CARDIOVASCULAR Flashcards

Question

What is a *Silent MI*? What % of patients present with it, and it what populations is it most common?

Answer 1

MI without chest pain 30% of case of MI present without chest pain. This is particularly important in: * Women * Those with diabetes * The elderly

Answer 2

Other symptoms associated with a silent MI include: Syncope Pulmonary oedema Epigastric pain Vomiting Acute confusional state Stroke Diabetic hyperglycaemia Significant historical features include: Shortness of breath – especially if on exertion (“SOBOE”) Generalised weakness Dizziness ***CHECK IF PATIENT HAS HAD CHEST PAIN IN THE LAST 12 HOURS, IF THEY ARE NOT HAVING CHEST PAIN NOW***

Answer 3

Pallor - due to sympathetic activity Sweating Tachycardia High or low blood pressure **Heart Murmurs** eg systolic murmur in Mitral regurg **S4 heart sound - due to impaired left ventricle diastole** Signs of Pulmonary Oedema Palpitations Raised Troponin ECG abnormalities

Answer 4

ECG, as soon as possible Blood Troponin Levels FBC, Blood glucose, Count Platelets -(due to Thrombocytopaenia, (low blood platelets) potentially occurring Chest x-ray to look at other causes of central chest pain Do a cardiac examination for Pulse BP JVP Murmurs

Answer 5

Measure High sensitivity cardiac troponin with **1 hour**. there will be no dynamic rise above the 99th percentile in patients with unstable angina

Answer 6

Troponin values <14ng/l normal = no MI, 14-30 ng/l = possible MI, >30ng/l = definite MI

Answer 7

**An absence** of ST elevation **typically no ECG changes** ST depression (indicates a worse prognosis), transient ST elevation, and T-wave changes may be seen May also be Normal!!! **can be similar to NSTEMI** Gold standard test used to diagnose this condition - Angiography

Answer 8

**An absence** of ST elevation T-wave inversion Hyper-acute T waves **ST depression** May also be Normal!!! **Same as unstable angina** Distinguish with High Sensitivity cardiac troponin testing. Will be elevated in NSTEMI *picture source unknown*

Answer 9

Measure Troponin **twice, 2 hours apart, with in 3 HOURS of onset of chest pain** A single negative troponin test is acceptable as a ‘rule out’ (for ACS) if it is >3 hours since the onset of pain - aka Unstable angina A positive test is defined as an increase in troponin between the two tests. - On average, and **20% rise is accepted for a diagnosis of NSTEMI** In MIs , you expect Troponin levels **to rise** In other conditions that can raise troponin, the troponin levels won't change much as the issue is ongoing ***Peoples troponin levels vary, so look at change in level other level itself***

Answer 10

Causes include: Renal failure Myocarditis PE Pericarditis Heart failure Arrhythmia

Answer 11

Peaked T wave (very tall T wave) **Raised ST-segment** - this can return to normal within a few hours Signs of a **New LBBB** ---> M shaped waves in V6 - LBBB - become and change shape (wiLLiaM) For any patient with new onset chest pain and LBBB on ECG you need to compare to an old ECG to see if the LBBB is new. If none is available, consider STEMI until proven otherwise. *taken from osmosis*

Answer 12

a) Inverted T waves – this may or may not persist ST segment returns to normal. **Raised ST segments may persist if a left ventricular aneurysm develops** b) Pathological Q waves form – these may resolve in 10% of cases **Q wave is pathological if it is >25% of the height of the R wave**, and/or it is **greater than 1small square** in width, and/or greater than 2 square squares in height Q waves are also a sign of a previous MI – the changes in Q waves are generally permanent *picture credit - unknown*

Answer 13

Cardiac * Angina * Pericarditis * Myocarditis * Aortic dissection Pulmonary * PE * Pneumothorax * Anything that causes pleuritic chest pain Oesophageal * Oesophageal reflux * Oesophageal spasm * Tumour * Oesophagitis Any of the other 2 conditions in ACS *Taken from almostadoctor*

Answer 14

MONA Morphine - For pain relief Oxygen - **ONLY IF SATS ARE LESS THAN 94%** - *don't need to give it if not!* Nitrates (GTN SPRAY) - typically fondaparinux in Sheffield - **A GTN, Glyceryl Trinitrate** Aspirin 300mg chewed to increase absorption Urgent ECG, IV access, Take history

Answer 15

Nitrates like GTNs decrease amount of oxygen being used by heart. ==> Helps to reduce the workload on heart, prevents further damage to heart muscle. Also help to open up the blood vessels, increasing blood flow to the heart **BUT don’t give with systolic BP <90, or with a HR <50, or left ventricular heart failure** As they lower blood pressure -

Answer 16

Refer to cardiology urgently First line, definitive **Percutaneous Coronary Intervention** - ***only suitable if done within 2 HOURS OF ONSET*** If PCI/angioplasty is not Available/over 2 hours - **give Fibrinolysis with IV Tenecteplase** - **Aspirin**, ***AND*** a **PY12 inhibitor**, eg clopidogrel/ticagrelor Give Heparin (anticoagulant) Give Glycoprotien IIb inhibitor *Do not give anticoagulant therapy if the patient is likely to be eligible for primary PCI.* *BUT – DONT GIVE FIBRINOLYSIS/THROMBOLYSIS TO THOSE WITHOUT ST ELEVATION*

Answer 17

Only offer a PCI if the patient is presenting within 12 hours on symptoms onset, and the PCI can be delivered within 120 mins Can consider it if presneting more tahn 12 hours after symptoms if still continuing with myocardial ischaemmia or cardiogenic shock

Answer 18

You need to get urgent input from seniors to arrange immediate **invasive coronary angiography** (with the intent to perform revascularisation) for any patient who has suspected NSTEMI and is clinically unstable - *it looks at the vessels of the heart with a dye* Do not wait for the results of troponin testing. Thrombolysis is NOT INDICATED for NSTEMI

Answer 19

Suspected NSTEMI and Clinically unstable - This includes any patient with: **Ongoing or recurrent pain despite treatment** Haemodynamic instability (low blood pressure or shock); see our topic Shock Dynamic ECG changes Left ventricular failure **A life-threatening arrhythmia (ventricular tachycardia or ventricular fibrillation)**

Answer 20

The urgent use of PCI (Percutaneous Coronary intervention) known as angioplasty blood vessel open. A balloon tipped catheter is entered into the body, normally in femoral or radial artery A guiding catheter is passed up the coronary artery, so radiopaque iodine based dye can be passed through the coronary arteries so they can be viewed on x-ray A balloon tipped catheter is placed and inflated in the right place and usually a stent in placed in the artery and is expanded by the pressure of the inflating balloon

Answer 21

PCSK9 attaches itself to the LDL receptor (LDLR) found on liver and other cellular membranes and causes it to break down, preventing it from receiving LDL particles from outside of the cell and reducing the amount of LDL particles in circulation.

Answer 22

They are monoclonal antibodies that inhibit PCSK9 protein in the liver which leads to improved clearance of cholesterol from the blood. Therefore used to treat Hypercholesterolaemia

Answer 23

The second line treatment for STEMI Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. *From zerotofinals*

Answer 24

GRACE SCORE This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI: <5% Low Risk 5-10% Medium Risk >10% High Risk If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease. *Taken from zerotofinals*

Answer 25

* If the history is convincing, but the investigations are normal, consider unstable angina * Consider a risk score – **such as the HEART score** to help you decide whether or not to discharge home, or refer to cardiology for admission Patients should **undergo ECG stress testing (‘treadmill test’)**

Answer 26

Clopidogrel or equivalent - STOP PLATELET ACTIVAATION Beta Blocker or ACE inhibitor or Angiotensin II receptor antagonist Statins Monitor Blood Glucose in Diabetic Patients

Answer 27

Exercise, Smoking cessation Reduction in weight Reduction in alcohol intake Dietary modifications - eg High in oily fish, fibre, fresh fruit and veg, Low in Saturated fat Also don't fly for 2 months, no sex for a month

Answer 28

COBRA-A C – Clopidogrel – antiplatelets O – Omacar – Omega 3 B – Bisoprolol – β-blocker R – Ramipril – ACE-i A – Aspirin A – Atorvastatin – very potent statin!

Answer 29

DREAD: Death, Rupture of septum or papillary muscles (which could lead to ischaemic MR), oEdema (Heart failure), Arrhythmia and Aneurysm, Dressler’s syndrome.

Answer 30

30% out of hospital 15% in hospital

Answer 31

Diuretics, ACEI, beta blocker, aldosterone antagonist (spironolactone, epleronone

Answer 32

beta blocker, nitrates, calcium antagonist

Answer 33

Cardiac Myxoma - have a bias towards the atria. Often harmless, but can be very bad if they block the mitral valve.

Answer 34

Inflammation of the Pericardium It is characterised clinically by a triad of **chest pain, pericardial friction rub, and serial ECG changes**.

Answer 35

1. Fibrous Pericardium - This is the outermost layer and is composed of dense connective tissue. 2. Parietal Pericardium - This is the middle layer and is composed of serous membrane. 3. Visceral Pericardium/Epidcardium - This is the innermost layer and is composed of serous membrane. It is also known as the epicardium. The fluid is located between the Parietal and Visceral Pericardium layers.

Answer 36

* Fixes the heart in the mediastinum and limits its motion * Prevents overfilling of heart, inextensible fibrous layer prevents the heart from increasing in size too rapidly * Lubrication from the thin film of fluid between the two layers of serous pericardium reduces friction generated by the heart as it moves Protection from infection – the fibrous pericardium serves as a physical barrier between the muscular body of the heart and adjacent organs prone to infection e.g. the lungs

Answer 37

Acute pericarditis is more common in adults (typically between 20 to 50 years old) and in men. In the UK, pericarditis is most commonly secondary to viral infection or MI

Answer 38

Viral Infection Acute MI Dressler's Syndrome Autoimmune Conditions - **Rheumatoid arthirits, SLE** Trauma/Surgery Bacterial infections - Malignancy Metabolic disorders (uraemia)

Answer 39

Streptococcus viridans is the commonest cause in patients from developing countries with an absence of other specific risk factors. *alpha haemolytic* Staph. epidermidis is a more likely causative organism of infective endocarditis if the patient has prosthetic valves -*coagulase negative* Staph. aureus is now the commonest cause in the developed world and is particularly likely if the patient is an intravenous drug user as is the case in this scenario. - *coagulase positive*

Answer 40

coxsackie B virus, influenza, adenovirus and echovirus * HIV – these patient may get **staphylococcal** pericarditis – which is often fatal

Answer 41

**Post MI Pericarditis** - occurs in about 20% of MI patients, most commonly with *anterior MI and MIs with Massive ST elevation - (But reduced in Thrombolysis)* **Dressler's Syndrome** - Pericarditis secondary to myocardial/pericardial damage, an autoimmune reaction by the body to damage Myocardium from a MI *(Antimyocardial antibodies are often found. Can occur anytime from few weeks to 2 years from an MI)*

