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Phase 2a diseases > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are the two different types of ischaemic heart disease?

A
  • Angina pectoris

- Myocardial infarction

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2
Q

What is angina pectoris?

A

Central chest tightness/pain caused by myocardial ischaemia. Often shortened to just “angina”.

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3
Q

What are the 4 different categories of angina pectoris and what are the criteria for each category?

A
  • Stable: Induced by effort, and relieved by rest. Each attack lasts less than 20 mins.
  • Unstable: Continuous pain of increasing severity, often caused by minimal exertion. Each attack lasts longer than 20 mins.
  • Decubitus: Pain when lying flat.
  • Prinzmetal (or vasospastic): Occurs during rest (such as sleeping).
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4
Q

What is the clinical presentation of angina pectoris?

A
  • Tightness or heaviness in chest on exertion, rest, emotion, cold, heavy meals etc.
  • May radiate to: one or both arms, neck, jaws or teeth.

Other symptoms include: Dyspnoea, nausea, sweatiness, faintness.

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5
Q

What is the pathophysiology of angina pectoris (except for vasospastic angina?)

A
  • Atheroma, leading to the obstruction or narrowing of coronary vessels.
  • Angina will also be rarely caused by other conditions such as anaemia.
  • The thickening of the myocardial wall (Hypertrophic cardiomyopathy), aortic stenosis, and hypertension can all result in an increased demand for oxygen, leading to angina.
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6
Q

What is the pathophysiology of vasospastic angina?

A

Coronary artery spasm, with no correlation to exertion.

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7
Q

What is the aetiology of Angina (excluding vasospastic angina)?

A
  • Atheroma (or atherosclerosis)

- Stenosis (often caused by the atheroma).

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8
Q

What is the aetiology of vasospastic angina?

A

Functional disease, so no organic aetiology.

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9
Q

Which layer of the heart do stable angina and vasospastic angina normally affect?

A
  • Stable angina affects subendocardium most commonly.

- Vasospastic angina affects all layers of the heart (transmural ischaemia).

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10
Q

What are the diagnostic tests for angina pectoris?

A
  • ECG. The ECG will usually be normal, but there could be some ST depression would occur in subendocardial ischaemia (so in stable/ unstable angina).
  • Some ST elevation would occur in transmural ischaemia (so in vasospastic angina).
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11
Q

What is the treatment for unstable angina?

What is the treatment for stable angina?

A

UNSTABLE ANGINA

1st line:
DEFINITELY
- Aspirin (Anti-platelet)
- P2Y12 inhibitor (clopidogrel)
- GTN (Nitrate) or morphine (if GTN not analgesic enough).
- Anti-emetic (metoclopramide)
- PCI

STABLE ANGINA

1st line:
DEFINITELY
- Discuss lifestyle changes (healthy diet, lowering alcohol intake, stop smoking etc.)
- Aspirin (+ clopidogrel after an acute attack)
- Statin (atorvastatin)
- B-blocker (or CCB 2nd line)
- ACEI
-GTN for any future angina attacks.
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12
Q

What are the potential complications of angina?

A
  • Sudden death (possibly due to MI, as angina is probably a risk factor for MI).
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13
Q

What is myocardial infarction?

A

Death (necrosis) of heart tissue (usually muscle, otherwise known as the myocardium) due to an ischaemic event.

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14
Q

What are the two main types of myocardial infarction?

A
  • STEMI (ST-elevated myocardial infarction).

- NSTEMI (Non ST-elevated myocardial infarction).

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15
Q

What is the clinical presentation of myocardial infarction?

A
  • Crushing chest pain, radiating to left arm.
  • Sweating/ fever
  • Nausea
  • Vomiting
  • Dyspnoea
  • Fatigue
  • Heart palpitations.
    SIGNS:
  • Fever
  • Hyper/hypotension
  • 3rd/4th heart sounds (sounds during diastole).
  • Signs of congestive heart failure.
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16
Q

Which types of myocardial infarction are a medical emergency?

A

Both STEMI and NSTEMI are medical emergencies.

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17
Q

What is the pathophysiology of myocardial infarction?

A
  • A thrombus has blocked a coronary artery. As a result, part of the cardiac tissue has become ischaemic and died (necrosis).
  • The location of the necrosis depends on the location of the blockage.
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18
Q

What is the aetiology of myocardial infarction?

A
  • Atheroma/ extreme stenosis.
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19
Q

What is the epidemiology of MI?

A
  • 3x more likely in men.

- Approx 0.5% incidence rate in the population.

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20
Q

What are the diagnostic tests for MI?

A
  • DO NOT DELAY TREATMENT FOR DIAGNOSTIC TESTS IN THE EVENT OF MI.
  • ECG: If STEMI, there will be at least 1-2mm of ST elevation. NSTEMI will show no ST-elevation.
  • Shortly after MI, there might be peaked T-waves (within the first 30 mins).
  • After 12-24 hours, T-wave inversion, new Q waves (Q waves in V2 or V3) and new conduction defects may be developed as a result of ischaemic heart injury.
  • FBC: Rules out anaemia.
  • Cardiac enzyme testing: Troponin T/I (TropT/TropI) are markers for cardiac damage, and are released into the bloodstream following an MI. These are usually the way an NSTEMI is picked up, as it will not show up on an ECG.
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21
Q

What is the treatment for a myocardial infarction?

A 
STEMI and NSTEMI
1st Line:
"MONA"
Morphine
Oxygen (if sats below 94%)
Nitrates (GTN)
Aspirin

Arrange PCI surgery if possible, or CABG is more vessels are occluded/PCI will not achieve full revascularisation.

FOLLOWING THE MI:

  • Continue dual antiplatelet therapy (Aspirin + Prasugrel/clopidogrel)
  • Start/continue B-blocker (Bisoprolol). ONLY START CCB IF B BLOCKER CONTRAINDICATED (Amlodipine).
  • ACEI (ramipril)
  • Statin (atorvastatin)
  • Lifestyle changes (cardiac rehab).
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22
Q

What are the complications of myocardial infarction?

