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My Phase 2a > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is atherosclerosis

A

The buildup and hardening of cholesterol in the blood vessels

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2
Q

What are the potential consequences of atherosclerosis

A
  • heart attack
  • stroke
  • gangrene of the extremities
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3
Q

What is the best known factor for coronary heart disease

A

Age

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4
Q

How does tobacco smoking affect atherosclerosis formation

A

Nicotine damages the endothelial layer

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5
Q

How does diabetes affect atherosclerosis formation

A
  • high blood glucose damages the endothelial layer
  • changes/ fluctuations in glucose also damages the vessels
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6
Q

How does hypertension affect atherosclerosis formation

A

Repeated damage to the endothelium through high blood flow/ shear forces

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7
Q

T/F
Family history is a risk factor for atherosclerosis

A

T
Plays a role but is not fully understood

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8
Q

Where does atherosclerosis typically occur AND
Describe the distribution of atherosclerotic plaques

A
  • found in peripheral and coronary arteries
  • focal distribution along the artery length
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9
Q

What factors determine the distribution of atherosclerotic plaques

A

haemodynamic factors
- Changes in flow or turbulence (eg at bifurcations) cause the artery to alter endothelial cell function.
- Wall thickness is also changed leading to neointima - a new intima layer

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10
Q

T/F
The blood vessels have an epithelial layer

A

FALSE
Blood vessels have an ENDOthelial layer

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11
Q

What components make up an atheroscleortic plaque

A
  • lipid
  • necrotic core
  • connective tissue
  • fibrous cap
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12
Q

What are 2 possible outcomes of an atherosclerotic plaques

A
  • vessel occlusion ➡️ restriction of blood flow = angina
  • rupture of the plaque ➡️ thrombus formation ➡️ clot and stroke/ MI
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13
Q

How does injury to endothelial cells cause atherosclerosis

A
  • Injury ➡️ endothelial dysfunction ➡️ chemoattractants released from endothelial cells signal circulating leukocytes
  • chemoattractants are released from the site of injury ➡️ conc. gradient which the leukocytes follow.
  • this causes leukocytes accumulation and they migrate into the vessel wall ➡️ inflammation
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14
Q

Role of LDL in atherosclerosis

A

It can pass in and out of the arterial walls in excess. Within the wall it undergoes oxidation and glycation

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15
Q

Summarise leukocyte recruitment to a vessel wall

A
  1. Capture: the leukocyte sticks “loosely” to the endothelial layer via selectins
  2. They then slow down and begin rolling along the endothelial surface
  3. They roll down the conc. gradient of chemoatttractants until peak conc is reached where they bind to integrins ➡️ firm adhesion to the endothelial layer
  4. At this point the leukocytes enter the vessel wall via transmigration
    • this is made easier by erosion ➡️ Loss of endothelial cells ➡️ increased gaps and opportunity for transmigration
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16
Q

Summarise the key points of atherosclerosis progression

A
  1. Fatty streaks
    • appear at a v early age ~10yrs
    • consist of lipid-laden macrophages [foam cells] + T-lymphocytes within the intima layer
  2. Intermediate lesions
    • made of layers of foam cells, vascular smooth muscles cells + T-lymphocytes.
    • platelets adhere and aggregate on the endothelial wall
  3. Fibrous plaques or advanced lesions
    • blood flow is restricted and the plaque is prone to rupture
    • Contains: smooth muscle cells, macrophages and foam cells and T lymphocytes
    • covered by fibrous cap that is made of collagen and elastin for strength and flexibility.
  4. Plaque rupture
    • thrombus clot formations
    • the fibrous cap is resorbed and redeposited in order to be maintained. If this balance shifts e.g. due to resp. Infection ➡️ weakening and rupture
  5. Plaque erosion
    • Second most prevalent cause of coronary thrombosis
    • A thickened fibrous cap may lead to collagen triggering thrombosis rather than tissue factor
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17
Q

T/F
Diet is the most influential factor on a persons cholesterol level

A

FALSE
Genetic is, thus starting cholesterol lowering drugs is key

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18
Q

Main differences between plaque rupture and plaque erosion

A
  • rupture has a large lipid core while erosion has a small one
  • ruptures have a red thrombus and erosions have a white thrombus
    • Red thrombus = rbcs and fibrin, white thrombus platelets and fibrinogen
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19
Q

What is plaque erosion

A

When a thickened fibrous cap has exposed collagen ➡️ thrombosis being triggered ➡️ platelet rich clot forming [white thrombus]
(usually tissue factor exposure tiggers clot formation)

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20
Q

Define ACS

A
  • Acute coronary syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery.
  • a range of different conditions, including: unstable angina and different myocardial infarctions
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21
Q

Symptoms of unstable angina

A
  • cardiac chest pain at rest
  • cardiac chest pain with a crescendo pattern
  • new onset angina
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22
Q

How is unstable angina diagnosed

A
  • pt history
  • ECG
  • troponin - no significant rise indicates unstable angina as opposed to MI
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23
Q

2 main types of acute MI

A
  • STEMI : can usually be diagnosed on ECG at presentation
  • NSTEMI : retrospective diagnosis made after troponin results and sometimes other investigation results are available.
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24
Q

What is a Q-wave MI

A

An MI where new Q-waves develop on the ECG

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25
Q

Symptoms of myocardial infarction

A

Cardiac chest pain that:
- Is unremitting
- usually severe but may be mild or absent
- occurs at rest
- associated with sweating, breathlessness, nausea and/or vomiting
- one third occur in bed at night

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26
Q

Initial MI management

A
  • get to hospital ASAP
  • direct to primary PCI centre for transfer if paramedics detect ST elevation
  • take 300mg aspirin immediately
  • pain relief if needed
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27
Q

Hospital management of MI

A
  • make diagnosis -ECG
  • bed rest
  • oxygen therapy if hypoxic
  • pain relief - opiates or nitrates
  • dual anti platelet tx - aspirin +/- platelet P2Y12 inhibitor
  • beta blocker
  • other anti anginal therapy
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28
Q

