IHD Flashcards
(99 cards)
1
Q
Break down the word atherosclerosis
A
Atheroma= fatty deposits in artery walls Sclerosis= process of hardening or stiffening of blood vessels
2
Q
What is atherosclerosis caused by?
A
Chronic inflammation and activation of the immune system in the artery wall which causes deposition of lipids
3
Q
What three things do fibrous atheromous plaques lead to?
A
- Stiffening - leads to hypertension and strain of heart pumping against resistance 2. Stenosis - leads to reduce blood flow (eg. Angina) 3. Plaque rupture- giving off a thrombus that blocks a distal vessel leading to ischaemia (eg. Acute conorary syndrome)
4
Q
Atherosclerosis non-modifiable risk factors
A
- Older age 2. Family history 3. Male
5
Q
Atherosclerosis modifiable risk factors
A
- Smoking 2. Alcohol consumption 3. Poor diet (High sugar and trans-fat and reduced fruit and vegetable and omega 3 consumption) 4. Low exercise 5. Obesity 6. Poor sleep 7. Stress
6
Q
Medical co-morbidities that increase the risk of atherosclerosis
A
- Diabetes 2. Hypertension 3. Chronic kidney disease 4. Inflammatory conditions (rheumatoid arthritis) 5. Atypical antipsychotic medications
7
Q
Complications of atherosclerosis
A
- Angina 2. Myocardial infarction 3. Transient ischaemic attacks 4. Stroke 5. Peripheral vascular disease 6. Messenteric ischaemia
8
Q
Two types of prevention of cardiovascular disease?
A
- Primary prevention - for patients that have never had cardiovascular disease in the past 2. Secondary prevention - for patient that have had angina, myocardial infarction, TIA, stroke or peripheral vascular disease
9
Q
How to change modifiable risk factors?
A
- Advice on diet, exercise and weight loss 2. Stop smoking 3. Stop drinking alcohol 4. Tightly treat co-morbities (diabetes)
10
Q
Primary prevention of cardiovascular disease?
A
- Perform a Q-risk 3 score 2. Over 10% risk of having heart attack or stroke in the next ten years? Offer a statin (Current NICE = atorvastatin 20mg at night)
11
Q
Nice guidelines to statin prescription?
A
- check lipids at 3 months- aim for increasing dose to aim for 40% reduction in non-HDL Cholesterol- always check adherence first!
- Check LFTs within 3 months and at 12 months, don’t need to be checked again if normal
- Statins can cause a transient and mild raise in ALT and AST in first few weeks of use and don’t need stopping if rise is less than 3 times the upper limit of normal
12
Q
Secondary prevention (drugs) for cardiovascular disease?
A
4 As:
- Aspirin (plus second anti platelet like clopidogrel for 12months)
- Atorvastatin 80mg
- Atenolol (or other beta-blocked - commonly bispropol - titrated to maximum tolerated dose)
- ACE inhibitor (commonly ramipril) (tritated to max tolerated dose)
13
Q
Notable side effects of statins
A
- Myopathy (check creative kinase in patients with muscle pain or weakness) 2. T2DM 3. Haemorrhagic strokes (very rarely) Usually benefits far outweigh risks and newer statins are mostly very wel tolerated
14
Q
What’s a Q-risk 3 score?
A
-Predicts risk of CVD in 10 upcoming years -Factors include: Age SBP BMI Socieconomic status Ethnicity -Score of ten plus (10% + risk in the next ten years) is an indication to start 1° lipid lowering therapy (statins)
15
Q
What is atorvastatin an example of?
A
Lipid lowering therapy
16
Q
Which arteries does atherogenesis affect most commonly?
A
LAD Circumflex RCA
17
Q
Risk factors for IHD
A
Age Smoking Obesity, high serum cholesterol Diabetes Hypertension Family history M>F Cocaine use Stress Physical inactivity
18
Q
Symptoms of stable angina pain?
