CVS 9 Flashcards by Alyssa Conte

What is the simple definition of the following:

Angina
Unstable angina
STEMI
NSTEMI

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What is Ischaemic Heart Disease?

an umbrella term that covers a whole spectrum of problems caused by reduced blood flow to the heart muscle

imbalance between oxygen supply to myocardium and demand
could happen when blood vessels become narrow or blocked due to atherosclerosis
encompasses coronary artery diseases such as stable and unstable angina, STEMI/NSTEMI, silent ischaemia, chronic IHD

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List the 4 things which oxygen SUPPLY to the heart depend on.

List 4 things which oxygen DEMAND depends on.

supply:
- coronary blood flow: narrowed arteries reduce this
- hB content: anaemia means less oxygen delivered
- perfusion pressure: low BP reduces coronary perfusion
- coronary artery resistance: spasms or plaque raise resistance

demand:
- heart rate: faster = more oxygen needed
- contractility: stronger squeeze = more oxygen needed
- pre-load (venous return/filling): more stretch = higher workload
- after-load: higher pressure = higher oxygen use

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What does this diagram show/explain?

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What is atherosclerosis?

What is the pathophysiology?

coronary artery disease

progressive disease of arterial wall characterised by plaque formation which contains: lipid, fibrous tissue, inflammatory cells

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The heart receives blood supply from coronary arteries (mostly) during which phase of the cardiac cycle?

diastole

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What happens to diastole when HR is high? What does this mean?

when HR is high, diastole SHORTENS - less time for blood to flow so less oxygen supply to the heart muscle

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What happens when myocardial oxygen demand exceeds supply?

myocardial ischaemia -> angina or infarction

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Why does diastole shorten more than systole when HR increases?

systole has a fixed minimum duration, so higher HR reduces diastolic filling time -> less coronary perfusion

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Which layer of the heart is most vulnerable to ischaemia, and why?

subendocardium - furthest from coronary supply and under highest intraventricular pressure

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What are the three layers of the heart wall (from inside to out)?

endocardium, myocardium, epicardium

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Which layer is made of cardiac muscle and responsible for pumping?

myocardium

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Which layer forms the smooth inner lining of the heart and valves?

endocardium

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Which part of the myocardium is most vulnerable to ischaemia? Why?

subendocardium - furthest away from coronary arteries and under the highest LV pressure

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What does a subendocardial infarction look like on an ECG?

ST depression (NSTEMI)

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What does a transmural infarction look like on an ECG?

ST elevation (STEMI)

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What structure surrounds the heart and has visceral and parietal layers?

pericardium

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Which layer contains the coronary arteries?

Which layer is affected in infective endocarditis?

epicardium

endocardium (valves)

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Which local metabolites can cause vasodilation?

adenosine, K+, H+

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What is the difference between stable angina and unstable angina?

(explain in details)

STABLE ANGINA >70% OCCLUSION
- coronary artery is narrowed by an atherosclerotic plaque
- at rest blood flow may just be enough to meet oxygen demand
- during exertion increased HR and increased contractility = oxygen demand rises -> narrowed arteries cannot supply enough blood = ischaemia only on exertion
- predictable, gets better when exercise stops or with GTN

UNSTABLE ANGINA - 90% OCCLUSION
- artery is so narrowed that even at rest, oxygen supply cannot meet demand
- ISCHAEMIA AT REST
- part of ACS spectrum and can progress to NSTEMI/STEMI

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Why does stable angina cause chest pain during exertion?

during exertion increased HR and increased contractility = oxygen demand rises -> narrowed arteries cannot supply enough blood = ischaemia only on exertion

transient ischaemia causes pain

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In regards to stable angina, unstable angina and MI, answer the following:

Site
Onset
Characteristics
Radiation
Associated symptoms
Timing
Exacerbating/relieving factors
Severity

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Where is the pain typically felt in angina/MI?

central chest/retrosternal, sometimes localised to the left

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What is the onset pattern in stable angina?

gradual - brought on by exertion

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What is the onset pattern in unstable angina?

at rest (anytime)

