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Yr 3 - Core Conditions > CVS > Flashcards

CVS Flashcards

1
Q

Give some red flag symptoms for chest pain

A
  • SOB
  • Not relieved by rest
  • Not relieved by GTN spray
  • Weight loss
  • New dyspepsia
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2
Q

What is acute coronary syndrome?

A

A sudden reduction in blood flow to the heart.

It encompasses a variety of diagnoses and can be subcategorised into:

  1. ST-elevation ACS (STEMI)
  2. Non ST elevation ACS (NSTEMI)
  3. Unstable angina
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3
Q

What is the cause of ACS?

A

ACS is caused by a mismatch between myocardial oxygen demand and myocardial oxygen delivery

In some cases, myocardial supply and demand mismatch may be caused by conditions that only indirectly affect the coronary arteries (e.g. severe anaemia, hypotension, tachycardia, aortic stenosis, PE) → address underlying cause

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4
Q

Give some risk factors for ACS

A
  • These include any factors which increase the risk of coronary artery atherosclerosis
  • Modifiable:
    • Obesity
    • Smoking
    • Longstanding hypertension
    • Hyperlipidaemia
  • Non-modifiable:
    • Male sex
    • Older age
    • Diabetes
    • Renal insufficiency
    • Previous history of ACS/ischaemic heart disease
    • FH of ACS/ischaemic heart disease
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5
Q

Give some differentials for ACS

A
  • VTE
  • MSK
  • Respiratory; pneumothorax, pneumonia
  • GI symptoms; heartburn
  • Anxiety
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6
Q

Give some pathologies that can cause myocardial damage in the absence of coronary artery pathology and thus present with a raised serum troponin and ECG changes

A
  • Myocarditis
  • Pericarditis
  • PE
  • Aortic dissection
  • Acute heart failure
  • Arrhythmias
  • Sepsis
  • Cardiotoxic agents
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7
Q

Give the red flag symptom of ACS

A

Chest pain

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8
Q

What investigations would be required in ACS

A

Bedside:

  • 12-lead ECG
  • Blood glucose

Labs:

  • Troponin
  • FBC
  • U&Es
  • Glucose

Imaging:

  • Coronary angiography
  • Echocardiogram
  • CXR
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9
Q

What is troponin?

A

a structural protein solely found in cardiac myocytes

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10
Q

What does the presence of troponin in the blood indicate?

A

myocardial necrosis

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11
Q

What troponin levels are indicative of myocardial damage?

A

Troponin 3x standard deviations from normal range

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12
Q

Why is an FBC useful in the context of ACS?

A

Low Hb → underlying anaemia can exacerbate ACS (increase risk of negative outcomes) or be indicative of an occult bleed

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13
Q

Why is it vital to check kidney function in ACS?

A

Cardiac troponin levels are challenging to interpret among patients with CKD → raised troponin levels and non-coronary artery related myocardial damage can be seen in CKD patients

CKD is also a risk factor for coronary artery disease

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14
Q

Why is it essential to check blood glucose in ACS?

A

Hyperglycemia is a frequent condition in patients ACS → caused by an inflammatory and adrenergic response to ischaemic stress, when catecholamines are released and glycogenolysis induced.

Hyperglycaemia can lead to poorer outcomes

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15
Q

Why should a CXR be conducted in ACS?

A

rule out other potential causes of chest pain e.g. pneumothorax, pneumonia

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16
Q

Aetiology of a STEMI?

A

Mismatch almost always caused by total occlusion of a coronary artery from atherosclerotic plaque rupture and subsequent thrombus formation

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17
Q

What are the diagnostic features for unstable angina?

A

Cardiac chest pain + abnormal/normal ECG + normal troponin

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18
Q

What are the diagnostic features for NSTEMI?

A

Cardiac chest pain + abnormal/normal ECG (but not ST elevation) + raised troponin

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19
Q

What are the diagnostic features for STEMI?

A

Cardiac chest pain + persistent ST elevation/new LBBB

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20
Q

ACS may atypically present with no pain. Who is this more common in?

A

Elderly, diabetics

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21
Q

Give some atypical presentations of ACS

A
  • Epigastric pain
  • No pain (more common in elderly and patients with diabetes)
  • Acute breathlessness
  • Palpitations
  • Acute confusion
  • Diabetic hyperglycaemic crisis
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22
Q

Location of ST elevation → leads II, III and aVF

a) what area of myocardium?
b) which coronary artery?

A

area → inferior

coronary artery → right coronary artery

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23
Q

Location of ST elevation → V1-V2

a) what area of myocardium?
b) which coronary artery?

