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Phase 2a > Cardio > Flashcards

Cardio Flashcards

1
Q

What is an ECG?

A

A representation of the electrical events of the cardiac cycle.

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2
Q

What can ECG’s can identify?

A
  • Arrhythmia’s
  • Myocardial ischaemia and infarction
  • Pericarditis
  • Chamber hypertrophy
  • Electrolyte disturbances
  • Drug toxicity
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3
Q

What is the SA node?

A

It is the dominant pacemaker with an intrinsic rate of 60-100 bpm.
The fastest depolarising tissue.

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4
Q

What is the AV node?

A

The back-up pacemaker with an intrinsic rate of 40 - 60 bpm.

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5
Q

What are ventricular cells?

A

The back-up pacemaker with an intrinsic 20-45 bpm.

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6
Q

What is the impulse conduction pathway?

A

Sinoatrial node –> AV node –> Bundle of His –> Bundle branches –> Purkinje fibres

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7
Q

What are the normal time durations for depolarisations/ repolarisations/ node delays?

A

AV node delays: 0.12-0.2s
Atrial depolarisation: 0.08-0.1s
Ventricular depolarisations: 0.06-0.1s

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8
Q

Describe the PQRST wave…

A

P wave: atrial depolarisation (every lead apart from aVR)
PR interval: time taken for atria to depolarise and electrical activation to get through AV node
QRS complex: ventricular depolarisation
ST segment: interval between depolarisation and repolarisation
T wave: ventricular repolarisation

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9
Q

What is tachycardia?

A

increased heart rate

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10
Q

What is bradychardia?

A

decreased heart rate

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11
Q

What is dextrocardia?

A

heart is on the right side of the chest instead of the left

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12
Q

What is seen on an ECG for an acute anterolateral myocardial infarction?

A

ST segments are raised in anterior (V3 -V4) and lateral (V5 - V6) leads

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13
Q

What is seen on an ECG for an acute inferior MI?

A

ST segments are raised in inferior (II, III, aVF) leads

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14
Q

Why is atrial repolarisation not seen on an ECG?

A

Atrial repolarisation is usually not evident on an ECG since it occurs at the same time as the QTS complex so is hidden.

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15
Q

What are the box representations on the ECG paper?

A 
Horizontally: 
- One small box = 0.04s
- One large box = 0.20s
Vertically:
- One large box = 0.5mV
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16
Q

What is the cardiac definition of the left ventricle?

A

Palpated in the 5th intercostal space and mid-clavicular line, responsible for the apex beat.

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17
Q

What is the definition of stroke volume?

A

The volume of blood ejected from each ventricle during systole.

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18
Q

What is the definition of cardiac output?

A

The volume of blood each ventricle pumps as a function of time (litres per min).
CO (L/min) = SV (L) x HR (BPM)

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19
Q

What is the total peripheral resistance?

A

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

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20
Q

What is the definition of preload?

A

The volume of blood in the left ventricle which stretches the cardiac myocytes before left ventricular contraction. Vol. of blood in ventricles before it pumps.
Decreased by vein dilation.

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21
Q

What is the definition of afterload?

A

The pressure the left ventricle must overcome to eject blood during contraction.
Dilated arteries decrease afterload.

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22
Q

What is the definition of contractility?

A

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

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23
Q

What is the definition of elasticity?

A

Myocardial ability to recover recover normal shape after systolic stress.

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24
Q

What is the definition of diastolic dispensibility?

A

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

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25
Q

What is the definition of compliance?

A

How easily the heart chamber expands when filled with blood volume.

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26
Q

What is Starlings law?

A

Force of contraction is proportional to the end diastolic length of cardiac muscle fibre.
The more the ventricle fills, the harder it contracts.

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27
Q

Explain the relationship of end diastolic volume, preload, sarcomere stretch, stroke volume and force of contractions…

A

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

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28
Q

What is the effect of standing on the cardiac output and what other effects does this have?

A

Standing decreases venous return due to gravity, so cardiac output decreases, causing a drop in blood pressure, stimulating baroreceptors to increase blood pressure.

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29
Q

Explain the heart sounds…

A

S1 - mitral cand tricuspid valve closure
S2 - aortic and pulmonary valve closure
S3 - in early diastole during rapid ventricular filling, associated with mitral regurgitation and heart failure, normal in children and pregnant women
S4 - “Gallop”, in late diastole, blood being forced into still hypertrophic ventricle - associated with left ventricular hypertrophy

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30
Q

In ischaemic heart disease, what coronary arteries commonly develop atheroscerosis?

A

Circumflex, Left anterior descending (LAD), Right coronary arteries

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31
Q

What are the risk factors for atherosclerosis?