Answer 42

male sex age 20 to 50 years transmural myocardial infarction *A heart attack that affects the entire thickness of heart wall* cardiac surgery neoplasm viral and bacterial infections systemic autoimmune disorders

Answer 43

* Central chest pain ○ Severe ○ Worsened on deepened breathing ○ Sharp and **pleuritic** (without constricting crushing character of ischaemic pain) ○ Releived by leaning forwards and sitting up * Dyspnoea * Hiccups – phrenic involvement * Fever

Answer 44

**Bear in mind there is no specific diagnostic test.** Diagnoses should be based **on clinical history** – e.g. recent viral infection (+/- absence of risk factors for cardiovascular disease) - Listen to chest - look for **Pericardial friction Rub** **ECG** **FBC** – there may be leukocytosis or lymphocytosis due to viral or bacterial infection **Echocardiogram** - best **CXR**

Answer 45

**High pitched superficial scratching or crunching sound** produced by movement of the pericardium. *It is diagnostic for pericarditis.* Usually heard in systole but may also be heard in diastole. * It is classically heard in three, or two (‘to and fro’ rub) phases – i.e. this means it is heard 3 times or twice during one cardiac cycle * The rubs are **typically heard best with the diaphragm at the left lower sternal edge at full expiration**

Answer 46

**Saddled ST elevation** - distributed in both inferior and anterior leads – thus this helps to distinguish it from MI **PR depression** *If both of these are present it is diagnostic of pericarditis*

Answer 47

Treat the underlying cause! **Colchicine** - inhibits migrations of neutrophils to site of inflammation to reduce risk of occurrence * 500mcg BD for 3 months * PLUS *Oral NSAID’s * Ibuprofen or Aspirin * Do not use NSAID’s in the first few days after MI – as they associated with increased risk of myocardial rupture

Answer 48

* Pericardial effusion – Accumulation of fluid in the pericardial sac * Cardiac tamponade – When there is enough pericardial effusion in the pericardium that it restricts diastolic ventricular filling (ability for heart to expand) and causes reduced BP and CO * Chronic constrictive pericarditis – persistent inflammation of acute pericarditis causes the heart to be encased with a **rigid fibrotic pericardial sac** which prevents adequate diastolic filling of the ventricles

Answer 49

In-between the two layers of serous pericardium, (Parietal and Visceral) where there is lubricating fluid - here there is **potential space** *Pericardial effusion is when the potential space of the pericardial cavity fills with fluid. This creates an inward pressure on the heart, making it more difficult to expand during diastole*

Answer 50

**Increased venous pressure** - so drainage from pericardial cavity is reduced -*seen in Congestive heart failure/Pulmonary hypertension* **Exudative effusions** - seen in inflammatory processes, such as in the causes of **pericarditis**

Answer 51

a) Cardiac Tamponade b) **THINK - FULLNESS IN CHEST, COMPRESSING LOCAL STRUCTURES** aka Chest pain Shortness of breath A feeling of fullness in the chest Orthopnoea (shortness of breath on lying flat) Phrenic nerve compression - Hiccups Recurrent laryngeal nerve compression - hoarse voice Osesphagus compression - Dysphagia

Answer 52

Quiet heart sounds **Pulsus paradoxus** (an abnormally large fall in blood pressure during inspiration, notably when palpating the pulse) Hypotension Raised JVP Fever (with pericarditis) Pericardial rub (with pericarditis)

Answer 53

CXR – large heart ECG – low voltage QRS complexes and sinus tachycardia Echocardiogram

Answer 54

Treatment of the underlying cause (e.g., infection) Drainage of the effusion (where required) *eg Needle pericardiocentesis (echocardiogram guided), Surgical drainage* Treat the pericarditis if necessary Management: Most pericardial effusions resolve spontaneously If effusion recurs, **excision of pericardial segment allows fluid to be absorbed through plural and mediastinal lymphatics**

Answer 55

Cardiac Tamponade is a condition where the heart become compressed by excess fluid in the pericardium. Compression causes reduced diastolic filling of the heart, which can cause cardiac arrest. *taken from almost a doctor*

Answer 56

**Traumatic injury** – particularly penetrating injury – can lead to accumulation of blood in the pericardial sac. *In trauma emergency setting it is life threatening* **Pericarditis, pericardial effusion** **Cancer** Iatrogenic - occur after cardiothoracic surgery

Answer 57

Becks Triad – occurs in about 1/3 of patients with cardiac tamponade Hypotension Distended Neck Veins Muffled Heart Sounds *Taken from almostadoctor*

Answer 58

Dyspnoea Elevated Jugular Venous pressure Distant heart sounds Tachycardia Hypotension Reduced exercise tolerance **Pulsus Paradoxus** ***-Pulse fades/systolic BP decreases >10mmHg on inspiration***

Answer 59

a) anti-inflammatory treatment plus gastroprotection plus observation b) emergency pericardiocentesis c) effusion recurs, excision of pericardial segment allows fluid to be absorbed through plural and mediastinal lymphatics

Answer 60

Where a needed is inserted into the pericardium and fluid is drawn out. The most common approach for pericardiocentesis is between the **xiphoid and the left costal margin.** Initially, the needle is inserted at a 15-degree angle to pass under the costal margin. The needle is then lowered to a plane parallel with the chest and slowly advanced towards the tip of the left scapular, **while aspirating** *taken from bmjbestpractise*

Answer 61

Infection of the heart valves and/or other endocardial structures within the heart e.g. septal defects, pacemaker leads, surgical patches etc. **Can increase the risk of embolism!!**

Answer 62

In the past was most commonly seen in children with Rheumatic heart disease - *Autoimmune condition, where body attacks heart* Nowadays, seen in ○ The elderly (in an ageing population) ○ IV drug abusers (IVDU) ○ Children with congenital heart disease ○ Anyone with prosthetic heart valves or pacemakers ○ Those with bad dental hygiene More common in males **Fever + new murmur = endocarditis until proven otherwise. Any fever lasting >1wk in those known to be at risk must prompt blood cultures.**

Answer 63

Developing world/Dentist - Viridins group strep Surgery/Proestetic valve - Stap Epidermis Developed world/IVDU - Staph Aureus - most common ***Candida (Fungal)*** - infected long lines / hickman lines in patient with immunocompromise - **also for new valves** More rarely, **pseudomonas, pneumococcus, aspergillus** - patients with immunocompromise

Answer 64

a) Staph Aureus b) Coagulase negative stapylococci (eg staph Epidermidis c) **α-haemolytic streptococci, (Strep viridans)**

Answer 65

* Previous Rheumatic heart disease (rare in the western world) * Age related valvular degeneration * Prosthetic valve (both mechanical and bioprostheses) IV drug use **Fever + new murmur = endocarditis until proven otherwise. Any fever lasting >1wk in those known to be at risk must prompt blood cultures.**

Answer 66

The tricuspid valve is the first heart valve to be encountered after blood has returned from the systemic circulation, so bacterial seeding is most common here – the tricuspid is the primary effected valve in ~50% of patients, with the mitral and aortic being less common (both at ~20%), although there is often a mixed picture.

Answer 67

The damage of the endocardium leads to thrombi formation, made of platelets and fibrin, it often causes in areas of high haedynamic pressure where there are shearing forces - **aka around valves** **Bacteria are able to colonise** the thrombi, creating a **Vegetation** leading to Infective endocarditis. These infected thrombi can become large enough to form an obstruction, or they may also break off to form emboli. This emboli can go to affect **CNS, lungs, spleen, kidney** **Fever + new murmur = endocarditis until proven otherwise. Any fever lasting >1wk in those known to be at risk must prompt blood cultures.**

Answer 68

Depends on site where embolism is affecting, so potentially could have - Stroke, PE, Kidney dysfunction Valve dysfunction, new murmurs General septic signs, like Fever, sweating, malaise, Rigors, splenomegaly, clubbing A INR that has shot up *international normalised ratio, measure of blood clotting time)*

Answer 69

a) Janeways lesions small, painless, red-brown lesions that appear on the palms of the hands and soles of the feet. b)Roth spot - Roth spots are red-centered retinal hemorrhages, usually found in the peripheral retina. c) Osler's Nodes - small, tender, raised bumps on the hands and feet. d) Splinter haemorrhages are tiny linear or needle-like streaks of blood that can be seen under the fingernails or toenails **Taken from Prof Chico IE Lecture, 2023**

Answer 70

- how you diagnose Infective Endocarditis - has two criteria, major and minor Major (2) - Pathogen grown from 2 separate blood cultures -Evidence of endocarditis on echo, or new valve leak Minor (5) a) Predisposition ie **Cardiac lesion, IVDU** b) Positive blood cultures that don’t meet major criteria c) **Fever** d) Immune phenomena - **glomerulonephritis**, Roth spot ,Osler’s nodes e) Vascular phenomena - aka major arterial emboli, septic pulmonary infarcts, conjunctival/intracranial haemorrhages, **Janeway lesions** **PPFIV** Definite IE 2 majors, or 1 major and 3 minors, or all 5 minors Possible IE 1 major and 1 minor 3 minor

Answer 71

**Transoesophageal Echo (TOE) - DIAGNOSTIC** ○ Generally safe but risk of perforation or aspiration ○ Easiest if ventilated (but never ventilate just for TOE) * Transthoracic echo (TTE), safer, but lower sensitivity * ECG *Urinalysis *FBC - look for elevated leukocytes, or elevated CRP (C Reactive protein), Increased INR * CXR – cardiomegaly * Blood cultures - **take 3 cultures, from 3 different sites, at different times**

Answer 72

Antimicrobials!! Treat complications, *aka arrhythmias, Heart failure, heart block, stroke* Surgery - if can't be cured with anbtx, there are complications, to remove **infected devices, or replace valves** Also can use surgery to remove large vegetations before they embolise

Answer 73

Acute presentation – flucloxacillin, gentamycin Subacute presentation – benzylpenicillin, gentamycin Prosethetic valve / resistant organism – triple therapy of vancomycin, gentamycin and rifampicin In cases of penicillin allergy, then vancomycin (a glycopeptide – other example is teicoplanin) is the usual substitute. **Fever + new murmur = endocarditis until proven otherwise. Any fever lasting >1wk in those known to be at risk must prompt blood cultures.**

Answer 74

Staphs—native valve: **flucloxacillin** - If allergic or MRSA: **vancomycin + rifampicin.** Staphs—prosthetic valves: **flucloxacillin + rifampicin + gentamicin**

Answer 75

* Streps—fully sensitive to penicillin: benzylpenicillin, or if less sensitive: **benzylpenicillin + gentamicin** * Enterococci: **amoxicillin + gentamicin,** if penicillin allergic = **vancomycin + gentamicin**

Answer 76

When the heart can't supply enough blood to meet the body's demands Either by systolic Heart failure, where **heart’s ventricles can’t pump blood hard enough during systole** (not squeezing enough( or by Diastolic heart failure, where **or not enough blood fills the ventricles during diastole** (not filling enough) (reduced preload)

Answer 77

Blood backs up into the lungs, causing congestion or fluid build-up, which is why it’s also often known as congestive heart failure, or just CHF.