A

area → septum

artery → proximal left anterior descending artery (LAD)

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24
Q

Location of ST elevation → V3-4

a) what area of myocardium?
b) which coronary artery?

A

area → anterior

artery → LAD

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25
Q

Location of ST elevation →V5-6

a) what area of myocardium?
b) which coronary artery?

A

area → lateral/apex

artery → distal LAD, left circumflex artery (LCx), right coronary artery (RCA)

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26
Q

Location of ST elevation → leads I, aVL

a) what area of myocardium?
b) which coronary artery?

A

area → lateral

artery → left circumflex artery

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27
Q

Serum troponin levels typically rise how long after MI begins?

A

3 hours

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28
Q

What do low levels of troponin indicate? Differentials?

A

No myocardial death

Patient not having MI but may be having unstable angina

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29
Q

What do mildly raised levels of troponin indicate? Differentials?

A
  • This is an equivocal result and may be due to other non-MI related factors
  • These patients need a 6-12 hour repeat test:
    • If repeat troponin is raised → having an MI
    • If repeat troponin is stable or falling → unlikely to be having an MI
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30
Q

What do definitely raised levels of troponin indicate? Differentials?

A

MI confirmed

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31
Q

Give some non-ACS causes of a raised troponin

A
  • Pericarditis
  • Myocarditis
  • Arrhythmias
  • Defibrillation
  • Acute heart failure
  • Pulmonary embolus
  • Type A aortic dissection
  • Chronic kidney disease
  • Prolonged strenuous exercise
  • Sepsis
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32
Q

Acute management steps of a STEMI?

A
  1. Oxygen (aim for sats >90%)
  2. Aspirin 300mg (protocols often also call for 2nd antiplatelet e.g. clopidogrel 300mg or ticagrelor 180mg)
  3. Sublingual GTN spray
  4. IV morphine/diamorphine
  5. Primary percutaneous coronary intervention (PPCI) if possible
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33
Q

Purpose of GTN spray in STEMI?

A

Symptom relief

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34
Q

Purpose of IV morphine/diamorphine in STEMI?

A
  • Symptom relief
  • Also causes vasodilation reducing preload on heart
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35
Q

Who is eligible for PPCI?

A

Those who present within 12 hours of onset of pain

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36
Q

Acute management of NSTEMI (and unstable angina)?

A
  1. Oxygen
  2. Aspirin 300mg and fondaparinux
  3. Sublingual GTN spray
  4. IV morphine/diamorphine
  5. Start antithrombin therapy e.g. LMWH or fondaparinux if they are for an immediate angiogram
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37
Q

What is fondaparinux?

A

A synthetic anticoagulant

Similar to low molecular weight heparins, it is an indirect inhibitor of factor Xa, but it does not inhibit thrombin at all.

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38
Q

In all post MI patients, what 5 drugs should they be offered?

A
  1. Aspirin 75mg OM + 2nd antiplatelet
  2. Beta blockers (bisoprolol)
  3. ACEi (ramipril)
  4. High dose statin (e.g. atorvastatin 80mg ON)
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39
Q

Why should all post-MI patients have an echocardiogram?

A

to assess systolic function and any evidence of heart failure should be treated

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40
Q

Aetiology of a STEMI?

A

Complete occlusion of a coronary artery from atherosclerotic plaque rupture and subsequent thrombus formation

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41
Q

Aetiology of an NSTEMI?

A

Severe but incomplete stenosis/occlusion of a coronary artery:

a) Partial coronary artery occlusion from a rupture plaque (most common)
b) Partial occlusion from a stable plaque
c) Coronary artery vasospasm (Prinzmetal’s angina)
d) Coronary arteritis

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42
Q

What is Dressler’s syndrome?

A

A post-infarction pericarditis that tends to occur 2-6 weeks following an MI

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43
Q

What is the presumed pathophysiology behind Dressler’s syndrome?

A

Thought to be autoimmune reaction against antigenic proteins formed as the myocardium recovers

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44
Q

Presentation of Dressler’s syndrome?

A

Fever, pleuritic chest pain, pericardial effusion, & raised ESR

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45
Q

Management of Dressler’s syndrome?

A

high dose aspirin

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46
Q

What is the most common cause of death following an MI?

A

Ventricular fibrillation

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47
Q

How can an MI lead to cardiogenic shock?

A

If a large part of the ventricular myocardium is damaged in the infarction, the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock

Other causes of cardiogenic shock include ‘mechanical’ complications e.g. left ventricular free wall rupture

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48
Q

How can MI lead to congestive heart failure?

