Angina Flashcards

Question

What are re-vascularisation options?

Answer 1

- **Percutaneous coronary intervention (PCI):** a ****balloon is inflated in a stenosed vessel and a stent is placed to ensure the lumen remains open. - Administer a combination of aspirin and clopidogrel for a minimum of 12 months to reduce the risk of thrombosis. - **Coronary artery bypass graft (CABG):** involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis. - Associated with a better overall outcome, however,as it is an open procedure it is associated with greater perioperative risks.

Answer 2

- **Lifestyle changes**: exercise, dietary alterations, lipid, diabetes and hypertension management, smoking cessation - **Aspirin** 75mg daily and a **statin** (e.g. atorvastatin 80mg daily) - **Angiotensin-converting enzyme inhibitors** (ACEi): if the patient has angina and diabetes

Answer 3

- After patient has been treated for a number of months / years - Coronary angioplasty PCI: Percutaneous coronary Intervention - CABG- highly invasive procedures, Mammary artery from chest and leg vessel, have to be moderately fit to undergo this procedure

Answer 4

- Reassure - Changes in lifestyle factors - Diet - Excercise - Smoking - Weight - Advice for emergency

Answer 5

- Anaemia - Tachycardia - Thyrotoxicosis

Answer 6

- GTN Spray - Beta blocker - slow heart and reduce the force of contraction. REDUCES HEART RATE AND CONTRACTILITY WHICH REDUCES CARDIAC OUTPUT AND REDUCES OXYGEN DEMAND. - Risks/ side effects - Bradycardia - Cold hands and feet - Erectile dysfunction - Tiredness, nightmares - Never give to someone with severe asthma - can cause bronchoconstriction - Bradycardic pATIENTS - slow resting heart rate - Heart Block patients - Long acting Nitrates: Venodilators - reduce preload by venodilitation? and dilating healthy coronary arteries - Vasodilator so thumping headache - goes away after several days. - Ca channel blockers - amlodipine - Swollen ankles - Postural hypertension - Antiplatelet agent - Dyspenisa - Caution - gastric ulcers - Statins - Inhibit endogenous production of ldl cholesterol In the liver by 30-40% - Ace inhibitors - reduce vasoconstriction and sodium and water retention by the kidney. Useful for remodelling of the left ventricle after heart attack - Cough - Can cause renal impairment - Aspirin Dihydropyridine

Answer 7

- Cardiovascular complications - eg, unstable angina and myocardial infarction. - **Myocardial Infarction:** a plaque may continue growing until the coronary artery is completely obstructed - **Chronic heart failure:** the ****underlying causes of ischaemic heart disease are also associated with an increased risk of chronic congestive heart failure - **Stroke:** atherosclerosis may also develop within the cerebrovascular system - Anxiety and depression. - Reduced general health and quality of life.

Answer 8

- Demographic risk factor - **Increasing age** - **Sex (male)** - **Ethnicity** - Genetics (**family history** of coronary heart disease )

Answer 9

- Lifestyle risk factors - **Smoking** - Diet - Physical activity - Sedentary lifestyle - **Stress** - **Drug use (cocaine)** - Clinical risk factors - **Hypertension** - Lipids - **Diabetes** - **Obesity** - **Hypercholesterolaemia** - Environmental risk factors - Air pollution - Chemicals

Answer 10

1. Coronary prone behaviour pattern 2. Depression and anxiety and CHD 3. Psychocial work characteristics 4. Social support

Answer 11

1. Type A pattern behaviour is not a personality trait (fixed trait or disposition). It is a modifiable behaviour pattern. 2. Extreme competitiveness, striving for achievement, hostileness and a sense of urgency 3. Identified by cardiologist Friedman and Rosenman (1959) Evidence concluded that: a reduction in type A behaviour reduces morbidity and mortality in post infarction patients. More recent research identifies the hostility dimension as a key risk factor - Feelings of anger - Annoyance and resentment - Verbal or physical aggression

Answer 12

1. Type A pattern behaviour is not a personality trait (fixed trait or disposition). It is a modifiable behaviour pattern. 2. Extreme competitiveness, striving for achievement, hostileness and a sense of urgency 3. Identified by cardiologist Friedman and Rosenman (1959) Evidence concluded that: a reduction in type A behaviour reduces morbidity and mortality in post infarction patients. More recent research identifies the hostility dimension as a key risk factor - Feelings of anger - Annoyance and resentment - Verbal or physical aggression

Answer 13

1. High demand low control jobs - significant association to MI 1. These types of jobs are also associate with lower employment grades. They are also low reward and less secure which are additional sources of psychological stress. 2. Longer working hours

Answer 14

1. Both quantity and quality of social relationships 2. Loneliness

Answer 15

- Pericarditis/Myocarditis - Myocardial ischaemia - Pulmonary Embolism - Chest infection - GORD - Dissection of the aorta - Anxiety - Anaemia

