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2a > Ischaemic heart disease, heart failure, hypertension > Flashcards

Ischaemic heart disease, heart failure, hypertension Flashcards

1
Q

What is ischaemic heart disease?

A

Heart disease due to insufficient perfusion of cardiac tissues. It includes angina pectoris, acute coronary syndromes and myocardial infarction.
Lecture 9/1/18

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2
Q

What is angina pectoris?

A

Central chest tightness or heaviness due to myocardial ischaemia, brought on by exertion and relieved by rest
(OHCM)

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3
Q

How does Poisueille’s law relate to angina symptoms?

A

Radius affects blood flow to the 4th power, so diameter has to fall by 75% before a person experiences symptoms.

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4
Q

What is Prinzmetal’s angina?

A

Arteries go into vasospasm which increases resistance and causes reduction in blood flow.
(9/1/18 lecture)

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5
Q

Give a non-modifiable risk factor for angina.

A

Age, sex

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6
Q

Give a modifiable risk factor for angina.

A

Smoking, exercise, weight

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7
Q

What is unstable (crescendo) angina?

A

Angina of increasing frequency or severity, occurring on minimal exertion or at rest, with normal troponin. (OHCM)

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8
Q

What are the 3 key characteristics of angina pain?

A
  1. Heavy, central, tight chest pain, radiation to arms, jaw and neck
  2. Precipitated by exertion
  3. Relieved by rest/ sublingual GTN. (9/1/18 lecture)
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9
Q

How does GTN spray work?

A

It dilates arteries.

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10
Q

What would you see on an ECG in angina?

A

ECG is often normal but there may be signs of IHD such as ST depression, T wave inversion and bundle branch block. (lecture 9/1/18)

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11
Q

What would the treadmill test show with angina?

A

The person walks on a treadmill which gets incrementally steeper. Look for ST segment depression on ECG. This is no longer on the NICE guidelines but can still be used.

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12
Q

What is the gold-standard diagnostic test for angina?

A

Invasive angiogram, which shows the luminal narrowing.

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13
Q

How does CT angiography work and why is it used?

A

A contrast-rich dye is injected into the arteries and CT scanning produces detailed images. It has a higher NPV than PPV so it is good for excluding CAD in young, low-risk patients. There are lots of false positives.

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14
Q

What is a stress echo?

A

A functional test which uses dynamic imaging with and without pharmacological stress, looking for regional wall motion abnormalities. Requires expertise so not done as often as it could be. (9/1/18 lecture)

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15
Q

What is a SPECT and what is it used for?

A

SPECT = Single photon emission CT. Radio labelled tracer taken up by metabolising tissues, to give an idea of the degree of ischaemic myocardia. AKA myoview.

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16
Q

What factors affect choice of investigation for angina?

A

Patient choice, pre-test probability of CAD, invasive or non-invasive, allergies, intolerances, clinician preferences.

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17
Q

What is primary prevention of angina?

A

Exercise, stop smoking, antihypertensive, good control of diabetes.

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18
Q

What are the first-line anti-anginal drugs and how do they work?

A

Beta-blockers such as bisoprolol and atenolol reduce oxygen demand and work of the heart.
Nitrates are venodilators, reduce preload and vasospasm.
Lecture 9/1/18

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19
Q

Give a side-effect of beta-blockers.

A

Bradycardia, worsening of asthma and coronary spasm.

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20
Q

What is PCI and why would it be used? What are the risks?

A

Percutaneous coronary intervention/ stenting to remove narrowing and restore blood flow. Used for patients with troponin elevation or unstable angina. Risks of restenosis and thrombosis, but less invasive than CABG. (lecture 9/1/18)

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21
Q

What might a blood test show in angina?

A

Anaemia

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22
Q

Is angina more common in men or women?

A

5% men, 4% women.

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23
Q

What investigation could you use to check the pulmonary vessels and heart size?

A

Chest X ray

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24
Q

What drug can be used to treat angina if a person has asthma?

A

Calcium channel blockers.

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25
Q

What is an example of a second-line anginal drug and how does it work?

A

Ivabradine - cardiotonic; reduces cardiac pacemaker activity, so it slows HR selectively and allows more time for blood to flow to the myocardium. This makes it a good drug for HFREF.

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26
Q

What is a CABG and what are the advantages and disadvantages?

A

Surgical intervention to divert blood around narrow or clogged arteries to major arteries. Good prognosis but longer recovery. Contraindicated in frail patients. (PTS)

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27
Q

What are acute coronary syndromes?