A
  • Age; increasing age = increased risk
  • Tobacco smoking; leads to endothelium erosion
  • High serum cholesterol
  • Obesity; more pericardial fat = increase in inflammation
  • Diabetes; hyperglycaemia damages the endothelium
  • Hypertension
  • Family history
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32
Q

Where is atherosclerosis plaque distributed?

A
  • Found within peripheral and coronary arteries

- Focal distribution along the artery length

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33
Q

Describe the structure of an atherosclerotic plaque…

A

A complex lesion of:

  • lipid
  • necrotic core
  • connective tissue
  • fibrous “cap”
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34
Q

What can be the effects of atherosclerotic plaque?

A

Plaque will either occlude the vessel lumen resulting in a restriction of blood flow (ANGINA), or it may rupture (thrombus formation and subsequent death)

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35
Q

Describe the process of atherosclerosis formation…

A
  1. Initiated by an injury to the endothelial cells, resulting in endothelial dysfunction.
  2. Chemoattractants are released from endothelium to attract leukocytes, which then accumulate and migrate into the vessel wall.
  3. Chemoattractants are released from site of injury and concentration gradient is produced.
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36
Q

What inflammatory cytokines are found in plaques?

A

IL-1 (most important)
Il-6
IFN-gamma

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37
Q

What are fatty streaks in the context of atherosclerosis?

A
  • Earliest lesion of atherosclerosis
  • Appear at a very early age (less than 10)
  • Consist of aggregations of lipid-laden macrophages and T lymphocytes within the intimal layer of the vessel wall
38
Q

What are intermediate lesions in atherosclerosis composed of?

A
  • Foam cells (lipid laden macrophages)
  • Vascular smooth muscle cells
  • T lymphocytes
    Adhesion and aggregation of platelets to the vessel wall.
39
Q

What rug inhibits platelet aggregation?

A

Aspirin

40
Q

What do fibrous plaques/advanced lesions in atherosclerosis do? Structure? Appearance?

A
  • Impede blood flow
  • Prone to rupture
  • Covered by dense fibrous cap
  • Made up of extracellular matrix proteins including collagen (strength) and elastin (flexibility) provided y smooth muscle cells that overly lipid core and necrotic debris (within cap)
  • May be calcified
41
Q

What do fibrous plaques/advanced lesions contain?

A
  • Smooth muscle cells
  • Macrophages and foam cells
  • T lymphocytes
  • Red cells
42
Q

What are foam cells?

A

Lipid laden macrophges

43
Q

What is the plaque within advanced lesions filled with?

A

Fibrin

44
Q

describe the process of plaque rupture…

A
  • Plaque is constantly growing and receding
  • Hence fibrous cap needs to be resorbed and redeposited in order to be maintained
  • If balance shifts, the cap can become weak and the plaque ruptures
  • Rupture causes basement membrane, collagen and necrotic . tissue exposure
  • Also causes haemorrhage of vessel within the plaque
  • Resulting in thrombus (clot) formation and subsequent vessel occlusion
45
Q

What is angina?

A

A chest pain or discomfort as a result of reversible myocardial ischaemia.
Implies narrowing of one or more of the coronary arteries.
Exacerbated by exertion.
Relieved by rest.

46
Q

What are the different types of angina?

A

Stable angina; induced by effort and relieved by rest

Unstable (crescendo) angina; - Angina of recent onset (less than 24 hours)

  • Deterioration in previously stable angina, symptoms occurring at rest
  • Angina of increasing frequency or severity, occurring at minimal exertion or even at rest (form of acute coronary syndrome)

Prinzmetal’s angina; caused by coronary artery spasm (rare)

47
Q

When does myocardial ischaemia result in angina?

A
  • Myocardial ischaemia resulting in angina occurs when there is a mismatch between blood supply and metabolic demand, due to:
  • Atheroma/stenosis of coronary arteries; impairing blood flow
  • Valvular disease
  • Aortic stenosis
  • Arrhythmia
  • Anaemia; less O2 is transported
48
Q

Epidemiology of angina

A

More common in men

49
Q

What produces pain in angina?

A

Ischaemic metabolites including adenosine, stimulate nerve endings, producing pain.

50
Q

What are the risk factors for angina?

A
  • Smoking
  • Sedentary lifestyle
  • Obesity
  • Hypertension
  • Diabetes Mellitus
  • Family History
  • Genetics
  • Age
  • Hypercholesterolaemia
51
Q

What is the initiation stage of angina?

Pathophysiology

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 oxidase lipoproteins occurs
  • Mural thrombi on surface and subsequent healing and repeat of cycle
52
Q

What is the adaptation stage of angina?

Pathophysiology

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
53
Q

What is the clinical stage of angina?

Pathophysiology

A
  • Plaque continues to build up into the lumen and runs the risk of haemorrhage or exposure of tissue HLA-DR antigens (which can stimulate T cell accumulation)
  • Drives inflammatory reaction against part of the plaque contents
    Complications develop including:
  • ulceration, fissuring, calcification and aneurysm change
54
Q

What are the different pathological stages of angina?

