Cardiovascular Station Assignment PDF

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Just some questions regarding the cardiovascular system that is relevant for clinical exam of the cardiovascular system....

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1. a. How to interpret ECG Basic understanding of the ECG: 1. 12 leads = 6 chest leads (V1-V6) and 6 limb leads (I, II, III, aVR, aVL, aVF) 2. Each large box represents 0.20s and there are five small boxes in each large box (each small box = 0.04s) 3. The standard 12-lead ECG is a 10-second strip. Then there must be 50 large boxes. The standard approach to interpreting an ECG: 1. Examining the rate a. The normal heart rate is 60-100 bpm. Tachycardia: HR > 100bpm. Bradycardia: HR < 60bpm. b. 1 minute = 60s = 1500 small squares (60/0.04) = 300 large squares (60/0.2) c. The rate can be calculated by counting the numbers of large squares between two consecutive R waves and dividing 300 by it. d. Another way to calculate the rate is based on the fact that the entire ECG is 10 seconds. So by counting the number of QRS complexes and multiplying by 6, the number per minute can be calculated (since 10 seconds times 6 is 60 seconds or 1 minute). 2. Examining the rhythm a. Sinus rhythm refers to the origination of electrical activity from the sinoatrial node and it is an upright P wave in lead II and biphasic P wave in lead V1. b. Heart rhythm can be regular or irregular. This can be evaluated by marking out several R-R intervals and moving them along the rhythm strip to check if subsequent intervals are similar 3. Examining the axis a. Normal heart axis is when QRS complex is upright in both lead I and lead II. b. Normal QRS axis should between -30 and +90 degrees. Left axis deviation is when it falls between -30 and -90 degrees. Right axis deviation is when it falls between +90 and +180. Indeterminate axis is between +/-180 and -90 degrees. 4. Examining everything else a. P waves – absence with irregular rhythm may suggest atrial fibrillation b. PR interval – should be between 3-5 small squares c. QRS complex d. ST segment – should be an isoelectric line e. T waves f. Extra – U waves

References: https://geekymedics.com/how-to-read-an-ecg/ https://edlaunceston.files.wordpress.com/2019/02/abc-of-clinical-ecg.pdf

1. b. ECG Findings in ST elevation MI

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The first change ECG change during STEMI is “hyper-acute T waves” which appear peaked and are related to localized hyperkalaemia 1 mm of ST elevation in 2 contiguous leads is required to diagnose STEMI

Reference: https://www.ecgmedicaltraining.com/what-is-a-stemi/ 2. ECG that suggests anterior/ anteroseptal/ inferior/ posterior/ right sided/ lateral MI Anterior MI - Worst prognosis due to larger infarct size - How to recognize on ECG: o o

ST element elevation with Q wave formation in precordial leads (V1-6) ± the high lateral leads (I and aVL) Reciprocal ST depression in the inferior leads (mainly III and aVF)

Example:

Extensive anterior MI (“tombstoning’ pattern) - Massive ST elevation with “tombstone” morphology is present throughout the precordial (V1-6) and high lateral leads (I, aVL) - Pattern is seen in proximal LAD occlusion and indicates a large territory infarction with a poor LV ejection fraction and high likelihood of cardiogenic shock and death. Reference: https://litfl.com/anterior-myocardial-infarction-ecg-library/

Anteroseptal MI Example:

Hyper-acute Anteroseptal STEMI - ST elevation is maximal in anteroseptal leads (V1-4) - Q waves are present in the septal leads (V1-2) - Some subtle ST elevation in I, aVL, and V5, with reciprocal ST depression in lead III - Hyper-acute (peaked) T waves in V2-4 Reference: https://litfl.com/anterior-myocardial-infarction-ecg-library/ Inferior MI Example:

Inferior STEMI - ST elevation in II, III and aVF. - Q-wave formation in III and aVF - Reciprocal ST depression and T wave inversion in aVL - ST elevation in lead II = lead III and absent reciprocal change in lead I (isoelectric ST segment) suggest a circumflex artery occlusion

Reference: https://litfl.com/inferior-stemi-ecg-library/ Posterior MI -

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Usually occurring in the context of an inferior or lateral infarction Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed. Posterior extension of an inferior or lateral infarct implies a much larger area of myocardial damage, with an increased risk of left ventricular dysfunction and death. How to spot: o Posterior myocardium is not directly visualised by standard 12-lead ECG, so reciprocal changes of STEMI are sought in anteroseptal leads V1-3 o Changes in V1-3 that suggests posterior MI: ▪

Horizontal ST depression

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Tall, broad R waves (>30ms)

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Upright T waves

▪ Dominant R wave (R/S ratio > 1) in V2 o Posterior infarction is confirmed by presence of ST elevation and Q waves in posterior leads (V7-9) Example: Posterior extension suggested by: - Horizontal ST depression (V1-3) - Tall, broad R waves (V2-3) - Dominant R wave (V2) - Upright T waves (V2-3)

