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Medicine Phase 2a > CVS > Flashcards

CVS Flashcards

1
Q

Where is apex beat

A

5th left intercostal space and mid-clavicular line

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2
Q

Stroke Volume

A

Volume of blood ejected from each ventricle during systole

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3
Q

Cardiac output

A

Volume of blood each ventricle pumps as a function of time (litres per minute)

Stroke Volume (L) x Heart rate (BPM)

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4
Q

Total Peripheral Resistance

A

The total resistance to flow in systemic blood vessels from beginning of aorta to vena cava - arterioles provide the most resistance

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5
Q

Preload

A

Volume of blood in the left ventricle which stretches the cardiac myocytes before left ventricular contraction

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6
Q

What is effect on preload when veins dilate?

A

Decreased preload since venous return decreases (decrease in P in right atrium)

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7
Q

End-Diastolic Volume

A

How much blood is in the ventricles before it pumps

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8
Q

Afterload

A

The pressure the left ventricle must overcome to eject blood during contraction

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9
Q

What is effect on after load from a dilation of arteries

A

Decreased afterload

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10
Q

Contractility

A

Force of contraction and the change in fibre length (how hard the heart pumps).

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11
Q

When cardiac muscle contracts what is effect on length of:
Myofibrils
Sarcomere

A

When muscle contracts myofibrils stay the same length but the sarcomere shortens - force of heart contraction that is independent of sarcomere length

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12
Q

Elasticity

A

Myocardial ability to recover normal shape after systolic stress

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13
Q

Diastolic dispensability

A

The pressure required to fill the ventricle to the same diastolic volume

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14
Q

Compliance

A

How easily the heart chamber expands when filled with blood volume

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15
Q

Starlings law

A

Force of contrition is proportional to the end diastolic length of cardiac muscle fibre (the more ventricle fills the harder it contracts).

↑ venous return = ↑ end diastolic volume = ↑ preload = ↑ sarcomere stretch = ↑ force of contraction thus = ↑ stroke volume and force of contractions

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16
Q

What is effect of standing on cardiac output?

A

Standing decreases venous return due to gravity, thus cardiac output decreases.
Causes a drop in blood pressure, stimulating baroreceptors to increase BP

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17
Q

What is effect on force of contraction if cardiac muscle is below optimal length (e.g. at rest)

A

Decreased force of contraction

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18
Q

Heart sounds: What is S1 (Lub)

A

mitral and tricuspid valve closure

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19
Q

Heart sounds: What is S2 (dub)

A

aortic and pulmonary valve closure

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20
Q

Heart sounds: What is S3 and when would you hear it

A

In early diastole during rapid ventricular filling, normal in children and pregnant women, associated with mitral regurgitation and heart failure

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21
Q

Heart sounds: What is S4

A

‘Gallop’, in late diastole, produced by blood being forced into a stiff hypertrophic ventricle - associated with left ventricular hypertrophy

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22
Q

Name risk factors for atherosclerosis

A
  • Age - increases with age
  • Tobacco smoking - leads to endothelium erosion
  • High serum cholesterol
  • Obesity - since more pericardial fat and thus increase in inflammation - Diabetes - hyperglycaemia damages endothelium
  • Hypertension
  • Family history
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23
Q

Describe structure of an atherosclerotic plaque

A 
A complex lesion consisting of:
• Lipid
• Necrotic core
• Connective tissue 
• Fibrous “cap”
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24
Q

Eventually a plaque can occlude the vessel lumen - what can result from this?

A 
Restriction of blood flow (angina)
May rupture (thrombus formation and subsequent death)
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25
Q

What initiates atherosclerosis formation

A

Endothelial dysfunction as a result of injury to endothelial cells

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26
Q

What is released from damaged endothelial cells to attract leukocytes

A

chemoattractants

concentration gradient of this also produced

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27
Q

Give examples of inflammatory cytokines found in plaques/promote atherogenesis

A 
IL-1(B)
IL-6
IL-8, IL-4, IL-12
IFN-gamma
TNF-alpha
MCP-1
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28
Q

Give examples of cytokines that suppress atherosclerosis production

A

IL-5
IL-10
TGF-beta

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29
Q

What 2 coagulation factors help convert prothrombin to thrombin

A

Xa

Va

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30
Q

Macrophages engulf fat cells to form what cells in atherogenesis

A

(Lipid-laden) foam cells

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31
Q

What are fatty streaks

A

Earliest lesion of atherosclerosis

Consist of aggregations of foam cells and T-lymphocytes in the intimal layer of the vessel wall

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32
Q

What makes up intermediate lesions?

A 
Composed of layers of:
-Foam cells
-Vascular smooth muscle cells
-T lymphocytes 
Also adhesion of platelets to vessel wall
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33
Q

What drug can inhibit platelet aggregation?

A

Aspirin (anti-coagulant)

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34
Q

In fibrous.advanced plaques, what makes up the dense fibrous caps

A

Extracellular matrix proteins including collagen (strength) and elastin (flexibility) laid down by smooth muscle cells that overly lipid core and necrotic debris

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35
Q

What two ways can a thrombus form?

A

1 - Superficial endothelial injury. Involved denudation of the endothelial covering over the plaque. Sub-endocardial connective tissue matrix then exposed and platelet adhesion occurs due to reaction with collagen.
Thrombus adherent to surface of the plaque.