A

Consequence of impairment of heart muscle function 2ary to ischaemia

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49
Q

Pharmacological management of congestive heart failure 2ary to MI?

A
  • Loop diuretics (furosemide) to decrease fluid overload
  • ACEi & beta-blockers have been shown to improve long term prognosis
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50
Q

Heart (AV) block is more common following what type of MI (i.e. what area)? Why?

A

Inferior MI → as the RCA supplies the SA node

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51
Q

Dressler’s syndrome vs post-MI pericarditis?

A

Pericarditis → typically within first 48 hours

Dresslers → within 2-6 weeks

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52
Q

Features of pericarditis?

A
  • Pain worse on lying flat
  • Pericardial tub may be heard
  • Pericardial effusion may be seen on echo
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53
Q

How can an MI lead to a LV aneurysm?

A

Aneurysm can occur following an anterior MI where the myocardium can be susceptible to wall stress, leading to aneurysm formation

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54
Q

What are the potential complications of a LV aneurysm?

A

Thrombus may form within aneurysm – increasing risk of stroke, acute limb ischaemia, mesenteric ischaemia

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55
Q

Treatment of LV aneurysm?

A

Anticoagulation

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56
Q

How can an MI lead to LV free wall rupture? What are the complications of this?

A

Necrosis of the free walls of either ventricle can lead to rupture, allowing blood into the pericardial space.

Leads to rapid tamponade and often cardiac arrest/death within seconds

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57
Q

How can an MI lead to acute mitral regurgitation?

A

May be due to ischaemia or rupture of papillary muscle

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58
Q

What type of murmur is heard in acute mitral regurgitation?

A

Pansystolic murmur heart best at apex (rolling patient to their left with stethoscope over mitral area in CVS exam)

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59
Q

What 3 features define stable angina?

A
  1. Brought on by physical activity
  2. Alleviated by rest or GTN spray within minutes
  3. Constriction like pain in chest/neck/arm/jaw
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60
Q

Bedside tests for stable angina?

A
  • CVS exam – heart sounds, signs of heart failure, BMI
  • 12-lead ECG → this will be normal
  • Pregnancy test
  • Glucose
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61
Q

Lab tests for stable angina?

A
  • FBC → exclude anaemia (can exacerbate angina), infection
  • TFTs → exclude hyperthyroidism (can exacerbate angina)
  • LFTs (prior to statins)
  • Lipid profile
  • HbA1c
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62
Q

What is the gold standard imaging for angina? Why?

A

CT coronary angiography

This gives a detailed view of the coronary arteries, highlighting any narrowing

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63
Q

What is the pharmacological 1st line management for stable angina?

A

Aspirin

Statin

Beta blocker (or rate limiting CCB)

Sublingual GTN spray

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64
Q

What side effects of GTN spray should patients be warned about?

A

headaches, flushing, dizziness

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65
Q

How should GTN spray be used?

A
  • Initial dose when symptoms come on
  • 2nd dose after 5 minutes if still symptomatic
  • Call ambulance if pain not subsided after 2 doses → may indicate ACS
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66
Q

2 surgical management options for angina?

A
  1. Percutaneous coronary intervention (PCI)
  2. Coronary artery bypass graft (CABG)
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67
Q

Define unstable angina

A

An ACS that is defined by the absence of biochemical evidence of myocardial damage:

  • Prolonged (>20 minutes) angina at rest
  • New onset of severe angina
  • Angina that is increasing infrequency, longer in duration, or lower in threshold
  • Angina that occurs after a recent episode of MI
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68
Q

What is atrial fibrillation?

A

: A cardiac arrhythmia characterised by disorganised electrical activity within the atria resulting in ineffective atrial contraction and irregular ventricular contraction (due to delay at the AV node so that only some of the atrial impulses are conducted to the ventricles).

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69
Q

What is the most common sustained cardiac arrhythmia?

A

AF

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70
Q

What is fast AF?

A

When the ventricular rate is >100bpm

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71
Q

Define paroxysmal AF

A

episodes last >30 seconds but <7 days; are self-terminating and recurrent

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72
Q

What type of arrhythmia is AF?

A

supraventricular cardiac arrhythmia

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73
Q

Where does AF often originate from?

A

the left atrial myocytes which extend as sleeves around the pulmonary veins

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74
Q

How does AF affect ventricular contraction?

A

Irregular ventricular contraction - depends on speed of AVN conduction

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75
Q

Why can AF predispose to systemic embolic complications?

A

Presence of chaotic electrical activity → ineffective atrial contraction → blood stasis within atria → increased chance of thrombosis and subsequently embolic complications

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76
Q

What are the 2 most common cardiac causes of AF in the UK?