A

A spectrum of disease progressing from unstable angina to STEMI, with the main underlying pathology of plaque buildup and rupture leading to thrombosis and inflammation.

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28
Q

What is troponin and what is it used for?

A

Regulator of actin-myosin contraction. Sensitive marker of cardiac injury. Used to diagnosed NSTEMI, not specific for ACS (also positive in sepsis, heart failure etc)

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29
Q

What can cause ST elevation, tall T waves and possibly a new LBBB?

A

STEMI

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30
Q

How is NSTEMI diagnosed?

A

Retrospectively using troponin. ST depression seen on ECG. (PTS)

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31
Q

What changes would be seen on an ECG in someone with ischemia?

A

ST-T changes: The ST segment can be depressed or elevated, and the T wave can be up (hyperacute T wave), down (flattening) or inverted.
https://ecgwaves.com/topic/ecg-myocardial-ischemia-ischemic-changes-st-segment-t-wave/

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32
Q

What features of chest pain may suggest MI?

A

Chest pain - unremitting, usually severe, at rest; associated with sweating, breathlessness, nausea and vomiting.

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33
Q

What is the difference between Q wave and non-Q-wave MI - what might you see on ECG?

A

Non-Q-wave: Poor R wave progression, STE, biphasic T wave. Q-wave - pathological Q waves.

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34
Q

What is a silent MI?

A

MI without ECG signs or symptoms. Seen in elderly and diabetics. lecture 9/1/18; PTS

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35
Q

Who is at higher risk of death from ACS?

A

Increasing age, diabetes, renal failure, LVSD (lecture 9/1/18)

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36
Q

What is the initial management of MI?

A 
AMONA: 
Ambulance (admission)
Morphine (analgesia)
Oxygen if hypoxic
Nitrates
Aspirin 300mg
If STE, primary PCI 
Bed rest 
Lecture 9/1/18
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37
Q

What causes ACS?

A

Mainly rupture of atherosclerotic plaque, but can also be caused by vasospasm, drug abuse eg cocaine, and coronary artery dissection related to connective tissues disease.
(lecture 9/1/18)

38
Q

How does aspirin reduce risk of ACS?

A

Aspirin inhibits thromboxane formation.

39
Q

Give an example of a fibrinolytic drug and an indication for use.

A

Streptokinase, alteplase.
Indicated for MI, greatest benefit in those with ST elevation (esp anterior infarction) and BBB.

https://bnf.nice.org.uk/treatment-summary/fibrinolytic-drugs.html

40
Q

How are ACS treated pharmacologically?

A

Dual antiplatelet therapy:
1. Aspirin - inhibits thromboxane formation
2. Clopidogrel/ticagrelor/prasugrel - inhibit P2Y12
Anticoagulant eg heparin
Anti-anginal - beta blocker, nitrates, calcium antagonist.

41
Q

GbIIb/ IIIa antagonists - example, mechanism, use?

A

Used for patients with STEMI undergoing primary PCI. Eg, tirobifan. Inhibit fibrinogen formation?
Lecture 9.1.18

42
Q

Other than obstruction, what could cause ACS?

A

The plaque ruptures and then the thrombus clears before angioplasty;
Stress-induced (Tako-tsubo) cardiomyopathy related to surge in catecholamines.

43
Q

What is a disadvantage of clopidogrel?

A

A person’s response to clopidogrel varies according to their weight, age, and genetics. It has a slower onset and offset than ticagrelor so surgical bleeding is more severe/common.

44
Q

What is an advantage of ticagrelor?

A

More rapid onset (after first death) and offset (after last dose) than clopidogrel, so less risk of death. More effective so more bleeding, but rapid offset means risk of surgical bleeding is still less than clopidogrel.

45
Q

What investigations would you do for unstable angina and why?

A

FBC to check for anaemia which aggravates angina
Troponin test to exclude infarction
ECG which would show ST depression during angina
Coronary angiography to look for artery narrowing.
(PTS)

46
Q

What happens in myocardial infarction?

A

A clot occludes a coronary artery causing myocardial cell death and inflammation.

47
Q

What are the symptoms of MI?

A
  1. Acute central chest pain radiating to jaw or shoulder lasting >20 mins (unless silent)
  2. Nausea
  3. SOB
  4. palpitations
48
Q

What are the signs of MI?