What is the onset pattern in MI?

sudden, unprovoked

Describe the pain in an MI.

crushing, severe, heavy pressure

Where can cardiac chest pain radiate?

jaw, neck, shoulders, down the left arm

What relieves stable angina?

rest or GTN

Name three associated symptoms of angina/MI.

dyspnoea nausea sweating (palpitations, vomiting, syncope)

What do you think is the most likely diagnosis? Why?

stable angina - intermittent central chest discomfort - tight and pressure-like - mainly when climbing stairs or on exertion - resolves within 5-10 mins of rest

age: 58 year old man 20 pack year smoking history hypertension hyperlipidemia family history of CAD

According to NICE guidance, what is the most appropriate next diagnostic investigation for suspected stable angina in this patient?

CT coronary angiography

What clinical assessment would you do when suspecting stable angina? What diagnostic tests would you do?

What modifiable risk factors can be seen in Mr Addam's results?

What is the gold standard tool to diagnose stable angina? List one benefit of this.

What is the most appropriate initial management strategy?

GTN, aspirin, statin and either a beta-blocker or calcium-channel blocker

What is the 1st line management of stable angina?

optimal medical therapy - GTN - aspirin - statin - beta-blocker or calcium-channel blocker

What is the medical management of stable angina?

anti-aginal - reduce workload of heart - improve blood supply to heart - GTN for symptom relief - first line: b-blockers or CCB - second line: b-blockers + CCB secondary prevention - prevent further cardiovascular events and episodes of angina - treat modifiable factors like HTN and hyperlipidaemia - antiplatelet therapy: aspirin 75mg daily / clopidogrel if contraindicated - lipid lowering therapy: atorvastatin - ACE inhibitors/ARBs

In regards to the medical management of angina, what comes under anti-aginal?

In regards to the medical management of angina, what comes under secondary prevention?

If someone presents with angina and symptoms persists despite OMT, what must then be done/considered?

Label the image.

LM: left main coronary artery LCX: left circumflex DIAG: diagonal branch LAD: left anterior descending SPs: septal perforators OM: obtuse marginal branch

What does Acute Coronary Syndrome consist of?

unstable angina OR NSTEMI OR STEMI - all are medical emergencies

List 2 features about each of the following.

UNSTABLE ANGINA - non-occlusive thrombus - ischaemia without myocardial necrosis NSTEMI - partially occlusive thrombus - subendocardial ischaemia (partial thickness) STEMI - completely occlusive thrombus - transmural ischaemia (full thickness of ventricular wall)

What type of ACS involves a completely occlusive thrombus with transmural ischaemia?

STEMI

What type of ACS involves a partially occlusive thrombus with subendocardial ischaemia?

NSTEMI

What kind of ACS involves a non-occlusive thrombus and ischaemia with no myocardial necrosis?

unstable angina

A 70-year-old woman has central chest pain. Her ECG shows ST depression, and troponin is elevated. What does this indicate? (what kind of thrombus and what kind of ischaemia)

NSTEMI -> partially occlusive thrombus causing subendocardial ischaemia

A 62-year-old man has chest pain at rest. ECG is normal, and troponin is not elevated. What is the likely diagnosis? (what kind of thrombus and what kind of ischaemia)

unstable angina -> non-occlusive thrombus causing ischaemia without necrosis

A 55-year-old smoker has sudden severe chest pain. ECG shows ST elevation in V2–V5. What’s the diagnosis? (what kind of thrombus and what kind of ischaemia)

STEMI -> completely occlusive thrombus, causing transmural infarction

1. What type of thrombus is present in unstable angina? 2. What type of ischaemia is seen in NSTEMIs? 3. What type of ischaemia is seen in STEMIs?

1. non-occlusive thrombus 2. subendocardial (partial thickness) ischaemia 3. transmural (full wall thickness) ischaemia

What further investigations do would you want to do at this time?