What causes ACS

A

Most cases caused by atherosclerotic plaques

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29
Q

What is troponin + What is it made of
What is its role

A
  • A protein complex made of 3 subunits Tropnin T, I + C
  • regulates actin:myosin contraction
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30
Q

High troponin indicates …

A

Cardiac muscle injury
- troponin T and I are highly sensitive indicators of cardiac muscle injury

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31
Q
  • T/F
    High troponin is always a marker of permanent cardiac muscle injury
A
  • FALSE
  • May not represent permanent muscle damage
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32
Q
  • T/F
    High troponin is always a marker of ACS
A

False troponin is non-selective
troponin is also positive in
- gram negative sepsis
- pulmonary embolism
- myocarditis
- heart failure
- arrhythmias
- chronic renal failure
- aortic dissection
- cytotoxic drugs

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33
Q

What is a psychosocial factor

A

Factors influencing psychological responses to the social environment and pathophysiological changes

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34
Q

Name 5 types of risk factors

A
  1. Clinical risk factors (hypertension, lipids, diabetes)
  2. Lifestyle/ behavioural risk factors (smoking, diet, physical inactivity)
  3. Environmental risk factors (air pollution, chemicals)
  4. Demographic risk factors (age, sex, ethnicity, genetic)
  5. Psychosocial risk factors (behaviour pattern, depression/anxiety, work, social support)
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35
Q

What is coronary prone behaviour?

A
  • “Type A” behaviour
  • competitive, hostile and impatient
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36
Q

How might you assess behaviour patterns

A
  • clinical interview
    • Speech, Answer content
    • Psychomotor, Non-verbal
  • questionnaires
  • assessment usually done in psychological settings not day to day medical practice
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37
Q

name a soluble platelet agonist

A

ADP

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38
Q

what is th erole of ADP in platelet aggregation

A
  • ADP is released by damaged endothelium –> platelet adhesion and secretion of more ADP
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39
Q

what are the effects platelet activation

A
  1. shape change
  2. fibrinogen release which promotes blood clotting by forming bridges between platelets via GPIIb/IIIa - an integrin
  3. thromboxane release which amplifies platelet activation + recruits more platelets.
  4. dense granule formation -> ADP release -> amplification of platelet activation via P2Y1 and P2Y12 receptors
  5. thrombin generation which converst fibrinogen –> fibrin to form a more stable fibrin basaed clot.
  6. alpha granule formation -> release of coagulation factos and inflammatory mediators.
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40
Q

what are the acute coronary syndromes

A
  1. unstable angina
  2. STEMI
  3. NSTEMI
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41
Q

Why do you get myocardial ischamia

A

An imbalance between the heart’s oxygen demand and supply, usually caused by an increased demand coupled with a limitation of supply

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42
Q

Predisposing factors to ischaemic heart disease

A
  1. Age
  2. Cigarette smoking
  3. Diabetes mellitus
  4. Family history
  5. Male
  6. Hyperlipidemia
  7. Hypertension
  8. Obesity
  9. Kidney disease
    10 physical inactivity
  10. Stress
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43
Q

What factors can exacerbate angina

A

factors affecting O2 supply
- anaemia
- hypoxemia

factors affecting O2 demand
- hypertension
- tachycardia
- valvular heart disease
- hyperthyroidism
- hypertrophic cardiomyopathy

environmental factors
- exercise
- cold weather
- heavy meals - blood is diverted to the stomach
- emotional stress

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44
Q

At what point is there a rapid decline in coronary flow ➡️ symptoms?

A

When diameter stenosis reaches 70%

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45
Q

What is crescendo angina

A

Angina pain that has been steadily getting worse over prior weeks and months, due to coronary heart disease

Serious and requires hospitalisation

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46
Q

What is unstable angina

A

Angina pain at rest, due to coronary hear disease
Serious and requires hospitalisation

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47
Q

What is Prinzmetal’s angina

A

Coronary spasm that narrows the coronary arteries ➡️ symptoms of angina
RARE

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48
Q

What is micro vascular angina

A
  • The micro vessels are at fault , meaning they can’t relax to reduce the resistance and increase blood flow ➡️ angina
  • The main coronary arteries apparently normal
  • mostly affects females
  • Cause unknown
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49
Q

High prevalence and low incidence says what about the prognosis of a condition

A
  • The prognosis is not bad as those that are diagnosed with the condition go on to live with it for a while
  • Prevalence = the number of people with a condition
  • Incidence = the number of people that develop a condition
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50
Q

Information to acquire when taking a history in IHD

A

Personal details (demographics, identifiers)
Presenting complaint
History of PC + risk factors
Past medical history
Drug history, allergies
Family history -1st degree relative <60years old
Social history
Systematic enquiry

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51
Q

What are the symptoms of stable angina

A
  • Chest pain / tightness/ discomfort / heaviness on exertion
  • Breathlessness
    • No fluid retention (unlike heart failure)
    • Palpitation (not usually)
    • Syncope or pre-syncope (very rare)
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52
Q

What questions should you ask about the pain a pt with stable angina experiences

A

OPQRST
Onset
Position (site)
Quality (nature / character)
Relationship (with exertion, posture, meals, breathing and with other symptoms)
Radiation
Relieving or aggravating factors
Severity
Timing

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53
Q

Differential diagnosis of chest pain

A
  • MI
  • pericarditis/ myocarditis
  • pulmonary embolism / pleurisy
  • chest infection
  • Gastro-oesophageal (reflux, spasm, ulceration)
  • Musculo-skeletal
  • Psychological
  • Aorta dissection - severe tearing pain

the description of the pain is helpful

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54
Q

Broad treatment plan for stable angina / IHD

A
  • Lifestyle
    • smoking
    • Weight
    • Exercise
    • diet
  • Advice for emergency
  • Medication
  • Revascularisation
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55
Q