A
  • Recurrent infarction in the future.
  • Post-infarction angina.
  • Left ventricular dysfunction, leading to heart failure.
  • Ventricular septal rupture.
  • Free wall rupture, leading to bleeding into the pericardium and cardiac tamponade.
  • False aneurysm (So the ventricular wall is structurally compromised) in ventricular wall.
  • Acute mitral regurgitation (as a result of ischaemic damage to the papillary muscles).
  • Arrhythmias: Ventricular tachycardia/brachycardia, ventricular fibrillation, total AV block.
  • Thrombus formation in ventricle wall.
  • DVT and PE.
  • Pericarditis (common if infarction was anterior).
  • Depression (20% of patients after an MI).
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23
Q

What are the potential sequelae of MI?

A
  • Cardiogenic shock/ heart failure

- Pericarditis

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24
Q

What is cardiac failure?

A

The heart is unable to pump enough blood around the body to meet it’s needs for blood and oxygen.

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25
Q

What are the signs and symptoms of cardiac failure?

A

Left side cardiac failure:

  • Dyspnoea
  • Tachypnea
  • Crackling lungs (usually starts in inferior aspect of lungs and spreads upwards as disease progresses).
  • Wheezing
  • Cyanosis (occurs later in the course of disease).
  • Frothy, pink sputum (blood in sputum).

SIGNS

  • Laterally displaced apex beat.
  • Gallop rhythm
  • Heart murmurs.
Right side cardiac failure:
- Peripheral oedema.
- Ascites (fluid buildup in abdomen)
- Liver enlargement
- Raised JVP (Jugular venous pressure).
(All of these symptoms are as a result of blood backup into the venous system due to inadequate ability of the heart to pump blood effectively).
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26
Q

What is the pathophysiology of heart failure?

A

Left side heart failure - Blood backs up into the pulmonary circulation

Right side heart failure - Blood backs up into the systemic circulation.

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27
Q

What is the aetiology of heart failure?

A

If the heart failure is diastolic (heart cannot relax properly between beats):
- Tamponade, constrictive pericarditis, hypertension.

If heart failure is systolic (heart isn’t contracting well during heartbeats):
- IHD, MI, cardiomyopathy.

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28
Q

What is the epidemiology of heart failure?

A
  • 1-3% in general population have heart failure.
  • 10% of elderly have HF.
  • Prognosis is poor. Approx 25%-50% die within 5 years of diagnosis.
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29
Q

What investigations are used for heart failure?

A
  • BNP (Brain natriuretic hormone, secreted by the cardiomyocytes in the ventricles) will be high in people with heart failure. 1ST LINE ESPECIALLY IN PRIMARY CARE FOR SUSPECTED HEART FAILURE.
  • ECG
  • CXR: Bat wing alveolar oedema, Kerley B lines (faint white lines at the base of the lungs), cardiomegaly, dilated/prominent upper lobe vessels, pleural effusion.
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30
Q

What lifestyle changes should a person with heart failure make?

A

Lifestyle:

  • Stop smoking
  • Eat healthily
  • Exercise
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31
Q

What is the treatment for chronic heart failure?

A

1st line:

  • Ramapril (ACEI)
  • Lifestyle changes (Lower sodium intake, reasonable fluid intake, exercise).
  • Bisoprolol (B-blocker).
  • IF FLUID RETENTION OCCURING furosemide (loop diuretic).
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32
Q

What is the treatment for the different types of acute heart failure and how does it work?

A

CARDIOGENIC SHOCK (<90mmHg systolic, hypotensive):
1st line:
- Treat underlying cause (Infection, tamponade, PE, MI etc.)
- Give O2 if needed hypoxic
- Refer to specialist

HYPERTENSIVE CRISIS:
1st line:
- Treat underlying cause (MI, angina, tachycardia etc.)
- Loop diuretic (furosemide)
- GTN for vasodilation.
- Refer to specialist

HAEMODYNAMICALLY STABLE:
1st line:
- Treat underlying cause
- Refer to specialist

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33
Q

What is valvular heart disease?

A

Disease affecting the valves of the heart.

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34
Q

What are the 4 main types of valvular heart disease?

A
  • Mitral stenosis
  • Mitral regurgitation
  • Aortic Stenosis
  • Aortic regurgitation
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35
Q

What is the clinical presentation of mitral stenosis?

A
  • Pulmonary hypertension, often causing dyspnoea.
  • Pink, frothy sputum (bloody sputum).
  • Left atrial dilation.
  • Right ventricular hypertrophy.
  • Heart palpitations.
  • Malar flush (butterfly rash) due to CO2 retention.
  • Sounds: Opening “snap” and MID DIASTOLIC MURMUR.
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36
Q

What is the clinical presentation of mitral regurgitation?

A
  • Haemodynamic effects are variable.
  • Deviated apex beat (suggests change of heart shape).
  • Sounds: PANSYSTOLIC (persists throughout systole) MURMUR, mid-systolic click, and late systolic murmur in mitral prolapse (occurs during systole, and suggests blood is passing back through the mitral valve into the left atrium.
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37
Q

What is the clinical presentation of aortic stenosis?

A
  • EARLY (as blood is initially ejected) SYSTOLIC MURMUR.
  • Left ventricular hypertrophy.

“SAD”

  • Syncope.
  • Angina.
  • Dyspnoea.
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38
Q

What is the clinical presentation of aortic regurgitation?

A
  • EARLY DIASTOLIC MURMUR as blood flows back into the left ventricle straight after systole.
  • Wide pulse pressure (Big gap between systolic and diastolic blood pressure).
  • Collapsing pulse (Pulse with very high peaks and steep drops again.
  • Angina
  • Left ventricular failure
  • Austin Flint murmur (a rumbling diastolic murmur caused by fluttering of the mitral valve due to regurgitant bloodstream.)
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39
Q

What are the 7 main structural heart defects?

A
  • Atrial septal defect
  • Ventricular septal defect
  • Coarctation of the aorta
  • Bicuspid aortic valve
  • Fallot’s tetralogy
  • Patent ductus arteriosus
  • Patent foramen ovale.
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40
Q

What is an atrial septal defect?