ECG, FBC, trop, U&Es, lipid profile

Mr. Patel, a 58-year-old man with a history of type 2 diabetes and stable angina, presents to A&E with the sudden onset of crushing central chest pain radiating to his left arm and jaw. The pain began 45 minutes ago while he was resting and has not improved with his usual GTN spray. He is sweaty, nauseous, and mildly short of breath. On examination, his BP is 140/85 mmHg, HR 95 bpm. His ECG is shown below. What does the ECG show and what is the most appropriate immediate management for this patient?

ECG shows STEMI - dual antiplatelet therapy and arrange urgent primary PCI

Mr. Patel, a 58-year-old man with a history of type 2 diabetes and stable angina, presents to A&E with the sudden onset of crushing central chest pain radiating to his left arm and jaw. The pain began 45 minutes ago while he was resting and has not improved with his usual GTN spray. He is sweaty, nauseous, and mildly short of breath. On examination, his BP is 140/85 mmHg, HR 95 bpm. During angiography, based on the ECG, which vessel is most likely found to be occluded?

right coronary artery - ST elevation in INFERIOR leads II, III, aVF, reciprocal depression in lateral leads I and aVL (but ST elevation greater in lead III than lead II which suggest RCA, if elevation in lead II > III = LCx occlusion)

Which ECG leads show ST elevation in an inferior STEMI? Which artery usually supplies in the inferior wall of the LV?

leads II, III, aVF RCA in about 80% of people, LCx in about 20%

Which ECG clue suggests an RCA infarct rather than LCx?

ST elevation greater in lead III than lead II

Which ECG leads show ST elevation in an anterior STEMI? What artery is usually involved in an anterior STEMI?

V1-V4 - LAD

What causes the ST elevation in STEMIs?

occluded coronary artery -> no oxygen -> ATP production drops -> Na+/K+ ATPase pump fails = intracellular K+ leaks out of injury cells = raises extracellular K+ around the damaged area

List the heart area and the ECG leads for the following:

List the artery and the heart area for the following ECG leads:

List the artery and ECG leads for the following heart areas:

Mrs. Williams, a 65-year-old woman with a history of hypertension, hyperlipidaemia, and smoking (10 pack-year history), presents with central chest tightness that started 45 minutes ago, lasting 30 minutes on rest. The pain improves partially whilst in ED but recurs intermittently. On examination: BP 130/80 mmHg, HR 90 bpm. What two things could this be and what would be needed to differentiate the two?

ACS specifically NSTEMI or unstable angina - no ST elevation so not a STEMI - ST depression in leads V4-V6, aVF (lateral and inferior leads) - T wave inversion in lead aVF (isolated T wave inversion in lead III can sometimes be a normal variant) TROPONIN NEEDED to distinguish the two (elevated trop = NSTEMI)

Where is T-wave inversion normal on ECGs?

- always inverted in aVR - can be inverted in V1 and V2 - can be inverted occasionally in lead III as a normal variant

1. Is T-wave inversion in aVF normal? 2. Is T-wave inversion in lead III normal?

1. no, usually suggest pathology e.g inferior ischaemia 2. yes sometimes can be normal variant

Which feature differentiates NSTEMI from unstable angina? Which features can be present in both unstable angina and NSTEMIs?

elevated troponin = myocardial necrosis -> diagnostic of STEMI ST changes, chest pain, pain at rest, hypertension

Troponin T peaks during what hours? What needs to be ruled out if trop levels are normal?

12-48 hours post cardiovascular event acute myocardial infarction

What is troponin?

protein found in cardiac muscle which is released from damaged myocytes

What is the risk stratification tool which guides the management for ACS? What does it predict/estimate?

GRACE score (global registry of acute coronary events) estimates the risk of in-hospital and 6 month mortality

What variables are included in the GRACE score?

What would be considered a high GRACE score and what does it indicate? What would be considered a low GRACE score and what does it indicate?