A
  1. Ischaemic heart disease
  2. Hypertension
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77
Q

What is the most common cardiac cause of AF in developing countries?

A

Rheumatic heart disease

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78
Q

Give the 3 major risk factors for AF

A
  1. HTN
  2. Obesity
  3. Alcohol
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79
Q

Most common complication of AF?

A
  • Thromboembolic events:
    • Ischaemic stroke
    • Mesenteric ischaemia
    • Acute limb ischaemia
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80
Q

How can AF lead to a risk of bleeding?

A

Due to anticoagulants

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81
Q

Give 2 medications that may cause AF?

A

Bronchodilators

Thyroxine

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82
Q

Symptoms of AF?

A
  • Some patients can be asymptomatic, even when causing tachycardia and so may eb an incidental finding on clinical examination or when doing a 12-lead ECG
  • SOB
  • Palpitations
  • Chest discomfort
  • Syncope/dizziness: due to bradycardia (particularly in paroxysmal AF)
  • Light-headedness
  • Reduced exercise tolerance
  • Malaise
  • Remember – a TIA or stroke can be the presenting complaint!!!
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83
Q

Signs of AF?

A
  • Irregularly irregular pulse
  • Radial-apical deficit/delay
  • Tachycardia
  • Co-existing heart failure symptoms
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84
Q

12-lead ECG features of AF?

A
  • Absent P-wave with a chaotic baseline
  • Fibrillation waves (vest seen in lead II and V1)
  • Tachycardia
  • Irregularly irregular rhythm – irregular R-R intervals
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85
Q

Lab tests in AF?

A
  • FBC – assess for reversible causes e.g. acute infection (raised WCC)
  • U&Es – assess for reversible causes e.g. hypokalaemia/hyponatraemia
  • LFTs – establish baseline hepatic function before giving anticoagulants
  • TFTs – rule out/in hyper/hypothyroidism (raised T4 & low TSH  hyperthyroidism)
  • CRP – assess for reversible causes e.g. acute infection (raised CRP)
  • Clotting screen – before giving anticoagulants
  • BP – assess for underlying heart failure (N.B. AF can cause raised BNP without evidence of heart failure)
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86
Q

Imaging in AF?

A
  • Echocardiogram – US of heart can help identify other heart-related problems e.g valve disease
  • CXR: Can assess for changes associated with heart failure e.g. cardiomegaly, pleural effusion)
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87
Q

Why is a CXR useful in AF?

A

Can assess for changes associated with heart failure e.g. cardiomegaly, pleural effusion)

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88
Q

What are the 3 1st line pharmacological management steps for AF?

A
  1. Rate control
  2. Rhythm control
  3. Anticoagulants
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89
Q

Who should rate control drugs NOT be offered to in the context of AF?

A
  • Whose AF has reversible cause
  • Who have heart failure thought to be primarily caused by AF
  • New onset AF
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90
Q

What 2 classes of drugs can be used to control rate in AF?

A
  1. Beta blockers e.g. bisoprolol
  2. Rate limiting CBB e.g. verapamil, diltiazem (note NOT amiodarone)
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91
Q

What are beta blockers contraindicated in?

A

Asthma

COPD

Hypotension

92
Q

What are CCBs contraindicated in?

A

Heart failure

93
Q

If neither beta blockers nor CCBs are appropriate for rate control in AF, which drug can be used?

A

Digoxin

94
Q

What are the 2 methods to control rhythm in AF?

A
  1. Electrical cardioversion
  2. Pharmacological cardioversion
95
Q

Give 3 examples of drugs that can be used to control rhythm in AF

A
  1. Flecainide
  2. Amiodarone
  3. Sotalol
96
Q

What class of drug is Flecainide?

A

Class I antiarrhythmic

97
Q

What is sotalol?

A

Beta blocker with additional K channel blocker action

98
Q

Why is long term anticoagulation needed in AF?

A

the main complication of AF is embolic stroke.

99
Q

Give 3 possible anticoagulants to use in the long term management of AF

A
  1. DOACs
  2. Warfarin
  3. LMWH
100
Q

Which anticoagulant is generally considered the one of choice in AF?

A

DOACs

101
Q

Half life of DOACs?

A

12-hour half-lives (patients not covered if miss a dose)

102
Q

What does warfarin initially require cove with for the first 5 days?

A

LLMWH - warfarin is initially prothrombotic

103
Q

What is the only oral anticoagulant licensed for valvular AF?