2 - Deep endothelial fissuring, which involves an advanced plaque with a lipid core.
Plaque cap tears, allowing blood from lumen to enter inside of plaque. Core is highly thromogenic and thrombus can form in plaque, expanding its volume and distorting its shape. Thrombus can extend into the lumen.

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36
Q

Why is plaque core highly thrombogenic?

A

Contains lipid-lamellar surfaces and tissue factor (which triggers platelet adhesion and activation) that is produced by macrophages and exposed collagen

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37
Q

What cells release cytokines in atherosclerosis and what is result of this?

A

Monocytes
Macrophages
Damaged endothelium
Promotes further accumulation of macrophages as well as smooth muscle migration/proliferation.

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38
Q

What is released by proliferating smooth muscle in atherogenesis

A

Collagen

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39
Q

*Give examples of cytokines released in atherosclerosis

A

Platelet-derived growth factor
Interleukin-1
Transforming Growth Factor-1

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40
Q

What is angina

A

Chest pain, often also spreading to the shoulders, arms, and neck, owing to an inadequate blood supply to the heart.

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41
Q

Describe different types of angina

A

Stable angina - induced by effort and relieved by rest.

Unstable angina - recent onset (<24 hours) or deterioration in previously stable angina, with symptoms frequently occurring at rest. Angina of increasing frequency/severity, occurring on minimal exertion or at rest. Form of acute coronary syndrome.
Crescendo pattern.

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42
Q

Myocardial ischaemia resulting in angina occurs when there is a mismatch between blood supply and metabolic demand. What can cause this?

A
  • Atheroma/stenosis of coronary arteries thereby impairing blood flow - most common cause
  • Valvular disease
  • Aortic stenosis
  • Arrhythmia
  • Anaemia - thus less O2 can be transported
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43
Q

Give example of an ischaemic metabolite and what do they do?

A

Adenosine

Stimulate nerve endings and produce pain

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44
Q

Give examples of angina risk factors

A
  • Smoking
  • Sedentary lifestyle
  • Obesity
  • Hypertension
  • Diabetes mellitus
  • Family history
  • Genetics
  • Age
  • Hypercholesterolaemia
    (also more common in men)
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45
Q

Describe initiation of atherosclerosis

A
  • Endothelial dysfunction and injury around sites of sheer and damage with subsequent lipid accumulation at sites of impaired endothelial barrier
  • Local cellular proliferation and incorporation of oxidise lipoproteins occurs
  • Mural thrombi on surface and subsequent healing and repeat of cycle
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46
Q

Describe when is meant by adaptation in atherosclerosis

A
  • As plaque progresses to 50% of vascular lumen size the vessel can no longer compensate by re-modelling and becomes narrowed
  • This drives variable cell turnover within the plaque with new matrix surfaces and degradation of matrix
  • May progress to unstable plaque
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47
Q

As plaque continues to encroach on the lumen, exposure of what? can stimulate T cell accumulation

A

Tissue HLA-DR antigens

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48
Q

Describe the clinical stage of atherosclerosis (follows adaption stage)

A

• The plaque continues to encroach upon the lumen and runs the risk of haemorrhage or exposure of tissue HLA-DR antigens which might stimulate T cell accumulation
• This drives an inflammatory reaction against part of the plaque contents
• Complications develop including ulceration, fissuring, calcification and
aneurysm change

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49
Q

What is a fatty streak?

A

Macrophages filled with abundant lipid (foam cells) and smooth muscle cells with fat

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50
Q

Describe the intimal cell mass of an atheroma

A

Collections of muscle cells and connective tissue

without lipid - “cushions”

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51
Q

What can you do to see if someone has a local haemorrhage

A

Local haemorrhage may mean iron deposition and calcification

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52
Q

Why are complicated plaques prone to rupture

A

Show calcification and mural thrombus, making them vulnerable to rupture

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53
Q

Complications of Plaque rupture

A
  • Acute occlusion due to thrombus
  • Chronic narrowing of vessel lumen with healing of the local thrombus
  • Aneurysm change
  • Embolism of thrombus +/- plaque lipid content
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54
Q

*Describe clinical presentation of angina

A
  • Central chest tightness or heaviness
  • Provoked by exertion, especially after meal or in the cold windy weather or by
    anger or excitement
  • Relieved by rest or GTN spray
  • Pain may radiate to one or both arms, the neck, jaw or teeth
  • May be dyspnoea, nausea, sweatiness and faintness
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55
Q

*Describe scoring of angina (stable)

A
    1. Have, central, tight, radiation to arms, jaw & neck
    1. Precipitated by exertion
    1. Relieved by rest or spray GTN
  • 3/3 = Typical angina
  • 2/3 = Atypical pain
  • 1/3 = Non-anginal pain
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56
Q

Differential diagnosis of angina

A
  • Pericarditis/myocarditis
  • Pulmonary embolism
  • Chest infection
  • Dissection of the aorta
  • GORD
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57
Q

Diagnosis of angina

A 
12 lead ECG
Treadmill test/exercise ECG
CT scan Calcium scoring
SPECT/myoview
Cardiac catheterisation
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58
Q

*Describe 12 lead ECG of angina patient

A
  • Often normal
  • May show ST depression
  • Flat or inverted T waves
  • Look for signs of past MI
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59
Q