Diagnostic tests for coronary heart disease

A
  • CT Coronary Angiography
  • exercise testing
  • myoview scan
  • stress echo
  • perfusion MRI = GOLD STANDARD.
  • coronary angiography
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56
Q

What does ST depression indicate

A

Ischaemia

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57
Q

What is CT coronary angiography

A
  • CT Coronary Angiography - good at ruling out and spotting severe disease.
  • Shows the anatomy of the heart nor the function.
  • much less invasive than traditional angiogram
  • Long waiting times
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58
Q

What is exercise testing

A
  • Pt walks on treadmill while hooked up to ECG continuously and the intensity is gradually increased.
  • Dependent on pts ability to walk on treadmill
  • diagnostic tool for IHD
  • useless in disabled, elderly, obese, arthritic etc
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59
Q

what is a myoview scan and what is it used for

A
  • small dose of radiolabel circulates through the heart and imaged using a gamma camera to determine which parts of the heart have low perfusion when stressed and if perfusion returns on rest.
  • Uses pharmacological stressor to Increase HR and CO
  • a diagnostic tool for IHD
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60
Q

What is a stress echo

A
  • diagnostic tool for IHD
  • Pharmacological stressor administered and a highly skilled operative looks for a regional wall abnormality.
  • Not used often
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61
Q

What is the best non-invasive test for IHD

A
  • perfusion MRI = GOLD STANDARD.
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62
Q

what is a coronary angiography

A
  • A catheter is inserted and guided to heart and contrast administered
  • X-ray taken to look at the coronary arteries - also treatment planning tool as a stent can be administered immediately if appropriate
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63
Q

What is the cholesterol reduction target when initiating statins in IHD

A

Reduce the cholesterol by 30%

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64
Q

What drugs are used to treat stable angina

A
  • aspirin
  • Beta-blocker or Calcium channel blocker [2nd line]
  • statin
  • nitrates - GTN and long acting
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65
Q

What affect do Beta blockers have on the heart

A
  • negatively inotropic [rate] and chronotropic [contractility] ➡️ reduced cardiac output and reduced oxygen demand
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66
Q

Side effects of beta blockers

A
  • bradycardia
  • nightmares - depending on w=if water soluble or not
  • cold peripheries
  • erectile dysfunction
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67
Q

How do nitrates work in IHD

A
  • mainly act on venous return by causing expansion of venous capacitance vessels, causing the veins to relax ➡️ reduced preload on the heart.
  • dilates the coronary arteries
  • dilates the arterioles
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68
Q

Side effect of nitrates

A

A headache caused by vasodilation - should stop within 3 days of use

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69
Q

How do CCBs work in IHD

A
  • negatively inotropic ➡️ less left ventricular contraction
  • negatively chronotropic ➡️ lower heart rate
    • together this reduces the work the heart does and therefore the oxygen demand
  • lowers BP ➡️ reduced after load
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70
Q

Side effects of CCBs

A
  • flushing
  • postural hypotension
  • swollen ankles
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71
Q

Main side effect of aspirin

A

Gastric ulceration

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72
Q

How do statins work

A

They inhibit the enzyme HMG CoA reductase
This prevents the production of cholesterol

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73
Q

Pros and cons of PCI

A

pros
- Less invasive
- Convenient
- Repeatable
- Acceptable

cons
- Risk stent thrombosis
- Risk restenosis
- Can’t deal with complex disease
- Dual antiplatelet therapy

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74
Q

Pros and cons of CABG

A

Pros
- Prognosis
- Deals with complex disease

Cons
- Invasive
- Risk of stroke, bleeding
- Can’t do if frail, comorbid
- One time treatment
- Length of stay
- Time for recovery

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75
Q

What is a CABG

A

Coronary artery bypass graft
The internal mammary artery is diverted from the chest back to the LAD beyond the blockage
A graft from the leg [saphenous vein] is placed to another blockage

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76
Q

When would you use PCI

A
  • STEMI
  • NSTEMI
  • stable angina
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77
Q

When would you use CABG

A
  • NSTEMI
  • complex stable angina
    never use for STEMI
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78
Q

d

A

c

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79
Q

what are the branches of the aorta

A
  • brachocephalic trunk → right common carotid and right subclavian
  • left common carotid artery
  • left subclavian artery
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80
Q

what is the pericardium, how many layers/subdivisions

A

a double layered sac covering the heart.

  • inner layer = serous pericardium: has simple squamous epithelium
    • visceral serous pericardium [epicardium] lines the outer surface of the heart
    • parietal serous pericardium lines the fibrous pericardium and secretes fluid.
  • outer layer = fibrous pericardium
    • tough connective tissue that anchors the heart to the mediastinum.
  • outside → in = FPSV
    • Fibrous, parietal serous, SPACE, visceral serous
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81
Q

what is the significance of level T4/T5?

A

sternal angle

point at which the trachea bifurcates

end of the aortic arch and begining of the thoracic aorta.

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82
Q

what surface marking marks the apex of the heart

A

midclavicular line of the 5 intercostal space

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83
Q

where can you hear the aortic valve

A

the 2nd intercostal space at the right sternal margin

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84
Q

where can you hear the pulmonary valve

A

2nd intercostal space of the left sternal margin

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85
Q

where does the right coronary artery originate from

A

the ascending aorta

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86
Q

where is the right coronary artery located

A

on the anterior surface of the heart in the atrioventricular sulcus.

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87
Q

what are the main branches of the right coronary artery?

A

the right marginal artery

posterior interventricular artery - present in 90% of people.

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88
Q

where does the left coronary artery originate from

A

the ascending aorta

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89
Q

what are the main branches of the left coronary artery?

A
  • left anterior descending
  • the left marginal artery / obtuse marginal artery
  • Circumflex artery
  • diagonals
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90
Q

what are the potential sources of blood in the posterior interventricular arterty

A
  • 90% of people have PIV supplied by the right coronary artery
  • 30% of people have the PIV supplied by the circumflex artery
  • 20% of people have TWO PIVs supplied by each
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91
Q

the Posterior interventricular artery supplies …

A

the atrioventricular node recieves blood supply from..