Answer 78

Ejection fraction <40% (SV/EDV) Caused by IHD MI Hypertension Cardiomyopathy

Answer 79

Inability to relax and fill There is **reduced preload because there is abnormal filling of the LV** Ejection fraction >50% Caused by Constrictive pericarditis Cardiac tamponade Hypertension

Answer 80

50-70% of blood in the ventricles being pumped out the heart in ventricular systole. 40% or under would indicate systolic heart failure *40% (SV/EDV)*

Answer 81

Biventricular heart failiure

Answer 82

Often by systolic HF, as damage to the myocardium means heart can't contract as forcefully and pumped blood as efficiently Ischemic heart disease caused by **coronary artery atherosclerosis, or plaque buildup**, is the most common cause. In this case, less blood and oxygen gets through the coronary artery to the heart tissue, which damages the myocardium. *===> In severe cases MI lead to scar tissue, which would also lead to this*

Answer 83

Because systemic hypertension makes it harder for the left ventricle to pump blood out into that systemic circulation. To compensate, the left ventricle **goes under hypertrophy** so that the ventricle can contract with more force. The increase in muscle mass means that ***there is a greater demand for oxygen*** and, to make things even worse, the ***coronaries get squeezed down by the this extra muscle so that even less blood’s delivered to the tissue.*** **Leads to more demand and reduced supply** means that some of the ventricular muscle starts have weaker contractions—leading to systolic failure. *taken from osmosis video*

Answer 84

Signs: Cardiomegaly (displaced apex beat) Pulmonary Oedema 3rd and 4th heart sounds Pleural effusion Crepitations in lung bases Tachycardia Reduced BP Cool peripheries Heart murmur

Answer 85

Left sided heart failure Cardiomyopathy is a chronic disease of the heart muscle which **causes the heart to become weak and enlarged., as it attempts to increase preload and stroke volume via Frank-starling law** This can lead to heart failure, where the heart is unable to effectively pump enough blood to meet the body's needs.

Answer 86

The hypertrophy that is created by hypertension is concentric, which means that the new sarcomeres are generated in parallel with existing ones. This means that heart muscle **encroaches on the ventricular chamber space, resulting in less room for blood** in there -> *Can't fill up as much* ==> Therefore contributes to systolic but can also cause diastolic heart failure

Answer 87

Group of disease of myocardium that affect mechanical or electrical function of heart

Answer 88

Hypertrophic cardiomyopathy *(can be caused by hypertension, see card on it)* Dilated cardiomyopathy Arrhythmogenic Cardiomyopathy Restrictive cardiomyopathy

Answer 89

Walls either normal or thin 🡪 weak contraction 🡪 less pumped out 🡪 biventricular congestive HF

Answer 90

**Desmosome gene mutations** Lead to arrhyhmias Arrhythmogenic cardiomyopathy (ARVC/ALVC) – Arrhythmia main feature of arrhythmogenic cardiomyopathy

Answer 91

Restrictive physiology – ventricles stiffer and less compliant 🡪 less CO 🡪 HF

Answer 92

decreases blood flow to the kidneys, activates the renin-angiotensin-aldosterone system, ultimately causing fluid retention. Which fills the heart a bit more during diastole and increases preload, which increases contraction strength again by the Frank Starling mechanism. **leads to fluid retention, aka oedema**

Answer 93

LSHF leads to increased pulmonary blood pressure, due to fluid build up. increased pulmonary blood pressure makes it harder for the right side to pump blood into. In this case the heart failure would be biventricular, since both ventricles are affected.

Answer 94

Hypertension Pulmonary stenosis Lung disease (cor pulmonale) Atrial/ventricular septal defects

Answer 95

It allows blood to flow from the higher-pressure left side to the lower-pressure right side, which **increases fluid volume on the right side** Eventually leads to concentric hypertrophy of the right ventricle, making it more prone to ischemia— *(Systolic Failure)* ....and have a smaller volume and become less compliant - *(Diastolic failure)*

Answer 96

Right sided heart failure caused by chronic arterial pulmonary hypertension, due to lung diseases, Pulmonary vascular disorders, neuromuscular and skeletal diseases

Answer 97

Hypoxia due to the disease causes Pulmonary arterioles constrict 🡪 increase pulmonary BP 🡪 harder for RV to pump against 🡪 hypertrophy and failure

Answer 98

a) - the lungs b) the systemic veins - leading to **Systemic vein congestion** - *think raised JVP

Answer 99

Blood back up into jugular vein Raised JVP, – JVP distension - b) leads to Hepatomegaly and Splenomegaly *(Hepatosplenomegaly)*- In extreme cases and lead to cirrhosis of liver, known as cardiac cirrhosis c) Fluid build up in peritoneum leads to **Ascites** and weight gain d) leads to **Pitting oedema** – sacral/leg oedema in bed-bound patients which causes a “pit” when pressed

Answer 100

Raised JVP – JVP distension Hepatomegaly/Splenomegaly Pitting oedema – sacral/leg oedema in bed-bound patients which causes a “pit” when pressed Ascites Weight gain (fluid)

Answer 101

paroxysmal nocturnal dyspnoea orthopnoea Exertional dyspnoea

Answer 102

shortness of breath (and must say specifically at least one of; paroxysmal nocturnal dyspnoea, orthopnoea), Ankle swelling, Fatigue

Answer 103

Exertional dyspnoea Fatigue Weight loss **Paroxysmal nocturnal dyspnoea** – attacks of severe SOB and coughing at night Nocturnal cough – pink, frothy sputum **Orthopnoea** – dyspnoea (SOB) that occurs when lying down

Answer 104

*think about what it backs up into! (left side backs up into lungs)* Cardiomegaly (displaced apex beat) Pulmonary Oedema **3rd and 4th heart sounds** Pleural effusion Crepitations in lung bases Tachycardia Reduced BP Cool peripheries Heart murmur

Answer 105

ECG Chest X ray BNP B-type Natriuretic Peptide levels Echocardiogram

Answer 106

Should be performed on all suspected heart failure patients **May indicate the underlying cause of the heart failure such as**; Myocardial infarction/ischemia Bundle Branch Block Ventricular hypertrophy Pericardial disease Arrhythmias Signs of previous MI - pathological Q waves ***A normal ECG makes heart failure unlikely (sensitivity 89%)*** *taken from almostadoctor*

Answer 107

ABCDE Recommended for all suspected HF patients Alveolar oedema - seen in Bat wing shadowing Kerley B Lines *interstitial oedema* Cardiomegaly Dilated upper lobe vessels of lungs *(prominent upper lobe veins)* Effusions (pleural) A normal CXR does not exclude the possibility of Heart Failure

Answer 108

thickened, horizontal lines that radiate from the costophrenic angle - they are the **interlobular septa** *(that separate lobes of the lungs)* that have become filled with fluid Basically oedema within the interlobular septa - interstitial oedema

Answer 109

B-type Natriuretic Peptide (BNP) are peptides that cause natriuresis, diuresis and vasodilation. HF - released in response to increased pressure on heart - BNP signals to the body that it needs to **reduce the amount of fluid in the body, and help reduce the strain on the heart.** == **They are the body’s “natural defence” against hypervolaemia** A marker of heart failure Released when the myocardial walls are under stress Levels directly correlated to ventricular wall stress and severity of heart failure **RELEASED FROM THE VENTRICLES**

Answer 110

***ECHOCARDIOGRAM*** Can confirm the diagnosis Can calculate the **ejection fraction, ventricular wall thickness** etc *An ejection fraction (EF) of <40% strongly indicated heart failure EF of 41-49% is not diagnostic, but suggestive of heart failure* Can confirm any underlying structural abnormalities – such as valve disease Helps to **stratify the type of HF present and therefore guides management**

Answer 111

BASED ON LIMITATIONS Class I: No limitation (Asymptomatic) Class II: Slight limitation (mild HF) Class III: Marked limitation (Symptomatically moderate HF) Class IV: Inability to carry out any physical activity without discomfort (symptomatically severe HF 1- Nothing, 2 -Mild, 3 - Moderate, 4 - Severe

Answer 112

Exercise more Reduced salt intake and processed foods, monitor weigh Fluid restriction in severe cases Reduce alcohol, stop smoking Get flu vaccination

Answer 113

A diuretic, like furosemide

Answer 114

A diuretic, like furosemide **The following flashcards will be asking about heart failure medication for when there is a** ***reduced*** **ejection fraction**

Answer 115

- an ACE inhibitor, like **Ramipril**, and **Beta blockers, like Bisoprolol** ***Start low, progress slow!*** - monitor BP and heart rate ABAL *(can consider giving an Angiotensin 2 receptor blocker eg Candesartan if intolerant of ACE-i)*

Answer 116

A mineralocorticoid receptor antagonist - eg Spironolactone

Answer 117

K+ sparing diuretic, like Spironolactone - Aldosterone receptor antagonist ABAL Also a drug like ***Digoxin*** - good for arrhythmias and AF, and helps symptoms of **LVSD** *(Left Ventricular Systolic Dysfunction.)* ---> *Helps strengthen heart muscle contractions*

Answer 118

Digoxin - used AF **CAN ALSO CAUSE HYPERKALAEMIA** Spironolactone - an aldosterone receptor antagonist (Not used in heart failure, but anabolic steroids and antipsychotics *that inhibit dopamine and therefore nothing to restrict prolactin* can also cause Gynaecomastia)

Answer 119

Hypertension Heart failure Diabetic nephropathy eg RAMIPRIL, ENALAPRIL, PERINDOPRIL, TRANDOLAPRIL

Answer 120

Think - **Due to reduced angiotensin II formation!! (duh)** a. Hypotension b. Acute renal failure c. Hyperkalaemia d. Teratogenic effects in pregnancy **Also due to** ***increased Kinin production*** a. Cough b. Rash c. Anaphylactoid reactions

Answer 121

Hypertension Diabetic nephropathy Heart failure **(when ACE-I contraindicated)** eg CANDESARTAIN, VALSARTAIN, LOSARTAN

Answer 122

Symptomatic hypotension (especially volume deplete patients) Hyperkalaemia Potential for renal dysfunction Rash Angio-oedema Contraindicated in pregnancy (aka not safe for pregnancy) Generally very well tolerated

Answer 123

Hypertension Ischaemic heart disease (IHD) – angina Arrhythmia (tachycardia) eg AMLODOPINE, FELODIPINE, VERAPAMIL, DILTIAZEM

Answer 124

Ischaemic heart disease (IHD) – angina Heart failure Arrhythmia Hypertension eg BISOPROLOL, PROPRANOLOL, ATENOLOL, NADOLOL

Answer 125

**Calcium channels blockers, with the exception of Amlodipine**, are generally avoided in heart failure, and verapamil in particular can worsen heart failure.