Describe exercise ECG/treadmill test

A
  • Put ECG on patient, then make them run on treadmill uphill - trying to induce ischaemia
  • Monitor how long patient is able to exercise for
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60
Q

Describe exercise ECG/treadmill test result on an angina patient

A
  • If you see ST segment depression then this is a sign of late-stage ischaemia
  • Many patients unsuitable e.g. can’t walk, very unfit, young females and bundle branch block
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61
Q

Describe CT scan calcium scoring for angina diagnosis

A

CT the heart and if there is atherosclerosis in the arteries then the calcium will light up white - if there is significant calcium then this would indicate angina

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62
Q

Describe SPECT/myoview and what it can show

A

Radio-labelled tracer injected into patient.
It’s taken up by the coronary arteries where there is good blood supply - this will light up.
Where there is little blood supply these areas will not light up.
If there is no light after exercise then this is indicative of myocardial ischaemia.

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63
Q

Describe treatment of angina

A

Modify risk factors - stop smoking, encourage exercise, weight loss
Treat underlying conditions
Pharmacological - Aspirin, Statins, Betablockers, GTN spray, Ca2+ channel blocker
Revascularisation

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64
Q

*What is purpose of revascularistion and when would it be used?

A

To restore patent coronary artery and increase flow reserve

Done when medication fails (most) or when high risk disease is identified

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65
Q

*What are the 2 types of revascularisation?

A

Percutaneuos Coronary Intervention (PCI)

Coronary Artery Bypass Graft (CABG)

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66
Q

Describe Percutaneous Coronary Intervention (PCI - revascularisation)

A
  • Dilating coronary atheromatous obstructions by inflating balloon within it
  • Insert balloon and stent, inflate balloon and remove it, stent persists and keeps artery patent
  • Expanding plaque = make artery bigger
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67
Q

Pros of Percutaneous Coronary Intervention

A

less invasive
convenient
short recovery
repeatable

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68
Q

Cons of Percutaneous Coronary Intervention

A

risk of stent thrombosis, not good for complex disease

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69
Q

Describe example of Coronary Artery Bypass Graft (CABG)

A

Left Internal Mammary Artery (LIMA) used to bypass proximal stenosis (narrowing) in Left Anterior Descending (LAD) coronary artery

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70
Q

Pros of Coronary Artery Bypass Graft (CABG)

A

good prognosis, deals with complex disease, one time treatment

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71
Q

Cons of Coronary Artery Bypass Graft (CABG)

A

invasive
risk of stroke or bleeding
one time treatment, but
need to stay in hospital - long recovery

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72
Q

Give example of aspirin

A

salicylate

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73
Q

Describe how aspirin works

A

Antiplatelet effect (inhibits platelet aggregation) in coronary arteries thereby avoiding platelet thrombosis.

COX inhibitor - reduces prostaglandin synthesis including thromboxane A2 resulting in reduced platelet aggregation

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74
Q

*Side effect of aspirin

A

Gastric ulceration

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75
Q

Example of statin

A

Simvastatin

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76
Q

*How do statins work

A
  • HMG-CoA reductase inhibitors - Reduces cholesterol produced by liver
  • Reduce events and LDL-cholesterol
  • Anti-atherosclerotic
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77
Q

*How do beta blockers work?

A

Act on B1 receptors in the heart as part of the adrenergic sympathetic pathway.
B1activation→Gs→cAMP to ATP→contraction

Reduce force of contraction

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78
Q

What is the effect on the heart by beta blockers

A

Reduces HR (-vely chronotropic)
Reduces left ventricle contractility (-vely inotropic)
Reduces cardiac output

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79
Q

Side effects of beta blockers

A 
Tiredness
Nightmares
Bradycardia
Erectile dysfunction
Cold hands and feet
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80
Q

*When should you not give beta blockers?

A

Asthma
Heart failure/heart block
Hypotension
Bradyarrhythmias

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81
Q

What are 1st line antianginal drugs

A

Glyceryl Trinitrate spray

Beta blockers

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82
Q

Effects of Glyceryl Trinitrate spray

A
  • Nitrate that is a venodilator
  • Dilates systemic veins thereby reducing venous return to right heart
  • Reduces preload
  • Thus reduces work of heart and O2 demand
  • Also dilates coronary arteries
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83
Q

Side effects of Glyceryl Trinitrate spray

A

Profuse headache immediately after use

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84
Q

Example of a calcium channel blocker

A

Verapamil

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85
Q

How do calcium channel blockers work?

A
  • Primary arterodilators
  • Dilates systemic arteries resulting in BP drop
  • Thus reduces afterload on the heart
  • Thus less energy required to produce same cardiac output
  • Thus less work on heart and O2 demand
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86
Q

Acute coronary syndrome is an umbrella term that includes what?