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92
Q

describe the consequence of disease in the PIV

A

as the PIV supplies the AVN, disease could limit O2 supply → electrical blockage in the heart.

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93
Q

the atrioventricular node recieves blood supply from..

A

the Posterior interventricular artery supplies …

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94
Q

describe the conducting system of the heart

A
  1. An excitation signal (an action potential) is created by the sinoatrial (SA) node.
  2. The wave of excitation spreads across the atria, causing them to contract.
  3. Upon reaching the atrioventricular (AV) node, the signal is delayed.
  4. It is then conducted into the bundle of His, down the interventricular septum.
  5. The bundle of His and the Purkinje fibres spread the wave impulses along the ventricles, causing them to contract
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95
Q

what is the SAN and where is it located?

A

the sinoatrial node is a collection of pacemaker cells, located in the upper wall of the right atrium, at the junction where the superior vena cava enters.

96
Q

where is the AVN located

A

located within the right atrioventricular septum, near the opening of the coronary sinus.

97
Q

What area does each coronary artery supply

A
  • right coronary artery = right atrium and ventricle
  • LAD = right and left ventricles and interventricular septum
  • obtuse / left marginal artery = left ventricle
  • circumflex = left atrium and ventricle
  • Right marginal = right ventricle and apex
98
Q

RBC lifespan

A

120 days

destroyed as they have no nucleus for self maintainance

99
Q

difference between primary and secondary phases of haemostasis

A

phase 1 = platelet plug formation

phase 2 = coagulation - stabilising the plug

100
Q

how many pathways in the coagulation pathway

A

3:

  1. intrinsic: triggered by surface contact with collagen
  2. extrinsic: triggered by endothelial damage
  3. common
101
Q

5 main steps of platelet plug formation

A
  1. endothelial injury
  2. exposure
  3. adhesion
  4. activation
  5. aggregation
102
Q

how is the SAN activated

A

it’s not activated by any other cell, it is in an automatic, constant cycle

103
Q

effect of sympathetic stimulation on the heart

A
  • Increases heart rate (positively chronotropic)
  • Increases force of contraction (positively inotropic)
  • Increases cardiac output
104
Q

effect of parasympathetic stimulation on the heart

A
  • Decreases heart rate (negatively chronotropic)
  • Decreases force of contraction (negatively inotropic)
  • Decreases cardiac output
105
Q

sympathetic stimulation is controlled by

A

Adrenaline and noradrenaline + type 1 beta adrenoreceptors

  • Increases adenylyl cyclase → increased cAMP
106
Q

parasympathetic stimulation is controlled by

A

ACh and M2 receptors

– inhibit adenyl cyclase → reduced cAMP

107
Q

what is a refractory period

A

the time in which the cell cannot depolarise again

108
Q

what happens at each stage of the ecg pathway

A
  • P wave
  • atria fills with blood → SA node firiing → atrial contraction
    • atrial systole occurs partway through the P wave
    • P-R = atrial systole / ventricle diastole
    • P-Q segment = time it takes for signal to pass from SAN → AVN
  • QRS complex
  • represents firing of AVN and depolarisation of the ventricles
  • R-S = isovolumetric contraction
    • AV valves are shut and semilunar valves are shut BUT the ventricle has started contracting
  • ST segment
  • represents the plateau in myocardial action pd = Ca2+ influx → contraction
  • Thus ST segment = ventricular contraction - systole
  • T wave
  • ventricular repolarisation and diastole
  • end of T wave represents isovolumetric relaxation
109
Q

what is troponin

A
  • a protein that holds tropomyosin in place on actin and is involved in myocyte contraction
  • it has 3 subunits
    1. TNI - inhibitory to prevent in actin and myosin interaction
    2. TnT tropomyosin binding
    3. TnC calcium binding
110
Q

what causes the first and second heart sounds

A
  1. Mitral valve shutting
  2. aortic valve shutting
111
Q

what is preload and what factors affect it

A

the degree of ventricular stretch at the end of diastole - a volume

venous blood pressure and rate of venous return

112
Q

what is afterload and what factors affect it

A

the pressure which the ventricles must overcome to eject blood

i.e. systemic pressure and pulmonary pressure

113
Q
  • When a thrombus forms in a fast flowing artery it is made up mostly of…
  • how does this influence treatment
A
  • platelets
  • anti-platelet therapy is used
114
Q

Right Coronary Artery (RCA) curves around the right side and under the heart and supplies the:

A

Right atrium
Right ventricle
Inferior aspect of left ventricle
Posterior septal area

115
Q

Circumflex Artery curves around the top, left and back of the heart and supplies the:

A

Left atrium
Posterior aspect of left ventricle

116
Q

Left Anterior Descending (LAD) travels down the middle of the heart and supplies the:

A

Anterior aspect of left ventricle
Anterior aspect of septum

117
Q

What symptoms are associated with ACS

A

Nausea and vomiting
Sweating and clamminess
Feeling of impending doom
Shortness of breath
Palpitations
Pain radiating to jaw or arms

118
Q

What diagnostic tests should be carried out on a pt presenting with ACS symptoms

A
  1. ECG carried out to determine if there is ST elevation or new left bundle branch block
  2. Blood test for troponin levels to determine if there was an MI
119
Q

High troponin levels and ECG changes indicate

A

NSTEMI

120
Q

PT presents with central chest pain radiating to jaw and arms
Normal troponin levels and no pathological change on an ECG
What does this suggest

A

Unstable angina
Or another cause of chest pain such as MSK chest pain

121
Q

What ECG changes are seen in an NSTEMI

A

ST segment depression in a region
Deep T Wave Inversion
Pathological Q Waves (suggesting a deep infarct – a late sign)

122
Q

What are alternative causes of raised troponin

A

Chronic renal failure
Sepsis
Myocarditis
Aortic dissection
Pulmonary embolism

123
Q

Acute treatment for a STEMI

A
  • Primary PCI (if available within 2 hours of presentation)
  • Thrombolysis (if PCI not available within 2 hours)
    • Using fibrinolytic drug to dissolve the clot such as alteplase, streptokinase or tenectplase
124
Q

Acute NSTEMI treatment

A

BATMAN

B – Beta-blockers unless contraindicated

A – Aspirin 300mg stat dose

T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)

M – Morphine titrated to control pain

A – Anticoagulant: Fondaparinux (unless high bleeding risk ➡️ heparin)

N – Nitrates (e.g. GTN) to relieve coronary artery spasm

Give oxygen only if their oxygen saturations are dropping (i.e. <95%).

