Phase 2 v2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

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1
Q

What are the three main types of acute coronary syndrome?

A
  • Unstable angina.
  • STEMI.
  • NSTEMI.
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2
Q

How are acute coronary syndromes classified?

A
  • ST elevated? STEMI.
  • ST not elevated? NSTEMI or unstable angina.

If non-ST elevated:
Troponin raised? NSTEMI.
Troponin normal? unstable angina.

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3
Q

What is the clinical presentation of acute coronary syndromes?

A
  • Acute onset, crushing chest pain radiating to arm/shoulder.
  • Nausea/vomiting.
  • Sweating.
  • Breathlessness.
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4
Q

What is the difference between stable and unstable angina?

A
  • Unstable angina occurs at rest/ during extremely light exercise.
  • Stable angina occurs under exertion, and resolve with rest.
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5
Q

What is are the risk factors for acute coronary syndrome?

A
  • Hypertension.
  • Diabetes.
  • Obesity.
  • Old age.
  • Smoking.
  • Hyperlipidemia (high cholesterol/LDL).
  • Raised GFR (kidney disease).
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6
Q

What is the pathophysiology of acute coronary syndrome? (Thrombosis)

A

ACS involves formation of a thrombus within the coronary vessels:

1) Injury to endothelial wall of vessel.
2) Exposes collagen, triggering the intrinsic pathway.
3) Clotting factors released (coagulation cascade) and platelets aggregate at the site of injury.
4) Thrombus forms, containing: RBC’s, platelets, neutrophils and is surrounded by a fibrin mesh.

If the thrombus is fully occlusive, this will cause an MI.

If the thrombus is partially occlusive, this will cause unstable angina.

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7
Q

What are the investigations used for ACS?

A

12 lead ECG as soon as suspected ACS:
- ST elevation suggests STEMI.

Troponin testing:

  • Raised troponin suggests MI (with ST elevation = STEMI, without ST elevation = NSTEMI).
  • Normal troponin + normal ECG suggestive of unstable angina.
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8
Q

What is the initial treatment as soon as ACS suspected?

A
  • Initial loading dose of aspirin.
  • GTN to relieve symptoms (morphine if required).
  • O2 if O2 sats are <90%.
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9
Q

What is the treatment immediately after ACS confirmed?

A
  • PCI/CABG.
    (In the case of STEMI, PCI should be urgently carried out within 2 hours).
  • If PCI/CABG not possible, use altepase (a thrombolytic).
  • Commence dual antiplatelet therapy (clopidogrel/prasugrel + aspirin).
    DON’T ADMINISTER P2Y12 INHIBITOR IF IMMEDIATELY HAVING PCI/CABG - THIS WILL BE DONE IN THEATRE.
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10
Q

What is the long term management of ACS?

A

FOR ALL ACS:

  • B blocker (bisoprolol).
  • Dual antiplatelet therapy (aspirin + clopidogrel).
  • Statin (atorvastatin).
FOR MI (STEMI OR NSTEMI):
- ACEI (ramapril) or ARB 2nd line (losartan).

FOR UNSTABLE ANGINA:

  • GTN for any future episodes of angina.
  • ACEI (ramapril) ONLY IF: DIABETIC, CKD OR HEART FAILURE PRESENT.
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11
Q

What is stable angina?

A
  • A form of ischaemic heart disease.

- Angina that occurs on exertion, and is relieved by rest.

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12
Q

What is the clinical presentation of STABLE angina?

A
  • Substernal pain (in some cases can radiate to the jaw/neck).
  • PROVOKED BY EXERCISE/EMOTIONAL STRESS.
  • RELIEVED BY REST/GTN.
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13
Q

What are the risk factors for stable angina?

A
  • Old age.
  • Smoking.
  • Obesity.
  • Diabetes.
  • Hypertension.
  • Male.
  • Raised LDL.
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14
Q

What is the pathophysiology of stable angina?

A
  • Development of lipid-dense plaques in the arterial wall.
  • The plaques cause stenosis.
    When 70-80% stenosis is achieved, stable angina may occur.
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15
Q

What are the investigations used for stable angina?

A
  • Ensure the condition is stable.

Then:
- ECG is 1st line. Usually normal (>50%) but sometimes will be abnormal and give clues to pathological cause.

  • EchoCG is GS, but not always used.
  • Lipid profile (check for hyperlipidemia).
  • Haemoglobin (check for anaemia which can cause angina symptoms).
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16
Q

What is the treatment for stable angina?

A
  • Low dose aspirin.
  • GTN to relieve symptoms.
  • Statin (atorvastatin) to lower LDL.
  • B blocker (bisoprolol) /ACEI (ramapril) to control BP.
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17
Q

What is the major complication of angina?

A
  • MI.
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18
Q

What is the definition of heart failure?

A

The heart is unable to pump enough blood around the body to meet demands for blood and oxygen.

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19
Q

What is the definition of congestive heart failure?

A
  • Heart failure with breathlessness and oedema (due to increased sodium and water levels).
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20
Q

What is the clinical presentation of congestive heart failure?