LOW < 109 = mortality <2% = can be managed medically or with delayed angiography if stable HIGH > 140 = mortality >5% = early invasive strategy (angiography within 72 hours)

Mr Jones, a 72-year-old man with a history of hypertension, type 2 diabetes, and stable angina, presents to A&E with recurrent episodes of central chest tightness at rest over the past 12 hours. Each episode lasts around 10 minutes and resolves spontaneously. He reports an increasing frequency of chest pain compared with previous months. FBC: - hB normal - WCC normal - platelets normal U&Es - sodium 138 (133-146) - potassium 4.2 (3.5-5.1) - creatinine 85 (50-120) - eGFR 75 (>60ml/min) Trop: 10 (UK normal: <15 ng/L) Given his clinical history, ECG and blood results, what is the most likely diagnosis?

unstable angina - trop normal = not a STEMI or NSTEMI (yet, troponin only rises 3-6 hours after MI) - ST elevation in leads II, III, aVF - ischaemic symptoms + ECG changes + normal trop = unstable angina

What would be your immediate and long-term management of a patient with unstable angina?

secondary prevention: - ACE inhibitors and continue indefinitely - dual antiplatelet therapy: aspirin usually lifelong - beta-blockers - statin

What do statins do? What transports cholesterol around the body and to tissues? What returns excess cholesterol back to the liver?

HMG-CoA reductase inhibitors - they block the key enzyme in the liver that makes cholesterol which results in lower cholesterol production (more LDL receptors on hepatocytes -> more LDL cholesterol removed from blood) around body: LDL back to liver: HDL

1. What is the role of LDLs? 2. What is the role of HDLs? 3. What is the role of VLDL?

1. LDLs: the "bad" ones, carry cholesterol to tissues including arteries which leads to plaques 2. HDLs: the "good" ones, carry excess cholesterol and return it to the liver 3. they're made in the liver and carry endogenous triglycerides and cholesterol, they lose triglycerides via LIPOPROTEIN LIPASE then they become IDL then further into LDLs

What enzyme converts free cholesterol picked up by HDL into cholesteryl esters which then move into the core of HDL, allowing HDL to carry more cholesterol?

LCAT (lecithin-cholesterol acyltransferase)

What is the role of the enzyme LCAT (lecithin-cholesterol acyltransferase)?

What lipoproteins lose triglycerides via lipoprotein lipase and eventually become LDL?

VLDL

Statins also have pleiotropic effects, what does this mean?

As well as lowering cholesterol, statins improve endothelial function, stabilise atherosclerotic plaques, reduce inflammation and reduce thrombogenicity - this means they have what kind of effect?

means they have pleiotropic effects - they help prevent cardiovascular events beyond just lowering LDL

1. What is the heart rhythm (sinus or not, regular or not) 2. What is the heart rate? 3. Assess the P waves (is each followed by a QRS complex)? 4. Assess the PR interval 5. What is the cardiac axis? 6. Assess QRS complex 7. Assess QT interval 8. Assess ST segment 9. Assess the T waves DIAGNOSIS?

1. NOT sinus (P wave not present before each QRS complex), rhythm regular (consecutive R-R intervals) 2. 1500 divided 6 = 250 bpm (number of small squares between R-R intervals) 3. unable to assess P wave 4. unable to assess PR interval 5. lead I is positive deflection and aVF is positive deflection = normal axis (is the main deflection/bulk of QRS going upwards - above baseline or downwards - below baseline, UPWARD = positive, DOWNWARD = negative) 6. no pathological Q waves, narrow QRS, no features of LVH because height normal) 7. QT interval - normal (250-440ms for adult male, 350-460ms for women - rule of thumb is that normal QT is less than half preceding RR interval) 8. ST segment = isoelectric 9. no t or inverted T waves DIAGNOSIS: SVT

1. What else would you like to know about Maria's lifestyle? 2. What examinations would you like to conduct after taking a history from Maria?

1. does she smoke and if yes how much, alcohol intake, dietary habits, does she work out? 2. BMI, vital signs, JVP, apex beat, auscultation, look for oedema, urine dipstick

What factors regulate the movement of fluid between capillaries and tissues?

In someone with HF, why might their ankle be swollen by the evening but less so in the morning?

What does a raised JVP tell you about the pressures in someone with HF's CVS?

CVS 9 Flashcards

(86 cards)