Answer 126

B1 selective - Metoprolol, Bisoprolol in the middle - Atenolol B1/B2 non selective - Propranolol, nadol *The term “cardioselective” is often used to imply β-1 selectivity This is a misnomer since up to 40% of cardiac β-adrenoceptors are β-2*

Answer 127

Fatigue Headache Sleep disturbance/nightmares Bradycardia Hypotension Cold peripheries Erectile dysfunction Worsening of: Asthma (may be severe) or COPD PVD – Claudication or Raynaud’s Heart failure – if given in standard dose or acutely

Answer 128

Hypertension Heart failure Classes Thiazides and related drugs **(act on distal tubule)** Loop diuretics **(act on loop of Henle)** Potassium-sparing diuretics Aldosterone antagonists

Answer 129

a) **Bendroflumethiazide**, hydrochlorothiazide b) Furosemide, Bumetanide c) Spironolactone Amiloride

Answer 130

Hypovolaemia and hypotension - **Mainly caused by Loop diuretics** *eg furosemide* Low serum potassium (hypokalaemia) Low serum sodium (hyponatraemia) Low serum magnesium (hypomagnesaemia) Low serum calcium (hypocalcaemia) Raised uric acid (hyperuricaemia – gout) Erectile dysfunction and Impaired glucose tolerance - **Mainly thiazides** *eg Bendroflumethiazide,* spironolactone can cause gynecomastia

Answer 131

Released from atria and ventricles. Released by stretching of atrial and ventricular muscle cells, in Raised atrial or ventricular pressures or volume overload Actions **Increase renal excretion of sodium** (natriuresis) and **water** (diuresis) Relax vascular smooth muscle (except efferent arterioles of renal glomeruli) Increased vascular permeability Inhibit the release or actions of: Aldosterone, angiotensin II, endothelin, anti-diuretic hormone (ADH) *Counter-regulatory system to the renin-angiotensin system*

Answer 132

They are Arterial and venous dilators Reduction of preload and afterload Lower BP Ischaemic heart disease (angina) Heart failure MI

Answer 133

Isosorbide mononitrate GTN Spray GTN infusion *GTN = Glyceryl Trinitrate* Main adverse effects: Headache; GTN syncope (spray)

Answer 134

Ankle oedema (Augmented drug reaction)

Answer 135

S1 - CLOSING OF AV VALES, START OF SYSTOLIC CONTRACTION - STOPS BLOOD GOING OUT OF VENTRICLES AND BACK INOT ATRIA NORMAL

Answer 136

S2 - CLOSING OF THE SEMI LUNAR VALVES , WHEN SYSTOLE IS CONMPLETE - STOPS BLOOD FLOW BACK INTO VENTIRICLES NORMAL

Answer 137

S3 - HEARD 0.1S AFTER S2 SOUND SUBTLE - CAUSED BY THE RAPID VENTRICLE FILLING, MEANING THE CHORDI TENDONAE EXTEND TO FULL STRETCH AND TWANG

Answer 138

NORMAL IN YOUNG HEALTHY PATIENTS, heart fills and stretches easily CAN INDICATE HEART FAILURE IN OLDER PATIENTS, AS CHORDI TENODNAE ARE STIFF A WEAK - SO REACH STRETCHING LIMIT MUCH QUICKER THAN USUAL *eg old person bending over, and their hamstrings quickly tighten as they reach limit of stretch* Lub DeDub

Answer 139

S4 - HEARD DIRECTLY BEOFRE S1 - INDICATES A STIFF AND HYPERTROPHIC VENTRICLE - SOUND CAUSES BY TURBULENT FLOW OF AN ATRIA, THAT IS CONTRACTING AGAINST THE VENTRICLE THAT IS NOT RELAXED/NON COMPLIANT ===> ***TURBULENT FLOW***

Answer 140

ERB's POINT - 3rd Intercostal space, left sternal boarder - best place to listen to heart sounds S1-S4

Answer 141

If heart chamber is pushing against stenotic valve - **has to work a lot harder- aka will undergo hypertrophy** AKA if **mitral valve is stenotic, will get left atrial hypertrophy** Aortic stenosis = left ventricular hypertrophy

Answer 142

In a leaky valve, blood will **reenter back to the chamber it came from, stretching the muscle in it- leading to a dilated chamber** eg Aortic Regurgitation - blood flows back into left ventricle after systole when it shouldn't leads to left ventricular dilation

Answer 143

Aortic Stenosis

Answer 144

It is the narrowing and stiffening of the aortic valve - specifically of the 3 cusps that form it. **It is progressive**

Answer 145

Most common valve disease Presenting Patients are normally in their 70s or over

Answer 146

Calcification of the aortic valve over time Congenital issues - aka **having a** ***bicuspid aortic valve (2 cusps)*** **not 3** - *These are far more prone to calcification* Rheumatic fever is a rare cause

Answer 147

Think of it in any old person with the **classic triad of: - Syncope (can be on exertion) - Angina -Dyspnoea** Also think of it in heart failure

Answer 148

**causing an ejection systolic murmur** - *high pitched due to high velocity, turbulent blood flow* ***Will radiate up to carotid as turbulence radiates up to the neck*** *Murmur is also known as crescendo decrescendo - louder than quieter* Sounds like a *whoosh*

Answer 149

- Slow rising (pulsus tardus) and weak (pulsus parvus) carotid pulse - **loud ejection systolic murmur** at the aortic area, **radiating to both carotid arteries** - *can have a crescendo-decrescendo character* - Soft or absent S2 sound - as A2 (aortic sound) is far quieter - Can also observe **pathological S4 korsakoff heart sound** On Xray - **Cardiomegaly, dilated ascending aorta, pulmonary oedema, calcification of aortic valve**

Answer 150

* Surgical ○ **Aortic valve replacement** – in symptomatic patients as onset of symptoms associated with 75% mortality at 3 years ○ If not medically fit for surgery, then Transcatheter Aortic Valve Implantation (TAVI) with a balloon expandable stent **Balloon valvoplasty** * General ○ Dental hygiene/care – risk of infective endocarditis ○ IE prophylaxis *(IPC)* in dental procedures

Answer 151

Mitral leaflets fuse together, leading to obstruction of inflow to left ventricle = prevents proper filling during diastole, due to narrowing of mitral valve *(Normal mitral valve orifice is 4-6cm^2)*

Answer 152

More common in females, 40-50 years old

Answer 153

Rheumatic heart disease rheumatic fever from group A beta-haemolytic strep e.g. s. pyogenes Infective endocarditis Congenital deformation of mitral valve Carcinoid tumours

Answer 154

* History of rheumatic fever * Untreated streptococcus infections

Answer 155

LA hypertrophy = **PULMONARY HYPERTENSION, ARRHYTHMIAS** Thickening and immobility of valve leads to obstruction of blood flow from LA to LV ===> increased LA pressure, which can eventually lead to **pulmonary hypertension and right heart dysfunction** High Pressure in left atrium can also lead to Atrial fibrillation, which can lead to further *thrombi forming, can cause things like stroke* pulmonary hypertension can **pulmonary oedema**

Answer 156

**Mid diastolic low pitched, rumbling murmur** This is a **murmur after S2, due to the low velocity of the blood going through it into the ventricle** also A **Loud S1** *(Due to Thick mitral valve suddenly forcefully shutting)* eg LUB! DUBdurrrr *see picture*

Answer 157

**Malar flushes on cheek** –decreased CO can cause vasoconstriction which results in pinkish-purple patches on the cheeks **Loud first heart sound** due to increased pressure in LA, with a **tapping apex beat** loud P2, due to pulmonary Hypertension Diastolic murmur – heard when blood flows over a valve

Answer 158

Get them to lie on their left hand side

Answer 159

MVS - leads to LA hypertension, so can cause pulmonary hypertension/RSHF! * Progressive exertional dyspnoea * **Haemoptysis – coughing up blood due to rupture of bronchial vessels due to elevated pulmonary pressure** * Right HF ○ Fatigue ○ Weakness ○ Abdominal/lower leg swelling * Palpitations – due to AF * Chest pain

Answer 160

* Echocardiogram - **can see left atrial enlargement , thick and calcified mitral valve** * CXR – LA enlargement, **pulmonary hypertension** and sometimes a calcified mitral valve * ECG – **AF** and LA enlargement

Answer 161

Control symptoms that it has caused: * Rate control if patient has AF – **beta blockers, digoxin** * **Anticoagulation with warfarin** for AF patients to prevent clot formation and embolisation Diuretics for heart failure e.g. furosemide * Percutaneous mitral balloon valvotomy – access to mitral valve obtained via catheterisation through the femoral vein, RA and interatrial septum and a balloon is inflated to open the orifice

Answer 162

Aortic regurgitation (AR) occurs when there is a backflow of blood from the aorta into the left ventricle during ventricular diastole. *taken from geekymedics*

Answer 163

either acute or chronic: * Congenital bicuspid aortic valve - chronic * Rheumatic heart disease (rheumatic fever) - chronic Connective tissue diseases (e.g. Marfan’s syndrome) * Infective endocarditis - acute * Chest trauma - acute * Aortic dissection - acute (inner layer of aorta tears, so blood flows between layers of wall, forcing it apart

Answer 164

It leads to a combined volume and pressure overload in the left ventricles

Answer 165

Get them to sit up, lead forward, breathe out and hold it, then listen

Answer 166

an **early diastolic, soft murmur** - **Very subtle!** due to blood flowing straight back into left ventricle from aorta **during diastole** ==> because of this, also associated with a **collapsing pulse**

Answer 167

**WATERHAMMER PULSE** - Early diastolic murmur *due to backflow* - heard at left sternal edge 4th IC space - Ejection systolic murmur *due to more volume in left ventricle when it contracts* **Wide pulse pressure** *Quincke's Sign* *De Musset's sign* *Muller's Sign*

Answer 168

Water hammer pulse/*collapsing pulse* - get Pt to sit down and lie back, and raise up arm, Grab **Muscular part of forearm**, and will feel a **tapping pulse, as blood that is pumped into arm during systole is emptied into heart during diastole** Can be seen in Aortic regurgitation

Answer 169

* Quincke’s sign – capillary pulsation in nail beds * De Musset’s sign – head nodding with each heart beat Muller’s sign – visible pulsations of uvula *c for capillary = quinCke*

Answer 170

* Exertional dyspnoea * Orthopnoea - *struggling to breathe lying down* * Paroxysmal nocturnal dyspnoea - sudden onset of difficulty breathing at night * Palpitations * Angina Syncope

Answer 171

* Echocardiogram * ECG – shows evidence of LVH * CXR - shows a large heart (cardiomegaly) and occasional dilatation of the ascending aorta Cardiac MRI