A
  1. Clammy and pale
  2. 4th heart sounds
  3. pansystolic murmur
  4. may later develop peripheral oedema.
49
Q

Describe the acute management of a STEMI. (5 steps)

A
  1. 12-lead ECG, oxygen if <94%
  2. IV access for bloods and enzymes
  3. History, RFs, vital signs, JVP, murmurs, signs of heart failure
  4. Aspirin 300mg PO
  5. Morphine 5-10mg IV and anti-emetic
    (PTS)
    refer to PCT and thrombolysis if not contraindicated.
50
Q

Give 3 complications of MI.

A 
Death
Arrhythmia
Rupture
Tamponade
Heart failure
Valve disease
Aneurysm of ventricle
Dressler's syndrome
Embolism
Recurrence/mitral regurg
[oxfordmedicaleducation.com]
51
Q

What is heart failure?

A

Breathlessness, oedema and fatigue associated with a cardiac abnormality that reduced cardiac output.

52
Q

If there is evidence of heart failure in a normotensive patient, what drugs should you put them on?

A

Beta blockers if not CI, ACEI.

53
Q

What can cause heart failure?

A

Systolic: IHD; MI, CM
Diastolic: Constrictive pericarditis, cardiac tamponade, hypertension
L-sided causes R-sided. [PTS]

54
Q

What are the signs of HF?

A

NON-SPECIFIC, NON-SENSITIVE
Dyspnoea
Peripheral oedema
Fatigue
Usually HF, sometimes mitral regurgitation
Paroxysmal nocturnal dyspnoea and orthopnoea - frightens patient, they have to open the window.

55
Q

How is SOB classified?

A

NYHA classification.
Class 1 - no limitation or SOB
Class 2 - slight limitation, SOB on exertion
Class 3 - marked limitation, SOB on mild exertion
Class 4 - SOB at rest

56
Q

How is HF staged?

A 
ACC/AHA staging system.
A High risk
B asymptomatic
C symptomatic
D End-stage
57
Q

What are the complications of HF?

A 
Renal dysfunction
Rhythm disturbances
Systemic thromboembolism
DVT, Pe, LBBB, bradycardia
Hepatic dysfunction causing hepatomegaly
neurological and psychological complications
58
Q

What is the difference between systolic and diastolic HF?

A

Systolic = inability to contract, EF <40% (reduced), caused by IHD/MI/CM
Inability to relax and fill, EF >50% (preserved), caused by constrictive pericarditis/cardiac tamponade/hypertension.

59
Q

Describe the management of heart failure.

A

Lifestyle - control of weight, education, diet, smoking
Symptomatic: Loop diuretics eg furosemide
ACE inhibitors - improve symptoms and reduce mortality in HFREF.
beta blockers
aldosterone antagonists
calcium glycoside

60
Q

Describe the role of diuretics in HF and give an example of a thiazide and loop diuretic.

A

Symptomatic relief of oedema and dyspnoea. Thiazide (eg hydrochlorothiazide) and loop (eg furosemide) are both used for severe oedema.
NICE 2018

61
Q

Describe the role of ACEIs in HF and give an example. What patient group are they most effective in?

A

Reduce morbidity and mortality. Eg, ramipril. Offer in HFREF, most effective in those with LV dysfunction but may also be beneficial in those with normal LV systolic function.
https://patient.info/doctor/angiotensin-converting-enzyme-inhibitors

62
Q

Describe the role of aldosterone antagonists in HF and give an example. What are the main side-effects?

A

Reduce morbidity and mortality. Eg, spironolactone. Renal impairment and hyperkalaemia -Measure renal function and U&Es at one week and four weeks after starting/increasing the dose. Considered in all patients unless CI’d.
https://patient.info/doctor/heart-failure-management

63
Q

What is valvular heart failure?

A

Heart failure due to dysfunction of the valves such as stenosis or regurgitation.

64
Q

What is myopathic HF?

A

= Cardiomyopathy. The heart muscle becomes enlarged, rigid and weak so cannot pump enough blood around the body.

65
Q

What is hypertensive HF?

A

Increased blood pressure causes buildup of cholesterol and inflammation in the arteries and thickening and rigidity of the heart muscle causing heart failure.

66
Q

What is cor pulmonale?

A

Abnormal enlargement of the right side of the heart as a result of disease in the lungs or pulmonary vessels.

67
Q

What causes low-output HF?

A

In low output HF there is decreased CO which fails to increase with exertion. Pump failure, excessive pre-load, chronic increased afterload. [pts]

68
Q

What causes high-output HF?

A

Anaemia, pregnancy, hyperthyroidism.