A
- Central crushing chest pain radiating to neck/jaw 2. Brought on with exertion 3. Relieved with 5mins rest or GTN spray
19
Q
Four types of angina?
A
- Stable - normal three point definition
- Unstable - pain at rest, not relieved by inactivity or GTN spray + no ECG CHANGES
- Prinzmetal’s - due to coronary vasospasm (not due to cv vessel atherogenesis) Seen increasingly in cocaine users ECG shows ST elevation
- Microvascular angina due to narrowing only in small arteries
20
Q
Development of atherosclerosis
A
Atherogenesis: Endothelial injury attracts cells to site via chemokines (IL1, IL6, IFN-Y)
1. Fatty streak = Foam cells (lipid laden macrophages) and T-cells
2. Intermediate lesions = foam cells (bigger as taken up more lipid), t- cells and smooth muscle cells. Platelets also aggregate and adhere to site inside vessel lumen.
3. Fibrous plaques (advanced) = large lesions (foam cells, t-cells, smooth muscle, fibroblasts, lipids with a necrotic core) Develops a fibrous cap over lesion.
21
Q
Fibrous cap in stable angina?
A
Fibrous cap is strong and less rupture prone
22
Q
What happens if plaque is prone to rupture?
A
Prothrombotic state, platelet adhesion and accumulation leads to progressive luminal narrowing
23
Q
Difference between ischaemia and infarction?
A
Ischaemia= blood flow restricted Infarction= lumen fully occluded
24
Q
When do symptoms for stable angina start?
A
When 70 to 80% lumen occluded Due to poiseulle’s law, nothing much happens until the diameter stenosis reaches 70% and then there is rapid decline
25
Symptoms of IHD?
Central crushing chest pain radiating to jaw/neck, worsens with time (doesn't peak straight away )
Nausea
Sweating
Fatigue
Dyspnoeic weak breathing + hypotensive/tachycardic in ACS and impending sense of doom‚ and palpitations
26
How to diagnose stable angina?
1st line= ECG- resting and with exercise (to induce ischaemia) Coronary angiography- looks for stenoses and atherosclerotic arteries (~70-80% occluded) Gold standard but invasive so not first line
27
Treatment for stable angina?
-Symptomatic= GTN sublingual spray -Lifestyle modifying (decrease weight, stop smoking, exercise, diet etc) -Pharmacological (all patients=1st line) 1. CCB (CI heart failure) or B-b (CI Asthma)
Secondary anti platelet treatment is recommended (75mg aspirin) (eg if they have a stent but not necessarily for stable angina)
Potentially Revascularisation: PCI/CABG with an MDT meeting or coronary angiogram if symptoms not controlled
28
What does acute coronary syndromes cover?
Umbrella term for unstable angina, NSTEMI and STEMI
29
How to define different acute coronary syndromes?
Unstable angina- severe ischaemia NSTEMI- partial infarction + Q wave infarction STEMI- transmural infarct and ST elevation in local ECG leads +Non-Q infarction
30
What does an ECG after MI look like?
-hyperacute t wave -pathologically deep q waves - ST segment elevation
31
What’s the difference between types of MI?
T1 = traditional MI due to an acute coronary event (athermatous plaque rupture) T2 = secondary to ischaemia due to either increased oxygen demand or decreased supply (vasopasm, anaemia and sepsis)
32
Is troponin or creatine kinase mb a better indicator of cardiac damage long term?
Troponin has a shorter half life so CKMB is a better biomarker after a few days
33
Pathophysiology of ACS (angina)?
ACS is usually the result of a thrombus—> atherosclerotic plaque formation due to damage to arterial walls causing myocardial ischaemia When a thrombus forms in a fast flowing artery it is made up mostly of platelets. - why anti-platelet medications= key
34
Making a diagnosis of ACS? (Step by step) (primary investigations)
1) when patient presents with symptoms (eg chest pain) perform ECG
2) ST elevation or new left bundle branch block = STEMI
3) no ST elevation‚-> troponin blood tests: - increased troponin + changes (ST depression, t wave inversion or path Q waves) = NSTEMI -normal troponin + no ECG changes then unstable angina or another cause (musculoskeletal chest pain)
35
Symptoms of ACS?