A

Warfarin

104
Q

What is valvular AF

A

AFib is considered valvular when it’s seen in people who have a heart valve disorder or a prosthetic heart valve.

Nonvalvular AFib generally refers to AFib caused by other things, such as high blood pressure or stress.

105
Q

Options for permanent treatment of AF?

A

Atrial ablation or pacemaker insertion

106
Q

How does anaemia affect ACS?

A

Anaemia further potentiates this imbalance between myocardial oxygen supply and demand by both

a) reducing oxygen‐carrying capacity
b) simultaneously increasing myocardial oxygen consumption via increased cardiac output

107
Q

Define essential hypertension

A

HTN where no identifiable cause is found

108
Q

What is the most common type of hypertension?

A

Essential (90%)

109
Q

How common is hypertension?

A

Around ⅓ adults in UK

110
Q

Which ethnicities are at higher risk of HTN?

A

Black African and Black Caribbean origin are at higher risk

111
Q

What is the single biggest risk factor for CVS disease?

A

HTN

112
Q

What are some red flag symptoms of accelerated or malignant HTN?

A
  • Headache
  • Visual disturbances
  • Seizures
  • N&V
  • Chest pain
113
Q

What is ambulatory blood pressure monitoring (ABPM)?

A

BP during normal activities of daily life recorded using a 24-hour blood pressure monitor

114
Q

What does home blood pressure monitoring (HBPM) consist of?

A

recorded by patient 2x a day (morning & evening)

115
Q

What is the 1st line pharmacological management option for patients <55y who are not of Black African or African-Caribbean descent?

A

ACEi (ramipril)

116
Q

What is the 1st line pharmacological management option for patients with diabetes (regardless of ethnicity)?

A

ACEi (ramipril)

117
Q

What is the 1st line pharmacological management option for patients patients >55y (without diabetes) or of Black African or African-Caribbean descent (any age, without diabetes)?

A

Calcium channel blocker e.g. amlodipine

118
Q

What is offered is an ACEi is not tolerated in HTN?

A

Angiotensin II receptor blocker e.g. losartan

119
Q

PRESCRIBING for HTN:

A
120
Q

If a CCB is not tolerated in HTN, what can be offered instead?

A

Thiazide-like diuretic e.g. indapamide

121
Q

Define a DVT

A

The formation of a blood clot in the deep veins of a limb, most commonly affecting those of the legs or pelvis, which partially or completely obstructs blood flow

122
Q

DVTs can be provoked or unprovoked. What does this mean?

A

Provoked - presence of risk factors (80%)

Unprovoked - absence of risk factors

123
Q

What is thrombophilia?

A

a condition that increases your risk of blood clots.

124
Q

What is factor V Leiden?

A

A thrombophilia - mutation in factor V means it is unable to be degraded by protein C

125
Q

What is antiphospholipid syndrome?

A

An autoimmune condition in which the immune system mistakenly creates antibodies that attack tissues in the body. These antibodies can cause blood clots to form in arteries and veins.

126
Q

Give some inherited risk factors for DVT

A
  • Family history (1st degree relative with VTE)
  • Thrombophilia
  • Antiphospholipid syndrome
  • Factor V Leiden
127
Q

What is the most serious complication of a DVT?

A

PE – 10% of people with untreated DVT will develop PE

128
Q

Give some signs & symptoms of a PE

A

Pleuritic chest pain, SOB, tachycardia, syncope, hypotension, heart failure, sudden death

129
Q

What is the most common complication following a DVT?

A

Post-thrombotic syndrome (up to 50% will develop this)

130
Q

What is post-thrombotic syndrome?

A

chronic pain, swelling, and other symptoms in your leg in the months following a DVT

131
Q

Signs & symptoms of a DVT?

A
  • Unilateral leg pain (throbbing) and swelling
  • Pitting oedema
  • Tenderness over deep veins of leg
  • Heavy ache in affected area
  • Pain may be worse when dorsiflexing foot
  • Can be asymptomatic
  • Skin changes e.g. oedema, redness, warmth
132
Q

What screening test can be used to assess DVT risk?

A

Well’s score

133
Q

What Wells score indicates a d-dimer test?

A

Above or equal to 2

134
Q

Investigations in DVT?

A
  • Wells score
  • D-dimer
  • Leg circumference
  • Imaging → duplex US
  • Obs
  • Bloods - FBC, U&Es, d-dimer, LFTs
135
Q

How do you measure leg circumference in a potential DVT?

A

Measure circumference of leg 10cm below tibial tuberosity and compare with asymptomatic leg → a difference >3cm indicates DVT

136
Q

What is the 1st line imaging in a DVT?