69
Q

What compensatory changes occur during HF?

A
  1. Sympathetic stimulation: peripheral vasoconstriction increases afterload
  2. RAAS: salt and water retention, increases afterload and preload which increases volume and vasoconstriction.
  3. Cardiac changes: ventricular dilatation, myocyte hypertrophy.
70
Q

What are the symptoms of left-sided HF?

A

Exertional dyspnoea
Fatigue
Paroxysmal nocturnal dyspnoea
Nocturnal cough - pink frothy sputum

71
Q

What are the signs of left-sided HF?

A 
cardiomegaly causes displaced apex beat
3rd and 4th heart sounds
crepitations in lung bases
weight loss
reduced BP
tachycardia
cool peripheries
(PTS)
72
Q

What causes right-sided HF?

A

LVF, pulmonary stenosis, lung disease causing cor pulmonale

73
Q

What are the symptoms of right-sided HF?

A

Ascites
Nausea
Anorexia
Peripheral oedema

74
Q

Signs of right-sided HF

A

Hepatomegaly
Pitting oedema
ascites
(PTS)

75
Q

What investigations would you do if you suspect HF and why?

A

Bloods - B Natriuretic Peptide (BNP) - if normal, unlikely HF. FBC, LFTs, U&E, TFTs
ECG - if normal, unlikely HF. May indicate cause of HF eg IHD, MI, ventricular hypertrophy.
Cardiac enzymes - troponin, creatinine kinase
CXR
ECG
Echo (TransThoracic)

76
Q

What would a X ray show for heart failure?

A 
Alveolar oedema (bat's wings)
Kerley B lines (= septal lines; interstitial oedema)
Cardiomegaly
Dilated prominent upper lobe vessels
Effusions (pleural)
77
Q

What is the pharmacological treatment of chronic heart failure?

A

ACEIs eg ramipril, or ARB eg candesartan, aldosterone antagonists eg spironolactone
Beta blockers eg atenolol
CCBs and other vasodilators eg amlodipine
Diuretics eg furosemide, Digoxin

78
Q

BP=?

A

BP=PRx CO

79
Q

What is stage 1 HTN?

A

clinic BP > 140/90 (ambulatory is always LOWER)

80
Q

What is stage 2 HTN?

A

clinic BP > 160/100

81
Q

What is severe HTN?

A

clinic BP> 180/110

82
Q

How is hypertension diagnosed?

A

Clinic BP taken using sphygmomanometer. If over 140/90, confirm with 24h ambulatory BP monitor and multiple home BP monitoring.

83
Q

What investigations should you do if someone has hypertension?

A

Fundoscopy in severe htn,
overall CVD risk (CHADSVASC)
Cholesterol levels
ECG to look for past MI and LV hypertrophy
Urine analysis - look for proteinurea, haematuria
Bloods: FBC, U&E to exclude secondary hypertension
Hba1c

84
Q

What is the most common type of hypertension?

A

Essential hypertension (95%) which has a primary cause.

85
Q

What are secondary causes of hypertension?

A

CKD, Conn’s syndrome, pregnancy, coarctation, Cushing’s, hyperthyroidism, acromegaly.

86
Q

What is the non-pharmacological management of hypertension?

A

Lifestyle changes - stop smoking, low-fat diet, reduce alcohol and salt intake, control weight, exercise.

87
Q

Describe the pharmacological management of hypertension in someone who is 50 and asian. Give examples of each drug type.

A

First-line: They are under 55 and non afrocarribean so start on ACEI eg ramipril or ARB eg candesartan
Second-line: add CCB eg amlodipine if needed
Third-line: add thiazide-like diuretic eg hydrochlorothiazide if needed

88
Q

Describe the pharmacological management of hypertension in someone who is 58 and white.

A

First line: They are over 55 so start on CCB eg amlodipine.
Second-line: Add ACEI eg ramipril or ARB eg candesartan if needed
Third-line: add thiazide eg hydrochlorothiazide if needed.
This would be the same if they were under 55 and afro-carribean.

89
Q

What is resistant hypertension and how is it treated?

A

Remains high after 3 classes of antihypertensives have been tried. Treated with spironolactone/ alpha-blocker/ beta-blocker/ specialist centres.

90
Q

What are contraindications for ACEIs?

A

Pregnancy, asthma, chronic cough, CKD

91
Q

How does losartan work?

A

It is an ARB blocks angiotensin II receptors, which reduces blood pressure. Another example is candesartan.

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