Answer 172

* Vasodilators – ACE inhibitors e.g. Ramiprils only if symptomatic or hypertension * Surgical – replace valve before LV dysfunction

Answer 173

Imperfect closure of mitral valve during systole, leads to back flow into left atria

Answer 174

Degenerative mitral valve disease - most common cause in developed world Also: * Infective Endocarditis * Ischaemic mitral valve Dilated cardiomyopathy Connective disorders, like Maarfans In Developing world: Rheumatic heart disease – from rheumatic fever

Answer 175

Risk Factors * Female * Lower BMI * Advanced age * Renal dysfunction * Previous MI

Answer 176

* Pure volume overload due to leakage from LV into LA 🡪LA dilatation * Compensatory mechanisms: ○ **LA enlargement ○ LV hypertrophy** – since LV must put in same effort to pump less blood ○ Increased contractility ○ Progressive LA dilatation and RV dysfunction due to pulmonary hypertension ○ Progressive LV volume overload leads to dilatation and progressive HF ○ **LA enlargement can Lead to AF**

Answer 177

* Exertional dyspnoea * Fatigue and lethargy * Palpitations * Right sided HF and can lead to congestive heart failure **Symptoms of any heart valve defect**

Answer 178

Get a Pan systolic murmur - **murmur that is present throught the systolic period** - due to blood following back into the atria during ventricular contraction *It’s high pitched and whistling, due to the high velocity of blood flow back through the leak vale, from ventricular contraction*

Answer 179

* Collapsing pulse with **wide pulse pressure** * Hyperdynamic and displaced apex beat ○ Soft S1 Mitral stenosis - **Mid diastolic low pitched murmur,** after S2 Mitral regurgitation = **PAN SYSTOLIC MURMUR** - Due to blood going back into atria - *High pitched and whistling, due to high velocity of blood going back into atria - radiates to the axilla* *Any sound produced by the mitral valve will radiate to the axilla*

Answer 180

* ECG – P Mitrale – ‘*bifid’ (two-peaks) P waves* due to ***atrial hypertrophy*** * **Trans-Oesophageal Echocardiogram** – TOE – used to asses the level of valve damage, to check if suitable for valve repair / replacement * Doppler-Echo – assesses the site and size of the regurgitant jet

Answer 181

functional **mitral and tricuspid regurgitations.** This is because the enlarged ventricles cause an incomplete seal at the valves during diastole.

Answer 182

High Blood pressure! WHO classification – **140/90 mmHg** on *at least two readings on separate occasions*

Answer 183

The prevalence of high blood pressure in 2015 was reported as 31% among men and 26% among women, affecting more than 1 in 4 adults.

Answer 184

1.13 billion people have hypertension worldwide (defined as systolic blood pressure [BP] ≥140 mmHg and diastolic BP ≥90 mmHg) * Hypertension is more common in black Africans – 40-45% of adults

Answer 185

90-95% primary, 5-10% secondary

Answer 186

It has **multifactorial aetiology** Genetic factors – can run in families 40%-60% have a genetic component Foetal factors – low birth weight is associated with hypertension Obesity High alcohol Alcohol intake Insulin intolerance Lack of physical activity Metabolic Syndrome X *cluster of conditions, such as high insulin levels, glucose intolerance, low levels of HDLs, central obesity*

Answer 187

* Family history * Old age * Low birthweight * Male * Afro-Caribbean’s * Unhealthy diet * Lack of physical activity * Obesity

Answer 188

○ Renal e.g. CKD ○ Endocrine e.g. Conn’s syndrome, acromegaly, Cushing’s syndrome ○ Coarctation of the aorta ○ Pre-eclampsia occurring during third trimester of pregnancy

Answer 189

Hypertension - Causes arteries to common less compliant, and narrowing of the lumen Can lead to Hyaline arteriosclerosis, which is protein deposition in the arterial wall, Lead to atherosclerosis and aneurysms forming - stroke Endothelial damage = CAD, ACS

Answer 190

Asymptomatic – except in malignant hypertension May have the occasional general headache *although the reliability of this as a symptom is disputed*

Answer 191

Take BP reading, and Repeat BP in the other arm * Repeat again at the end of the consultation *If it remains high, then arrange home BP monitoring; either: **Ambulatory BP monitoring (ABPM)** – the patient is fitted with a BP recording device, which takes their BP every hour (or more) throughout a 24 hour period. -> *tell them to keep doing their daily activities* *Home blood pressure monitoring (HBPM)* – Ask the patient to keep a diary of their BP: * **Twice daily * For 7 days** * Take two consecutive readings and record the lowest * Discard the first day and take an average of the rest of the readings at a follow-up appointment

Answer 192

Look at retina! - Cotton wool spots - damage to nerve fibres - Silver/Copper wiring - walls of the arterioles become sclerosed causing increased reflection of the light. - Hard exudates leaking lipids into the retina. - Papilledema is caused by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margin - Retinal haemorrhages = releasing blood into the retina. *taken from zerotofinals*

Answer 193

- Urinalysis to check for Kidney damage (Proteins/blood in wee, Albumin to creatine ratio) - ECG/Echo for LV hypertrophy - Fundoscopy for retina damage - Bloods - Serum creatine, eGFR, Glucose (Hba1c) - Take clinical history Lipid Profile and QRISK

Answer 194

- Cardiac - MI, AAA, Atherosclorosis, AF, HF - Stroke - Renal failure Eye defects

Answer 195

* Lifestyle changes ○ Smoking cessation ○ Low-fat diet + high consumption of fruit and vegetables ○ Reduce alcohol and salt intake ○ Increase exercise Loss weight is obese

Answer 196

ACE-Inhibitor e.g. Ramipril (or angiotensin receptor blocker e.g. candesartan if contraindicated e.g. due to cough)

Answer 197

ACEi, eg Ramipril

Answer 198

eg Candesartan It's given instead of an ACE-inhibitor, if a ACE-i is contraindicated. You give ACE-i to anyone who is younger than 55, or not Black afro Caribbean, or someone with Diabetes at any age .

Answer 199

calcium channel blocker e.g. amlodipine

Answer 200

ACE-inhibitor + CCB Or if afro Caribbean - CCB and ARB

Answer 201

○ Third line = ACE-inhibitor + CCB + diuretics e.g. Bendroflumethiazide or furosemide

Answer 202

Calcium-channel blockers such as amlodipine commonly cause peripheral oedema

Answer 203

Fourth line – ACE-inhibitor + beta blocker *e.g. Bisoprolol* + CCB + diuretics

Answer 204

A DVT is a blood clot that forms in the deeper veins of the leg or pelvis, as opposed to the veins closer to the surface of the skin. If these clots appear in other areas of the body, such as the arm, it can point to a more serious condition *(eg Clotting disorder/Carcinoma)* and usually requires long-term treatment or prevention.

Answer 205

Blood from the superficial veins is **transferred into the deeper veins,** with the assistance of the skeletal muscle pump. The muscles surrounding the vein contract, pushing the blood onward, and the **valves in the vein** restrict the backflow of liquid.

Answer 206

So vwf FACTOR bind to collagen, and starts off either intrinsic or extrinsic pathway =PLATELET PLUG, PRIMARY HOMEOSTASIS Then is followed by secondary cascade is set off, which ends in FIBRONGEN BECOMING FIBRIN, leading to a mesh around the plug = SECONDARY HOMEOSTASIS **Intrinsic pathway , uncommon - 12 > 11 > 9 > 8 >10 Extrinsic pathway - more common 3 > 7 > 10 Both lead to common pathway, 10 > 5 > 2 > 1** *Factor 2 is called Prothrombin, when activated becomes thrombin, Factor 1 is called fibrinogen activated becomes fibrin* **10 is initiator of common pathway**

Answer 207

Plasmin cuts up fibrin into pieces known as D-dimers.

Answer 208

ANYTHING THAT LEADS TO EXCESS CLOTTING!! **Age** - Middle aged and over **Smoking** **Immoniliity in legs** - eg long flights, surgery, being bed bound **Pregnancy** **Polycythaemia** **Thrombophilia** e.g. antiphospholipid syndrome, antithrombin deficiency, protein C or S deficiency *Can be genetic* Having **Virchow's triad:** hypercoagulability, venous stasis, endothelial damage

Answer 209

deep veins of the leg start off at a spot situated just behind and above a venous valve. Above knee is more dangerous, more likely to embolise

Answer 210

* Unilateral swelling * Oedema * Tender and erythematous (red, flushed) * Distention of superficial veins * Phlegmasia cerulea dolens: occurs in a massive DVT, resulting in obstruction of venous and arterial outflow (rare). This leads to ischaemia and a blue and painful leg

Answer 211

* Red, swollen leg (particularly calf) * Tenderness * Pitting oedema * Fever

Answer 212

**Ultrasound scanning** - cheap and quick - 90% accurate above leg, but only 50% accurate below leg **Venography - GOLD STANDARD** - injection of a radio-opaque dye into the foot, allowing the path of the dye to be monitored as it travels up the leg **D-dimer levels** -D-dimer, a breakdown product of fibrin, is also used to diagnose DVT. A negative test result rules out DVT, however a positive result does not necessarily mean the patient has the condition **Leg Measurement**

Answer 213

This involves measuring the diameter of the calf on each leg, **usually 10cm below the tibial tuberosity.** A difference of more than **3cm** between the two legs can be an indication of DV

Answer 214

The Wells score calculates the risk of DVT and determines how the patient is investigated and managed. Those with a score ≥ 2 are deemed high risk **taken from OHCM 9th edition**

Answer 215

Active Cancer = 1 Bedridden or recent major surgery = 1 Calf swelling >3cm compared to other leg = 1 Superficial (non varicose) veins present = 1 Entire leg swollen = 1 Tenderness along veins = 1 Pitting oedema of the affected leg - 1 immobility of affected leg - 1 Previous DVT - 1 Alternative diagnosis likely = -2 points **taken from OHCM 9th edition**

Answer 216

Duplex ultrasound of leg within 4 hours: this is diagnostic (offer a D-dimer if the scan is negative); if an ultrasound is not possible to arrange within 4 hours: ○ Perform a D-dimer AND ○ Offer interim anticoagulation for 24 hours (ideally in a form that can be easily continued) AND ○ Arrange the ultrasound for the following day **taken from OHCM 9th edition**

Answer 217

D-Dimer with a result available within 4 hours: if D-Dimer results cannot be obtained within 4 hours, offer interim anticoagulation until the result is available ○ If D-Dimer is raised: perform a duplex ultrasound within 4 hours ○ If D-Dimer is normal: a DVT is unlikely and alternative diagnoses should be considered

Answer 218

No renal impairment § Offer apixaban or rivaroxaban *(Inhibits thrombin)* § If neither suitable, offer one of: □ LMWH for at least 5 days followed by dabigatran or edoxaban *(Inhibits thrombin)* Renal impairment (estimated creatinine clearance <15 ml/min) § Offer one of: □ LMWH *(Low Molecular Weight Heparin.)* □ Unfractionated heparin (UFH)