Same as stable angina but pain @ rest prolonged with no relief “impending doom” palpitations and Symptoms more severe
36
Alternative causes of raised troponin?
Gram negative sepsis
Myocarditis
Aortic dissection
Pulmonary embolism
Arrhythmias
37
Other investigations when considering ACS?
Those normally arranged for stable angina:
- physical examination (heart sounds, signs of heart failure, BMI)
- FBC (anaemia)
- U&Es (check for electrolyte imbalances prior to ACEi and other meds)
- LFTs (prior to statins)
- Lipid profile
- Thyroid function tests (hypo/hyperthyroid)
- HbA1c and fasting glucose (for diabetes)
- Plus:
- chest x ray to investigate other causes of chest pain and pulmonary oedema
- Echocardiogram after event to assess for functional damage
- Ct coronary angiogram to assess for coronary artery disease
38
Acute management of ACS generally?
MONAC Morphine + anti-emetic (metoclopramide) O2 (if stats <94% or 88-92% if COPD) Nitrates (GTN) Aspirin (300mg) Clopidogrel/Ticagrelor (75mg dual antiplatelet) or pasugrel if undergoing PCI (PY12 inhibitor) Anticoagulant: fondaparinux or heparin *not all patients require oxygen
39
What does GRACE score assess?
Mortality risk of patients with ACS from MI within the next 6 months to 3 years
40
Treatment for low risk NSTEMI/unstable angina
Monitor
41
Treatment for high risk NSTEMI/ unstable angina?
Immediate angiogram and consider PCI
42
Treatment for STEMI if presenting <12h of Sx and <2h of first medical contact?
-PCI (percutaneous intervention) (Insertion of a catheter via radial or femoral artery to open up blocked vessels using an inflated balloon (angioplasty) and a stent may also be inserted) -unfractionated heparin and glycoprotein IIb/IIIa inhibitor
43
Treatment for STEMI if presenting <12h Sx and more than 2h of first management?
Ineligible for PCI:-Fibrinolysis/ thrombolysis - IV administered alteplase or tenecteplase -antithrombin agent eg unfractionated heparin (bivalirudin and/or glycoproteins IIB/IIIa may also be considered) Offer ECG 60-90 mins after If shows residual ST elevation offer immediate angiography and PCI
44
Why are diabetics major culprits of Silent MIs?
-diabetic neuropathy -don’t feel the anginal pain and therefore may miss diagnosis and die from sudden collapse
45
Long term and secondary prevention after ACS?
6 As
-Atenolol (or other Beta blocker titrated to toleration) (life)
-Aspirin (initial dose 300mg -> 75mg life)
-Atorvastatin (80mg life)
-ACEi (eg ramipril titrated to 10mg) (life)
-Another antiplatelet (eg. clopidogrel (75mg for 12months)
-Aldosterone antagonist for those with clinical heart failure (ie eplerenone titrated to 50mg once daily)
Can add an opiate or GTN spray for pain relief
Dual antiplatelet duration will vary following PCI procedures (due to higher risk of thrombus formation in diff stents)
46
Acute complications of ACS (2 >= wk)
Heart failure due to ventricular fibrillation
Mitral incompetence
Left ventricle free wall rupture
Cardiogenic Shock
47
Other complications of ACS (2< weeks)
Dressler syndrome (autoimmune pericarditis)
Heart failure
LV aneurysm-heart literally becomes saggy :(
48
How to interpret GRACE score
<5% low risk 5-10% medium risk >10% high risk
49
Complications of MI
DREAD -Death -Rupture of heart septum or Papillary muscles -Edema (Heart failure) -Arrhythmia and Aneurysm -Dressler syndrome
50
Limits for diagnosing hypertension
>= 140/90 mmHg in clinic >= 135/85 mmHg at home (ambulatory blood pressure monitoring)
51
Primary vs secondary hypertension
1° = Essential hypertension (idiopathic/no known cause) 95% cases 2° = known underlying cause 5% cases
52
Causes of secondary hypertension
- Renal disease (CKD-most common cause due to diabetic nephropathy)
- Endocrine disorders (phaeochromocytoma, conn‚s, cushing‚s)
- Medication/iatrogenic : glucocorticoids, ciclosporin, atypical antipsychotics, combined oral contraceptive pill
- pregnancy
53
Non modifiable risk factors for hypertension
Age African heritage Family history
54
Modifiable risk factors for hypertension
Obesity Sedentary lifestyle Alcohol excess Smoking High sodium intake (>1.5g a day) Stress
55
Define the limits for stages of hypertension
(H) = clinic reading (A) = ambulatory Discrepancy of >= 20/10mmHg between clinic and ambulatory suggests “white-coat hypertension
56
Malignant (accelerated) hypertension?