Answer 16

- If lifestyle changes are made and the patient remains compliant with medication, 58% of patients are expected to be free of symptoms. - However, poor lifestyle and poor anti-anginal compliance can predispose a stable atheromatous plaque to become unstable, increasing the risk of myocardial infarction

Answer 17

- **Stable angina**: brought on by exertion, relieved by rest - **Unstable angina**: occurs on minimal exertion or at rest, with increasing frequency and severity (acute coronary syndrome) Usually caused by rupture of atherosclerotic plaque with thrombosis (blood clot forms on top of plaque). There is even less room left for blood to flow by, and the heart tissue is starved for oxygen even during rest. Unstable angina involves subendocardial ischaemia and should be treated as an emergency as patients are at a high risk of progressing to myocardial infarction. ECG = ST segment depression - **Decubitus angina**: induced by lying flat - **Prinzmetal angina**: coronary artery spasm; typically brief chest pain at rest (non-exertional) and seen in younger patients. There is transient ST-elevation which self-resolves and normal serial troponins. Ischaemia and resulting chest pain is due to coronary artery vasospasms (smooth muscles around the arteries constrict tightly and reduce blood flow). The underlying mechanism causing vasospasms isn’t well understood, but likely involves vasoconstrictors e.g. platelet thromboxane A2. In this case the coronary artery’s constrict so severely that all layers of the heart wall being supplied are affected - transmural ischaemia. Episodes of vasospastic angina don’t correlate with exertion and can happen anytime, including at rest. ECG = transient ST segment elevation - **Nocturnal angina:** occurs at night and may wake patient up

Answer 18

Acute coronary syndrome (ACS) encompasses unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI). An acute coronary syndrome typically manifests as sudden, new-onset angina, or an increase in the severity of an existing stable angina.

Answer 19

- STEMI = 5/1000 per annum in UK - M>F

Answer 20

- Non-modifiable risk factors: - **Age (>65 years of age)** - **Male** - **Family history of premature coronary heart disease** - **Premature menopause**

Answer 21

In general, the process underlying all three conditions is atherosclerotic plaque formation. - The first stage of atherosclerotic plaque formation involves the accumulation of low-density lipoprotein cholesterol in the inner layer of the blood vessel - Leukocytes adhere to the endothelium and gain entry into the intima, where they combine with the lipids to become foam cells - Artery remodelling and calcification, alongside the presence of foam cells, causes atherosclerotic plaques to form - Rupture of a plaque causes platelet activation, thrombus formation and coronary artery occlusion. (The thrombus is mainly made up of platelets) - This results in ischaemia and infarction In unstable angina and NSTEMI, the occlusion is partial. In STEMI, the occlusion is complete. In the case of a STEMI, ischaemia is initially just subendocardial, but eventually becomes transmural.

Answer 22

- **Hypotension** or **hypertension** - **Reduced 4th heart sound** - **Signs of heart failure:** e.g. increased JVP, oedema; ****red flag symptom - **Systolic murmur:** if mitral regurgitation or a ventricular septal defect develops - - **Chest pain** - Central, ‘heavy’, crushing pain - Radiation to the left arm or neck - Symptoms should continue at rest for more than 20 minutes - Certain patients e.g. diabetics or elderly, have atypical presentation and may not have chest pain (‘silent MI’) - May sometimes feel like **indigestion** - **Shortness of breath** - **Sweating and clamminess** - **Nausea and vomiting** - **Palpitations** - **Anxiety:** often described as a ‘sense of impending doom’

Answer 23

- **Chest pain** - Central, ‘heavy’, crushing pain - Radiation to the left arm or neck - Symptoms should continue at rest for more than 20 minutes - Certain patients e.g. diabetics or elderly, have atypical presentation and may not have chest pain (‘silent MI’) - May sometimes feel like **indigestion** - **Shortness of breath** - **Sweating and clamminess** - **Nausea and vomiting** - **Palpitations** - **Anxiety:** often described as a ‘sense of impending doom’

Answer 24

ECG: perform within 10 minutes. Aim to perform serial ECGs every 10 minutes to detect dynamic changes. - **Troponin:** for a STEMI and NSTEMI, troponin levels will begin to elevate 4-6 hours after injury and will remain elevated for roughly 10 days. In unstable angina, there is no elevation in troponin. -

Answer 25

- *ECG findings* - **Unstable angina:** non-specific changes - **NSTEMI:** ST-segment depression; T-wave inversion; pathological Q waves; a normal ECG may be seen - **STEMI:** ST-segment elevation; T-wave inversion; new left-bundle branch block

Answer 26

- Perform other tests that you would for stable angina e.g. - **Physical Examination** (heart sounds, signs of heart failure, BMI) - **Lipid profile** - **Thyroid function tests:** check for hypo / hyper thyroid - **HbA1C and fasting glucose:** check for diabetes - **Coronary angiogram:** aim to carry out angiography within 90 minutes if required; diagnostic investigation of choice - **FBC:** Hb and haematocrit may reveal a secondary cause in type 2 MI e.g. anaemia - **U&Es:** electrolyte imbalances may predispose the patient to cardiac arrhythmias; also done prior to ACEi and other meds - **LFTs:** done prior to statins - **Other biomarkers**: less commonly used biomarkers of cardiomyocyte injury include **creatine kinase-MB** (increases at 3-6 hours), and **myoglobin** (earliest to rise, usually within 2 hours) - **CXR:** to exclude other potential causes, if needed - **Echocardiogram** after the event to assess the functional damage