A

ST-elevation myocardial infarction
Unstable angina
Non-STEMI

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87
Q

Describe what causes a STEMI

A

• Develop a complete occlusion of a MAJOR coronary artery
previously affected by atherosclerosis
• This causes full thickness damage of heart muscle
• aka a Q-wave infarction - see a pathological Q wave

88
Q

How can you diagnose a STEMI

A

Can be diagnosed on ECG at presentation
Tall T waves
ST-elevation and subsequent pathological Q wave
May present as new Left bundle branch block (LBBB)

89
Q

What causes a NSTEMI

A

Developing a complete occlusion of a minor or partial occlusion of a major coronary artery previously affected by atherosclerosis.
Leads to partial thickness damage of heart muscle

90
Q

What can be seen on an ECG of a NSTEMI

A

Non-Q wave infarction

ST depression and/or T wave inversion

91
Q

*What is the difference between a NSTEMI and unstable angina

A

In a NSTEMI there is occluding thrombus which leads to myocardial necrosis and a rise in serum troponin (T) or creatine kinase-MB (CK-MB)

92
Q

Describe Type 1 MI

A

Spontaneous MI with ischaemia due to a primary coronary event e.g. plaque erosion/rupture, fissuring or dissection

93
Q

Describe type 2 MI

A

MI secondary to ischaemia due to increased O2 demand or decreased supply such as in coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension

94
Q

Describe type 3/4/5 MI

A

MI due to sudden cardiac death, related to PCI and related to CABG respectively

95
Q

Epidemiology in UK of STEMI

A

5/1000 per annum in UK

96
Q

Risk factors of acute coronary syndrome

A
  • Age
  • Male
  • Family history of Ischaemic Heart Disease (IHD) - MI in first degree relative below 55
  • Smoking
  • Hypertension, diabetes mellitus, hyperlipidaemia
  • Obesity & sedentary lifestyle
97
Q

Give brief overview of pathophysiology of acute coronary syndrome

A
  • Rupture or erosion of the fibrous cap of a coronary artery plaque
  • Leading to platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distal thrombus embolisation
  • The presence of a rich lipid pool within the plaque and a thin, fibrous cap is associated with an increased risk of rupture
  • Thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2 result in myocardial ischaemia due to reduction of coronary blood flow
  • Fatty streak → Fibrotic plaque → Atherosclerotic plaque → Plaque rupture/ fissure and thrombosis → MI or Ischaemic stroke or Critical leg ischaemia or Sudden CVS death
98
Q

Describe features of plaque causing unstable angina

A

plaque has a necrotic centre and ulcerated cap and the thrombus results in PARTIAL OCCLUSION

99
Q

Describe features of plaque causing myocardial infarction

A

plaque also has a necrotic centre but the thrombus results in TOTAL OCCLUSION

100
Q

Clinical presentation of unstable angina

A
  • Chest pain; new onset, at rest with crescendo pattern
  • Breathlessness
  • Pleuritic pain
  • Indigestion
101
Q

Clinical presentation of acute coronary syndrome

A 
Recent destabilisation of pre-existing angina with moderate or severe limitations of daily activities.
Acute central chest pain, lasting more than 20 minutes, associated with:
• Sweating
• Nausea and vomiting 
• Dyspnoea
• Fatigue
• Shortness of breath 
• Palpitations
  • Distress and anxiety
  • Pallor
  • Increased pulse and reduced BP
  • Reduced 4th heart sound
  • May be signs of heart failure (increase in jugular venous pressure)
  • Tachy/bradycardia
  • Peripheral oedema
102
Q

*When would acute coronary syndrome present without chest pain

A

Diabetics

Elderly

103
Q

*Give example of signs of heart failure (state 3)

A 
Increase in jugular venous pressure
Swelling in ankles, legs and feet
Dyspnoea (when exert or lie down)
Rapid or irregular heart beat
Reduced ability to exercise
Persistent cough or wheezing with white or pink blood-tinged phlegm
Fatigue and weakness
104
Q

Differential diagnosis of acute coronary syndrome

A
  • Angina
  • Pericarditis
  • Myocarditis
  • Aortic dissection
  • Pulmonary embolism
  • Oesophageal reflux/spasm
105
Q

Diagnosis of Acute Coronary syndrome

A

12 lead ECG
Biochemical markers: Troponin (T and I), CK-MB, Myoglobin
CXR

106
Q

What would 12 lead ECG of acute coronary syndrome look like?

A

Can be normal
ST depression and T-wave inversion (this tends to occur hours/days after) (NSTEMI) are highly suggestive of an ACS, particularly if associated with anginal chest pain
Can get hyperacute (tall) T waves

107
Q

What is the most sensitive and specific biochemical marker of myocardial necrosis

A

Troponin - T and I

108
Q

Decrease how concentration of Troponin T and I changes from the onset of chest pain

A

Serum levels increase within 3-12 hours from the onset of chest pain and peak at 24-48 hours
They then fall back to normal over 5-14 days

109
Q

What can Troponin T and I levels be used to determine

A

Can act as prognostic indicator to determine mortality risk and define which patients may benefit from aggressive medical therapy and early coronary revascularisation

110
Q

Describe levels of myoglobin after an MI

A

Becomes elevated very early in MI but the test has poor specificity since myoglobin is present in skeletal muscle

111
Q

What can Chest X-ray show

A

Cardiomegaly
Pulmonary Oedema
Widened mediastinum (aortic rupture)

112
Q

Describe treatment of acute coronary syndrome

A 
Pain relief (GTN spray or IV opioid)
Anti-emetic
Oxygen
Antiplatelets
Beta-blockers
Statins
ACE inhibitors
Coronary revascularisation
Risk factor modification
113
Q

What can be used as pain relief in acute coronary syndrome

A

GTN spray

Iv opioid

114
Q

What oxygen levels would you aim for in acute coronary syndrome?