A

A hole in the septum that connects the atria together

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41
Q

What are the two types of atrial septal defect?

A
  • Ostium primum (hole in the septum primum - wall of the left atrium)
  • Ostium secundum (hole in the septum secundum - wall of the right atrium).
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42
Q

What is the pathophysiology of atrial septal defects?

A

Failure of the septal tissue between the L and R atrium to form, creating a left to right shunt.

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43
Q

What is the aetiology of atrial septal defects?

A

Unknown, but influenced by genetics.

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44
Q

What is the epidemiology of atrial septal defects?

A

10% of all congenital abnormalities of the heart are atrial septal deficits.

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45
Q

What are the diagnostic tests for atrial septal defect?

A

Echocardiogram

ECG

  • RBBB in both
  • LAD (Left axis deviation) and prolonged PR interval for ostium primum.
  • Right axis deviation for ostium secundum.
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46
Q

What are the treatment options for atrial septal defects?

A

LEFT TO RIGHT SHUNT:

  • Observe
  • Close if the shunt doesn’t close.

RIGHT TO LEFT SHUNT:

  • Operate the close if the right to left shunt is reversible with pulmonary vasodilators.
  • Eisenmenger’s is incurable (irreversible changes to pulmonary vessels cause the shunt to reverse from left-to-right to right-to-left).
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47
Q

What are the potential complications of atrial septal deficits?

A
  • Eisenmenger syndrome.
  • Caused by pressure increase in pulmonary circulation due to septal defect (left to right shunt), which causes damage to pulmonary vessels.
  • Increases pressure in right side of heart, eventually leading to reversal of the shunt (now goes right to left) and as a result deoxygenated blood bypasses pulmonary circulation and mixes with the oxygenated blood.
  • Can be recognised as cyanosis.
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48
Q

What are the common clinical presentations of the two atrial septal deficits?

A
  • Ostium primium usually presents early, and is associated with AV valve abnormalities.
  • Ostium secundum presents later, and is associated with hypertension, cyanosis, arrythmia, haemoptysis (coughing up blood), and chest pain.
  • If the defect is big enough, ASD’s can cause shortness of breath on exertion.
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49
Q

What is a ventricular septal defect?

A

Hole connecting the ventricles.

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50
Q

What is the clinical presentation of ventricular septal deficit?

A
  • In infancy, if large, can cause severe heart failure.
  • However, if small, can go unnoticed (asymptomatic) and may be found incidentally.
  • Loud pansystolic mumur may be present.
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51
Q

What other heart abnormalities are associated with ventricular septal defects?

A
  • Valvular abnormalities.
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52
Q

What is the pathophysiology of a ventricular septal defect?

A

Blood shunts from right ventricle (high pressure) to left ventricle (low pressure) through septum.

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53
Q

What is the aetiology of ventricular septal defects?

A

Unknown, but thought to have a genetic component.

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54
Q

What is the epidemiology of ventricular septal defects?

A
  • Make up 25% of all congenital abnormalities of the heart.

- Affect 1:500 births.

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55
Q

How are ventricular septal defects investigated?

A
  • Echocardiogram (NOT THE SAME AS AN ECG).
  • Small VSD will not be detectable on an echoCG.
  • Medium VSD will show left axis deviation (ECG) and left ventricular hypertrophy.
  • Large VSD will show both left and right ventricular hypertrophy.
  • Chest X-ray. Shows pulmonary plethora (increased pulmonary perfusion), potentially cardiomegaly and large pulmonary arteries.
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56
Q

How are ventricular septal deficits treated?

A
  • Often will close spontaneously.

- Will be surgically closed if symptomatic, or the shunt is large enough.

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57
Q

What are the potential complications of ventricular septal deficits?

A
  • Aortic regurgitation
  • Infundibular stenosis (infundibulum refers to the funnel-shaped portion of the right ventricle that connects to the pulmonary artery).
  • infective endocarditis (due to high velocity of blood flow across the defect).
  • subacute bacterial endocarditis
  • pulmonary hypertension
  • cardiac failure
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58
Q

What is coarctation of the aorta?

A

Aortic narrowing at the level of the ductus arteriosus (a vessel that carries blood from the pulmonary artery to the aorta during foetal development).

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59
Q

What is the clinical presentation of coarctation of the aorta?

A
  • Hypertension in upper limbs, but this pressure decreases in vessels distal to the coarctation.
  • It is often asymptomatic.
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60
Q

What else is coarctation of the aorta associated with?

A

Other valvular defects such as bicuspid aortic valve.

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61
Q

What is the pathophysiology of coarctation of the aorta?

A

The aorta narrows, leading to increased LV pressure. To try and increase the blood flow through the aorta, the left ventricle may hypertrophy.

Other smaller blood vessels dilate to increase circulation to the lower parts of the body. For example, the intercostal arteries will dilate.

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62
Q

What is the aetiology of coarctation of the aorta?

A

Unknown but has a genetic component.

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63
Q

What is the epidemiology of coarctation of the aorta?

A
  • Is responsible for approx 6% of all congenital heart defects.
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64
Q

What investigations should be carried out for coarctation of the aorta? What are the key findings?

A

1st line:

  • ECG
  • CXR (will show rib-notching, due to dilation of the intercostal arteries).
  • Echocardiogram

2nd line:
CT/MRI - Coarctation will be visible.

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65
Q

What treatment is available for a patient with coarctation of the aorta?

A

Surgical intervention.

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66
Q

What are the possible complications someone with coarctation of the aorta might face?

A
  • Congestive heart failure
  • Intracerebral haemorrhage
  • Bacterial endocarditis (due to changes in blood flow, which promotes bacterial growth/survival).
  • Rupture of an aortic dissecting aneurysm (due to changes in blood flow dynamics).
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67
Q

What is a bicuspid aortic valve?

A

An aortic valve with two cusps.

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68
Q

What is the clinical presentation of bicuspid aortic valve?

A

Usually asymptomatic and discovered during other medical investigations.

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69
Q

How are athletes’ with bicuspid aortic valves monitored?

A

Yearly check-ups as bicuspid aortic valve complications are exacerbated during exercise.