Answer 219

* Compression stockings * Frequent calf exercises during long periods of immobilisation Prophylactic anticoagulation with LMWH e.g. in patients who have had surgery and will be immobilised for a long period of time

Answer 220

* Pulmonary embolism: increased pressure in the vein can cause a part of the main clot to break free. Therefore, there is a risk of an embolism to the lungs. Pulmonary embolism can be diagnosed with a CT pulmonary angiogram or ventilation–perfusion (VQ) scan. * Embolic stroke: seen in patients with **atrial septal defect** :, the clot may travel to the left atria and then the left ventricle. The clot can then embolise to any part of the body, including the brain causing an embolic stroke * Post-thrombotic syndrome: this is a long term complication caused by chronic obstruction of venous blood, leading to venous hypertension, with pain, swelling, and ulceration * Increased risk of bleeding: patients on anticoagulation are at risk of bleeding * Phlegmasia cerulea dolens: occurs in a massive DVT, resulting in obstruction of venous and arterial outflow (rare). This leads to peripheral limb ischaemia and a blue and painful leg

Answer 221

Normally a complication of venous thromboembolism from elsewhere in the body. The clot becomes dislodged, and goes via bloodstream to get dislodged in the lungs

Answer 222

Virchow's triad risk factors for PE Hypercoagulability - Due to Cancer, sepsis, Genetic conditions, Protein S and C deficiency Surgery, Contraceptive pill Endothelial damage - Smoking, Diabetes, Hypertension Venous stasis - Heart failure, DVT Recent surgery, bed bound or long haul flight *taken from https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.113.004586*

Answer 223

- **Right ventricular thrombus *(post-MI)* - **Septic emboli (right-sided endocarditis - bacterial vegetation)** Air Embolus Parasites Forgein Materail from IVDU Fat Emboli

Answer 224

**A piece of clot that have broken free** Can lead to Thromboembolism - Clog in a tiny artery leading to a **decrease in oxygen. Alveoli will receive air but no blood, leading V/Q mismatch** unable to produce surfactant, which leads to alveolar collapse and an increased lack of oxygen in the body (hypoxaemia).

Answer 225

*think RSHF?* -**Hypoxia** - **Cyanosis** may be present - **Deep vein thrombosis:** swollen, tender calf - **Pyrexia** may be present - **Tachypnoea and tachycardia** - **Crackles** - **Hypotension:** SBP <90 mmHg suggests a massive PE - **Elevated JVP:** suggests cor pulmonale - **Right parasternal heave:** suggests right ventricular strain

Answer 226

- **Pleuritic chest pain** - **Dyspnoea** - **Cough +/- haemoptysis** - **Fever** - **Fatigue** - **Syncope:** a red flag symptom *taken From https://www.verywellhealth.com/symptoms-of-pulmonary-embolus-4163779*

Answer 227

- **CXR:** performed to rule out alternative pathology. It is typically normal in a PE, although a wedge-shaped opacification may be seen - **ECG:** - **CT pulmonary angiogram** (**CTPA):** highlights the pulmonary arteries to demonstrate any blood clots. - **D-dimer:** detect fibrin breakdown products - Other investigations to consider - **ABG:** to quantify the degree of hypoxaemia; also respiratory alkalosis if there is hyperventilation that gets rid of CO2 - **V/Q scan**: involves using radioactive isotopes and a gamma camera to reveal areas of the lung that are ventilated but not perfused. Done in patients allergic to contrast, with severe renal impairment and also considered in pregnancy - **Pulmonary angiography**: **gold-standard** but more invasive and has higher complications

Answer 228

- **Compression stockings** - **Frequent calf exercises** during long periods of sitting still - Prophylactic treatment with **low molecular weight heparin**

Answer 229

Oxygen if Hypoxic, and morphine if needed Get IV access with LMWH or Fondaparinux Give Bolus 500ml IV fluid if hypotensive Haemodynamically unstable - **Thrombolysis, eg alteplase** - either IV or directly into pulmonary arteries with central catheter

Answer 230

No renal impairment § Offer apixaban or rivaroxaban *(Inhibits thrombin)* § If neither suitable, offer one of: □ LMWH for at least 5 days followed by dabigatran or edoxaban *(Inhibits thrombin)* Renal impairment (estimated creatinine clearance <15 ml/min) § Offer one of: □ LMWH *(Low Molecular Weight Heparin.)* □ Unfractionated heparin (UFH)

Answer 231

Heparin treatment = decrease in platelet count, known as hepatic-associated **thrombocytopaenia.** Obstruction of pulmonary vasculature= resulting in pulmonary hypertension and **subsequent strain on the right heart** ***=Cor Pulmonale.*** Pulmonary infarction, tissue necrosis. Sudden death due to **large pulmonary thromboembolism** Hyperventilation in response to the embolism can cause a rapid release of CO2, **resulting in respiratory alkalosis.** AVSD - Emboli can travel to brain, **and cause an embolic stroke**

Answer 232

A true aneurysm is one that affects all three layers of the arterial wall - the endothelial cells of the tunica intima, the smooth muscle of the tunica media, and the connective tissue of the tunica adventitia, On the other hand, a false/pseudo-aneurysm only involves one layer of the arterial wall, for example, the tunica intima in aortic dissection.

Answer 233

**fusiform aneurysms**, which are uniform in shape with symmetrical dilatation and involves the entire circumference of the aortic wall; **saccular aneurysms** = local outpouchings of only a portion of the aortic wall.

Answer 234

An abdominal aortic aneurysm (AAA) describes a dilatation in vessel wall diameter of >50%, which typically means a diameter of >3 cm

Answer 235

- **Increasing age** - **Male gender** - **Atherosclerosis** - **Smoking** - **Hypertension** - **Hyperlipidaemia** - **Diabetes** - **Connective tissue disorders**: such as Ehlers Danlos and Marfan syndrome, due to changes in the balance of collagen and elastic fibres - **Family history**

Answer 236

The abdominal aorta usually develops an aneurysm**below the renal artery level.** Below renal arteries, the aorta lacks the small blood vessels **(vasa vasorum)** in its adventitial layer which are necessary to supply the aorta with nutrients. Therefore, the middle layer of the aorta is prone to ischaemia, making an aneurysm more likely.

Answer 237

1. Tunica Interna (Endothelium): This innermost layer is composed of a single layer of flat, squamous endothelial cells that are supported by a thin basement membrane. 2. Tunica Media: This layer is composed of multiple layers of smooth muscle cells, separated by layers of elastic fibers. 3. Tunica Adventitia: This outermost layer is composed of connective tissue and collagen fibers that provide structural support for the artery wall.

Answer 238

Atherosclerosis Atherosclorosis - Enzymes released in inflammation lead to breakdown of extracellular matrix found in tunica media, === **weakens structure of aortic wall** Also the persistent inflammation weakens the arterial wall

Answer 239

Atheroma – persistent inflammation weakens the arterial wall Trauma Connective disorders **Inflammatory AAA** - so by smoking, atheroslcorosis, and vasculitis Maran's syndrome Ehlers-Danlos syndrome Infection

Answer 240

Inflammatory AAA = usually affects younger patients and is associated with smoking, atherosclerosis and vasculitis, accounting for 5-10% of aortic aneurysms cases. Presents similarly to a normal AAA but may also be associated with fever. Marfan’s – gene coding for fibrillin-1 affected (fibrillin-1 used in ECM structure)

Answer 241

***In general, aneurysms are not associated with any symptoms and are often found by chance. In contrast, signs and symptoms may be present if the aneurysm has ruptured or is likely to rupture.*** - Signs - **Pulsatile abdominal mass** - **Tachycardia and hypotension:** red flags signifying ruptured AAA - **Grey-Turner’s sign:** - **Cullen’s sign:**

Answer 242

- **Grey-Turner’s sign:** flank bruising secondary to retroperitoneal haemorrhage - **Cullen’s sign:** pre-umbilical bruising

Answer 243

- **Flank, back or abdominal pain** - **Pulsating abdominal sensation** Ruptured ones: **Shock, An** ***expansible abdominal mass*** **that rises and contracts** **Collapse** **intermittent or continuous abdominal pain**

Answer 244

**Abdominal ultrasound:** definitive diagnosis with high sensitivity (92-99%) and specificity (~100%)

Answer 245

- **FBC**: leaking AAA may cause anaemia, inflammatory AAA may cause leukocytosis - **U&Es**: baseline renal function is important prior to a CT angiogram as it requires contrast, whilst hypovolaemia may cause pre-renal acute kidney injury - **CRP/ESR**: raised in inflammatory AAA - **Group and save & crossmatch**: vital if a ruptured AAA is suspected in order to ensure blood is available for transfusion - **CT angiogram**: for more detailed anatomical information, particularly if near the renal arteries; it is also the test of choice for pre-operative planning - **MRI**: MRI is preferred over CT for females of child-bearing age and those allergic to iodinated contrast

Answer 246

The screening programme in England is offered to all males aged 65 and over **as a one-off abdominal ultrasound** and further surveillance is organised if the aneurysm exceeds 3 cm. <3 cm - discharge from screening 3 -4.4 cm - Annual Surveillance 4.5-5.4 cm - 3 monthly surveillance >5.5 cm - Refer to vascular surgeon to be seen within 2 weeks of a diagnosis

Answer 247

Treatment Lifestyle advice, Surveillance, BP control, Statins, controlling cardiovascular co-morbidities Or Surgery - eg **Endovascular Aortic repair** Antiinflammatorys if its inflammatory aka steroids of immunosuppressants

Answer 248

Summon a vascular surgeon, warn theatre - you **have to operate!** Do ECG, take blood for amylase Catheterise bladder Gain IV access with 2 large-bore cannulae Treat shock with ORh-ve blood, **but keep BP <100mmHg to avoid rupturing a contained leak** Take patient straight to theatre Give **prophylactic antibiotics**, eg co-amoxiclav** Surgery involves clamping the aorta above the leak, and inserting a tube graft

Answer 249

TUNICA INTIMA SPLITS, BLOOD FLOWS INTO FALSE CHANNEL BETWEEN TUNICA INTIMA AND MEDIA -- **MEDICAL EMERGNCY, CAN LEAD TO RUPUTRE**

Answer 250

- **Hypertension**: the most important risk factor - **Smoking** - **Family history of aortic aneurysm or dissection** - **Coarctation of the aorta:** narrowing of vessel - **Bicuspid aortic valve** - **Connective tissue disorders:** Marfan and Ehlers-Danlos syndrome - **Turner and Noonan syndrome** - **Trauma** - **Pregnancy:** increased blood plasma volume - **Syphilis** According to Haroon, obesity is not a risk factor for aortic dissection!!