A

Duplex US

137
Q

1st line pharmacological management in DVT?

A

DOACs (warfarin if these are contraindicated)

138
Q

Define chronic/congestive heart failure

A

When the heart is unable to pump sufficiently to maintain blood flow to meet the body’s needs.

139
Q

What are the most common causes of CHF in UK?

A
  1. Coronary artery disease
  2. Hypertension
  3. Valvular disease (commonly aortic stenosis)
  4. Arrhythmias (commonly AF)
140
Q

Which parasitic disease is a common cause of CHF in central/south america?

A

Chagas disease

141
Q

What is the equation for cardiac output?

A

Cardiac output (CO) = Heart rate (HR) x Stroke volume (SV)

142
Q

Systolic vs diastolic HF?

A

Systolic - impaired LV contraction

Diastolic - impaired LV relaxation and filling

143
Q

What is systolic HF also called?

A

HF with reduced ejection fraction

144
Q

What is diastolic HF also called?

A

HF with preserved ejection fraction

145
Q

Causes of diastolic HF?

A
  • Hypertrophic obstructive cardiomyopathy
  • Restrictive cardiomyopathy
  • Cardiac tamponade
  • Constrictive pericarditis
146
Q

Causes of systolic HF?

A
  • Ischaemic heart disease
  • Dilated cardiomyopathy
  • Myocarditis
  • Infiltration (e.g. in haemochromatosis or sarcoidosis)
147
Q

Does L or R HF cause venous congestion?

Does L or R HF cause pulmonary congestion?

A

L - pulmonary

R - venous

148
Q

Give some symptoms of pulmonary congestion caused by LHF

A
  • SOB on exertion
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Nocturnal cough (+/- pink frothy sputum)
149
Q

What is paroxysmal nocturnal dyspnoea (PND)?

A
  • Suddenly waking at night with a severe attack of SOB and cough (maybe wheeze)
  • Have to sit on side of bed or walk around and gasp for breath – feel they are suffocating
  • Symptoms improve over several minutes
150
Q

Give some signs of pulmonary congestion caused by LHF

A
  • Tachypnoea
  • Bibasal fine crackles on lung auscultation
151
Q

HF can also cause systemic hypoperfusion. Give some signs of this

A
  • Prolonged CRT
  • Cyanosis
  • Hypotension
  • Low O2 sats
152
Q

Give some symptoms caused by venous congestion caused by RHF

A
  • Ankle congestion (peripheral oedema)
  • Weight gain
  • Abdominal distention & discomfort (ascites)
  • Anorexia/nausea
153
Q

Give some signs caused by venous congestion caused by RHF

A
  • Raised JVP
  • Pitting ankle/sacral oedema
  • Tender smooth hepatomegaly
  • Ascites
  • Transudative pleural effusion (typically bilateral)
154
Q
A

Transudate is fluid buildup caused by systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system (lower protein)

Exudate is fluid buildup caused by tissue leakage due to inflammation or local cellular damage (higher protein)

155
Q

Important blood tests in HF?

A
  • BNP test
  • FBC
  • U&Es
  • LFTs
  • TFTs
  • Glucose & lipid profile
156
Q

What is BNP?

A

Brain natriuretic peptide (BNP) is a hormone secreted by cardiac cells in response to increased pressure within the heart i.e. released by ventricles in response to myocardial stretch

157
Q

Why is a FBC important in HF?

A

Anaemia (high output HF)

Infection

158
Q

Why are TFTs important in HF?

A

Hyperthyroidism (high output HF)

159
Q

Why are U&Es important in assessing HF?

A

Renal function

Assess for hyponatraemia

160
Q

What is the most common electrolyte disorder?

A

Hyponatraemia

161
Q

What causes hyponatraemia in heart failure?

A

HF increases anti-diuretic hormone (ADH/vasopressin) → reduced excretion of water → dilution of sodium

162
Q

Why are LFTs important in assessing HF?

A

Assessing hepatic congestion → Passive hepatic congestion due to increased central venous pressure may cause elevations of liver enzymes (ALP, ALT, AST) and both direct and indirect serum bilirubin.

Assessing acute hepatocellular necrosis → Impaired perfusion from decreased cardiac output may be associated with acute hepatocellular necrosis with marked elevations in serum aminotransferases (ALT).

163
Q

What imaging can be done in HF?

A
  • Echocardiogram
  • CXR
164
Q

What is the purpose of an echocardiogram in HF?

A

Confirm presence and degree of ventricular dysfunction which is measured by ejection fraction.

165
Q

How is ventricular dysfunction measured?