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70
Q

What is the pathophysiology of a bicuspid aortic valve?

A

Over time, the bicuspid aortic valve will degrade abnormally.

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71
Q

What is the aetiology of bicuspid aortic valve syndrome?

A

Unknown, but has a genetic component.

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72
Q

What is the epidemiology of bicuspid aortic valve?

A

Occurs in about 1-2% of the general population (relatively common).

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73
Q

What investigations can be carried out to confirm diagnosis of bicuspid aortic valve?

A
  • Echocardiogram

- MRI of chest

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74
Q

What treatment can be offered for a bicuspid aortic valve?

A
  • Valve replacement if/when complications occur.
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75
Q

What are some of the possible complications of having a bicuspid aortic valve?

A
  • Aortic regurgitation.
  • IE (Infective endocarditis/SBE (Subacute bacterial endocarditis).
  • Aortic dissection/dilation (due to changes in blood flow/turbulence).
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76
Q

What is Fallot’s tetralogy?

A

Fallot’s Tetralogy consists of 4 abnormalities:

  • Pulmonary infundibular stenosis.
  • Overriding aorta (the aorta is positioned directly over a ventricular septal defect, rather than just the left ventricle. Therefore, it receives blood from both the right and left ventricles)
  • Ventricular septal defect
  • Right ventricular hypertrophy
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77
Q

What is the clinical presentation of Fallot’s teralogy?

A

NOTE: The severity of presentation heavily depends on. the degree of pulmonary stenosis. Presentation consists of:

  • Cyanosis
  • Systolic murmur
  • Increased haemoglobin concentration (unknown reason).
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78
Q

What is the significance of the ductus arteriosus in Fallot’s tetralogy?

A
  • A potent ductus arteriosus keeps a patient with severe Fallot’s Tetralogy alive, as it allows blood to pass from the aorta to the pulmonary artery, maintaining adequate blood supply to the lungs.
  • If the ductus arteriosus closes as a baby develops and they have tetralogy of Fallot, their symptoms may get worse.
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79
Q

What is the pathology of tetralogy of Fallot?

A
  • Creates a right to left shunt of blood. (high pulmonary resistance -> hypertrophy of right ventricle -> increased right ventricular pressure.)
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80
Q

What is the aetiology of Tetralogy of Fallot?

A
  • Unknown, but has a genetic component.
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81
Q

What is the epidemiology of tetralogy of Fallot?

A
  • Most common form of complex congenital cardiac abnormality (10% of all complex congenital cardiac abnormalities).
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82
Q

What diagnostic test is used for tetralogy of Fallot?

A
  • CXR May show a boot-shaped heart.

- Echocardiogram will be able to assess the anatomy of and the degree of their pulmonary stenosis.

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83
Q

What is the treatment for tetralogy of Fallot?

A
  • Early surgical intervention.
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84
Q

What are the complications of tetralogy of Fallot?

A
  • Right heart failure is inevitable.
  • Bacterial endocarditis may occur.
  • Usually, death occurs before adult life.
85
Q

What is a patent ductus arteriosus?

A
  • Failure of the ductus arteriosus to close
86
Q

What is the clinical presentation of a patent ductus arteriosus?

A
  • Continuous machinery murmur, that will be loudest at the second heart sound.
  • Large shunt causes precordial impulses (Pulsations of the heart that are palpable/visible on the anterior chest wall of a patient).
87
Q

What is the pathophysiology of having a patent ductus arteriosus?

A
  • Abnormal shunt of blood from the aorta to the pulmonary artery. (Left to right shunt).
  • Pulmonary arterial and left heart flow increases.
  • Right side of the heart is unaffected (R atrium and ventricle).
88
Q

What is the aetiology of having a patent ductus arteriosus?

A
  • Unknown, but influenced by genetics.
89
Q

What is the epidemiology of having a patent ductus arteriosus?

A
  • Approx. 0.02% of live births have a patent ductus arteriosus (very rare).
90
Q

What investigation can be performed to diagnose patent ductus arteriosus?

A
  • An Echocardiogram.
91
Q

What treatment is available for a patent ductus arteriosus?

A
  • Hopefully will close naturally during early life.

- However, surgical intervention is possible if this doesn’t occur.

92
Q

What is a patent foramen ovale?

A

Failure of the foramen ovale to close.

93
Q

What is the usual clinical presentation of a patent foramen ovale?

A
  • Usually is asymptomatic.
94
Q

How often does a patent foramen ovale cause a patient health difficulties?

A
  • Not usually, unless the patient has other cardiological abnormalities.
95
Q

What is the pathophysiology of a patent foramen ovale?

A
  • Occurs when the foramen ovale doesn’t close properly in the weeks after birth.
96
Q

What is the aetiology of having a patent foramen ovale?

A
  • Unknown, but appears to have a genetic component.
97
Q

What is the epidemiology of patent foramen ovale?

A

Approx. 1/4 people will have a patent foramen ovale.

98
Q

What are the investigations used to diagnose patent foramen ovale?

A
  • Bubble test. (Inject a small amount of bubbly salt solution into the left side of the heart. If the bubbles appear on the left side, there must be a patent foramen ovale as the blood must have bypassed the pulmonary circulation, which would have filtered these bubbles out.
  • Echocardiogram
99
Q

What are the treatments for patent foramen ovale?

A
  • Usually, no treatment is given as the defect is usually asymptomatic.
  • Sometimes, cardiac catheter surgery is used to close the foramen, where the catheter is inserted in a leg vein and directed up to. the heart where it is used to close the hole.
100
Q

What are the potential complications of having a patent foramen ovale?

A
  • Usually there are none.
  • Very rarely, there may be a thromboembolic stroke (due to increased risk of thrombus development due to abnormal blood flow).
101
Q

What is cardiomyopathy?

A

Deterioration of the myocardium’s ability to contract (can be due to mechanical dysfunction and/or electrical dysfunction)

102
Q

What are the four types of cardiomyopathy?

A
  • Dilated cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Arrythmogenic right ventricular cardiomyopathy.
  • Restrictive cardiomyopathy..
103
Q

What is the clinical presentation of dilated cardiomyopathy?