A
  • Dyspnoea.
  • Tachycardia.
  • S3 gallop.
  • Cardiomegaly.
  • Rales (“rattling heart”).
  • Ankle oedema.
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21
Q

What are the risk factors for congestive heart failure?

A
  • Hypertension.
  • Male.
  • Diabetes mellitus.
  • Dyslipidemia.
  • Old age.
  • Obesity.
  • LV dysfunction/hypertrophy.
  • AF.
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22
Q

What is the pathophysiology of congestive heart failure?

A 
A chronic condition.
Usually associated with LV remodelling due to conditions such as:
- MI
- Cardiomyopathy (e.g. hypertrophic).
- Pulmonary hypertension.
- Valvular heart disease.
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23
Q

What are the investigations used for congestive heart failure?

A

ECG - Signs may be suggestive of underlying pathology (e.g. left axis deviation suggests LVH).

EchoCG. Can detect things like LVH (Diastolic heart failure) or Left ventricular dilation (systolic heart failure). Can also detect valvular heart diseases.

CXR - “ABCDE”. Alveolar oedema (Bat wings), Kerley B lines, Cardiomegaly, Dilated upper lobe vessels, Pleural effusion.

BNP - Increases in heart failure.

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24
Q

What is the treatment for congestive heart failure?

A
  • Lifestyle changes (increased exercise, better diet, weight loss etc.).
  • Loop diuretics (e.g. furosemide).
  • ACEI (ramapril) + B-blocker (bisoprolol).

If ACE not tolerated, ARB (losartan).