A

By ejection fractino

166
Q

What ejection fraction indicates HF?

A

<50%

167
Q

What does a >40% EF but a raised BNP indicate?

A

HF with preserved EF

168
Q

What signs can be seen on a CXR in HF (ABCDEF)

A

A - Alveolar oedema

B - Kerley B lines (caused by interstitial oedema)

C - Cardiomegaly (cardiothoracic ratio >0.5)

D - upper lobe Division

E - pleural Effusions

F - Fluid in the horizontal fissure

169
Q

What is the pharmacological first line management in HF? (ABAL)

A

A - ACEi (ramipril)

B - Beta blocker (bisoprolol)

A - Aldosterone antagonist when symptoms not controlled with A & B (spironolactone or eplerenone)

L - Loop diuretics (e.g. furosemide)

170
Q

What can ramipril be titrated up to in HF?

A

ramipril titrated as tolerated up to 10mg once daily

171
Q

What can be used in HF if an ACEi is not tolerated?

A

ARB e.g. candasartan

172
Q

Are ARBs or ACEi contraindicated in valvular heart disease?

A

ACEi

173
Q

What can bisoprolol be titrated up to in HF?

A

bisoprolol titrated as tolerated up to 10mg once daily

174
Q

What beta blocker is most often chosen in HF? Why?

A

Bisoprolol - one of the only cardio-selective bet blockers that has been shown to reduce mortality in HF

175
Q

How may spironolactone be useful in the management of HF?

A
  1. Lowers BP
  2. May reduce risk of volume overload which reduces risk of HF and CVS disease
176
Q

When giving a HF patient furosemide, what must be monitored carefully?

A

Kidney function

177
Q

What is high output HF?

A

Cardiac output is normal but there is an increase in peripheral metabolic demands which exceeds those that can be met with maximal cardiac output.

178
Q

Give some cause of output HF? (AAPPTT)

A

A - Anaemia

A - Arteriovenous malformation

P - Pregnancy

P - Paget’s disease

T - Thyrotoxicosis

T - Thiamine deficiency

179
Q

What occurs in LV failure?

A

LV is unable to adequately move blood through the left side of the heart and out into the body.

180
Q

How does LVF lead to pulmonary oedema?

A
  • This causes a backlog of blood that increases the amount of fluid stuck in the left atrium
  • As the vessels in this area are engorged with blood due to the increased volume and pressure, they leak fluid and are unable to reabsorb fluid from the surrounding tissues → pulmonary oedema
181
Q

Define pulmonary oedema

A

Where the lung tissues and alveoli become full of interstitial fluid which interferes with normal gas exchange, causing SOB, oxygen desaturation etc.

182
Q

Is the fluid seen in pulmonary oedema due to LVF transudative or exudative?

A

Transudative

183
Q

What type of respiratory failure does LVF cause?

A

Type 1 (low O2 without an increase in CO2 in blood)

184
Q

Give some triggers for LVF

A
  • Iatrogenic (e.g. aggressive IV fluids in frail elderly patient with impaired LV function)
  • Sepsis
  • MI
  • Arrythmias
185
Q

What causes Kerley B lines?

A

Fluid in septal lines

186
Q

Initial management for LVF and pulmonary congestion? (Pour SOD)

A

Pour away (stop) their IV fluids

Sit up (takes fluid to bases, leaving upper lungs clear for better gas exchange)

Oxygen - caution in patients with COPD

Diuretics e.g. IV furosemide

187
Q

What are higher levels of BNP associated with?

A

Poorer prognosis

188
Q

Give some factors that increase BNP levels

A
  • Left ventricular hypertrophy
  • Ischaemia
  • Tachycardia
  • Right ventricular overload
  • Hypoxaemia (including PE)
  • GFR <60 ml/min
  • Sepsis
  • COPD
  • Diabetes
  • Age >70 y/o
  • Liver cirrhosis
189
Q

Give some factors that decrease BNP levels

A
  • Obesity
  • Diuretics
  • ACE inhibitors
  • Beta-blockers
  • Angiotensin II receptor blockers (ARBs)
  • Aldosterone antagonists
190
Q

what are some signs to look for in the hands during a CVS exam?

A
  • Oslers nodes
  • Janeway lesions
  • Splinter haemorrhages
  • Pallor
  • Peripheral cyanosis
  • Tar staining
  • Clubbing
191
Q

what are some signs to look for in the eyes during a CVS exam?

A
  • Conjunctival pallor
  • Corneal arcus
  • Xanthelasma
  • Kayser-Fleicher rings
192
Q

what are some signs to look for in the mouth during a CVS exam?