125
Q

What is the GRACE score AND
What is it used for

A
  • A scoring system that gives a 6 months risk of death or repeated MI after an NSTEMI
  • It’s used to assess the need for PCI in NSTEMI
    • <5% Low Risk
    • 5-10% Medium Risk
    • > 10% High Risk
      • medium -high risk considered for early PCI for underlying coronary artery disease
126
Q

Complications of an MI

A

DREAD

D – Death

R – Rupture of the heart septum or papillary muscles

E – “Edema” (Heart Failure)

A – Arrhythmia and Aneurysm

D – Dressler’s Syndrome

127
Q

What is Dressler’s syndrome

A
  • post-myocardial infarction syndrome.
  • It usually occurs around 2-3 weeks after an MI.
  • It is caused by a localised immune response and ➡️ pericarditis
128
Q

Presentation of Dressler’s syndrome

A
  • pleuritic chest pain
  • low grade fever
  • pericardial rub on auscultation
129
Q

How is Dressler’s syndrome diagnosed

A
  • ECG ➡️ global ST elevation and T wave inversion
  • Echocardiogram ➡️ pericardial effusion
  • Raised inflammatory markers - CRP and ESR
130
Q

Secondary management of ACS

A

DASLAB
- D - Dual antiplatelet therapy - aspirin + clopidogrel or ticagrelor up to 12 months

  • A - Ace inhibitor
  • S - Statin - Astorvastatin 80mg
  • L - Lifestyle changes
  • A - Aldosterone antagonist for pts with clinical heart failure - eplerenone
  • B - Beta blocker titrated to max tolerated dose
131
Q

Describe the anatomy of the pericardium

A

2 continuous layers
- Visceral single cell layer adherent to epicardium
- Fibrous parietal layer 2mm thick
- ~50 ml of serous fluid in between for lubrication

132
Q

What structures lie within the pericardium

A
  • the great vessels
  • all of the heart EXCEPT the left atrium
133
Q

Function of the pericardium

A

To restrain the filling volume of the heart

134
Q

How do pericardial effusions occur

A
  • The pericardium is similar to rubber in that it is initially stretchy but becomes stiff at higher tensions
  • this means the sac can only take on a small amount of fluid before it stiffens. Thus, it has a small reserve volume.
  • pericardial effusions occur when fluid enters the sac and the reserve volume is exceeded ➡️ the pericardial sac stiffens and prevents the heart from filling as normal.
135
Q

What is tamponade physiology

A

A small increase or decrease in pericardial space fluid ➡️ dramatic effects on filling of the heart

136
Q

What is chronic pericardial effusion

A
  • Slow accumulation of fluid within the pericardium allows the parietal pericardium to adapt and stretch.
  • the increase in compliance of the parietal layer reduces the effect on filling of the chambers
  • this allows for large effusions to accumulate
  • slowly accumulation effusions rarely cause tamponade
137
Q

What is acute pericarditis

A

Acute pericarditis is an inflammatory pericardial syndrome with or without effusion

138
Q

What signs are needed for a clinical diagnosis of acute pericarditis

A

At least 2/4 of:
1. Chest pain
2. Friction rub
3. ECG changes
4. Pericardial effusion

139
Q

What is the aetiology of acute pericarditis

A

infectious
- viral - enteroviruses, herpes virus, adenovirus
- ** bacterial** - mycobacterium tuberculosis

Non-infectious
- autoimmune - common, e.g. Sjögren syndrome, rheumatoid arthritis, scleroderma,
- Neoplastic - secondary metastatic tumours
- metabolic - uraemia and myxoedema
- traumatic - direct or indirect injury
- iatrogenic
- amyloidosis, aortic dissection, CHF

140
Q

what is the clinical presentation of acute pericarditis

A
  • chest pain that is:
    • Severe
    • Sharp and pleuritic (without constricting crushing character of ischaemic pain)
    • Rapid onset
    • Left anterior chest or epigastrium
    • Radiates to arm more specifically trapezius ridge (co-innervation phrenic nerve)
    • Relieved by sitting forward exacerbated by lying down
  • dyspnoea
  • cough
  • hiccups
  • systemic disturbance
    • Skin rash, joint pain, eye Sx, weight loss (Cause)
    • Viral prodrome, Antecedent fever
  • past medical history of cancer, rheumatological conditions, MI or cardiac procedures.
141
Q

a clinical examination for acute pericarditis includes looking for…

A
  • pericardial rub: sounds like crunching snow or scratching on the left sternal edge
  • sinus tachycardia
  • fever
  • signs of effusion - pulsus paradoxus
  • Beck’s triad
    • elevated JVP
    • Hypotension
    • quiet heart sounds
142
Q

what is pericardial rub

A
  • a pathogonomic sign.
  • sounds like crunching snow or scratching in the left sternal edge
143
Q