Posterior leads recorded: Marked ST elevation in V7-9 with Q-wave formation confirms the involvement of posterior wall, making this and inferior-lateral-posterior STEMI

Reference: https://litfl.com/posterior-myocardial-infarction-ecg-library/

Right sided MI -

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Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon. o Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents. o Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated. How to spot: o In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of: ▪ ST elevation in V1 – the only standard ECG lead that looks directly at the right ventricle. ▪ ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle. o Right ventricular infarction is confirmed by the presence of ST elevation in the right-sided leads (V3R-V6R)

Example:

Right ventricular MI - There is an inferior STEMI with ST elevation in lead III > lead II. - There is subtle ST elevation in V1 with ST depression in V2. - There is ST elevation in V4R. Reference: https://litfl.com/right-ventricular-infarction-ecg-library/

Lateral MI -

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The lateral wall of the LV is supplied by branches of the left anterior descending (LAD) and left circumflex arteries. Infarction of the lateral wall usually occurs as part of a larger territory infarction, e.g. anterolateral STEMI. Isolated lateral STEMI is less common, but may be produced by occlusion of smaller branch arteries that supply the lateral wall, e.g. the first diagonal branch (D1) of the LAD, the obtuse marginal branch (OM) of the left circumflex arteries, or the ramus intermedius. Lateral STEMI is a stand-alone indication for emergent reperfusion. Lateral extension of an anterior, inferior or posterior MI indicates a larger territory of myocardium at risk with consequent worse prognosis. How to spot: o ST elevation in the lateral leads (I, aVL, V5-6). o Reciprocal ST depression in the inferior leads (III and aVF). o ST elevation primarily localised to leads I and aVL is referred to as a high lateral STEMI.

Example:

High Lateral STEMI - ST elevation is present in the high lateral leads (I and aVL). - There is also subtle ST elevation with hyper-acute T waves in V5-6. - There is reciprocal ST depression in the inferior leads (III and aVF) with associated ST depression in V1-3 (which could represent anterior ischaemia or reciprocal change). - This pattern is consistent with an acute infarction localised to the superior portion of the lateral wall of the left ventricle (high lateral STEMI). - The culprit vessel in this case was an occluded first diagonal branch of the LAD. Reference: https://litfl.com/lateral-stemi-ecg-library/

3. What cardiac enzymes to be sent at different point of time ● Usual scenario o Troponin (I or T) – elevated (positive) within a few hours of heart damage and remains elevated for up to two weeks. ● Patient recovering from MI and coming again with MI o CK-MB – increased CK-MB can usually be detected in someone with a heart attack about 3-6 hours after the onset of chest pain. The level of CK-MB peaks in 12-24 hours and then returns to normal within about 48-72 hours. If there is a second heart attack or ongoing damage, then levels may rise again and/or stay elevated longer. Reference: https://labtestsonline.org/tests/cardiac-biomarkers 4. When does each cardiac enzyme elevate, peak, disappear?

Enzymes CK-MB Troponin I Troponin T Myoglobin LDH AST

Initial rise 3-8h 3-8h 3-8h 1-3h 8-12h 6-12h

References: https://path.upmc.edu/cases/case735/dx.html https://www.ncbi.nlm.nih.gov/books/NBK545216/

Peak 10-24h 24-48h 72-100h 6-9h 72-144h 24-48h

Back to normal 2-3 days 3-5 days 5-10 days 1 day 8-14 days 4-6 days

5. Normal CXR Findings Rotation – Medial aspect of each clavicle should be equidistant from the spinous processes. The spinous processes should also be in vertically orientated against the vertebral bodies Inspiration – The 5-6 anterior ribs, lung apices, both costophrenic angles, and the lateral rib edges should be visible. Projection – If the scapulae are not projected within the chest, it’s PA. Exposure: The left hemidiaphragm should be visible to the spine and the vertebrae should be visible behind the heart ABCD approach: - Airway: trachea, carina, bronchi, hilar structures o Trachea should be normally located centrally with slight deviation to the right as it crosses the aortic arch. o The carina where trachea divides into left and right main bronchus should be clearly visible. The right main bronchus is generally wider, shorter and more vertical than the left main bronchus. o The hilar should be the same size, level with the T6–7 intervertebral space on either side of the mediastinum, The left hilum is often positioned slightly higher than the right. - Breathing: lungs and pleura o Lung fields should be equally translucent. Air on x-ray looks dark, healthy lungs should look quite dark to indicate a clear and healthy lungs. - Cardiac: heart size and borders o The heart should lie predominantly in the left hemithorax (right in the case of dextrocardia). Positioned with one-third of its diameter to the right and two-thirds to the left of the thoracic vertebrae spinous processes. o The width of the heart (cardiac shadow) should appear less than 50% of the diameter of the chest (thoracic width). - Diaphragm: including assessment of costophrenic angles o The right hemidiaphragm is higher than the left (due to liver). The diaphragm should be indistinguishable from the underlying liver. o The costophrenic angles should be clearly visible as a well-defined acute angle. References: https://geekymedics.com/chest-x-ray-interpretation-a-methodical-approach/ https://www.kenhub.com/en/library/anatomy/normal-chest-x-ray https://litfl.com/abc-of-cxr-interpretation/