A
  • Can be asymptomatic.
  • Congestive heart failure
  • Dyspnoea
  • Weakness
  • Fatigue
  • Oedema
  • Raised JVP (Jugular venous pressure)
  • Pulmonary congestion
  • Cardiomegaly
  • 3rd/4th heart sounds.
104
Q

What is the most frequent cause of heart transplant?

A
  • Dilated cardiomyopathy
105
Q

What is the pathophysiology of dilated cardiomyopathy?

A
  • Ventricular chamber enlargement, leading to contractile dysfunction and disruption to the hearts ability to pump blood effectively.
  • Starts with dilation of the left ventricle, and can spread to cause enlargement of the right ventricle.
106
Q

What is the aetiology of dilated cardiomyopathy?

A
  • Range of causes, such as ischaemia, genetic cause, alcoholism, thyrotoxicosis (too much T3 and T4/thyroxine produced by the thyroid gland).
  • There are many other potential causes too.
107
Q

What is the epidemiology of dilated cardiomyopathy?

A
  • 35/100,000 have disease.
  • Median age is 50
  • There is some minor genetic association
  • More common in males.
108
Q

What are the investigations used for dilated cardiomyopathy?

A

CXR - Will show cardiomegaly and pulmonary oedema, both indicative of dilated cardiomyopathy.
ECG: Tachycardia (often due to thyrotoxicosis).
Echocardiogram: Marked dilatation.

109
Q

What are the treatments for dilated cardiomyopathy?

A
  • Bed rest (reduce demand on heart).
  • Loop (Furosemide) and thiazide diuretics (loop diuretics are more potent than thiazide diuretics). These are used to reduce treat any oedema and lower blood pressure, to reduce strain on the heart.
  • ACEI (ramapril). Used to lower blood pressure.
  • Beta blockers (bisoprolol). Block the effects of epinephrine, otherwise known as adrenaline. This reduces blood pressure.
  • Potentially an ICD can be implanted surgically. (Used to manage arrhythmia, by sending an electrical impulse if heart rhythm becomes abnormal.)
110
Q

What are the potential complications for a person with dilated cardiomyopathy?

A
  • Progressive heart failure.

- Sudden cardiac death.

111
Q

What are the clinical signs of hypertrophic cardiomyopathy?

A

Usually asymptomatic. If symptomatic, symptoms are variable but can include:

  • Dyspnoea
  • Chest pain
  • Palpitations
  • Syncope (fainting/passing out) THIS IS A RISK MARKER FOR SUDDEN DEATH.

On examination:

  • Forceful apex beat
  • Systolic murmur related to late ejection, worsened when standing up.
  • Jerky carotid pulse.
  • Systolic thrill (vibration) at lower sternal border.
  • ATRIAL FIBRILLATION IS THE MOST COMMON SUSTAINED ARRHYTHMIA S SEEN IN HYPERTROPHIC CARDIOMYOPATHY.
112
Q

What is the pathophysiology of hypertrophic cardiomyopathy?

A
  • Hypertrophy of the LV and sometimes the RV too.

- Leads to a thickened wall, and impaired diastolic filling.

113
Q

What is the aetiology of hypertrophic cardiomyopathy?

A
  • Autosomal dominant
  • Most common genetic cardiovascular disease
  • Occurs due to mutation in genes responsible for coding the sarcomeric proteins.
114
Q

What is the epidemiology of hypertrophic cardiomyopathy?

A
  • 1/500 (0.2%) prevelance
  • Men and black people more likely
  • Most common cause of sudden cardiac death in young people.
115
Q

What are the investigations used to diagnose and manage hypertrophic cardiomyopathy?

A

ECG:

  • Evidence of left ventricular hypertrophy
  • ST segment changes
  • T wave inversion

CXR - Variable presentation:
- Left atrial enlargement, and mitral regurgitation due to potential damage caused to the mitral valve.

116
Q

What are the common treatments for hypertrophic cardiomyopathy?

A

1st line:
- B-blocker (atenolol/bisoprolol - inhibits action of epinephrine)

  • Prevention of sudden death. An implanted cardioverter defibrillator (ICD) may be inserted to control any chronic arrhythmias that occur.
  • Use amiodarone (cardioversion drug) or electrical cardioversion if there is an acute onset of AF (common in patients with HCM).
  • Severe hypertrophic cardiomyopathy. Treated with septal myectomy. Involves removal of excess septal myocardium to restore heart volume.
117
Q

What are the potential complications of hypertrophic cardiomyopathy?

A
  • Onset of severe arrhythmia

- Sudden death

118
Q

What is the typical clinical presentation of arrythmogenic right ventricular cardiomyopathy?
(Including how presentation progresses?)

A
  • 1/2 patients will have a normal physical examination.
  • Heart palpitations
  • Syncope/pre-syncope
  • Sudden death will potentially be the first time the arrythmogenic right ventricular cardiomyopathy will be diagnosed.

Progression of presentation:

1) Subtle changes in RV
2) Symptomatic changes in RV (arrythmia, heart palpitations, syncope).
3) RV failure
4) Biventricular pump failure, resulting in overall heart failure (mimics dilated cardiomyopathy at this stage).

119
Q

What is the pathophysiology of arrythmogenic right ventricular cardiomyopathy?

A
  • Associated with desmosomes.
  • Involves the replacement of RV cardiomyocytes with fibrous, fatty tissue.
  • This leads to impairment of RV muscle due to loss of cardiomyocytes.
120
Q

What is the aetiology of arrythmogenic right ventricular cardiomyopathy?

A
  • Unknown.
  • Seems to be a response to apoptosis of cardiomyocytes, side effect of chronic inflammation or due to genetics.
  • Probably multi-factorial.
121
Q

What is the epidemiology of arrythmogenic right ventricular cardiomyopathy?

A
  • 1/2000 (0.05%) prevalence
  • More common in males
  • Genetic predisposition in approx. 50% of cases.
122
Q

What investigations are used to diagnose and monitor arrythmogenic right ventricular cardiomyopathy?