A
  • Angular stomatitis
  • High arched palate
  • Central cyanosis
  • Dental hygiene
193
Q

What is rheumatic fever a delayed reaction to?

A

Strep A infection (most commonly Strep. pharyngitis)

194
Q

What is the most common valvular defect following rheumatic heart disease?

A

Mitral stenosis

195
Q

What type of murmur does mitral stenosis cause?

A

Mid-diastolic murmur heard over the apex (mitral valve)

196
Q

What heart condition can mitral stenosis lead to?

A

AF due to increases in left atrial pressure and concomitant atrial dilation

197
Q

What type of murmur does aortic stenosis cause?

A

Ejection systolic murmur that radiates to the carotid arteries

198
Q

Which valve pathology causes a narrow pulse pressure?

A

Aortic stenosis

199
Q

Which valve pathology causes a wide pulse pressure?

A

Aortic regurgitation

200
Q

What happens in aortic dissection?

A

Tear in tunica intima of wall of aorta, creating a false lumen which fills with large volumes of blood

201
Q

Classic pain felt in aortic dissection?

A

Tearing chest pain which radiates to back

202
Q

What may be seen on the CXR of someone with aortic dissection

A

A widened mediastinum

203
Q

How does amiodarone affect the P450 system?

A

Is an inhibitor

204
Q

How does amiodarone affect the risk of statin-induced rhabdomyolysis?

A

Increases risk as amiodarone is an enzyme inhibitor

205
Q

Which artery most likely supplies the AV node?

A

Right coronary artery

206
Q

What is heart failure with preserved ejection fraction?

A

This would lead to abnormal filling of the ventricles during diastole and a normal ejection fraction on the echo (>50%)

207
Q

What is heart failure with preserved ejection fraction typically 2ary to?

A

Usually caused by ventricular stiffness 2ary to long-standing HTN or ventricular hypertrophy

208
Q

Describe the ECG changes in hyperkalaemia

A
  • Small or absent P waves
  • Tall, tented T waves
  • Broad bizarre QRS complexes
209
Q

Describe the ECG changes in hypokalaemia

A
  • ST segment depression
  • U waves
  • Small or absent T waves (occasion ally inversion)
210
Q

What type of murmur is heard in aortic regurgitation? Why?

A

Early diastolic:

  • Aortic valve allows blood to flow back into the LV when the heat relaxes
  • As a result of the flow back into the ventricle, a murmur can be auscultated in the aortic area during diastole
211
Q

Give 3 features seen in aortic regurgitation

A
  1. Wide pulse pressure
  2. Early diastolic murmur
  3. Collapsing pulse
212
Q

Give 2 causes of aortic regurgitation

A

Infective endocarditis

Aortic dissection

213
Q

How do nitrates affect intracellular calcium?

A

Nitrates cause a decrease in intracellular calcium.

214
Q

How does NSAIDs affect the anti-hypertensive effects of ACEi?

A

NSAIDs reduce the anti-hypertensive effects of ACEi.

215
Q

What electrolyte abnormality can the combined use of PPIs and thiazide diuretics cause?

A

severe hyponatraemia

216
Q

Impact of thiazide diuretics and gout?

A

Thiazide-like diuretics can cause gout.

217
Q

What is the most common ECG sign in PE?

A
  • Sinus tachycardia (most common)
  • Signs of right heart strain
218
Q

Describe the volume of distribution of warfarin

A

Warfarin has a small volume of distribution as it is protein bound.

219
Q

How do antacids affect the absorption of ACEi?

A

Antacids reduce the absorption of ACEi

220
Q

What is Dressler’s syndrome?

A

A 2ary pericarditis that usually occurs 1-6 weeks post MI

221
Q

Symptoms of Dressler’s syndrome?

A
  • It is characterised by pleuritic chest pain, low-grade fever and pericarditis
  • Pain can radiate to left shoulder and is worse on lying down
222
Q

Management of Dressler’s syndrome?

A

high-dose aspirin

223
Q

How do NSAIDs affect the efficacy of diuretics?

A

When NSAIDs are taken with a diuretic the effect of the diuretic is reduced and any heart failure may be exacerbated

224
Q

Why are NSAIDs contraindicated in HF?

A

NSAIDs can lead to an elevation in blood pressure, especially in patients treated with drugs inhibiting RAAS.

Patients with congestive heart failure are at risk of the disease decompensation while taking NSAIDs.

225
Q

Effect of PPIs on sodium level?

A

hyponatraemia

Yr 3 - Core Conditions (33 decks)

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