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25
What are the main complications of congestive heart failure?
- Pleural effusion. | - AKI (contributed to by the use of loop diuretics/ACEI).
26
What is the mnemonic to remember the ECG changes seen in hyperkalaemia?
"Go, go wide, go tall, go long" - Small/absent P wave - Wide QRS complex - Tall tented T waves - Long PR interval
27
What is acute heart failure?
- Rapid onset/worsening of heart failure symptoms requiring urgent evaluation and treatment.
28
What is the presentation of acute heart failure?
- Dyspnoea. - Ankle oedema. - Raised JVP. - Fatigue. - Heart gallop (S3). - Cold extremities.
29
What are the risk factors for acute heart failure?
- Hypertension. - Old age. - Diabetes mellitus. - Smoking. - Arrhythmia (most commonly AF).
30
What are the investigations used in acute heart failure?
ECG. Usually abnormal (e.g. arrhythmia shown). CXR. "ABCDE" BNP. Raised. EchoCG. Will show underlying pathology, and allow measurement of the LVEF (key for management).
31
What is the management for acute heart failure?
- Prioritise the precipitating event (e.g. MI, SVT). For AHF: - Loop diuretics (e.g. furosemide). - ACEI (ramapril) + B-blocker (bisoprolol). If ACE not tolerated, ARB (spironolactone).
32
What is essential (primary) hypertension?
- Hypertension with no identifiable secondary cause.
33
How is essential hypertension normally diagnosed?
- Usually discovered during a routine blood pressure screening.
34
What are the risk factors for primary hypertension?
- Obesity. - High alcohol intake. - Diabetes mellitus. - Over 60 YO. - FH. - Black, non-hispanic.
35
What is the treatment for primary hypertension?
1st line: Lifestyle modification (stop drinking, exercise more, lose weight, improve diet). 2nd line: Drug treatment. ``` If: Non-diabetic AND black OR Non-diabetic AND over 55 Give amlodipine (CCB), or thiazide diuretic (hydrochlorothiazide) if not tolerated. ``` ``` If: Diabetic OR Under 55 and white Give ramipril (ACEI), or ARB (losartan) if not tolerated. ``` 3rd line: Add in the other drug: If on CCB/thiazide diuretic, add ACEI or ARB. If on ACEI/ARB add CCB or thiazide diuretic.
36
What is Raynaud's phenomenon?
- Vasospasm in the digits that reduces blood flow, causing colour change and pain.
37
What is the most common trigger of Raynaud's phenomenon?
- Cold weather.
38
What investigation is required for Raynaud's phenomenon?
- Just history and examination.
39
How does Raynaud's present?
- Fingers turn white (pallor) then blue (cyanosis) and then red (rubor) usually after exposure to cold temperatures. - Can be painful.
40
What is the treatment for Raynaud's phenomenon?
- Usually just lifestyle changes (keep hands warm, stop smoking). - If still uncontrolled and symptomatic, use nifedipine (CCB).
41
What are the diseases associated with secondary Raynaud's phenomenon? (3 examples).
Connective tissue diseases: - Rheumatoid arthritis. - SLE - Scleroderma (systemic sclerosis).
42
What is the heart sound for aortic stenosis?
- Crescendo-decrescendo ejection systolic murmur.
43
What is the heart sound for aortic regurgitation? | How is the pulse characterised?
- Early diastolic murmur. | - Collapsing pulse.
44
What is the heart sound for mitral stenosis?
- Mid-diastolic murmur.
45
What is the heart sound for mitral regurgitation?
- Pansystolic murmur.
46
If there is a pulmonary valve abnormality (right side of heart), when will it be best heard?
- Best heard during inspiration.
47
What is shock?
- Life threatening, acute circulatory failure. | - Causes inadequate delivery of oxygen to the cells.
48
How does shock present?
- Hypotension. - Cyanosis. - Cold peripheries. - Oliguria. - Dyspnoea.
49
What are the potential causes of shock?
- Septic shock. - Cardiogenic shock (e.g. MI, cardiac arrhythmia). - Obstructive shock (e.g. PE, tension pneumothorax). - Haemorrhagic shock (e.g. aortic dissection, GI bleeding).
50
What is the treatment for shock?
- ABCDE approach. - Secure airway. - Give O2 if sats are low. - Give fluids if BP low (saline usually, blood transfusion if haemorrhagic shock). - Then, concentrate on treating the underlying cause.
51
What is heart block/ AV block?
- Partial or complete interruption of signalling between the atria and ventricles.
52
What is the usual cause of heart block?
- Sclerosis/fibrosis of the conducting system.
53
How is heart block classified? How does each classification show on ECG?
First degree - Constant prolonged PR interval. Second degree (Mobitz type 1) - Progressive lengthening of PR interval until a QRS complex is dropped. Then the cycle repeats. Second degree (Mobitz type 2) - Constant PR interval with randomly dropped QRS complexes. Third degree/complete heart block - No association between the P waves and QRS complexes.
54
How is heart block treated?
Asymptomatic first degree and Mobitz type 1: - No treatment needed - just monitor. Symptomatic first degree and Mobitz type 1 OR asymptomatic Mobitz 2 and third degree: - Stop anti-AV conductive medications (B-blockers, CCBs) - Consider the use of a pacemaker. Symptomatic Mobitz 2 and third degree: - Stop anti-AV conduction medications (B-blockers and CCBs). - URGENT pacemaker.
55
What is bundle branch block?
- Blockage in either the left or right conducting bundle.
56
Where is are the bundles situated in the cardiac conduction system?
- Between the AV node and the purkinje fibres.
57
What is the ECG appearance of a BBB?
Left: Double R wave in V4-6. Right: Double R wave in V1, slurred S in V5-6
58
What is the management for BBB?
Usually no treatment is needed.
59
What is atrial fibrillation? | What is atrial flutter?
- Irregularly irregular atrial rhythm. | - Regular but extremely fast atrial rhythm (usually >200bpm).
60
What are the symptoms for both A fib and A flutter?
A fib may be asymptomatic. Symptoms of A fib and A flutter are: - Dyspnoea. - Chest pain. - Palpitations. - Fatigue.
61
What is the investigation used for A fib and A flutter? what are the findings?
ECG. A fib: Irregularly irregular HR; absent P waves. A flutter: "Saw-tooth pattern"; 2:1 AV block common.
62
What is the treatment for A fib/A flutter?
Haemodynamically unstable: DC cardioversion. Haemodynamically stable: - B blocker (rate control). If B-blocker not tolerated, other options are verapamil (ACEI) or digoxin (cardiac gluconate). - Warfarin (anticoagulation).
63
What is supraventricular tachycardia?
SVT - Signals re-enter the atria from the ventricles, causing a narrow complex tachycardia.
64
What does the ECG look like in SVT?
- Narrow complex tachycardia. | - QRS, P, QRS, P, QRS... with no gaps.
65
What is the treatment for SVT?
1st line: - valsalva manoeuvre. Stimulates the vagal nerve, hopefully restoring normal heart rhythm. - Carotid massage another option. 2nd line: - Adenosine IV (Class V anti-arrhythmic).
66
What are the three main types of cardiomyopathy?
- Hypertrophic cardiomyopathy. - Dilated cardiomyopathy. - Restrictive cardiomyopathy.
67
What is dilated cardiomyopathy? How is it diagnosed? How is it treated?
- Dilated LV leading to poor function and heart failure. - Diagnosed with echoCG - shows thickened LV wall. - Treated with B-blokcer/ACEI (heart failure).
68
What is hypertrophic cardiomyopathy? How is it diagnosed? How is it treated?
- Increased thickness of the LV wall. - Diagnosed with echoCG - shows thickened LV wall. - Treated with B-blocker/ACEI (heart failure).
69
What is dilated cardiomyopathy? | What is the epidemiology of dilated cardiomyopathy?
- Fibrosis of the myocardium. - More common in the elderly. - Presents as heart failure.
70
What is pericarditis?
- Inflammation of the pericardium, often constrictive and impairs diastolic function.
71
What is the presentation of pericarditis?
- Chest pain worse on inspiration and/or lying down. - Pericardial friction rub. - Fever (if infective).
72
How does pericarditis show on an ECG?
- ST elevation. | - PR depression.
73
What is the main complication of pericarditis?
- Cardiac tamponade. Fluid in the pericardial sack.
74
How does cardiac tamponade present?
- Muffled heart sounds. - Raised JVP. - Tachycardia.
75
What is the treatment for cardiac tamponade?
- Urgent pericardiocentesis.
76
What is the treatment for pericarditis?
- Usually, just NSAIDS and colchicine. | - If infective, IV antibiotics.
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