Answer 27

- Perform other tests that you would for stable angina e.g. - **Physical Examination** (heart sounds, signs of heart failure, BMI) - **Lipid profile** - **Thyroid function tests:** check for hypo / hyper thyroid - **HbA1C and fasting glucose:** check for diabetes - **Coronary angiogram:** aim to carry out angiography within 90 minutes if required; diagnostic investigation of choice - **FBC:** Hb and haematocrit may reveal a secondary cause in type 2 MI e.g. anaemia - **U&Es:** electrolyte imbalances may predispose the patient to cardiac arrhythmias; also done prior to ACEi and other meds - **LFTs:** done prior to statins - **Other biomarkers**: less commonly used biomarkers of cardiomyocyte injury include **creatine kinase-MB** (increases at 3-6 hours), and **myoglobin** (earliest to rise, usually within 2 hours) - **CXR:** to exclude other potential causes, if needed - **Echocardiogram** after the event to assess the functional damage

Answer 28

- **Oxygen:** only if SpO2 is <94%, and aim for 94-98% - **Analgesia:** morphine and sublingual glyceryl trinitrate - **Dual antiplatelets:** - **Aspirin** - The choice of the second antiplatelet agent depends on if the person is having PCI or not, and will vary based on local guidance: - **Prasugrel or ticagrelor or clopidogrel** if undergoing PCI - **Ticagrelor or clopidogrel** if not undergoing PCI - **Anticoagulation:** - **Fondaparinux:** offer to all patients unless undergoing immediate coronary angiography - **Unfractionated heparin:** an alternative to fondaparinux if the patient has renal failure - **Beta blockers:** e.g. atenolol or metoprolol, unless contraindicated - *Remember **‘MONA’: M**orphine, **O**xygen, **N**itrates, **A**spirin*

Answer 29

- **Oxygen:** only if SpO2 is <94%, and aim for 94-98% - **Analgesia:** morphine and sublingual glyceryl trinitrate - **Dual antiplatelets:** - **Aspirin** - The choice of the second antiplatelet agent depends on if the person is having PCI or not, and will vary based on local guidance: - **Prasugrel or ticagrelor or clopidogrel** if undergoing PCI - **Ticagrelor or clopidogrel** if not undergoing PCI - **Anticoagulation:** - **Fondaparinux:** offer to all patients unless undergoing immediate coronary angiography - **Unfractionated heparin:** an alternative to fondaparinux if the patient has renal failure - **Beta blockers:** e.g. atenolol or metoprolol, unless contraindicated - *Remember **‘MONA’: M**orphine, **O**xygen, **N**itrates, **A**spirin*

Answer 30

If the patient is clinically unstable they must be taken for PCI immediately. Otherwise, the remainder can be risk-stratified using the GRACE score (refer to 'other notes' below)

Answer 31

- **Oxygen:** only if SpO2 is <94%, and aim for 94-98% - **Analgesia:** morphine and sublingual glyceryl trinitrate - **Dual antiplatelets**: - **Aspirin** - The choice of the second antiplatelet agent depends on if the person is having PCI or not, and will vary based on local guidance: - **Prasugrel or clopidogrel** if undergoing PCI - **Ticagrelor or clopidogrel** if undergoing fibrinolysis

Answer 32

- **PCI**: first-line method of revascularisation; insertion of a catheter via the radial or femoral artery to open up the blocked vessels using an inflated balloon (angioplasty), and a stent may also be inserted - **Anticoagulation and further antiplatelet therapy** - **Unfractionated heparin** **and a** **glycoprotein IIb/IIIa inhibitor** - **Bivalirudin** may be used as an alternative to unfractionated heparin

Answer 33

- **Thrombolysis e.g. alteplase or tenecteplase** - IV administration of a fibrinolytic agent - Offered if symptom onset is greater than 12h OR PCI not available within 120 mins - **Anticoagulation** - An antithrombin agent such as unfractionated heparin is usually given alongside thrombolysis - **ECG:** if the ECG shows residual ST elevation after 60-90 minutes of thrombolysis, offer immediate angiography and PCI

Answer 34

- **Lifestyle changes**: exercise, diet change, smoking cessation, reducing alcohol intake - **Manage cardiovascular risk factors**: lipid, diabetes, hypertension management - **Antiplatelet therapy**: - Aspirin 75mg OD continued indefinitely - The second antiplatelet depends on the one chosen in the acute setting i.e. prasugrel, ticagrelor, or clopidogrel, and is usually continued for 12 months. - **Angiotensin-converting enzyme inhibitors** (ACEi) and **beta-blocker** - **Statin:** usually atorvastatin 80mg - **Cardiac rehabilitation**: must be offered following myocardial infarction