Answer 251

As the high-pressured blood continues to shear more and more of the tunica intima off the tunica media, **blood starts to pool between the two layers, increasing the outside diameter of the blood vessel.** The area where blood collects between intima and media is **called a false lumen.** This most commonly occurs around the **ascending aorta and aortic arch,** but can affect any part of the aorta.

Answer 252

***Sometimes, the lumen will be taken back into the primary lumen, = forms 'double-barrelled aorta' that may be stable yet may also rupture.*** Dissections can affect valves, if dissection reaches pericardium, will cause a **Hemopericardium** Dissection is a medical emergency and has to be treated asap. If the blood manages to escape through all the layers of the wall of the aorta, then rupture is the result.

Answer 253

**Stanford**: - **Type A**: dissection involves the ascending aorta with or without the involvement of the arch and descending aorta, *occurring proximal to the left subclavian artery (⅔ of cases)* - **Type B**: dissection does not involve the ascending aorta. Involves only the descending thoracic or the abdominal aorta, *occurring distal to the left subclavian artery (⅓ of cases)*

Answer 254

- **Weak downstream pulses**: radio-radial and/or radio-femoral delay - *Absent peripheral pulses* - **A difference in blood pressure between two arms:** >10 mmHg - **Hypertension** - **Tachycardia and hypotension:** as condition progresses - **Diastolic murmur:** due to aortic regurgitation - **Involvement of specific arteries** - Spinal arteries → paraplegia - Coronary arteries → angina - Distal aorta → limb ischaemia

Answer 255

- **Sudden onset, severe ‘tearing’ or ‘ripping’ chest pain** that may radiate to the back - **Syncope:** red flag symptom Pain usually follows the line of the dissection Ascending aorta – pain will be in the chest Descending aorta – pain often in the back Collapse (due to hypotension) Expansile (not pulsatile) mass in the abdomen Shock Hypotension Tachycardia Profound anaemia Sudden death Testicular pain Symptoms similar to renal colic Symptoms similar to diverticulitis Non-specific back pain – this results from gradual erosion of the vertebral bodies in patients with long-standing aneurysm.

Answer 256

CT/MRI angiography confirms diagnosis – contraindicated in patients with renal disease CXR – shows widened mediastinum/aorta Transoesophageal echocardiogram FBC: anaemia may be present ECG: non-specific changes such as T-wave inversion or ST-segment depression. ST-segment elevation may be seen in the inferior leads in some patients

Answer 257

- **Blood transfusion** - **Beta blocker e.g.** **IV labetalol**: aim for a systolic blood pressure of 100-120 mmHg; high pressures are associated with extension of the dissection - **Urgent surgical repair/ stenting**: open surgery with replacement of the ascending aorta should be performed immediately upon diagnosis *Type A - dissection involves ascending aorta, with or without involving the arch/descending aorta. Happens* ***Proximal to the left subclavian artery***

Answer 258

-Type B Conservative management - Bed rest Hardcore beta blocker, eg IV Labetalol - aim for systolic BP 100-120 - monitor closely in high dependency unit Open surgery, *(often still treatment of choice)* or Thoracic endovascular aortic repair *Type B - does not involve ascending aorta, only descending* ***Occurs distal to the left subclavian artery*

Answer 259

Aortic regurgitation: Dissection of the aorta causes weakening of the support of the leaflets of the valve. Myocardial infarction: Damage to the aorta that propagates in an upward direction can lead to an ST-elevation on the right side of the heart. Stroke: A tear in the aorta can interrupt the supply of blood to the brain. Renal failure: The false lumen created by the dissection can put pressure on the renal arteries, decreasing the flow of blood to the kidneys. Pericardial tamponade: Blood from the false lumen of the aorta can leak into the pericardial space, leading to a medical emergency known as pericardial tamponade. Haemorrhage and shock: Disruption of the walls of the aorta due to the dissection can cause the blood to rush out, leading to a rapid loss of blood and shock.

Answer 260

Peripheral vascular disease (PVD) is a long-term illness brought on by the narrowing of blood vessels in the arms and legs resulting from atherosclerosis. *The severity of the symptoms correlates with the degree of arterial blockage. The cause and risk factors for this condition are the same as for coronary artery disease (CAD).*

Answer 261

Hypertension Dyslipidaemia High LDL and low LDL levels Diabetes Obesity FHx of arterial disease Significant if a first degree relative had MI before the age of 55 Smoking Age Male gender

Answer 262

Aching in calves - claudication - relieved by taking a break Pain when legs are elevated, if bed bound - relieved when lowering **Claudication = think angina of the limbs**

Answer 263

Pale and cold leg on elevation - **(Beuger’s angle <20’)** – the leg will go pale and cold upon raising it 20’ off the couch. **Increased vascular filling time**– Upon lowering, the leg may become hot and red as reperfusion occurs. Perfusion time tends to be increased (>15s) Oedema is not usually present Evidence of poor skin health eg **ulcers, dry scaly skin, cool peripheries and reduced capillary refill time** **Absent (posterior tibial and dorsals pedis) pulses** represent an increased chance of peripheral vascular disease

Answer 264

‘Punched out’ ischaemic ulcers – usually on the toes and heels, rarely higher up the limb. These tend to occur after a localised traumatic event. . Gangrene – often black necrotic gangrenous tissue surrounds the punched out ulcer lesions. Infection of this areas can occur (wet gangrene). Reduced / absent peripheral pulses – start distally, and work your way up until you find the pulse Skin atrophy – in chronic disease Hair loss – in chronic disease Cyanosis Excessive sweating – due to overactivity of the sympathetic nerves Erectile Dysfunction – Amputation may be necesscary!

Answer 265

Ankle Brachial pressure index - Compares Blood pressure in Arms and legs, as reduced blood flow to legs is more common than arms in PVD. **Used alongside a suggestive examination and history to diagnose PVD**

Answer 266

Divide **systolic ankle pressure by systolic brachial pressure** A normal value is >1 A value of <0.9 is pathological for limb ischaemia (PVD). *lower the number, the greater the degree of PVD* Pain at rest – ABPI = <0.6 High Risk of gangrene – ABPI – <0.3, or ankle systolic pressure <55mmHg *CAUTION – in very severe arteriosclerosis the vessels are incompressible, and thus falsely high readings may be obtained (e.g. an ABPI >1.3)*

Answer 267

No medications proven to help with claudication **Walking therapies** and exercise encouragement! Statin (Atorvastatin) Ace Inhibitor - Ramipril Beta blockers - should be avoided, unless PAD is severe Antiplatelet agent - Aspirin, clopidogrel

Answer 268

Arterial ulcers develop as the result of damage to the arteries due to lack of blood flow to tissue. **Ischaemia** Venous ulcers develop from damage to the veins caused by an insufficient return of blood back to the heart. **(Stagnation of blood under pressure)**

Answer 269

Arterial ulcers Occur distally, affecting the toes or dorsum of the foot/lateral malleolus Are smaller and deeper than venous ulcers Well defined borders Have a “punched-out” appearance Are pale colour due to poor blood supply Are less likely to bleed Are painful Have pain worse at night (when lying horizontally), and on elevating, and then improved by lowering the leg

Answer 270

Occur in the gaiter area (between the top of the foot and bottom of the calf muscle), and medial malleolus Are **larger and more superficial**than arterial ulcers Have irregular, gently sloping border Are **more likely to bleed** Are less painful than arterial ulcers Have **pain relieved by elevation and worse on lowering** the leg

Answer 271

Lifestyle limiting claudication Pain at rest Gangrene Percutaneous Transluminal angioplasty – PTA

Answer 272

Angina refers to classic cardiac pain that is felt when there is a reduction in blood supply to the heart.

Answer 273

- **Non-modifiable**: increasing age, male gender, family history - **Modifiable**: hypertension, diabetes, obesity, hypercholesterolaemia, smoking, cocaine use, stress, sedentary lifestyle

Answer 274

reduced blood flow which causes ischaemia, leads to chest pain. It usually occurs when the patient has greater than or equal to 70% stenosis. --> *so can supply enough blood at rest to heart, but not enough during exertion* Patient's experience symptoms during these times of stress but symptoms are relieved with rest.

Answer 275

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.

Answer 276

Hypertrophic cardiomyopathy ( needs more O2) Aortic stenosis - Valvular disease - Arrhythmias - Embolus to the coronary artery - Vasculitis: causing aneurysm - Anaemia: less O2 is transported to the heart

Answer 277

- **Xanthomas or xanthelasma:** suggests hypercholesterolaemia - **Hypertension** - A risk factor for angina - **Retinopathy** may be seen on fundoscopy - **Evidence of peripheral vascular disease:** may coexist with ischaemic heart disease

Answer 278

If the pain doesn’t resolve within 5 minutes of cessation of activity, and/or with use of GTN spray, treat as ACS Angina can be precipitated by exertion, heavy meals, cold weather and emotion - Cardiac-sounding **chest pain** - Crushing, left-sided chest pain - Often radiating to neck, jaw, shoulders and left arm - **Dyspnoea** - **Nausea** - **Sweating**

Answer 279

Physical examination, ECG Chest X ray Exercise tolerance test CTCA - A type of high resolution CT scan, with contrast – injected through a peripheral cannula **A non-invasive test** takes about 10-15 seconds. Scan conducted whilst patient holds their breath, the contrast fills the coronary arteries and can indicate where they are narrowed Cardiac MRI Stress Echo

Answer 280

Stuff for symptom relief - GTN spray or tablet, a vasodilator - **1st line:** **β-blocker **calcium channel blocker**, aka verapamil - **2nd line**: dual therapy with dihydropyridine calcium channel blocker AND β-blocker - **3rd line**: add additional anti-anginal medication e.g. - Nitrates - Ivabradine - Nicorandil - Ranolazine

Answer 281

- **Lifestyle changes**: exercise, dietary alterations, lipid, diabetes and hypertension management, smoking cessation - **Aspirin** and a **statin** - **Angiotensin-converting enzyme inhibitors** (ACEi): if the patient has angina and diabetes

Answer 282

Angina due to coronary spasm, which can occur even in normal coronary arteries. Smoking is a risk factor for it, and cocaine/amphetamine use can trigger it. **Hypertensions and hypercholesterolaemia are not risk factors for it!!**

Answer 283

Avoid triggers Correct low magnesium Stop smoking Give GTN when needed Calcium channel blockers and/or long acting nitrates.

Answer 284

**Group A beta-haemolytic streptococcus, typically streptococcus pyogenes**, can cause tonsillitis which subsequently leads to rheumatic fever. The body's immune system produces antibodies to battle the infection, however, these antibodies also mistakenly **identify some of the individual's cells as foreign and attack them, resulting in a type 2 hypersensitivity reaction.** This delayed response usually occurs between 2 and 4 weeks after the onset of the initial infection.

Answer 285

It is rare in the UK due to early treatment of streptococcus with antibiotics.