What is Beck’s triad

A
  • 3 symptoms and signs that are indicative of pericardial tamponade
    • low blood pressure
    • High jugular vein pressure
    • muffled/ quiet heart sounds
144
Q

what is pulsus paradoxus

A
  • an exaggerated fall in a patient’s blood pressure during inspiration by greater than 10 mmHg caused by moderate or large effusions
  • paradox = the reduced cardiac output -> reduced volume of the peripheral pulse
145
Q

what does an investigation for pericarditis involve

A
  • Clinical examination
    • Pericardial rub – pathognomonic, crunching snow
    • Sinus tachycardia
    • Fever
    • Signs of effusion (pulsus paradoxus, Kussmauls sign)
  • ECG
  • Bloods
  • Chest X-ray - effusion may cause cardiomegaly
  • Echocardiogram
146
Q

key features of pericarditis on an ECGT

A
  • Saddle shaped ST elevation
  • Concave ST segment
  • diffuse ST elevation on ALL leads
147
Q

management of pericarditis

A
  • sedentary activity until resolution of symptoms and ECG and CRP
  • NSAID or aspirin at high dose - 2 weeks
  • colchicine - 3 months
148
Q

what is the most common cause of pericarditis

A

viral pericarditis
self-limiting conditions

149
Q

T/F bacterial pericarditis is a mild condition

A

FALSE
this causes a bad sickness and high mortality

150
Q

what causes Hypertrophic cardiomyopathy

A

Hypertrophic cardiomyopathy (HCM) caused by sarcomeric protein gene mutations

151
Q

what is Hypertrophic cardiomyopathy

A

unexplained primary cardiac hypertrophy

152
Q

symptoms of hypertrophic cardiomyopathy (HCM)

A

HCM may cause:
* angina
* dyspnoea
* palpitations
* dizzy spells or syncope.

153
Q

Dilated cardiomyopathy (DCM) what is a common cause of

A

Dilated cardiomyopathy (DCM) – often caused by cytoskeletal gene mutations

154
Q

what is a channelopathy

A

An Inherited arrhythmia caused by ion channel protein gene mutations.
usually relates to potassium, sodium or calcium channels.

155
Q

give 4 examples of channelopathies

A
  1. long QT
  2. short QT
  3. Brugada
  4. CPVT - Catecholaminergic polymorphic ventricular tachycardia
156
Q

features of channelopathies

A
  • Channelopathies have a structurally normal heart
  • Channelopathies may present with recurrent syncope
157
Q

what is the common cause of sudden cardiac death syndrome

A
  • usually caused by an inherited condition
  • If so this is most likely a cardiomyopathy or ion channelopathy
158
Q

Familial hypercholesterolaemia (FH) is…

A

an inherited abnormality of cholesterol metabolism

159
Q

consequences of familial hypercholesteraemia

A

FH leads to serious premature coronary and other vascular disease

160
Q

T/F
Aortic aneurysm or dissection is often inherited

A

True

161
Q

are inherited congenital condition usually dominant or recessive
what is their offspring’s chance of inheritance

A

ICCs are usually dominantly inherited – offspring have 50% risk of inheritance

162
Q

4 specific causes of pericarditis

A
  1. Viral pericarditis – most common cause in developed world
  2. Purulent bacterial pericarditis and effusion – rare and high mortality rate
  3. Tuberculous effusion TB pericarditis
  4. Dressler’s syndrome
163
Q

Why is it important to treat hypertension

A
  • it is an important preventable cause of premature morbidity and mortality as it is a major risk factor for numerous conditions
164
Q

What is hypertension a risk factor for

A

Stroke – ischaemic and haemorrhagic
Myocardial infarction
Heart failure
Chronic renal disease
Cognitive decline – dementia
Premature death

165
Q

What blood pressure is classed as hypertension

A

Clinic BP 140/90 mmHg or higher

166
Q

How is hypertension diagnosed

A
  • Pts with high BP in clinic are fitted with ambulatory BP monitoring to confirm a diagnosis
167
Q

What are the main drug targets for hypertension

A
  1. Cardiac output
  2. Peripheral resistance - KEY ISSUE IN HYPERTENSION
  3. Local vascular vasoconstrictor and vasodilator mediators
  4. Interplay between:
    a. Renin-Angiotensin-Aldosterone system
    b. Sympathetic nervous system (noradrenaline)
168
Q

ACEi clinical indications

A
  • hypertension
  • heart failure
  • diabetic nephropathy
169
Q

Main adverse effects of ACEi

A
  1. Related to reduced angiotensin II formation
    a. Hypotension
    b. Acute renal failure
    c. Hyperkalaemia
    d. Teratogenic effects in pregnancy – stop before conception if possible.
  2. Related to increased kinin production
    a. Cough
    b. Rash
    c. Anaphylactoid reactions
170
Q

What is an ARB

A

Angiotensin II Receptor Blockers

171
Q

What are the main indications for ARBs

A

Hypertension
Diabetic nephropathy
Heart failure (when ACE-I contraindicated)

172
Q

Main adverse reactions of ARBs

A

Symptomatic hypotension (especially volume deplete patients)
Hyperkalaemia
Potential for renal dysfunction
Rash
Angio-oedema

173
Q

T/F
ARBs are safe in pregnancy

A

FALSE It’s contraindicated

174
Q

Main clinical indications of CCBs

A

Hypertension
Ischaemic heart disease (IHD) – angina
Arrhythmia (tachycardia)

175
Q

What are the types of calcium channel blockers

A
  • Dihydropyridines
    • amlodipine etc
  • Non-dihydropyridines
    • Phenylalkylamines: verapamil
    • Benzothiazepines: diltiazem
176
Q

Action of dihydropyridines

A

Preferentially affect vascular smooth muscle
Peripheral arterial vasodilators

177
Q

Example of a phenylalkamine
What is its action

A
  • verapamil
  • mainly affects the heart - negatively chronotropic and inotropic
178
Q

Example of a benozthiazepine
What is its action

A
  • Diltiazem
  • effects on the heart and blood vessels
    • Negatively chronotropic
    • arterial vasodilation ➡️ reduced BP [increases smooth muscle relaxation
179
Q

Main side effects of CCBs

A
  1. Due to peripheral vasodilatation (mainly dihydropyridines)
    Flushing
    Headache
    Oedema - usually benign and can be ignored
    Palpitations
  2. Due to negatively chronotropic effects (mainly verapamil/diltiazem)
    Bradycardia
    Atrioventricular block
  3. Due to negatively inotropic effects (mainly verapamil)
    Worsening of cardiac failure
  4. Verapamil causes constipation
180
Q