Answer 35

- **Post-MI pericarditis:** inflammation of the pericardium usually occurs a few days post-MI due to irritation of the pericardium; usually benign - **Cardiac arrest/tachyarrhythmias:** most commonly ****due to ventricular fibrillation - Can lead to **sudden death** - **Bradyarrhythmias:** heart block is more common after an inferior myocardial infarction - **Cardiogenic shock:** extensive ventricular damage may lead to impaired ejection fraction and the development of cardiogenic shock - **Ventricular septal defect:** seen within the first week and may present with acute heart failure and a pansystolic murmur - **Mitral regurgitation:** most commonly due to ****papillary muscle rupture secondary to an inferior-posterior infarction, results in an early-mid systolic murmur - **Left ventricular wall rupture**: a rare but fatal complication which presents within a few weeks. Ischaemia leads to a weakened ventricular wall and rupture, presenting as cardiac tamponade and acute heart failure

Answer 36

Dressler’s syndrome: presents similarly to post-MI pericarditis but occurs 2-6 weeks post-MI, and reflects an autoimmune process against neo-antigens formed by the heart - **Heart failure:** ventricular dysfunction following extensive damage can lead to chronic heart failure - **Left ventricular aneurysm:** bulge or ballooning of a weakened area of the heart

Answer 37

**Diagnosis:** ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR). **Management:** NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). May need pericardiocentesis to remove fluid around the heart.

Answer 38

Unstable angina has a better outcome than an NSTEMI or STEMI. NSTEMIs and STEMIs have similar long-term outcomes. 5-10% of patients with ACS are predisposed to re-infarction. Poor prognostic factors include: increasing age, the magnitude of troponin rise, arrhythmias, left ventricular dysfunction, renal impairment, diabetes, anaemia, cerebrovascular disease

Answer 39

- **Type 1**: a classic MI and occurs due to atheromatous plaque rupture - **Type 2**: secondary to ischaemia due to **either** increased oxygen demand **or** decreased supply, such as vasospasm, anaemia and sepsis. Management involves treating the underlying cause. - **Type 3**: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event - **Type 4**: MI associated with PCI / coronary stenting / CABG

Answer 40

Aspirin - anti platelet: predominantly COX-1 inhibition, thus preventing the synthesis of thromboxane A2 Clopidogerol/prasugrel/ticagrelor: anti platelets - inhibit the binding of adenosine diphosphate (ADP) to its platelet P2Y12 Tirofiban/Abciximab/Eptifibatide: Antiplatelets: glycoprotein 2b/3a receptor antagonists (Gp2b/3a inhibitors) Enoxaparin (LMWH)/fondaparinux: Anticoagulants: activate antithrombin 2, thus causing the inhibition of clotting factor Xa Bivalirudin: anticoagulant: reversible direct thrombin inhibitor

Answer 41

The Global Registry of Acute Coronary Events (GRACE) score is recommended by NICE to risk-stratify patients with unstable angina and non-ST elevation myocardial infarction (NSTEMI). The GRACE score estimates admission to 6-month mortality.

Answer 42

Age, heart rate/pulse, systolic blood pressure, creatinine, cardiac arrest at admission, ST-segment deviation on ECG, abnormal cardiac enzymes killip class (signs and symptoms): - rales and/or jugular venous distension - pulmonary oedema - cardiogenic shock

Answer 43

Risk category - GRACE risk score - Admission to 6month mortality (%) 1. Low - 118 - >8

Answer 44

Intermediate- and high-risk patients with unstable angina or NSTEMI require coronary angiography during admission, whilst this can be delayed in low-risk patients. - **Clinically unstable:** immediate angiogram and percutaneous coronary intervention (PCI) - **Intermediate or high risk of cardiovascular event (>3%):** coronary angiography and percutaneous coronary intervention (PCI) within 72 hours of admission - **Low risk of cardiovascular event (<3%):** exclusively medical management

Answer 45

- Unstable angina is an acute coronary syndrome. - Continuous pain of Increasing severity. - Can be due to thrombus formation on top of thrombotic plaque - Can also happen at rest

Answer 46

- Cardiac chest pain at rest - Cardiac chest pain with crescendo pattern - New onset angina

Answer 47

Coronary heart disease due to atherosclerosis

Answer 48

- Unstable angina results when the blood flow is impeded(delayed) to the myocardium. - Blood flow obstacles cause a lack of perfusion to the myocardium. - Initial perfusion starts directly from the heart into the aorta and subsequently into the coronary arteries which supply their respective portions of the heart. - This block can be from intraluminal plaque formation, intraluminal thrombosis, vasospasm, and elevated blood pressure. - Often a combination of these is the provoking factor. --- - Angina represents an **imbalance** between myocardial oxygen supply and demand, resulting in myocardial ischaemia. - This is commonly due to ****atheromatous plaques. - Damage to arterial walls results in inflammation that promotes the formation of atheromatous plaques. - **Monocytes** scavenge lipids upon entry into the arterial wall, transforming into foam cells. - **Cytokines** are released by foam cells, promoting **smooth muscle migration** from the arterial media into the intima. Over time, plaques develop in size. - **Atheromatous plaques** obstruct coronary blood flow, reducing the amount of oxygen the heart receives. - Occasionally, transient angina may be **non-atheromatous** in nature, such as due to coronary artery vasospasm (Prinzmetal’s angina). - This is **not** associated with myocardial ischaemia. Anaemia is also a rare cause of angina.