A

94-98% oxygen saturation

88-92% in those with COPD

115
Q

What is an antiemetic

A

drug that prevents nausea and vomiting

116
Q

What risk factors need to be modified in patient with acute coronary syndrome

A
  • Stop smoking
  • Lose weight and exercise daily
  • Healthy diet
  • Treat hypertension & diabetes
  • Low fat diet with statins
117
Q

What method of revascularisation would you use in patient with high risk of mortality/in high risk group e.g. recent MI

A

CABG

118
Q

In an atheromatous plaque rupture, what allows platelet aggregation (and thus activation)

A

IIb/IIIa glycoproteins binding to fibrinogen (enables platelets to adhere to each other)

119
Q

What converts fibrinogen to fibrin?

What happens to fibrin in thrombosis

A

Thrombin
fibrin is insoluble and in atherosclerotic ruptures can result in the formation of a fibrin mesh over platelet plug and thus formation of a thrombotic clot

120
Q

Give examples of orally administered antiplatelets

A

Aspirin

P2Y12 inhibitors

121
Q

*How do P2Y12 inhibitors work?

A

Inhibit ADP-dependant activation of IIb/IIIa glycoproteins thereby preventing amplification response of platelet aggregation

122
Q

Give examples of P2Y12 inhibitors

A

Clopidogrel
Prasugrel
Ticagrelor

123
Q

When can you use P2Y12 inhibitors

A

if allergic to aspirin

can also be used alongside aspirin as a dual anti-platelet therapy

124
Q

Side effects of P2Y12 inhibitors

A

neutropenia (low neutrophils), thrombocytopenia (low platelets) and INCREASED RISK OF BLEEDING

also avoid if CABG planned

125
Q

Give example of only IV administered antiplatelet

A

Glycoprotein IIb/IIIa antagonists

126
Q

When could you give Glycoprotein IIb/IIIa antagonists

A

In patients with ACS undergoing Percutaneous Coronary Intervention in combination with aspirin and oral P2Y12 inhibitors

127
Q

*Main side effect of Glycoprotein IIb/IIIa antagonists

A

INCREASES RISK OF MAJOR BLEEDING

128
Q

Examples of Glycoprotein IIb/IIIa antagonists

A

Abciximab
Tirofiban
Eptifbatide

129
Q

Example of Beta blockers (in ACS)

A

Atenolol (IV then oral)

Metoprolol (IV then oral)

130
Q

Side effects of Beta blockers

A

Avoid with asthma, heart failure, hypotension and

bradyarrhythmias

131
Q

What enzyme is inhibited by statins

A

HMG-CoA reductase

132
Q

Examples of statins (oral)

A

Simvastatin
Pravastatin
Atorvastin

133
Q

Examples of ACE inhibitors (oral)

A

Ramipril

Lisonopril

134
Q

Define acute myocardial infarction

A

Necrosis of cardiac tissue (myocyte death) due to prolonged myocardial
ischaemia due to COMPLETE occlusion of artery by thrombus

135
Q

True or False:

STEMI is the most common medical emergency

A

True

136
Q

Risk Factors of acute MI

A
  • Age
  • Male
  • History of premature coronary heart disease
  • Premature menopause
  • Diabetes mellitus
  • Smoking
  • Hypertension
  • Hyperlipidaemia
  • Obesity and sedentary lifestyle
  • Diabetes mellitus
  • Family history of Ischaemic Heart Disease (IHD) - MI in first degree relative below 55
137
Q

Why is early reperfusion important in STEMI

A

May salvage regions of the myocardium - reducing future mortality and morbidity

138
Q

Describe pathophysiology of a STEMI

A
  • Rupture or erosion of vulnerable fibrous cap of coronary artery atheromatous plaque
  • This results in platelet aggregation, adhesion, local thrombosis, vasoconstriction and DISTAL THROMBUS EMBOLISATION resulting in PROLONGED COMPLETE ARTERIAL OCCLUSION resulting in myocardial necrosis within 15-30 minutes in a STEMI (since major artery occluded fully)
139
Q

How is a transmural Q wave produced in STEMI

A

Ischaemia of the sub-endocardial myocardium

transmural means occurring across the entire wall of an organ or blood vessel

140
Q

Describe clinical presentation of an acute MI

A
  • Severe, ongoing chest pain for more than 20 mins
  • Pain may radiate to the left arm, jaw or neck
  • Pain DOES NOT usually respond to sublingual GTN spray - opiate analgesia is required
  • Pain described as substernal pressure, squeezing, aching, burning or even sharp pain
  • Associated with; sweating, nausea, vomiting, dyspnoea, fatigue and/or palpitations
  • Breathlessness
  • Fatigue
  • Distress and anxiety
  • Pale, clammy and marked sweating
  • Significant hypotension (low BP)
  • Bradycardia or tachycardia
141
Q

Differential diagnosis of acute MI

A

Stable angina, unstable angina, NSTEMI, pneumonia, pneumothorax, oesophageal spasm, GORD, acute gastritis, pancreatitis and MSK chest pain