Severe increase in blood pressure >=180/120 mmHg (stage 3) with signs of retinal haemorrhage and/or papilloedema, associated with target organ damage = emergency assessment and treatment
57
Pathophysiology of hypertension
Ultimately all mechanisms will increase RAAS and SNS activity (CO) and TPR => increase in BP as BP=COxTPR
58
Signs of malignant hypertension
Hypertensive retinopathy Visual disturbances Cardiac symptoms eg chest pain Oliguira or polyuria Overall rare but scary and unrelated to cancer just very severe symptoms
59
Symptoms of hypertension
Mostly asymptomatic and found in screening May have pulsatile headache, classically occipital and worse in the morning
60
Signs of hypertension to consider
Signs of the underlying cause of secondary hypertension Eg phaeochromocytoma, hyperthyroidism or Cushing’s
61
How to diagnose hypertension
If bp reading in hospital is between 140/90 and 180/120 mmHg then offer ABPM to confirm diagnosis -bp is measured for 24h with at least 2 measurements per hour during waking hours -overall at least 14 measurements are required
62
Other investigations for hypertension?
Assess end organ damage (more damage = worse prognosis) : - Fundoscopy: assess for hypertensive retinopathy - 12- lead ECG: assess for LVH - Urinalysis and ACR: assess for renal dysfunction + diabetes risk - Bloods: HbA1c, U&Es, total cholesterol, HDL cholesterol
63
If a patient has T2DM and is black or 55+, would they take CCB or ACEi?
T2DM takes precedence and they should take ACEi BUT ARBs are preferred for black patients so that might be preferable
64
Complications for hypertension?
Heart failure Increased IHD risk CKD/Renal failure PVD Dementia Increased risk of cerebrovascular incident
65
Initial management of MI
Get in to hospital quickly- 999 call Paramedics-if ST elevation, contact primary PCI centre for transfer Take 300g aspirin immediately Pain relief
66
Causes of ACS
Rupture of atherosclerotic plaque and consequent arterial thrombosis is the main cause Uncommon causes: - stress induced cardiomyopathy - coronary vasospasm without plaque rupture - drug abuse
67
What is troponin?
Protein complex regulates actin:myosin contraction Highly sensitive marker for cardiac muscle injury Not specific for acute coronary syndrome May not represent permanent muscle damage
68
Examples of PY12 inhibitors
Clopidogrel Prasugrel Ticagelor
69
Why are GPIIb//IIa antagonists used selectively?
Increase risk of major bleeding But still used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS
70
Alternative treatment to PCI for NSTE ACS
CABG used in about 10% of patients But uncommonly, patients may have severe CAD not amenable to revascularisation
71
Pain relief used in ACS management?