Answer 49

The incidence is higher in men, but as individuals surpass the age of 75, the incidence of males and females becomes much closer.

Answer 50

Cardiac-sounding chest pain: - **Crushing, left-sided chest pain** or pressure - **Often radiating to left arm or jaw** - Pain or pressure in the back, neck, jaw, abdomen**,** shoulders or arms - **Sweating** - **Dyspnoea** - **Nausea**, vomiting - Dizziness or sudden weakness - Fatigue

Answer 51

Xanthomas or xanthelasma - Suggests hypercholesterolaemia Hypertension (A risk factor for angina) Evidence of peripheral vascular disease - May coexist with ischaemic heart disease Besides **exertion**, angina can also be precipitated by heavy meals, cold weather and emotion. --- - Diaphoresis (excess sweating) - Tachycardia or bradycardia

Answer 52

- **Unstable angina**: occurs on minimal exertion or at rest, with increasing frequency and severity (acute coronary syndrome) Usually caused by rupture of atherosclerotic plaque with thrombosis (blood clot forms on top of plaque). There is even less room left for blood to flow by, and the heart tissue is starved for oxygen even during rest. Unstable angina involves subendocardial ischaemia and should be treated as an emergency as patients are at a high risk of progressing to myocardial infarction. ECG = ST segment depression

Answer 53

**Typical angina** usually has all 3 characteristic features listed below, whilst **atypical angina** has 2 features and **non-anginal chest pain** has 0-1 features. - **Characteristic features of angina** - Discomfort to the chest, neck, jaw, shoulders or arms - Symptoms brought on by exertion: remember, unstable angina may occur at rest - Symptoms relieved within 5 minutes by rest or glyceryl trinitrate (GTN)

Answer 54

- Primary investigations - Investigation - **First line**: 12-lead ECG (ST segment depression) - 12 lead ECG - Usually normal - May show ST depression and T wave inversion - CT angiography (**gold standard**) - CT angiography - Shows narrowing of a coronary artery - Once narrowing is shown it is then possible to go in and open with a stent or balloon - **Second line:** functional imaging (stress echo, or cardiac MRI) is used if CT angiography is non-diagnostic - **Third line**: transcatheter angiography - **Non-anginal chest pain** - If the patient has ischaemic changes on 12 lead ECG, then consider investigations as per typical and atypical angina - If no changes are present on ECG, then no further cardiac investigations are required and non-cardiac causes should be considered - Investigations to consider - **FBC:** may reveal anaemia as an underlying cause of angina - **Fasting blood sugar and HbA1c**: diabetes is associated with an increased risk of ischaemic heart disease - **Fasting lipid profile:** hyperlipidaemia is associated with an increased risk of ischaemic heart disease - **Ambulatory blood pressure monitoring:** if hypertension is suspected in clinic - Thyroid function tests: check for hypo / hyper thyroid - U&Es: prior to ACEi and other meds - LFTs: prior to statins - High-sensitivity troponin - Chest x-ray

Answer 55

- Diagnosis - History - ECG - Troponin (There is no significant rise in unstable angina)

Answer 56

- **Immediate management** - **Oxygen:** only if SpO2 is <94%, and aim for 94-98% - **Analgesia:** morphine and sublingual glyceryl trinitrate - **Dual antiplatelets:** - **Aspirin** - The choice of the second antiplatelet agent depends on if the person is having PCI or not, and will vary based on local guidance: - **Prasugrel or ticagrelor or clopidogrel** if undergoing PCI - **Ticagrelor or clopidogrel** if not undergoing PCI - **Anticoagulation:** - **Fondaparinux:** offer to all patients unless undergoing immediate coronary angiography - **Unfractionated heparin:** an alternative to fondaparinux if the patient has renal failure - **Beta blockers:** e.g. atenolol or metoprolol, unless contraindicated - *Remember **‘MONA’: M**orphine, **O**xygen, **N**itrates, **A**spirin*

Answer 57

If the patient is clinically unstable they must be taken for PCI immediately. Otherwise, the remainder can be risk-stratified using the GRACE score (refer to 'other notes' below)

Answer 58

- Aspirin - Nitroglycerin - Clopidogrel - Supplemental oxygen - Anticoagulation with either low or high molecular weight heparin. - Beta blockers - Many trials have validated the use of statins in patients with unstable angina. Lifestyle and diet advice is recommended long term