142
Q

*Diagnosis of STEMI

A
  • Diagnosed on presentation
  • ST elevation
  • Tall T waves
  • L bundle branch block (LBBB)
  • T wave inversion and pathological Q waves follow
143
Q

*Diagnosis of a NSTEMI

A
  • Diagnosis is retrospective made after troponin results

* ST depression and T wave inversion

144
Q

Why is continuous monitoring required when in A and E and have MI

A

Due to high likelihood of significant cardiac arrhythmias

145
Q

What leads of an ECG show change in an acute MI of anterior heart

A

ST elevation in V1-3

146
Q

What leads of an ECG show change in an acute MI of inferior heart

A

ST elevation in leads II, III, aVF

Also Q waves and T wave inversion may also be present

147
Q

What leads of an ECG show change in an acute MI of lateral heart

A

Change in leads I, aVL, V5-V6

148
Q

What leads of an ECG show change in an acute MI of posterior heart

A

ST depression V1-V3
Dominant R wave
ST elevation in V5-V6

149
Q

What leads of an ECG show change in an acute MI of anterolateral heart

A

ST elevation in leads I, aVL and V3-V6 (pericardial leads)
Loss of general R wave progression in pericardial/V waves
May also be T wave inversion

150
Q

Occlusion of what vessels cause an acute anterolateral MI

A

Left anterior descending (LAD)

or LAD with RCA or LCx artery

151
Q

Occlusion of what vessels cause an acute inferior MI

A

Right coronary artery

152
Q

Occlusion of what vessels cause an acute right ventricular MI

A

Proximal coronary artery
Frequently associated with RBBB
(inferior-posterior wall)

153
Q

What leads of an ECG show change in an acute septal MI

A

ST elevation, Q wave formation and T wave inversion in the leads overlying the septal region of the heart (V2 and V3)

154
Q

When is hyperkalemia frequently seen

A

Renal failure

Those on K sparing diuretics

155
Q

Describe ECG of hyperkalemia

A

Mild hyperkalemia: Leads II, V2 and V4 demonstrate tall, tented, symmetrical T waves with a narrow base.

Moderate K overdose: QRS complex broadens and the S wave is widened in leads V3 - V6.
ST segment disappears.
P wave duration is increased, but amplitude is decreased.

Large K overdose: P wave duration and PR interval duration both increase until P wave disappears. QRS complex is broadened.

156
Q

ECG of hypokalemia

A

https://meds.queensu.ca/central/assets/modules/ECG/hypokalemia.html

157
Q

Evolution of STEMI on ECG

A
  • After the first few minutes, the T waves become tall, pointed and upright, and there is ST segment elevation
  • After the first few hours, the T waves invert, the R-wave voltage decreases and Q waves develop
  • After a few days, the ST segment returns to normal
  • After weeks or months, the T wave may return to upright but the Q WAVE REMAINS
158
Q

Other diagnosis of acute MI

A
  • Troponin I or T increased
  • Myoglobin increased
  • Transthoracic echocardiography (TTE) may be helpful to confirm MI, as wall-motion abnormalities are detected early in STEMI
159
Q

Describe prehospital treatment of acute MI

A
  • Aspirin 300mg chewable
  • GTN (sublingual)
  • Morphine
160
Q

Describe hospital treatment of acute MI

A
  • IV morphine
  • Oxygen if their sats are below 95% or are breathless
  • Beta-blocker - Atenolol
  • P2Y12 inhibitor - Clopidogrel
161
Q

Other treatment of acute MI (not usual/first prehospital or hospital)

A

Coronary revascularisation
Fibrinolysis
Risk factor modification

162
Q

When would you give coronary revascularisation to STEMI patient

A

Presented to all patients who present with an acute STEMI who can be transferred to a primary PCI centre WITHIN 120 MINUTES of first medical contact
- If not possible then give patient fibrinolysis and then transfer to PCI centre after infusion

163
Q

What is fibrinolysis

A

Enhance the breakdown of occlusive thromboses by the

activation of plasminogen to form plasmin

164
Q

Describe risk factor modifications of STEMI treatment

A
  • Stop smoking
  • Lose weight and exercise daily
  • Healthy diet
  • Treat hypertension & diabetes
  • Low fat diet with statins
165
Q

Describe secondary prevention of STEMI

A
  • Statins
  • Aspirin long term
  • Warfarin if large MI
  • Beta blockers
  • ACE inhibitors
166
Q

Complications of MI

A 
Sudden death - often within hours often due to ventricular fibrillation
Arrhythmias
Persistent pain
Heart failure
Mitral incompetence
Pericarditis
Cardiac rupture
Ventricular aneurysm
167
Q

Why do you get arrhythmias as a complication of a MI

A

Get them in the first few days due to electrical instability following infarction, pump failure and excessive sympathetic stimulation

168
Q

How long do you get persistent pain for after a MI and why

A

12 hours to a few days after due to progressive myocardial necrosis

169
Q

Why do you get heart failure as a result of an MI

A
  • When cardiac output is insufficient to meet the bodies metabolic demands
  • Due to ventricular dysfunction following muscle necrosis also resulting in
    arrhythmias
170
Q

Why do you get mitral valve incompetence?

