results in the lack of perfusion, Results in cardiac impairment .
In cardiogenic, tissue hypoperfusion from loss of cardiac output induces tissue inflammation

336
Q

What are the key presentations of shock?

A

Hypotension
Tachycardia
Skin changes
Oliguria
Fever
Chest pain
Dyspnoea
Hypoxaemia

337
Q

What are the signs of septic shock?

A

Fever
Tachycardia
High respiratory rate
Increased white cell count

338
Q

What are the signs of hypovolaemic shock?

A

inadequate tissue perfusion, clammy cold skin, tachycardia, sweating, tachycardia, then falling to hypotension and bradycardia

339
Q

What are the symptoms of septic shock?

A

pyrexia, nausea and vomiting, vasodilation and bounding pulse

340
Q

What investigations would you perform for a patient in shock?

A

Lactate levels (sepsis). Venous blood gas, full blood count, glucose, ECG, C-reactive protein

341
Q

How would you manage septic shock?

A

Sepsis
Give fluids for BP
Antibiotics
Community-acquired pneumonia – ceftriaxone
MRSA – vancomycin
Pseudomonas – cefepime + metronidazole

342
Q

How would you treat cardiogenic shock?

A

give IV fluids, loop diuretic, vasodilator

343
Q

What is the prognosis for shock?

A

Shock has a high mortality but this is dependent on cause. Septic shock has case-fatality rates of 40% to 50%, reaching up to 80%.

The odds of dying from a myocardial infarction increase by over 20-fold when it is complicated by shock. Hospital mortality of cardiogenic shock reaches around 60%.

Of these deaths, 70% to 80% occur in the first 30 to 60 days after onset of cardiogenic shock.

344
Q

What is a bicuspid aortic valve?

A

Affects 1-2% of live births

Pathology- Aorta usually has 3 cusped valve this has 2. Leads to aortic stenosis and regurgitation. Makes aortic dilation and dissection more common. Valve degenerates more quickly.

Investigation- Echocardiogram

Management- Surgical valve replacement

345
Q

What is an atrial septal defect?

A

It is an abnormal connection between the two atria.

346
Q

Describe what happens when an atrial septal defect is present

A

As the pressure is higher in the LA than RA the hole means blood shunts from the right to the left. This increases flow to the right side leading to right sided hypertrophy and distension

347
Q

What happens if a large atrial septal defect is left untreated?

A

left untreated than the patient can develop right heart overload and dilation. This will result in RV hypertrophy, Pulmonary hypertension- Eisenmenger’s complex and an increased risk of IE

348
Q

What is Eisenmenger’s complex?

A

Can occur in ASD or VSD. It is when there is a reversal of shunt due to pulmonary tension leading to right side hypertrophy, this will exacerbate the problem.

This causes de-oxygenated blood to skip the lungs and go back around the body. Once pulmonary HTN is high enough to cause reversal only transplant is curative. Will cause cyanosis, clubbing, heart failure, syncope and high RBC

349
Q

What are the signs and symptoms of ASD?

A

Pulmonary flow murmur
Fixed split-second heart sound
Dyspnoea
Exercise intolerance
Atrial arrhythmias from RA dilation

350
Q

What is the management of an ASD?

A

Surgical closure
Percutaneous (key hole technique)

351
Q

Describe the epidemiology of VSD?

A

Common the account for 20% of all congenital heart defects. Occur in 0.1-0.4% of births.

352
Q

What are the symptoms of a large VSD?

A

Will lead to Eisenmenger’s complex, a small breathless baby, poor feeding, failure to thrive
Increased Respiratory rate
Tachycardia
Big heart on X-ray
Murmur

353
Q

What are the symptoms of a small VSD?

A

Could be asymptomatic
Increases pulmonary blood flow only
Risk of endocarditis
Loud systolic murmur
Well grown
Normal heart rate
Normal heart size

354
Q

How would you manage a VSD?

A

Medically initially as the hole may close, if not then surgically. Medications include, furosemide, ACE inhibitor, Digoxin

355
Q

What is patent ductus arteriosus? (pda)

A

DA is the persistent communication between the proximal left pulmonary artery and the descending aorta. It Normally closes within a few hours of birth, premature may not close or maternal rubella.

This will result in an increased left ventricular volume, left ventricular output, and pulmonary over-circulation. Increased flow to the lungs leads to decreased pulmonary compliance and increased work of breathing. With the increased pre-load, the left ventricle dilates and left ventricular end diastolic pressures and left atrial pressures increase. The increase in left-sided pressure inhibits pulmonary venous return, furthering pulmonary congestion. In preterm infants, the effects of pulmonary over-circulation and systemic steal are more pronounced. Increased pulmonary blood flow not only leads to pulmonary oedema, but also to pulmonary haemorrhage, respiratory distress syndrome, and bronchopulmonary dysplasia

356
Q

symptoms of pda

A

Failure to thrive
Exercise intolerance
Tachypnoea
Low BP
Machine-like/Gibson murmur- This classic murmur, known as a Gibson murmur or machinery murmur, is best heard in the left infraclavicular area and peaks in late systole and continues through into diastole
Third heart sound at apex
Mid-diastolic murmur rumble at apex

357
Q

investigations for pda

A

CXR-large shunt may be prominent

ECG- may demonstrate defects due to LVH

Echocardiogram- gold standard test

358
Q

treatment for pda

A

Ibuprofen as they inhibit prostaglandins this is used in premature infants

For full term infants then surgery is the option either by surgical ligation or percutaneous catheter closure

359
Q

what is coarctation of the aorta? (CoA)

A

Is defined as the narrowing of the aorta. Most common at the site of the DA just to left of subclavian artery.

