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103 theme 3 > Ischaemic heart disease: prevalence, symptoms and principles of treatment > Flashcards

Ischaemic heart disease: prevalence, symptoms and principles of treatment Flashcards

1
Q

what is CVD

A

a disease of the heart or circulatory system which comprises

CHD, Cerebrovascular disease and peripheral vascular disease

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2
Q

What results from CVD

A

Marked increase in prevalence of CVD during 20th century in Western countries
UK’s second biggest killer – approx a 1/3 of deaths annually
Mainly heart attack and stroke
Significant economic burden

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3
Q

What is the framingham heart study

A

Ongoing, longitudinal study in 5209 healthy men and women 30-62 yrs in Framingham, MA
Begin in 1948, in 3rd generation of participants
Medical profession had little understanding of CVD prevention before Framingham
1957 high cholesterol and bp link to CHD
1961 Risk factors introduced
1962 smoking and CHD
1967 OBESITY
1972 DIABETES

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4
Q

what are controllable risk factors for CHD

A 
Cigarette smoking
Diabetes
Bp 
Cholesterol 
Obesity
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5
Q

what are noncontrollable risk factors for CHD

A

Age
Family history of premature CHD
Previous heart attack

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6
Q

what are the clinical manifestations of CHD

A

Athersclerosis (fatty streak, lipid deposition, intimal fibrosis)

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7
Q

what is IHD (or myocardial ischaemia)

A

occurs due to atherosclerotic plaque build-up within one or more arteries, obstructing myocardial blood flow
Imbalance between myocardial oxygen supply and demand
Restriction in normal increase in coronary blood flow which should occur with increasing myocardial oxygen demand

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8
Q

what are the clinical manifestations of IHD

A

Asymptomatic
Stable angina
Acute coronary syndromes – unstable angina, NSTEMI, STEMI
Long term – HF, arrythmias, sudden death

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9
Q

What is the pathology of stable angina

A

ischaemia due to fixed atheroma stenosis of one or more coronary arteries

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10
Q

What is the pathology of unstable angina

A

ischaemia caused by dynamic obstructions of a coronary artery due to plaque rupture with thrombosis

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11
Q

What is the pathology of myocardial infarction

A

acute occlusion of a coronary artery due to plaque rupture and thrombosis

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12
Q

What is the pathology of heart failure

A

Myocardial dysfunction due to infarction or ischaemia

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13
Q

What is the pathology of arrhythmia

A

altered conduction due to ischaemia or infarction

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14
Q

What is the pathology of sudden death

A

ventricular arrhythmia, asystole or massive infarction

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15
Q

what are the types of stable angina

A

typical, atypical, non-anginal

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16
Q

what are the symptoms of the types of stable anginas

A

typical meet all 3 of these characteristics
substernal chest discomfort of characteristic quality and duration
provoked by exertion or emotional stress
relieved by rest or nitrates in mins
atypical 2
non-anginal 1 or none

17
Q

how is stable angina measured

A

1st line
short acting nitrates and beta-blockers
2nd line if 1st not enough
then stent/CABG/lifestyle/education/aspirin/statins

18
Q

what are acute coronary symptoms characterised by

A

Includes unstable angina and acute MIs (stemi and nstemi)
All patients with acute MI have a rise in cardiac enzyme known as troponin, measured on a blood test
Troponin is released into bloodstream following an injury to heart muscle, diagnostic marker (elevated in acute MI but not unstable angina)

19
Q

what is the pathology of STEMI

A

ST elevation on ECG is a marker of complete coronary occlusion

20
Q

what is the pathology of NSTEMI

A

incomplete occlusion is associated with ST depression, variable T wave abnormalities or normal ECG

21
Q

What is the pathological progression to atherothrombosis

A

Plaque disrupted, thrombus results from
Adherence, activation and aggregation of platelets
Thrombin and fibrin produced via coagulation cascade (thrombin release from platelets)
Vasoactive molecules released from platelets which causes vasoconstriction

22
Q

what are the classical symptoms of ACS

A

Discomfort/pain in centre of chest for more than a few mins and recurs
Radiates to other areas eg left arm/jaw/back
Occur at rest or exertion
Not relieved immediately with sublingual GTN
Elderly/diabetic often present with
Breathlessness
Nausea or vomiting
Sweating or clamminess

23
Q

how can patients with suspected ACS be assessed

A

First – history, ECG, Physical exam

Then risk stratification and cardiac biomarkers (eg troponin)

24
Q

how can a history for suspected ACS be taken

A

Nature and site of pain
Time of pain onset and duration
History of CVD/risk factors

25
Q

what are therapeutic goals in ACS

A

Restore coronary artery patency (STEMI)
Limit myocardial necrosis (STEMI)
Control symptoms
Medical management
Anti-platelet therapy (aspirin, clopidogrel/prasugrel/ticagrelor)
Anti-ischaemic therapy (nitrates)
Secondary prevention therapy (statin, ACE inhibitors, beta blockers, stop smoking, lifestyle mod)

26
Q

what is key for treating STEMIs

A

Timely diagnosis key to successful management
Most critical time is early phase
Minimise delays to treatment associated with improved clinical outcomes

27
Q

how can STEMIs be treated rapidly

A

Importance of rapid treatment
Morphine and or nitrates
Anti-platelet agents
And emergency primary angioplasty (balloons or stents)
Clot busting drug (thrombolysis) if no primary angioplasty

28
Q

what is unstable angina

A

Angina at rest >20 mins
New onset <2 months exertional angina
Recent <2 months acceleration or progressions
Normal cardiac biomarkers

29
Q

what is an NSTEMI

A

No ST elevation but angina and elevated cardiac biomarkers

Pneumonia, pulmonary embolism, pericarditis, sepsis HF, uncontrolled tachycardia can raise troponin too

30
Q

What are high risk ACS patients

A 
Elevated troponin
Renal impairment 
Recurrent chest pain
Dynamic ST depression or T wave changes
Haemodynamic instability
Major arrythmias
HF 
Elderly
31
Q

how can NSTEMI be treated

A 
Analgesia
Anti platelet
Anti ischaemic
Statins
Early coronary angiography with view to revascularize (eg bypass)

103 theme 3 (20 decks)

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