A

Due to myocardial scarring preventing valve closure.

can happen in first few days or later

171
Q

Why do you get pericarditis after MI

A

Due to transmural infarct resulting in inflammation of pericardium
(more common in STEMI)

172
Q

Why do you get ventricular aneurysm after MI

A

Due to stretching of newly formed collagenous scar tissue

173
Q

Why do you get cardiac rupture after an MI (early or late)

A

Early rupture - the result of shearing between mobile and immobile myocardium

Late rupture - due to weakening of wall following muscle necrosis and acute inflammation

174
Q

Define cardiac failure

A

The inability of the heart to deliver blood and thus O2 at a rate that is commensurate with the requirement of metabolising tissue of the body

175
Q

Is cardiac failure a sign, a symptom, a syndrome or a diagnosis on its own?

A

Syndrome

176
Q

What can result in cardiac failure

A

Can result from any structural or functional cardiac disorder that impairs the hearts ability to function and meet the demands of supplying sufficient oxygen and nutrients to the metabolising body

177
Q

Epidemiology of cardiac failure

A

25-50% of patients die within 5 years of diagnosis
1-3% of general population
around 10% in the elderly

178
Q

Main cause of cardiac failure

A

Ischaemic heart disease

179
Q

Causes of cardiac failure

A

IHD
Cardiomyopathy (disease of heart muscles, where the walls have
become thickened, stiff or stretched)
Valvular heart disease e.g. aortic stenosis, aortic and mitral
regurgitation
Cor pulmonale
Hypertension
Alcohol excess
Any factor that increases myocardial work e.g. anaemia, arrhythmias, hyperthyroidism, pregnancy and obesity

180
Q

Risk factors of cardiac failure

A
  • 65 and older
  • African descent
  • Men (due to lack of protective effect provided by oestrogen resulting in the early onset of IHD in men
  • Obesity
  • People who have had an MI
181
Q

What is it called when heart failure progresses and the mechanisms to reduce effects of heart failure become overwhelmed and become pathophysiological?

A

Decompensation

182
Q

What are methods by body that try to maintain cardiac output and peripheral perfusion after heart failure, by physiological compensatory changes

A 
Venous return change (preload)
Outflow resistance (after load)
Sympathetic system activation
Renin Angiotensin Aldosterone system
183
Q

Describe changes in venous return after heart failure

A

Myocardial failure leads to a reduction of the volume of blood ejected with each heart beat, and an increase in the volume of blood remaining after systole
This increased diastolic volume/preload stretches the myocardial fibres and myocardial contraction is restored since the stretching of myocardial fibres will increase its force of contraction. (starlings law)
However, in heart failure, the failing myocardium actually doesn’t contract as much in response to increased preload meaning cardiac output cannot be maintained and may decrease.

184
Q

What is outflow resistance (after load)

A

Outflow resistance (afterload) is the load or resistance against which the ventricle contracts
Itismadeupof:
• Pulmonary and systemic resistance
• Physical characteristics of the vessel walls
• The volume of blood that is ejected

185
Q

Describe how outflow resistance/afterload changes following heart failure

A

When there is an increase in afterload, there is an increase in end- diastolic volume and a decrease in stroke volume and thus a DECREASE in cardiac output.

Increase of end-diastolic volume leads to dilatation of the ventricle itself (the more the ventricle is dilated the harder it must work i.e. the more resistance there is to contract against) which then further exacerbates the problem of afterload

186
Q

Where are baroreceptors located?

A

arterial wall of the aorta, carotid arteries and in the heart walls and major veins

187
Q

Describe decompensation of sympathetic nervous system from heart failure

A

Baroreceptors detects a drop in arterial pressure or increased venous pressure (due to blood back flow) and stimulates SNS.

Increase force of contraction (inotropic) and thus Stroke volume and heart rate and thus CO.

In HF, chronic sympathetic activation down regulates receptors that cause this. Means diminished effect of sympathetic activation and CO stops increasing in response to SNS activation.

188
Q

Describe decompensation of renin-angiotensin system from heart failure

A

Reduced CO means a diminished renal perfusion, thereby activating the renin-angiotensin system:
(angiotensinogen is converted to angiotensin I under the action of renin, angiotensin I is then converted to angiotensin II under the act of angiotensin converting enzyme (ACE), angiotensin II then stimulates the release of aldosterone from the adrenal cortex above the kidneys and ADH which stimulates water retention.
Angiotensin II and Aldosterone increase Na+ reabsorption and thus water reabsorption.)

Results in increased volume of blood -> increased BP -> increase venous pressure ->
Increases pre-load -> increases stretch of heart and thus force of contraction, SV and CO.

*However, with increased force of contraction the cardiac myocytes require more energy and thus more blood however in heart failure there will be no increase in blood and thus the cardiac myocytes will die resulting in a decrease in force of contraction and thus a decrease in stroke volume and a decrease in cardiac output.

189
Q

*What is systolic heart failure

A

Inability of the ventricle to contract normally resulting in a decrease in cardiac output.
Caused by ischaemic heart disease, myocardial infarction and cardiomyopathy (disease of heart muscle thus impairing function).