A

Echocardiogram:

  • Increased size of right ventricle.
  • Wall of right ventricle is abnormal.
  • Right ventricular wall is dysfunctional.

MRI:

  • RV enlargement
  • Fatty infiltration
  • Fibrosis
  • RV wall motion abnormalities.
123
Q

What treatment is given to patients with arrythmogenic right ventricular cardiomyopathy?

A

STANDARD HEART FAILURE MEDICATIONS:

  • Beta blockers (bisoprolol), even for asymptomatic patients.
  • ICD for high risk patients.
  • Heart transplant given to patients with refractory disease (heart not responding to the standard treatments).
124
Q

What are the complications of arrythmogenic right ventricular cardiomyopathy?

A
  • The disease is progressive
  • Can cause life-threatening arrhythmia
  • Can cause sudden death.
125
Q

What is the typical clinical presentation of hypertension?

A
  • Usually asymptomatic and found incidentally

- Search for end organ damage/ signs of renal disease etc. that could be causing the hypertension.

126
Q

What is primary hypertension?

A
  • Doesn’t have a known cause
127
Q

What is secondary hypertension?

A
  • Hypertension caused by another condition.
128
Q

What is the epidemiology of hypertension?

A
  • More common in the elderly
  • More prevalent in men than women.
  • Affects around 25% of adults.
129
Q

What are the diagnostic tests for hypertension?

A

Take blood pressure over several readings:

- Considered high at 140/90

130
Q

What are the treatment options for hypertension?

A
  • Offer lifestyle advice.

Drug therapy

If the patient has any of the following:

  • type 2 diabetes
  • is under 55 BUT NOT BLACK/AFRO-CARRIBEAN
  • 1st line is ACEi (ramipril)
  • If not tolerated (e.g. due to cough) give an ARB (e.g. olmesartan).
  • 2nd line is add in a CCB (a.g. amlodipine) OR a thiazide-like diuretic (a.g. metolazone).

If the patient is any of the following:

  • Aged over 55
  • No type 2 diabetes
  • Black/Afro-carribbean any age with no type 2 diabetes
  • 1st line is CCB (e.g. amlodipine).
  • If not tolerated (e.g. due to oedema) offer a thiazide-like diuretic (e.g. metolazone).
  • 2nd line is add ACEI (ramipril) or ARB (olmesartan) or thiazide-like diuretic (metolazone).

IF THERE IS AN UNDERLYING CAUSE AIM TO TREAT THIS.

131
Q

What are the potential sequale of hypertension?

A
  • Increased risk of MI.
132
Q

What are the 4 main types of cardiac arrhythmia?

A
  • Atrial fibrillation
  • Heart block
  • Supraventricular tachycardia (SVT)
  • Bundle branch block
133
Q

What is atrial fibrillation?

A

Uncoordinated atrial electrical activity, resulting in an irregularly irregular ventricular pulse (QRS).

134
Q

What is the clinical presentation of atrial fibrillation?

A
  • Breathlessness
  • Palpations
  • Syncope
  • Chest discomfort
  • IRREGULARLY IRREGULAR PULSE
135
Q

What is the pathophysiology of atrial fibrillation?

A

Atrial activity is chaotic and mechanically ineffective. This can lead to:
- Stagnation of blood, thrombus formation and risk of embolism/stroke.

  • Reduction in cardiac output, leading to heart failure (congestive).
136
Q

What is the aetiology of atrial fibrillation?

A
  • Hypertension
  • Coronary artery disease
  • Valvular heart disease (particularly mitral valve stenosis).
  • Cardiac surgery
137
Q

What is the epidemiology of atrial fibrillation?

A
  • Most common sustained arrhythmia

- Most common in males

138
Q

What investigations are used to diagnose atrial fibrillation?

A

ECG:

  • Irregularly irregular QRS complexes
  • Variability in RR intervals
  • Absent P waves
139
Q

What are the treatment options for atrial fibrillation?

A
  • B-blockers (bisoprolol) for rate control
  • Warfarin (dependant on CHA2DS2-VASc score). Treat co-presenting disease.

If there is an underlying cause, aim to treat this.

140
Q

What is heart block?

A
  • Disrupted electrical impulses leading to bradycardia.
141
Q

What is the clinical presentation of heart block?

A
  • Bradycardia.

- Third degree heart block (complete) can cause dizziness and blackouts).

142
Q

What are the different classifications of heart block and what are they?

A

First degree. Delayed atrioventricular conduction, without disruption.

Second degree. Some atrial impulses fail to reach the ventricles, known as “dropped beats”. There are two types of second degree heart block:

  • Mobitz I. Progressive prolongation of the PR interval until a beat is eventually dropped.
  • Mobitz II. PR interval is constant, but there is a sudden dropped beat due to random failure of the His-purkinjee cells to conduct the impulse.
  • Third degree. Signals between atria and ventricles are completely blocked. This leads to no relationship between the P and QRS complexes on the ECG.
143
Q

What is the aetiology of heart block?

A
  • Coronary artery disease
  • Cardiomyopathy
  • Fibrosis of the conducting tissues (more common in the elderly).
144
Q

What investigations and results would be expected for a person with heart block?

A

ECG

1st degree - Prolonged PR interval (>200 ms)

2nd degree (Mobitz I) - Progressively prolonging PR interval, followed by a dropped QRS.

2nd degree (Mobitz II) - Sustained PR intervals with an occasional dropped QRS.

3rd degree - Complete dissociation of P and QRS.

145
Q

What treatments are offered for the different types of heart block?

A

1st degree:
- None needed

2nd degree (mobitz I AND II):

  • Monitor
  • Potentially needs a pacemaker.

3rd degree:

  • If issue is with His bundle, atropine (1st line) or pacemaker (2nd line).
  • If issue is Purkinje fibres, permanent pacemaker.
146
Q

What is supraventricular tachycardia (SVT)?

A
  • Rapid heart rhythm originating at or above the AV node.
147
Q

What are the two types of supraventricular tachycardia?