Main indications for beta blockers

A

Ischaemic heart disease (IHD) – angina
Heart failure
Arrhythmia
Hypertension

181
Q

T/F beta blockers can be cardio selective

A

FALSE
Selectivity is relative not absolute
B2 receptors are found in the heart so no such thing as cardioselectivity.
NEVER give any BB to asmatics regardless of se;ectivity claim

182
Q

Main adverse effects of beta blockers

A

Fatigue
Headache
Sleep disturbance/nightmares
Bradycardia
Hypotension
Cold peripheries
Erectile dysfunction

183
Q

What conditions are worsened by beta blockers

A
  • asthma - severely worsened NEVER give to these pts
  • peripheral vascular disease - Claudication or Raynauds
  • heart failure IF given a standard dose - must start on a low dose and slowly uptitrate.
184
Q

Main indication for diuretics

A
  • hypertension
  • heart failure
185
Q

4 main classes of diuretics

A
  1. Thiazide like diuretics
  2. Loop diuretics
  3. Potassium sparing diuretics
  4. Aldosterone antagonists
186
Q

Examples of thiazide like diuretics

A
  • bendroflumethiazide
  • indapamide
  • metolazone
  • chorthalidone
  • hydrochlorothiazide
187
Q

Examples of loop diuretics

A
  • furosemide
  • bumetanide
188
Q

Examples of K+ sparing diuretics

A
  • amiloride
  • triamterine
  • spironolactone
  • eplerenone
189
Q

T/F
K+ sparing diuretics are weak diuretics

A

TRUE
- they are mainly used in conjunction with thiazide or loop diuretics in pts with hypOkalaemia instead of K+ supplements

190
Q

Examples of aldosterone antagonists

A

Spironolactone and eplerenone
They intrinsically act on the RAAS system. Thus they are disease modifying and prevent K+ loss, making them K+ sparing diuretics too

191
Q

Main adverse effects of diuretics

A
  • hypovolaemia and hypotension [ mainly loop diuretics]
  • hypokalaemia
  • hyponatraemia
  • hypomagnesaemia
  • hypocalcaemia
  • hyperuricaemia ➡️ gout
  • Impaired glucose tolerance [mainly loop diuretics]
  • erectile dysfunction [mainly thiazides]
192
Q

Examples of centrally acting anti-hypertensives

A
  • Moxonidine
  • methyldopa
193
Q

Examples of direct renin inhibitor

A

Aliskerin

194
Q

Example of alpha blocker

A

Doxazosin

195
Q

Describe the treatment pathway for hypertension

A
196
Q

Types of heart failure

A
  1. Chronic heart failure - caused by:
    • Left Ventricular Systolic Dysfunction LVSD
    • Diastolic failure - heart failure with preserved ejection fraction HFPEF.
  2. Acute heart failure
    • caused by MI
197
Q

What is heart failure and what is its most common cause

A

Heart failure is a complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired.
It is caused by structural or functional abnormalities of the heart.

Most common cause is coronary artery disease

198
Q

What are the best and worst drug targets for heart failure

A

Best
- Vasodilator therapy
- neurohumoral blockade of the RAAS-SNS systems
- reduces peripheral resistance AND cardiac output

Worst
- Left ventricle stimulant
- heart failure treatment aims to address the response to the impaired heart function rather than the heart function itself

199
Q

Summarise treatment for heart failure

A
  1. Symptomatic treatment for relief of oedema - usually loop diuretics
  2. Disease influencing treatment via neurohumoral blockade - inhibition of RAAS-SNS systems
    1. 1st line = ACE inhibitors and beta blocker therapy [Low dose and slow up-titration]
      1. Give ARB if ACEi intolerant
      2. give hydralazine/ nitrate combo if intolerant to ACEi + ARB
    2. Add aldosterone antagonist [MRA] if no response
    3. consider addition of digoxin, ivabradine or sacubitril/valsartan depending on preserved ejection fraction if poor response
200
Q

Is the heart an endocrine organ - yes or no
Expand

A

YES
- it produces natriuretic peptides in response to stretch
- Atrial natriuretic peptide (ANP) - from the atria
- B-(Brain) natriuretic peptide (BNP) – from the ventricles

  • stretching can be caused by raised atrial or ventricular pressures OR volume over load
201
Q

What are the main effects of ANP + BNP

A

Increase renal excretion of sodium (natriuresis) and water (diuresis)
Relax vascular smooth muscle (except efferent arterioles of renal glomeruli)
Increased vascular permeability
Inhibit the release or actions of:
Aldosterone, angiotensin II, endothelin, anti-diuretic hormone (ADH)

Counter-regulatory system to the renin-angiotensin system

202
Q

What is neprilysin

A
  • The enzyme that breaks down the cardiac natriuretic peptides
  • Neutral Endopeptidase = NEP = neprilysin
203
Q

What are the cardiac natriuretic peptides

A

Atrial natriuretic peptide (ANP) - atria
B-(Brain) natriuretic peptide (BNP) – ventricles

204
Q

What is sacubitril
How does it work +
What is it used for

A
  • A neprilysin inhibitor
  • it increases the levels of natriuretic peptides ➡️ the inhibition of release or action of RAAS:
    • Aldosterone, angiotensin II, endothelin, anti-diuretic hormone (ADH)
  • Heart failure with <35% ejection fraction preserved
205
Q

T/F
SGLT2 inhibitors can be used in heart failure

A

True
Preserves ejection fraction and is cardioprotective

206
Q

Mechanism of action of nitrates

A
  • arterial and venous vasodilators
  • reduce preload and after load
  • lower BP
207
Q