Answer 59

- **Myocardial infarction:** a plaque may continue growing until the coronary artery is completely obstructed. - **Chronic heart failure:** the ****underlying causes of ischaemic heart disease are also associated with an increased risk of chronic congestive heart failure - **Stroke:** atherosclerosis may also develop within the cerebrovascular system - Mental health issues such as depression - Arrhythmias

Answer 60

- Demographic risk factor - **Increasing age** - **Sex (male)** - **Ethnicity** - Genetics (**family history** of coronary heart disease )

Answer 61

- Clinical risk factors - **Hypertension** - Hyperlipidaemia - **Diabetes Mellitus** - **Obesity** - **Hypercholesterolaemia** - Lifestyle risk factors - **Smoking** - Diet - Physical activity - Sedentary lifestyle - **Stress** - **Drug use (cocaine,** amphetamine abuse**)** - Environmental risk factors - Air pollution - Chemicals

Answer 62

Yes - name them!

Answer 63

- Clinical interview - Speech and answer content - Psychomotor, Non verbal

Answer 64

- If lifestyle changes are made and the patient remains compliant with medication, 58% of patients are expected to be free of symptoms. - However, poor lifestyle and anti-anginal compliance can predispose a stable atheromatous plaque to become unstable, increasing the risk of myocardial infarction.

Answer 65

- Angina due to **coronary artery spasm** (rare). (spasm is a sudden involuntary muscular contraction) - The pain usually occurs during **rest** and resolves rapidly with short acting nitrates (e.g. GTN spray). - ECG during pain shows **ST segment elevation** - Avoid triggers - Prognosis is usually very good.

Answer 66

Coronary artery spasm; typically brief chest pain at rest (non-exertional) and seen in younger patients. There is transient ST-elevation which self-resolves and normal serial troponins.

Answer 67

- Prinzmetal’s angina is caused by spasms of the coronary arteries, or the arteries that bring blood and oxygen to the heart. - Medications that are intended to constrict blood vessels, such as migraine treatments like sumatriptan or decongestants that contain ephedrine - Use of drugs like marijuana and cocaine - Smoking tobacco - Stress - Exposure to cold - Exercise

Answer 68

Transient angina may be **non-atheromatous** in nature, such as due to coronary artery vasospasm (Prinzmetal’s angina). This is **not** associated with myocardial ischaemia. Anaemia is also a rare cause of angina. --- - The underlying mechanism in the development of coronary artery spasm is multifactorial. - One mechanism that might generate the spasm is an increased reactivity of the vessels to vasoconstrictive stimuli and subsequent high-grade stenosis in a segment of the coronary or creating low coronary flow and with this myocardial injury due to ischemia. - The causes of the hyperreactivity of the coronary vessels is unclear but could be related to: - Endothelial dysfunction and primary smooth muscle cells of the coronary vessels that might have impaired regulatory mechanism for vasoconstriction and vasodilation. - Balances within the sympathetic and parasympathetic tone is also an important factor that regulates flow in the coronaries. - The balance between sympathetic and parasympathetic activity determines heart rate. - Imbalance in this system can predispose exaggerated vasoconstriction.

Answer 69

- Cocaine user, young women, smokes, methamphetamine, history of migraines takes amitriptyline - Incidence and prevalence of Prinzmetal angina is unknown. - The reason for this is the possible misdiagnosis or confusion with other conditions that might present with the same systems, and further evaluation is not sought. - Some studies show that the Japanese population has an increased risk of developing it when compared to the caucasian population. - The risk of the Japanese is a three times higher risk.

Answer 70

- A chronic pattern of episodes of chest pain at rest that last 5 to 15 minutes, from midnight to early morning. - Typically, the chest pain is not triggered by exertion or alleviated with rest as is typical angina. - Sweating - Nausea and/or dizziness

Answer 71

- Patients have ischemic ST segment changes on an electrocardiogram during an episode of chest discomfort, which returns to baseline on symptom resolution. - **Pain decreases with the use of short-acting nitrates.**

Answer 72

- Patients have ischemic ST segment changes on an electrocardiogram during an episode of chest discomfort, which returns to baseline on symptom resolution. - **Pain decreases with the use of short-acting nitrates.**

Answer 73

- Stress test - Coronary angiography - Electrocardiogram

Answer 74

- Treatment is focused on decreasing episodes of angina and preventing complications like myocardial injury and arrhythmia. - Pharmacological - **Calcium antagonist (blocker)** - This is a first line treatment due to vasodilation effect in the coronary vasculature - Long acting nitrates - Effective in preventing vasospastic events. - Fluvastatin - This is a statin that had been shown to be effective in preventing coronary spasm. - Lifestyle changes - Smoking cessation - Avoid substances that cause spasms - Healthy diet - exercise Avoid beta blockers

Answer 75

- Arrhythmia - Sudden death - Myocardial infarction

Answer 76

- Cigarette smoking - Inflammatory states determined by high sensitivity C reactive protein - The metabolic disorder insulon resistance has also been associated with Prinzmetal’s angina. Other typical cardiovascular risk factors have not been directly associated with the presence of Prinzmetal’s angina.