A
  • Re-entrant. This is where there is a congenital extra electrical connection in the heart, disrupting conduction.
  • Automatic. Caused by the pathological generation of electrical signals in the heart.
148
Q

What is the clinical presentation of SVT?

A

Vary:

  • Some have minimal symptoms.
  • Paroxysmal attacks (sudden occurrence of symptoms).
  • Syncope
  • Palpitations
  • TACHYCARDIA.
149
Q

What is the pathophysiology of SVT?

What is the difference between re-entrant SVT and automatic SVT?

A
  • The gating mechanism in the AV node is being bypassed.
  • Re-entrant SVT involves a bypass tract existing to get around the AV node (Wolff-Parkinson-White syndrome).
  • Automatic SVT involves an impulse being created that will never encounter the AV node (so created by cells other than the pacemaker ones).
150
Q

What is the aetiology of SVT?

A
  • Drugs
  • Alcohol
  • Caffeine
  • Congenital
  • Stress
  • Smoking
151
Q

What are the risk factors associated with developing SVT?

A
  • Previous MI
  • Mitral valve prolapse
  • Rheumatic heart disease
  • Pericarditis
152
Q

What is the investigation and findings from this investigation used to diagnose SVT?

A

ECG

  • P waves may not be visible
  • Rapid and paroxysmal palpitations.
  • Short PR interval.
153
Q

What are the treatment options for SVT?

A
  • Valsalva manoeuvre if acute (stimulates vagal nerve to correct heart rhythm) 1st line.
  • 2nd line is IV adenosine (class V antiarrhythmic).
154
Q

What is bundle branch block?

A
  • Heart block in the ventricular bundle branches, leading to slower electrical conduction in the ventricles.
155
Q

What are the symptoms of bundle branch block?

A
  • Usually asymptomatic

- Possibly syncope.

156
Q

What are the two types of bundle branch block, and what is the pathophysiology of each?

A

Left bundle branch block (LBBB):

  • Left bundle branch no longer conducts impulse.
  • Therefore, right ventricle receives impulse prior to left and contracts first.
  • Creates a second R wave in in the left ventricular leads (V4-6).

Right bundle branch block (RBBB):

  • Right bundle no longer conducts an impulse.
  • Therefore, left ventricle receives impulse prior to right, and contracts first.
  • Creates a second R wave on the right ventricular/septal lead (V1).
157
Q

What is the potential aetiology of BBB?

A
  • Cardiac pathology
  • LVH (for LBBB)
  • RVH (for RBBB)
158
Q

What are the ECG findings for LBBB and RBBB respectively?

A

LBBB:

  • Secondary R wave present in I, AVL and V4-6
  • Slurred S in V1 and V2 (rounded S wave).

RBBB:

  • Secondary R wave in V1
  • Slurred S wave in V5 and 6.
159
Q

What is the treatment for BBB?

A
  • Treat underlying cause (if possible)
  • Treat symptoms (Blood pressure, cardiac failure etc.)
  • Potentially pacemaker.
160
Q

What are the two main types of aortic dysfunction?

A
  • Aortic aneurysm

- Aortic dissection

161
Q

What are the 4 classifications of aortic aneurysm?

A
  • Abdominal unruptured
  • Abdominal ruptured
  • Thoracic unruptured
    Thoracic ruptured
162
Q

What is the typical clinical presentation of aortic aneurysms?

A
  • If unruptured, usually asymptomatic. Can potentially cause pain in the location of the aneurysm. SEVERE PAIN INDICATES IMMINENT RUPTURE.
  • A ruptured abdominal aneurysm will present with hypotension, back pain, syncope, shock, collapse.
  • A ruptured thoracic aneurysm will present with acute pain, collapse, shock, and potentially sudden death.
163
Q

What is the prognosis for unruptured aortic aneurysms?

A
  • Could potentially rupture.

- Risk of rupture is proportional to the diameter of the aneurysm.

164
Q

What is the prognosis of ruptured aortic aneurysms (both thoracic and abdominal)?

A

Abdominal
- 80% mortality, both die before reaching the hospital.

Thoracic
- 94% mortality. Death usually within 6 hours.

165
Q

What is the aetiology of aortic aneurysm?

A
  • Degradation of the elastic lamellae, followed by leukocytic infiltration and smooth muscle loss.
  • This results in stretching of the aortic wall, and blood compiling inside to form an aneurysm.
  • Bursting can then occur spontaneously.
166
Q

What are the risk factors associated with aortic aneurysm?

A
  • Atherosclerotic damage
  • Smoking
  • Family history (genetic links)
  • Hypertension
  • COPD
  • Males
167
Q

What investigations are used for an abdominal aortic aneurysm?

A
  • If unruptured, ultrasound

- If ruptured, medical emergency so no investigation needed.

168
Q

What investigations are used for a thoracic aortic aneurysm?

A
  • If unruptured, ECG, lung function tests and ultrasound.

- If ruptured, ECG and CT scan with contrast.

169
Q

What are the treatment options for aortic aneurysm?

A
  • Surgical repair (immediate if ruptured).

- If unruptured, consider insertion of supportive stent.

170
Q

What is a false aortic aneurysm?

A
  • Damage to the aortic wall resulting in bleeding into the surrounding tissues, rather than stretching of the tunica lamina.
171
Q

What is aortic dissection?

A

Tear in the tunica intima, resulting in blood building up between the layers of the aortic wall.

172
Q

What is the clinical presentation of an aortic dissection?

A
  • “ripping pain” followed by pulse loss.

- The pain experiences usually migrates as the dissection progresses.

173
Q

Where are the most common sites for an aortic dissection to occur?

A
  • Near the aortic valve

- Distal to the left subclavian artery in the descending aorta.

174
Q

What is the pathophysiology of an aortic dissection?

A
  • Initial tear in the intima allows blood to enter the aortic wall.
  • This forms a haematoma, seperating the intima from the adventitia and creating a false lumen.
  • The false lumen will spread a variable distance in either direction under the high pressure present in the aorta.
175
Q

What is the aetiology of aortic dissection?

A
  • Atherosclerotic plaque buildup
  • Prolonged inflammation
  • Trauma
176
Q

What are the risk factors associated with aortic dissection?