190
Q

*What is diastolic heart failure

A

Inability of the ventricles to relax and fill fully thereby decreasing stroke volume and decreasing cardiac output

191
Q

Causes of diastolic heart failure

A

Hypertrophy (due to chronic hypertension which results in increased blood pressure thereby increasing afterload so heart pumps against more resistance and thus cardiac myocytes grow bigger to compensate for this) of ventricles resulting in there being less space for blood to fill in and thus decreased cardiac output.
Also caused by Aortic Stenosis (the narrowing of the aortic valve) which also increases afterload and thus decreases CO

192
Q

What characterises acute heart failure (not chronic)

A

Pulmonary and/or peripheral oedema with or without signs of peripheral hypotension

193
Q

What classification system can be used for assessment of severity of symptoms of heart failure

A

New York Heart Association (NYHA) classification

194
Q

*Describe the New York Heart Association (NYHA) classification for severity of symptoms of heart failure

A

Class I: No limitation (asymptomatic) - exercise = no fatigue, dyspnoea or palpitation

Class II: Slight limitation (mild HF (heart failure)) - comfortable at rest, normal activity = fatigue, dyspnoea and palpitations

Class III: Marked limitation (moderate HF) - comfortable at rest, gentle activity = fatigue, dyspnoea & palpitations

Class IV: Inability to carry out any physical activity without discomfort
(severe HF) - symptoms occur at rest

195
Q

On NYHA classification of severity of heart failure, what is the main difference between Class II and Class III

A

Class II (mild) - slight limitation: comfortable at rest, normal activity gives fatigue, dyspnoea and palpitations

Class III (moderate) - marked limitation: comfortable at rest also, but GENTLE activity gives fatigue, dyspnoea and palpitations

196
Q

*What are 3 cardinal symptoms of cardiac failure? (main symptoms)

A

Shortness of breath
Fatigue
Ankle swelling

197
Q

Clinical presentation of heart failure - less common symptoms

A

a persistent cough, which may be worse at night
wheezing
a bloated tummy
loss of appetite
weight gain or weight loss
confusion
dizziness and fainting
a fast heart rate (tachycardia)
a pounding, fluttering or irregular heartbeat (palpitations)
some people with heart failure may also experience feelings of depression and anxiety

198
Q

Signs of heart failure

A
  • Dyspnoea especially when lying flat (orthopnoea)
  • Cold peripheries
  • Raised jugular venous pressure (JVP)
  • Murmurs and displaced apex beat
  • Cyanosis
  • Hypotension
  • Peripheral or pulmonary oedema due to back flow resulting from the decreased cardiac output
  • Tachycardia
  • Third & fourth heart sounds
  • Ascites
  • Bi-basal crackles
199
Q

Diagnosis of heart failure

A

Blood tests
Chest X-ray
ECG
Echocardiography

If BNP and ECG normal then heart failure is unlikely, but if both abnormal, go to an echocardiogram

200
Q

Diagnosis of heart failure: Describe blood tests that can be done

A

Brain natriuretic peptide (BNP)

  • secreted by ventricles in response to increase mycocardial wall stress
  • increased in patients with heart failure
  • levels correlate with ventricular wall stress and severity of heart failure

also FBC, U and Es and liver biochem

201
Q

Diagnosis of heart failure: What would be looked for on a chest x-ray

A
  • Alveolar oedema
  • Cardiomegaly
  • Dilated upper lobe vessels of lungs
  • Effusions (pleural)
202
Q

Diagnosis of heart failure: What would be looked for on an Echocardiogram

A
  • Assess cardiac chamber dimension
  • Look for regional wall motion abnormalities, valvular disease and cardiomyopathies
  • Look for sign of MI
203
Q

Treatment after HF

A

Lifestyle changes
Diuretics
ACE inhibitors
Beta-blockers (start at a low dose and titrate up)
Digoxin
Inotropes
Revascularisation
Surgery to repair (mitral valve repair, aortic or mitral valve replacement)
Heart transplant (young)
Cardiac resynchronisation - improve the coordination of atria and ventricles

204
Q

Give examples of lifestyle changes to treat HF

A

avoid large meals, lose weight, stop smoking, exercise, vaccination

205
Q

Why give diuretics as heart failure treatment

A

Promote sodium and thus water loss thereby reducing ventricular filling pressure (preload) decreasing systemic and pulmonary congestion.
Symptomatic relief

206
Q

What are different diuretics that could be given

A
  • Loop diuretic - furosemide
  • Thiazide diuretic - bendroflumethiazide (inhibit sodium reabsorption in the distal convoluted tubule)
  • Aldosterone antagonist (thereby inhibiting ADH release resulting in water loss) - spirolactone but beware of renal impairment and hyperkalaemia
207
Q

Example of a loop diuretic

A

Furosemide

208
Q

Example of a thiazide diuretic

A

Bendroflumethiazide

209
Q

Example of an aldosterone antagonist

A

Spirolactone

Epelerone

210
Q

Examples of ACE inhibitors

A

Ramipril
Enalipril
Captopril

211
Q

ACE inhibitor side effects

A

Cough, hypotension, hyperkalaemia and renal dysfunction

212
Q

*Why does ACE inhibitor cause you to cough

A

since inhibit ACE and thus the breakdown of substance P and bradykinin which results in cough

213
Q

*Alternative to ACE inhibitor if cough is a problem

A

Angiotensin Receptor Blocker e.g. Canderstan or Valsartan

214
Q

Example of a beta-blocker

A

Bisoprolol

Nebivolol

215
Q

What patients can NOT be given beta-blockers

A

Asthmatics

Medicine Phase 2a (22 decks)

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