Main clinical indications for nitrates

A
  • Ischaemic heart disease - angina
  • heart failure
208
Q

Main adverse effects of nitrates

A
  • headache
  • GTN syncope - with the spray
    Dizziness
209
Q

Describe the treatment for chronic stable angina

A
  1. All pts receive
    • antiplatelet therapy - aspirin or clopidogrel
    • statins to lower cholesterol
    • GTN spray for acute attacks
  2. 1st line treatment =
    • Beta Blockers or CCBs
    • if intolerant ➡️ switch
    • if not controlled ➡️ combine
  3. If pt still uncontrolled or intolerant consider mono therapy or combinations with:
    • Long acting nitrate
    • Ivabradine (inhibits If current)
    • Nicorandil (K channel activator)
    • Ranolazine (inhibits late inward sodium current)
210
Q

Describe the drug treatment for STEMI + NSTEMI

A
  1. Pain relief: GTN spray, Opiates – diamorphine
  2. Dual antiplatelet therapy: Aspirin plus ticagrelor or prasugrel or clopidogrel
  3. Antithrombin therapy: Fondaparinux
  4. Consider Glycoprotein IIb IIIa inhibitor high risk cases: tirofiban, eptifibatide, abciximab
  5. Background angina therapy: beta blocker, long acting nitrate, calcium channel blocker
  6. Lipid lowering therapy: Statins
  7. Therapy for LVSD/heart failure as required: ACE-I, beta blocker, aldosterone antagonist
211
Q

What type of drugs are in the Vaughan Williams classification
Summarise the classification

A

Antiarrhythmic drugs

212
Q

What type of drug is digoxin

A

A cardiac glycoside
Antiarrhythmic drug

213
Q

Digoxin’s mechanism of action

A

Inhibit Na/K pump [ leads to increased Ca++ in the heart ➡️ increased vagal tone ]

214
Q

Effects of digoxin on the heart

A

Bradycardia (increased vagal tone)
Slowing of atrioventricular conduction (increased vagal tone)
Increased force of contraction (by increased intracellular Ca)

215
Q

main adverse effects of digoxin

A
  • N+V
  • confusion
  • Diarrhoea
  • dizziness
216
Q

What is digoxin used for
What precautions must be taken

A
  • Used in atrial fibrillation (AF) to reduce ventricular rate response
  • Used in severe heart failure as positively inotropic
  • has a narrow therapeutic index so frequent monitoring required
217
Q

What is amiodarone used for

A

Treatment of arrhythmias e.g. QT prolongation and Polymorphic ventricular tachycardia

218
Q

Adverse effects of amiodarone

A

Interstitial pneumonitis
Abnormal liver function
Hyperthyroidism / Hypothyroidism
Sun sensitivity
Slate grey skin discolouration
Corneal microdeposits
Optic neuropathy

Many DDIs

219
Q

which group of pts are more susceptible to silent MIs

A
  • diabetic pts
  • elderly pts
220
Q

causes of hypertension

A
  • Essential (Primary origin) – 95% cases
  • Secondary causes
    • Renal e.g. CKD
    • Endocrine e.g. Conn’s syndrome, acromegaly,
    • Cushing’s syndrome
    • Coarctation of the aorta
    • Pre-eclampsia occurring during third trimester of pregnancy
    • Drugs – oestrogen-containing oral contraceptives, NSAIDs, vasopressin
221
Q

what is malignant hypertension

A

Rapid rise in BP leading to vascular damage

222
Q

symptoms of malignant hypertension

A

Headache
Visual disturbance

223
Q

signs of malignant hypertension

A
  • Severe hypertension
    • Systolic > 200 mmHg
    • Diastolic > 130 mmHg
  • Bilateral renal haemorrhage = exudates = papilloedema
224
Q

complications of malignant hypertension

A

Hypertensive emergencies e.g:
- acute kidney injury,
- HF
- encephalopathy

225
Q

treatment for malignant hypertension

A

Sodium nitroprusside

226
Q

what is Prinzmetals angina

A
  • Angina due to coronary artery spasm, which can occur even in normal coronary arteries.
  • The pain usually occurs during rest and resolves rapidly with short-acting nitrates (eg GTN spray).
  • ECG during pain shows ST segment elevation.
227
Q

T/F
Prinzmetals angina presents with ST elevation

A

TRUE
during an episode of pain ST elevation is seen on the ECG

228
Q

treatment for prinzmetal’s angina

A
  • avoid triggers + quit smoking
  • correct low magnesium
  • PRN GTN spray
  • CCBs
  • long acting nitrates
  • AVOID non-selective BB, aspirin and triptans
229
Q

what factors are considered to calculate QRISK2

A
  1. BP
  2. Age
  3. Smoking status
  4. Cholesterol
  5. Rheumatoid Arthritis
  6. Diabetes Mellitus
  7. Anti-hypertensives
  8. BMI
  9. Ethnicity
230
Q

what is QRISK2

A

QRISK2 score predicts risk of CVD in next 10 years, considers:

231
Q

what is the most common cause of CHF

A

coronary arterial disease which causes myocardial dysfunction.

232
Q

what are the symptoms of heart failure

A
  • Breathlessness
  • Tiredness
  • Cold peripheries
  • Leg swelling
  • Increased weight
233
Q

what are the signs of heart failure

A
  • Tachycardia
  • Laterally Displaced apex beat
  • Raised JVP
  • Added heart sounds and murmurs
  • Hepatomegaly, especially if pulsatile and tender
  • Peripheral and sacral oedema n Ascites
234
Q

what is seen on an ECG of a pt with atrial fibrillation

A
  • loss of P-waves which show atrial depolarisation, due to contraction triggered by ectopic sites as well as SA node.
  • irregular rhythm on ECG due to irregular stimulation of the AV node from ectopic sites.
235
Q

key difference between atrial fibrillation and ventricular ectopics on an ECG

A
  • AF causes loss of P-wave whereas ventricular ectopics doesn’t.
  • both still cause palpitations + an irregular pulse
236
Q

ECG features of pericarditis

A

PR segment depression and widespread ST elevation with reciprocal changes in aVR (occurs during the first couple of weeks)

Associated T wave flattening can also be seen from weeks 1 to 3.

Sinus tachycardia is also seen in some cases due to the chest pain.

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