Answer 77

- Acute pericarditis - Angina pectoris - Anxiety disorders - Aortic dissection - Cocaine toxicity - Esophageal spasms - Gastroesophageal reflux disease - Myocardial infarction - Panic disorder - Unstable angina

Answer 78

Transmural ischaemis afecets all 3 layers of the heart = st elevation ? PRINZMETALS ANGINA

Answer 79

Acute myocardial infarction AKA a heart attack, is a life-threatening condition that occurs when blood flow to the heart muscle is abruptly cut off, causing tissue damage. - This is usually the result of a blockage in one or more of the coronary arteries There are 2 types: - STEMI - NSTEMI

Answer 80

Myocardial infarction is an acute coronary syndrome. - ST elevation - Tall T waves - Might present as a new LBBB (Left bundle branch block**)** (WilliaM) - **Pathological Q waves**

Answer 81

Atheroma Atherogenesis and atherothrombosis

Answer 82

- Almost always due to a **rupture** of an atherosclerotic plaque which leads to clot formation which then occludes one of the coronary arteries causing myocardial cell death and inflammation - So basically, plaque rupture 🡪 development of thrombosis 🡪 total occlusion of coronary artery 🡪 myocardial cell death

Answer 83

- Most common cause of death in developed countries - 1/3 cases occur at night - 600/100,000 for men. - 200/100,000 for women

Answer 84

- Crushing central chest pain similar to that occurring in angina – described as “elephant sitting on chest: Chest pain - 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 - Sweating - SOB/Dyspnoea - Fatigue - Nausea - Vomiting - Palpitations

Answer 85

- **Occurs at rest** - Last longer than 20 minutes - **Not relived by GTN spray** - Pain may radiate to left arm, neck and/or jaw - Pulse and BP may vary between being up or down - Patient appears pale, sweaty and grey - **4th heart sound** – due to forceful contraction of the atria to overcome a stiff or dysfunctional ventricle - Pansystolic murmur – due to papillary muscle dysfunction or rupture Heart muscle damage Myocardial infarction usually causes per infant heart muscle damage although this may not be detectable in small MI’s.

Answer 86

- Clinical history - ECG - STEMI - ST elevation - Tall T waves - LBBB - Pathological Q waves follow - NSTEMI - ST depression and/or T wave inversion - Cardiac enzymes – troponin T, creatine kinase, myoglobin are markers for cardiac damage - CT angiography - CXR - FBC —> rules out anaemia - U&E - Blood glucose and lipids

Answer 87

**If there is ST elevation or new left bundle branch block (LBBB) the diagnosis is *STEMI.*** - ST elevation myocardial infarction can be usually diagnosed on ECG at presentation - Non ST elevation myocardial infarction is a retrospective diagnosis made after troponin results and sometimes other investigation results are available

Answer 88

- Stable/unstable angina - Pericarditis - Aortic aneurysm - Endocarditis - Pulmonary Embolism - Pneumothorax - Cardiac – ACS, Aortic dissection, pericarditis, myocarditis - Respiratory – PE, pneumonia, pleurisy, lung cancer - MSK – rib fracture, chest trauma, costochondritis (inflammation of the cartilage between the ribs and sternum) - GORD - Oesophageal spasm - Anxiety/panic attacks

Answer 89

- Acute (initial management) - Get to hospital immediately - 999 call for ambulance which has defibrillator - Paramedics - if ST elevation, contact primary PCI centre for transfer - MONA - Morphine - Oxygen (if sats are <94%) - Nitrates – typically fondaparinux in Sheffield - Aspirin 300mg – chewed in order to increase absorption - Take aspirin 300mg immediately - 12 lead ECG and cardiac monitor - Beta blocker IV – contraindicated in hypotension, HF, bradycardia and asthma - Refer for PCI, thrombolysis (IV alteplase) or CABG ASAP as long as it’s not contraindicated - Subsequent (secondary prevention) - Modification of risk factors - Diabetes - Smoking - Hypertension - Hypercholesterolaemia - Exercise - Diet – high in oily fish, fruit and veg, low in saturated fats - Aspirin – 75mg daily - Clopidogrel/ticagrelor (for dual antiplatelet therapy) - Statins - Beta blocker – if contraindicated give ACE-I - ACE inhibitors – use angiotensin receptor blocker if intolerant e.g. valsartan - Advice - Return to work after 2 months – not all professions e.g. airline pilots, divers, air traffic controllers - No air travel for 2 months - No sex for 1 month

Answer 90

- Make diagnosis - Bed rest - Oxygen therapy if hypoxic - Pain relief - opiates / nitrates - Aspirin and a platelet P2Y12 inhibitor - Consider beta blocker - Consider other anti Angola therapy - Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy.