A
  1. Fatty streak
  2. Intimal cell mass
  3. The atheromatous plaque
  4. Complications of plaque rupture.
55
Q

What is the fatty streak pathological stage of angina?

A
  • These show macrophages filled with abundant lipid (foam cells)
  • Also show smooth muscle cells with fat
56
Q

What is the intimal cell mass pathological stage of angina?

A
  • Collections of muscle cells and connective tissue without lipid - “cushions”
57
Q

What is the atheromatous plaque pathological stage of angina?

A
  • Distorted endothelial surface containing lymphocytes, macrophages, smooth muscle cells
  • Local necrotic and fatty matter with scattered lipid rich macrophages
  • Evidence of local haemorrhage may be seen with iron deposition and calcification
    Complicated plaques = show calcification and mural thrombus, making them vulnerable to rupture
58
Q

What complications arise with 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
59
Q

What is the clinical presentation of angina?

A
  • Central test 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
  • Dyspnoea, nausea, sweatiness, faintness
60
Q

What is the scoring of the clinical presentation of angina?

A
  1. Have central, tight, radiation to arms, jaw and neck
  2. Precipitated by exertion
  3. Relieved by rest or spray GTN.
    3/3 = typical angina
    2/3 = atypical angina
    1/3 = non-anginal pain
61
Q

When presented with the clinical presentation of angina, what can be the differential diagnosis?

A
  • Pericarditis/myocarditis
  • Pulmonary embolism
  • Chest infection
  • Dissection of the aorta
  • GORD
62
Q

Appearance of 12 lead ECG with angina?

A
  • Often normal
  • May show ST depression
  • Flat or inverted T waves
  • Look for signs of past MI
63
Q

Diagnosis of angina; treadmill test/ exercise ECG?

A
  • Put ECG on patient, make them run uphill in efforts to induce ischaemia
  • Monitor how long patient is able to exercise for
  • ST segment depression = sign of late-stage ischaemia
  • However many patients unsuitable for this
64
Q

Diagnosis of angina; CT scan Calcium scoring?

A
  • CT the heart,
  • Atherosclerosis - calcium will light up white
  • Significant calcium = indication of angina
65
Q

Diagnosis of angina; SPECT/myoview?

A
  • Radio-labelled tracer injected into patient
  • Is taken up by the coronary arteries (good blood supply) - this will light up
  • Little blood supply - areas will not light up
  • No light after exercise, indicative of myocardial ischaemia
66
Q

What is the treatment for angina?

A 
Modify risk factors:
- Stop smoking 
- Encourage exercise 
- Weight loss
Treat underlying conditions
Pharmacological: 
- Aspirin 
- Statins 
- Beta-blockers 
- GTN spray 
- Ca2+ channel antagonists/blocker
Revascularisation; PCI 
CABG - Coronary Artery Bypass Graft
67
Q

What is the effect of Aspirin for angina treatment?

A
  • Anti-platelet effect (inhibit platelet aggregation ad avoid platelet thrombosis)
  • COX inhibitor; reduce prostaglandin synthesis = reduced platelet aggregation
    Side effects: gastric ulceration
68
Q

What is the effect of statins for angina treatment?

A
  • HMG-CoA reductase inhibitors; reduce cholesterol produced by liver
  • Reduce LDL cholesterol
  • Anti-atherosclerotic
69
Q

What is the effect of beta-blockers for angina treatment?

A
  • Negatively ionotropic (reduce left ventricle contractility)
  • Negatively chronotropic
  • Reduce cardiac output
  • Act on B1 receptors in the heart as part of the adrenergic sympathetic pathway
    Side effects: tiredness, nightmares, bradycardia, erectile dysfunction, cold hands and feet
    DO NOT GIVE in asthma, heart failure/ heart block, hypotension, bradyarrythmias
70
Q

What is the effect of Glyceryl Trinitrate spray?

A
  • Nitrate = venodilator
  • Dilates systemic veins, so reduces venous return to right heart
  • Reduces preload
  • So reduces work of heart and O2 demand
  • Dilates coronary arteries
    Side effect: profuse headache immediately after use
71
Q

What is the effect of Ca2+ channel antagonists/blockers in treatment for angina?