360
Q

what is the epidemiology of CoA

A

Coarctation of the aorta is a common congenital heart defect, constituting about 6% to 8% of all congenital heart defects. It occurs more frequently in males than in females. Most cases are sporadic, although recent evidence shows a familial link with non-syndromic left ventricular outflow tract obstructive lesions.

361
Q

what is the pathophysiology of CoA

A

The effects depend on the severity of the narrowing and resultant elevated after-load on the left ventricle. Severe narrowing presents in the neo-natal period with low output cardiac failure and shock once the DA shuts. This patients require prostaglandin E1 infusion to maintain DA and surgical repair.

Mild to moderate narrowing can be clinically silent for many years however there may be hypertension associated with it. Collateral blood vessels often enlarge and provide a route for blood to bypass the narrowed segment of the aorta. Indications for repair are congestive heart failure, systolic hypertension, or a peak pressure gradient >20 mmHg across the coarctation measured by Doppler echocardiography or catheterisation

362
Q

diagnostic factors of CoA (signs symptoms etc)

A

Hypertension at young age

Diminished pulse

Differential upper and lower pulses

Ejection systolic murmur

363
Q

risk factors for CoA

A

DiGeorge syndrome

Turner syndrome

Young age

364
Q

investigations for CoA

A

ECG

Chest x-ray

Echocardiogram

365
Q

treatment for CoA

A

Critical coarctation management:
Give a prostaglandin to maintain ductal patency plus surgical repair

Non critical repair:
Surgical repair and if recurrent then balloon angioplasty

366
Q

what is tetralogy of fallot (TOF)

A

Tetralogy of Fallot (TOF) is a congenital cardiac malformation. The key morphological abnormality is anterior and cephalad deviation of the muscular outlet of the ventricular septum, which causes the 4 classic findings:
(1) a mal-alignment ventricular septal defect (VSD),
(2) aorta over-riding the VSD,
(3) right ventricular outflow tract obstruction,
(4) secondary concentric right ventricular hypertrophy.

367
Q

Key diagnostic factors for TOF

A

Hypercyanotic episodes (Tet spells)

Harsh systolic ejection murmur

Cyanosis

Tachypnoea

368
Q

pathology of TOF

A

Degree of right ventricular outflow obstruction- can be below pulmonary valve, at the level of the valve, and above the valve. Mild= less cyanotic episodes

Pulmonary artery anatomy

Non-restrictive, mal-alignment VSD

369
Q

what are the different types of TOF

A

Cyanotic TOF (also know as blue tet): infants with TOF and moderate to severe pulmonary obstruction are cyanotic at birth due to right-to-left shunting of de-oxygenated blood from the right ventricle across the ventricular septal defect (VSD) to the body.

Acyanotic TOF (also know as pink tet): infants with TOF and mild pulmonary obstruction are commonly acyanotic because there is little or no right-to-left shunting of blood at the ventricular level. These patients still undergo complete intracardiac repair.

Pulmonary atresia/VSD: sometimes referred to as TOF with pulmonary atresia and is anatomically and physiologically very different. It is often associated with malformation of the central pulmonary arteries.

Absent pulmonary valve syndrome: sometimes referred to as TOF with absent pulmonary valve. It is often associated with tracheobronchial compression and malformation.

370
Q

management of TOF

A

Infant should be kept calm and maneuvers tried to increase the amount of blood exiting the right ventricle through the pulmonary vasculature instead of to the aorta.

Infant should be held in the parent’s arms and positioned with the knees to the chest.

Consider medications to control symptoms e.g., beta-blocker

Main management is complete surgical repair

371
Q

complications of TOF

A

Cyanotic spells

Paradoxical emboli

Atrial arrhythmias

Sudden cardiac death

Congestive heart failure

372
Q

prognosis of TOF

A

Surgical outcomes are excellent with survival rates of 100% at 1 month, 93% at 1 year, and 93% at 5 years after complete repair. Freedom from reoperation rates were 100% at 1 month, 89% at 1 year, and 58% at 5 years.[31]

Once the patient has undergone complete surgical repair, the prognosis and any problems that occur may be related to the patient’s individual anatomy and type of surgical repair, as well as any associated conditions. One study of survivors of the first year after surgical repair showed actuarial survival rates of 97% at 10 years, 94% at 20 years, 89% at 30 years, and 85% at 36 years.[

373
Q

Describe each of the different murmurs

A

The two most common murmurs:
aortic stenosis → ejection-systolic murmur
mitral regurgitation → pansystolic murmur

The two less common murmurs:
aortic regurgitation → early diastolic murmur
mitral stenosis → mid-diastolic murmur

374
Q

have you finished cardio

A

yes

Phase 2A Tom (15 decks)

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