Answer 91

DREAD - Myocardial rupture - Rupture of ventricular septum 🡪 right HF - LV wall 🡪 cardiac tamponade - Papillary muscle rupture 🡪 mitral regurgitation/prolapse - Arrhythmias - Tachycardia – Sinus, VF, AF - Brachycardia – Sinus, AV block - Pericarditis —> Common after anterior infarct. Dressler's syndrome (presents as pericarditis). - Dressler’s syndrome – pericarditis following cardiac intervention/surgery - Death - Mitral incompetence – due to myocardial scarring - Depression: 20% of patients following MI have depression issues

Answer 92

Age - Male - History of premature coronary heart disease - Diabetes mellitus - Hypertension - Hyperlipidaemia - Family history

Answer 93

- Non-ST-Elevation Myocardial Infarction - Type of heart attack - Will see ST depression and/or T wave inversion - no progression to Q wave - partial blockage of coronary artery

Answer 94

- NSTEMI is a result of an acute imbalance between myocardial oxygen demand and supply, most commonly due to a reduction in myocardial perfusion. - Atherosclerosis Atherogenesis and atherothrombosis - Coronary artery narrowing - Plaque rupture - Arterial inflammation - Obstruction - Drugs

Answer 95

- NSTEMI is a result of an acute imbalance between myocardial oxygen demand and supply, most commonly due to a reduction in myocardial perfusion. - Atherosclerosis Atherogenesis and atherothrombosis - Coronary artery narrowing - Plaque rupture - Arterial inflammation - Obstruction - Drugs

Answer 96

- Partial blockage of one of the coronary arteries, causing reduced flow of oxygen-rich blood to the heart muscle. - For most patients, the heart damage caused by NSTEMI is less serious than from [**STEMI**](https://ukhealthcare.uky.edu/gill-heart-vascular-institute/conditions/heart-attack/ST-elevation-myocardial-infarction) - Both STEMI and NSTEMI patients are said to have acute coronary syndrome.

Answer 97

Chest pain - 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 - dizziness - lightheadedness - nausea - sweating - shortness of breath - pressure, tightness, or discomfort in your chest - pain or discomfort in your jaw, neck, back, or stomach

Answer 98

- New murmurs - Sweating Heart muscle damage Myocardial infarction usually causes per infant heart muscle damage although this may not be detectable in small MI’s. Levine Tachycardia

Answer 99

- Blood test - Elevated levels of creatine kinase-myocardial band (CK-MB), troponin I, and troponin T. These markers are evidence of possible damage to the heart cells - ECG - Patterns of ST waves-identify if heart attack happened or not and if so, what type

Answer 100

- ST elevation myocardial infarction can be usually diagnosed on ECG at presentation - Non ST elevation myocardial infarction is a retrospective diagnosis made after troponin results and sometimes other investigation results are available

Answer 101

Acute NSTEMI treatement: BATMAN/PACMAN B - beta-blockers unless contraindicated A - aspirin 300mg stat dose T - Ticagrelor 180mg stat dose (clopidogerol 300mg is an alternative if higher bleeding risk) M - morphine titrated to control pain A - anticoagulant: fondaparinux (unless high bleeding risk) N - nitrates (e.g. GTN) to relieve coronary artery spasm Give oxygen only if their oxygen saturations are dropping (i.e. <95%) - Ticagrelor - Contraindicated in active bleeding or a history of intercranial haemorrhage

Answer 102

- Initial management - Arrive at hospital quickly - 999 call for ambulance which has defibrillator - Paramedics - if ST elevation, contact primary PCI centre for transfer - Take aspirin 300mg immediately - Pain relief

Answer 103

- Lifestyle changes - Pharmaceuticals - ACE inhibitors - Anticoagulants - Antiplatelets - ARBs (angiotensin receptor blockers) - Beta-blockers - Statins

Answer 104

- Hospital management - Make diagnosis - Bed rest - Oxygen therapy if hypoxic - Pain relief - opiates / nitrates - Aspirin and a platelet P2Y12 inhibitor - Consider beta blocker - Consider other anti Angola therapy - Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy.

Answer 105

- Hospital management - Make diagnosis - Bed rest - Oxygen therapy if hypoxic - Pain relief - opiates / nitrates - Aspirin and a platelet P2Y12 inhibitor - Consider beta blocker - Consider other anti Angola therapy - Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy.

Answer 106

- Acute heart failure - Aneurysm - Cardiac arrythmias - Depression

Answer 107

- Overweight/Obese - Lack of exercise - Smoking - Diabetes - High blood pressure - High cholesterol - Family history of heart disease or stroke

Answer 108

Aspirin: Clopidogerol/plausgrel/ticagrelor: Tirofiban/Abciximab/eptifibatide: Enoxaparin (LMWH)/Fondaparinux: Bivalirudin:

Answer 109

when blood flow to the heart muscle (myocardium) is obstructed by a partial or complete blockage of a coronary artery by a buildup of plaques (atherosclerosis). If the plaques rupture, you can have a heart attack (myocardial infarction).

Answer 110

Supply - too little supply = Anemia, Hypoxia - Demand - excessive demand - Left ventricular hypertrophy - Environmental - Increase cardiac output so need more oxygen.

Angina Flashcards

(136 cards)