A
  • Primary arterodilators
  • Dilate systemic arteries = BP drop
  • So reduce afterload on the heart
  • So less energy is required to produce the same cardiac output
  • Meaning less work on the heart and O2 demand
72
Q

Explain revascularisation as a treatment for angina:

A
  • Restore patent coronary artery and increase flow reserve

- Done when medication fails or when high risk disease is identified

73
Q

Explain the process of Percutaneous Coronary Intervention:

A
  • Dilating coronary atheromatous obstructions by inflating balloon within it
  • Insert balloon and stent, inflate balloon and remove it
  • Stent persists and keeps the artery patent
  • Expanding plaque = make artery bigger
    Pros; less invasive, convenient, short recovery time, repeatable
    Cons; risk of stent thrombosis, not good for complex disease
74
Q

Explains the process of a Coronary Artery Bypass Graft:

A
  • Left Internal Mammary Artery (LIMA) is used to bypass proximal stenosis in the Left Anterior Descending coronary artery
    (LIMA for LAD)
    Pros; good prognosis, deals with complex disease
    Cons; invasive, risk of stroke or bleeding, one time treatment and need to stay in hospital - long recovery time
75
Q

What is Acute coronary syndrome?

A 
Umbrella term that includes: 
- STEMI
- Unstable (crescendo) angina 
- NSTEMI
Difference between the 3 is that in a NSTEMi there is occluding thrombus which leads to myocardial necrosis and a rise in serum troponin or creatine kinase-MB.
76
Q

What is a STEMI?

A

ST elevation myocardial infarction

  • develop a complete occlusion of a major coronary artery (previously affect by atherosclerosis)
  • causes full thickness damage of heart muscle
  • can usually be diagnosed on ECG at presentation
  • Will produce a pathological Q wave some time after MI (also called Q wave infarction)
77
Q

What is an unstable (crescendo) angina?

A
  • Angina of recent onset (less than 24 hours)
  • Or cardiac chest pain with crescendo pattern
  • Deterioration in previously stable angina, symptoms occurring frequently at rest
  • Angina of increasing frequency or severity, occurring at minimal exertion or even at rest
78
Q

What is a NSTEMI?

A

Non-ST elevation myocardial infarction

  • Occurs by developing a complete occlusion of a minor or a partial occlusion of a major coronary artery (previously affected by atherosclerosis)
  • Retrospective diagnosis made after troponin results
  • Causes partial thickness damage of heart muscle
  • Non-Q wave infarction, will see ST depression and/or T wave inversion
79
Q

When does a myocardial infarction occur?

A

MI occurs when cardiac myocytes die due to myocardial ischaemia.

80
Q

How many types of MI are there?

A

Five types

81
Q

What is Type 1 MI?

A

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

82
Q

What is Type 2 MI?

A

MI secondary to ischaemia due to increased O2 demand or decreased supply.
Seen in coronary spasm, coronary embolism, anaemia, arrhythmia’s, hypertension or hypotension

83
Q

What is Type 3,4,5 MI?

A

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

84
Q

STEMI epidemiology?

A

5/1000 per annum in UK of STEMI

85
Q

STEMI risk factors?

A
  • Age
  • Male
  • Family history of Ischaemic Heart Disease (IHD) - MI in first degree relative below 55
  • Smoking
  • Hypertension, diabetes Mellitus, hyperlipidaemia
  • Obesity and sedentary lifestyle
86
Q

STEMI pathophysiology?

A
  • Rupture or erosion of the fibrous cap of a coronary artery plaque
  • Leads to platelet aggregation and adhesion, localised thrombosis, vasoconstriction, distal thrombus embolisation
  • Rich lipid pool within the plaque and a thin fibrous cap = 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

Unstable angina, plaque has a necrotic centre and ulcerated cap, thrombus results in partial occlusion
In myocardial infarction, plaque also has necrotic centre but thrombus results in total occlusion.

87
Q

Clinical presentation of Acute Coronary Syndrome:

A

Angina:
- Chest pain; new onset, at rest with crescendo pattern
- Breathlessness
- Pleuritic pain
- Indigestion
New Onset Angina
Recent destabilisation of existing angina (w/ moderate/ severe limitations of daily activity)
- Acute central chest pain, lasting more than 20 minutes, associated with sweating, nausea and vomiting, dyspnoea, fatigue, shortness of breath, palpitations
Silent infarct - can present without chest pain
Distress and anxiety
Pallor
Increased pulse, reduced BP
Reduced 4th heart sound
Tachy/bradycardia
Peripheral oedema

88
Q

Acute coronary syndrome; differential diagnosis…

A
  • Angina
  • Pericarditis
  • Myocarditis
  • Aortic dissection
  • Pulmonary embolism
  • Oesophageal reflux/ spasm
89
Q

Acute coronary syndrome; diagnosis with 12 lead ECG:

A
  • Can be normal
  • ST depression and T wave inversion (NSTEMI) are highly suggestive of an ACS (especially if in association with anginal chest pain)
  • Hyperacute (tall) T waves
  • STEMI; complete occlusion results in persistent ST-elevation, hyperacute T waves or new left bundle branch block pattern (days after MI pathological Q waves can be seen)
90
Q

What are the biochemical markers of ACS?

A
  • Troponin (T and I)
  • CK-MB (creatine kinase - MB)
  • Myoglobin

Phase 2a (8 decks)

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