Opiates (can delay absorption of P2Y12 inhibitor so only if necessary) Nitrates for unstable angina/coronary vasospasm (GTN spray) (may be ineffective for MI)
72
Clopidogrel vs prasugrel
Prasugrel is much more reliable and useful because it has a direct liver breakdown pathway while clopidogrel effectiveness relies on genetics alongside other factors
73
Ticagrelor vs clopidogrel
Ticagrelor decreases risk of myocardial infarction and cardiovascular death in comparison to clopidogrel
74
Exacerbating factors for IHD
Supply: -Anemia -hypoxemia Demand: -hypertension -tachycardia -valvular heart disease
75
Environmental exacerbating factors for IHD
Exercise Cold weather Heavy metals Emotional stress
76
Physiology of IHD
Myocardial ischemia occurs when there is an imbalance between heart’a oxygen demand and supply, usually from an increase in demand accompanied by limitation of supply: 1) impairment of blood flow by proximal arterial stenosis 2) increased distal resistance eg. Left ventricular hypertrophy 3) reduced oxygen-carrying capacity of blood eg. Anaemia
77
What is microvascular angina (syndrome X)
‘ANOCA’ Angina with apparently normal (main) coronary arteries Females mostly Cause unknown
78
Which risk factor drastically increases incidence of IHD
Age
79
Symptoms that don’t associate with angina
No fluid retention (unlike heart failure) Palpitation (not usually) Syncope or pre-syncope (very rare)
80
How to assess chest pain?
OPQRST Onset Position (site) Quality (nature/character) Relationship (with exertion, posture, meals, breathing and with other symptoms) Radiation Relieving or aggravating factors Severity Timing Treatment
81
Differential diagnosis for myocardial ischemia
Pericarditis/myocarditis Pulmonary embolism/pleurisy Chest infection/ pleurisy Gastro-oesophageal (reflux/spasm/ulceration) Musculoskeletal Physcological
82
Treatment for myocardial ischemia
Reassure Lifestyle - smoking - weight - exercise - diet Advice for emergency Medication Revascularisation
83
Advantages and limitations of CT angiography (fuzzier than normal angiography)
Good diagnostic test and at spotting severe disease Not so good at moderate disease Anatomical, not functional
84
Advantages and drawbacks to exercise testing
Good functional test Relies on patients ability to walk on a treadmill (useless for elederly, obese, arthritis etc)
85
Side effects of beta blockers
Tiredness, nightmares Erectile dysfunction Bradycardia Cold hands and feet
86
Contraindication for beta blockers?
Asthma- do not give
87
Side effect of aspirin
Gastric ulceration
88
Pros and cons of PCI
Pro: - less invasive - convenient - repeatable - acceptable Cons: - risk stent thrombosis - can’t deal with complex disease - dual antiplatelet therapy
89
Pros and cons of CABG
Pros: - prognosis - deals with complex disease Cons: - invasive - risk of stroke - can’t do if frail - one time treatment -time for recovery
90
Which veins can a CABG use?
Internal mammary artery (from chest) Saphenous vein (from leg)
91
If you don’t get chest pain when you run.. how likely is IHD?
Very low probability
92
What reduction do you expect with a full dose of any single drug?
Systolic: 8-10mmHg Diastolic: 4-6mmHg
93
Thresholds for treatment for hypertension?
Low CVD risk 160/100mmHg High CVD risk 140/90mmHg (Clinic thresholds)
94
Targets for blood pressure after treatment?
- Routine <140/90 mmHg - Previous stroke, Heavy proteinuria, CKD and Diabetes <130/80mmHg - older patients <150/90mmHg
95
How many drugs are generally needed to control blood pressure?
Mostly one or two
96
Can you lower blood pressure with lifestyle changes?
Yes: -Weight loss -Salt restriction -Exercise -Alcohol
97
Why would blood pressure treatment be withheld?
During general anaesthesia hypotension can be a problem and antihypertensives block attempts to increase BP ==> ACEi + ARBs temporarily stopped
98
Side effect of GTN spray?
Excruciating headache
99
Reasons for imperfect blood supply to the heart?
- Atherosclerosis - Thrombosis - Thromboemboli - artery spasm - blood pressure/ cardiac output/ heart rate - Arteritis