A
  • Connective tissue disorders
  • Hypertension (main one)
  • Cocaine use
  • Aortic aneurysm
  • Smoking
  • High cholesterol
  • Male aged 50-70
177
Q

What are the investigations used when there is a suspected aortic dissection?

A 
Urgent CT (1st line):
- Can be used to assess the site and extent of the aortic dissection.

ECG:
- May show evidence of cardiac ischaemia and/or an MI.

Troponin may be tested to exclude the occurrence of an MI.

178
Q

How is aortic dissection treated?

A
  • Surgical repair (either open or stentgraft).
179
Q

What is the prognosis for an aortic dissection?

A
  • If the dissection ruptures, 80% mortality.
180
Q

What is peripheral vascular disease?

A

Narrowing of the arteries distal to the aortic arch.

181
Q

What are the symptoms of peripheral vascular disease?

A

Variable. Could be:

  • Asymptomatic
  • Intermittent claudication (pain in buttock, thigh or calves).
  • Pain at rest (critical limb ischaemia).
  • Skin may ulcerate or even gangrene.
182
Q

What are the signs of peripheral vascular disease?

A
  • Gangrene
  • Absent femoral, popliteal or foot pulses
  • Cold, white legs.
183
Q

What is the prognosis for peripheral vascular disease?

A
  • 50% mortality at 5 years

- 70% mortality at 10 years

184
Q

What is the pathophysiology of peripheral vascular disease?

A
  • Atherosclerosis causing stenosis of the peripheral arteries.
185
Q

What is the prevalence of peripheral vascular disease?

A
  • 4-12% of people between 50 and 70.

- 15-20% of people over the age of 70.

186
Q

What investigations are used to diagnose and assess peripheral vascular disease?

A

Ankle-brachial index (1st line)

  • 100% specificity and 95% sensitivity.

Consider Doppler ultrasonography to assess the location and extent of the peripheral vascular disease.

187
Q

What is the treatment for peripheral vascular disease?

A
  • Antiplatelet therapy (aspirin + clopidogrel)
  • Lifestyle modification

To manage claudication:

  • consider use of cilostazol (another antiplatelet).

In the event of acute limb ischaemia:

  • Urgent revascularisation if possible, or urgent amputation.
188
Q

What is pericarditis?

A

Inflammation of the pericardium.

189
Q

What are the 3 types of pericarditis and what are they?

A
  • Acute. Infection of the pericardium causes buildup of fluid.
  • Chronic effusive. Chronic infection of the pericardium causes buildup of fluid. Usually occurs as sequelae to acute pericarditis.
  • Chronic constrictive. Chronic inflammation of the pericardium causes damage and subsequent calcification and thickening. As a result, there is reduced space for the heart and it is functionally impaired.
190
Q

What is the clinical presentation of acute pericarditis?

A
  • Rapid onset chest pain that is substernal/precordial (in front of the heart, behind the sternum).
  • Pain is aggravated by inspiration, swallowing, or lying flat.
  • Pain relieved by sitting up

SIGNS:

  • Pericardial friction rub
  • Large drop in systolic BP
  • Could include tachypnoea, tachycardia and/or fever.
191
Q

What is the clinical presentation of chronic effusive pericarditis?

A
  • Pericardial friction rub
  • Dyspnoea on exertion
  • Chest pain
  • Low systolic BP

SIGNS:

  • Hypotension
  • Raised JVP
  • Muffled heart sounds.
192
Q

What is the clinical presentation of chronic constrictive pericarditis?

A
  • Dyspnoea
  • Peripheral oedema
  • Raised JVP
  • Pulsatile hepatomegaly
  • PERICARDIAL KNOCK
  • Potentially a history of cardiac surgery
193
Q

What is the aetiology of pericarditis?

A
  • Many causes
  • Can be idiopathic
  • TB can cause pericarditis
194
Q

What are the investigations used for pericarditis?

A

Echocardiogram - 1st line

ECG - picks up around 50% of pericarditis

195
Q

What is the treatment for pericarditis?

A

1st line:
- NSAIDS (aspirin)
- PPI (omeprazole) to protect the gastric mucosa from high doses of NSAIDs.
Colchicine (unless TB is suspected cause).

TREAT UNDERLYING CAUSE

196
Q

What are the risks associated with effusive pericarditis?

A
  • The effusion may become haemorrhagic.
197
Q

What is septic shock?

A
  • Hypovolaemic shock as a result of sepsis.
198
Q

What is the clinical presentation of septic hypovolaemic shock?

A
  • Low BP (systolic <90)
  • Dizziness
  • Confusion
  • Diarrhoea
  • Cold, clammy skin
  • Tachypnoea
  • Fever
199
Q

What causes septic hypovolaemic shock?

A
  • Bacterial damage to blood vessels, leading to fluid leakage into the surrounding tissues.
200
Q

What are the clinical investigations used to diagnose septic hypovolaemic shock?

A

ABG:
- Metabolic acidosis with raised lactate.

ESR/CRP:
- Shows inflammation

201
Q

What is the treatment for septic hypovolaemic shock?

A

Don’t wait for investigations to confirm diagnosis:

  • ABC’s
  • Broad spectrum antibiotics.
  • IV fluids.
  • Vasopressors (such as vasopressin) to increase BP.
202
Q

What does the ABCD2 score indicate?

A
  • Risk of stroke after a TIA.
203
Q

What does the HAS-BLED score indicate?

A
  • Risk of bleeding for a patient on anticoagulation.
204
Q

What does the QRISK3 score indicate?

A
  • Risk of a patient having a stroke or heart attack in the next 10 years.
205
Q

What does Well’s criteria indicate?

A
  • Risk of a PE.
206
Q

What does the CHA2-DS2-VASc score indicate?

A
  • Risk of stroke in a patient with AF.
207
Q

How is aortic stenosis investigated?

A
  • Use an echoCG.
208
Q

What disease is common following a CABG surgery?

A
  • Pericarditis.
209
Q

What is the first drug given for anaphylactic shock?

A
  • Adrenaline.

Phase 2a diseases (18 decks)

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