6. Cardiac failure / Acute pulmonary edema CXR Findings Cardiac failure ● Chest x-ray findings include pleural effusions, cardiomegaly. Kerley B lines (horizontal lines in the periphery of the lower posterior lung fields, upper lobe pulmonary venous congestion, and interstitial edema. ฀ A – Alveolar edema (bat wing opacities) ฀ B – Kerley B lines ฀ C – Cardiomegaly ฀ D – Dilated upper lobe vessels ฀ E – Pleural effusion. Bat wing opacities: bilateral perihilar opacities due to alveolar edema

Kerley B lines: fluid leakage into peripheral interlobular septa due to interstitial edema

Dilated upper lobe vessels

References: https://radiopaedia.org/articles/heart-failure-summary?lang=gb#nav_radiographic-features

https://radiologyassistant.nl/chest/chest-x-ray/heart-failure Acute pulmonary edema ● Upper lobe pulmonary venous diversion (stag's antler sign) ● Increased cardiothoracic ratio/cardiac silhouette size: useful for assessing for an underlying cardiogenic cause or association ● Features of pulmonary interstitial edema: i. Peri-bronchial cuffing and perihilar haze ii. Septal (Kerley) lines iii. Thickening of interlobar fissures ● Features of pulmonary alveolar edema: i. air space opacification classically in a batwing distribution ii. may have air bronchograms ● Pleural effusions and fluid in interlobar fissures (including 'vanishing' pulmonary pseudo-tumor)

References: https://radiopaedia.org/articles/pulmonary-oedema https://www.emnote.org/emnotes/cxr-of-chf-with-pulmonary-edema

7. How to differentiate characteristic of different chest pain Questions to help differentiate chest pain: - Cause (any past cardiac problems or other medical history etc.) - Onset of pain (intermittent, continuous etc.) - Characteristic of pain (sharp, dull, heavy, tight etc.) - Location of pain (any radiation to jaw, shoulder, throat etc.) - Associated symptoms (sweating, nausea, vomiting, dyspnea etc.) - Aggravating factors (on exertion or provoked by posture etc.) - Relieving factors (relieved by nitrates or rest etc.) Causes of chest pain and typical features Pain Causes Cardiac pain Myocardial ischemia or infarction Vascular pain Aortic dissection Pleuro-pericardial Pericarditis, myocarditis pain Infective pleurisy Pneumothorax Pneumonia Autoimmune disease Mesothelioma Metastatic tumor Chest wall pain Persistent cough Muscular strains Intercostal myositis Thoracic zoster Coxsackie B virus infection Thoracic nerve compression Rib fracture Rib tumor Tietze’s syndrome Gastrointestinal Gastro-esophageal reflux pain Diffuse esophageal spasm Airway pain Tracheitis Central bronchial carcinoma Inhaled foreign body Central pain Panic attacks Mediastinal pain

Mediastinitis Lymphoma

Typical features Central, tight or heavy; may radiate to jaw or left arm Very sudden onset, radiates to the back Pleuritic pain, worse when lying down Pleuritic pain Sudden onset, sharp, a/w dyspnea Often pleuritic, a/w fever and dyspnea Pleuritic pain Severe and constant Severe and constant, localized Worse with movement, chest wall tender Worse with movement, chest wall tender Sharp, localized, worse with movement Severe, follows nerve root distribution, rash Pleuritic pain Follows nerve root distribution History of trauma, localized tenderness Constant, severe, localized Costal cartilage tender Worse when patient lies down – common Relieved by swallowing (eg. warm water) Pain in throat, breathing painful

Often preceded by anxiety, a/w breathlessness and hyperventilation

Differential diagnosis of chest pain Favors angina Favors pericarditis or pleurisy Tight or heavy Onset predictable with exertion Relieved by rest Relieved by nitrates

Sharp or stabbing Not exertional Present at rest Unaffected by nitrates

Not positional

Worse supine (pericarditis)

Unaffected by respiration

Worse with respiration

Differential diagnosis of chest pain Favors myocardial infarction (acute coronary syndrome) Onset at rest Severe pain Sweating Anxiety No relief with nitrates Associated symptoms (nausea, vomiting) Favors myocardial infarction Central chest pain Subacute onset (minutes) Severe pain Favors myocardial ischemia Exertional Occurs with exertion Brief episodes Diffuse No chest wall tenderness Reference: Talley and O’Connor’s Clinical Examination

Favors esophageal reflux pain Burning Not exertional Present at rest Unaffected unless spasm Onset may be when supine Unaffected by respiration

Favors angina Onset with exertion Moderate pain or discomfort No sweating Mild or no anxiety Rapid relief with nitrates Associated symptoms absent Favors aortic dissection Radiates to back Instantaneous onset Very severe pain, tearing quality Favors chest wall pain Positional Often worse at rest Prolonged Localized Chest wall tenderness...