Answer 286

The typical presentation of rheumatic fever occurs 2 – 4 weeks following a streptococcal infection, such as tonsillitis. Symptoms affect multiple systems, causing: Fever Joint pain Rash Shortness of breath Chorea Nodules Heart involvement, nervous system involvement

Answer 287

can lead to Carditis, or inflammation throughout the heart, with pericarditis, myocarditis and endocarditis, leads to: Tachycardia or bradycardia Murmurs from valvular heart disease, **typically mitral valve disease** Pericardial rub on auscultation Heart failure

Answer 288

Skin **Subcutaneous nodules** = Firm painless nodules occur over extensor surfaces of joints, such as the elbows. **Erythema marginatum** == rash pink rings of varying sizes affecting the torso and proximal limbs Chorea is the key nervous system symptom. This involves irregular, uncontrolled and rapid movements of the limbs. This is also known as Sydenham chorea and historically as St Vitus’ Dance.

Answer 289

Throat swab for bacterial culture ASO antibody titres Echocardiogram, ECG and chest xray can assess the heart involvement A diagnosis of rheumatic fever is made using the Jones criteria (see below). *Anti-streptococcal antibodies (ASO) are antibodies against streptococcus. They indicate a recent streptococcus infection and can be helpful in supporting a diagnosis of rheumatic fever.*

Answer 290

Patients with clinical features of rheumatic fever should be referred immediately for specialist management. Management involves medications and follow up: NSAIDs (e.g. ibuprofen) are helpful for treating joint pain Aspirin and steroids are used to treat carditis Prophylactic antibiotics (oral or intramuscular penicillin) are used to prevent further streptococcal infections and recurrence of the rheumatic fever. These are continued into adulthood. Monitoring and management of complications

Answer 291

Tonsillitis caused by streptococcus should be treated with **phenoxymethylpenicillin (penicillin V)** for 10 days.

Answer 292

Restrictive cardiomyopathy describes when the heart muscle becomes stiffer and less compliant. However, the muscles and size of the ventricles stay roughly the same size, or only get slightly enlarged When blood fills restricted ventricles, however, they can’t expand as much. This means the ventricles **fill with less blood and therefore pump out less blood.** This eventually leads to heart failure

Answer 293

- **ECG:** low amplitude QRS - **ECHO** - **CXR** - **MRI** - **Cardiac catheterisation**

Answer 294

**Amyloidosis** - amyloid deposition in the heart - **Sarcoidosis** - Formation of granulomas in the heart - **Haemochomatosis** - iron overload = iron in the heart **Scerloderma** - chronic connective tissue disease leading to hardening

Answer 295

Dilated cardiomyopathy refers to when all 4 chambers of the heart dilate (but don't get thicker).

Answer 296

Most often idiopathic - **Autosomal dominant** - familial - **Certain genetic conditions** e.g. Duchenne Muscular Dystrophy and haemochromatosis - **Infection** e.g. coxsackievirus B or Chagas disease, a protozoal infection - **Alcohol abuse:** alcohol and its metabolites have a direct toxic effect on the myocardium - **Chemotherapy drugs** e.g. doxorubicin and daunorubicin - **Drugs** e.g. cocaine - **Thyroid disorder** - **Peripartum cardiomyopathy:** dilated cardiomyopathy can develop in the third trimester of pregnancy

Answer 297

Pathophysiology New sarcomeres added, however walls remain thin **Leads to weak contractions, and a lower stroke volume** - leads to ***Biventricular heart failure*** Also, enlarged chambers press on valves, leading to **regurgiation/systolic murmur**, and stretching of walls **can lead to arrhythmias** blood rushing and slamming into the dilated ventricular wall during diastole --> **S3 heart sound**

Answer 298

- **Larger heart seen on imaging** - **Systolic murmur:** due to regurgitation - **S3 gallop:** due to blood rushing hitting the dilated ventricular wall during diastole - **Increased pulse** - **Decreased BP** - **Arrhythmias** - **Signs of heart failure** e.g. pulmonary oedema, increased JVP

Answer 299

- **Bloods:** BNP elevated; low Na+ implies poor prognosis - **CXR:** cardiac enlargement; pulmonary oedema - **ECG:** tachycardia, non-specific T wave changes and poor R-wave progression; may be AF or VT - **ECHO:** shows dilated heart and low ejection fraction

Answer 300

- **Bed rest** - **Diuretics:** to deal with oedema - **Beta blockers:** to control heart rate - **ACE inhibitors:** dilate vessels to improve blood flow - **Anticoagulation:** due to increased risk of thrombus - **Biventricular pacing** - **ICD** - implantable cardioverter defibrillator - **Left ventricular assist device (LVAD):** mechanical pump that assists the heart in distributing blood - **Heart transplant**, in extreme cases

Answer 301

Hypertrophic cardiomyopathy (HCM) is a genetic disorder characterised by **left ventricular hypertrophy** (LVH). IT IS AUTOSOMMAL DOMINANT CONDITION *It is a primary form of cardiomyopathy i.e. not in response to other underlying disease e.g. hypertension or valvular disease*

Answer 302

IT IS AUTOSOMMAL DOMINANT CONDITION - Walls take up more room so the cavity is smaller and less able to fill with blood. - Walls are more stiff and less compliant so can't stretch to fill with more blood. - This means less blood is pumped out of the heart - stroke volume is reduced. This can lead to heart failure. Muscle growth of IV septum, obstructs blood leaving LV and pulls anterior leaflet of mitral valve down ==> **leads to crescendo-descrendo murmur** Bigger heart means more O2 needed ( ==> **ischaemia**) and more disarray of myocytes (==> **Arrhythmias**)

Answer 303

- **Ejection systolic murmur:** crescendo-decrescendo character due to blood flowing through the obstructed left ventricular outflow tract. - **Bifid pulse:** two pulses due to mitral valve moving towards outflow tract mid-systole and causing further obstruction - **S4 sound:** due to atria contracting and pushing blood into a non-compliant ventricular wall during diastole. - **Systolic thrill** may be felt - **Arrhythmias** - **Hypertrophy seen on imaging**

Answer 304

- **ECG:** progressive T wave inversion and deep Q waves; may also be AF, WPW syndrome, ventricular ectopics, left axis deviation - **Echocardiogram:** shows ventricular hypertrophy and a small left ventricular cavity; mid-systolic closure of aortic valve; anterior movement of mitral valve mid-systole - **MRI** **Exercise test** **Genetic analysis** can confirm diagnosis since most cases are autosomal dominant and familial

Answer 305

Beta blockers or calcium channel blockers: control heart rate. *(Don't give digoxin as can increase force of contraction which can worsen condition)* - **Anti-arrhythmic medication** e.g. amiodarone - **Consider defibrillator** if at high risk of arrhythmias - **Anticoagulation:** if AF is present as there is higher risk of thrombus formation - **Septal myectomy:** surgery to remove part of septum causing obstruction

Answer 306

Calcium channel blockers are medications used to lower blood pressure. They **work by preventing calcium from entering the cells of the heart** and arteries. Calcium causes the heart and arteries to squeeze (contract) more strongly. By blocking calcium, calcium channel blockers allow **blood vessels to relax and open.**

Answer 307

Pulmonary stenosis **Right Ventricular hypertrophy** Ventricular septal defect Overriding aorta *It is the most common form of congenital cyanotic heart disease*

Answer 308

TETROLOGY OF FALLOT - Pulmonary stenosis - **leads to RV hypertrophy** as it has to push harder to get blood through VSD - blood shunts from **right to left due to RV hypertrophy** - *Deoxygenated blood enters circulation* Overriding Aorta - Entrance to aorta is further right then normal, above VSD - so more deoxygenated blood enters aorta when the RV contracts upwards

Answer 309

YES! There is a greater pressure in the RV than the LV and so blood is shunted into the LV -> CYANOSIS!

Answer 310

- **Neonates and babies**: typically manifests at around 1-2 months of life - **Family history of congenital heart disease** - **Rubella infection** - **Increased age of the mother** (over 40 years) - **Alcohol consumption in pregnancy** - **Diabetic mother** - **Down syndrome**: trisomy 21

Answer 311

- Signs - **Ejection systolic murmur:** due to pulmonary stenosis - **Reduced SpO2,** particularly when distressed - **Respiratory distress** - **Cyanosis** - **Clubbing** - Symptoms - **Poor weight gain or ‘failure to thrive’** - **Difficulty feeding** - Hypercyanotic or ‘tet’ spells: **cyanosis, breathlessness and syncope**, particularly when crying or feeding - **Squatting posture**

Answer 312

- **ECG:** evidence of right ventricular hypertrophy, such as right axis deviation - **Echocardiogram + doppler flow studies:** definitive investigation and will reveal right ventricular outflow obstruction, right ventricular hypertrophy, a ventricular septal defect and an overriding aorta **WILL ALSO SEE A "BOOT SHAPED" HEART**

Answer 313

Coarctation of the aorta is defined as a narrowing in the aorta. There is an infant (70%) and an adult form (30%). Turner's Syndrome is a risk factor for this

Answer 314

Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing. So narrowing of aorta is often just before or after the ductus arteriosus

Answer 315

In severe cases: Complete or almost complete obstruction of aortic flow Patient collapses with heart failure In moderate Cases; Raised BP Systolic murmur from collateral vessels – best heard over left scapula (scapula bruit)

Answer 316

Hypertension Early coronary artery disease Early strokes Sub arachnoid haemorrhage Re-coarctation requiring repeat intervention Aneurysm formation at the site of repair teenager with high blood pressure - think coarction of the aorta

Answer 317

Signs and Symptoms: Often asymptomatic for many years Right arm hypertension Radio-femoral pulse delay – will feel radial pulse BEFORE femoral pulse Discrepant BP in upper and lower body Bruits (buzzes) over the scapulae and back from collateral vessels **Mid systolic murmur** **teenager with high blood pressure - think coarction of the aorta** Headaches and nose bleeds (due to hypertension)

Answer 318

Management Surgical repair Percutaneous repair Balloon dilation (preferred for re-coarctation) and stenting RISK OF ANEURYSM FORMATION AT SITE OF REPAIR

Answer 319

Ventricular Septal Defect When the ventricular septum has a gap in it. This can vary in size from tiny to the entire septum, forming one large ventricle.

Answer 320

Oxygenated blood then enters the left atrium and then the left ventricle. Here, blood travels from the high pressure LV to the low pressure RV (left to right shunt). The blood flowing through the VSD causes a holosystolic murmur At this point, patient's are acyanotic as there is no deoxygenated blood entering the systemic circulation.

Answer 321

Overtime, this causes increase of blood in Right sided circulation = **causing an increase in pressure.** Now **shunt is reversed** = **deoxygenated blood enters the systemic circulation** via the aorta and cause cyanosis - this is known as **Eisenmenger syndrome**.

Answer 322

- Signs - **Pansystolic murmur** at the lower left sternal border - May be a **systolic thrill on palpation** - **Cyanosis:** due to deoxygenated blood in systemic circulation - **Tachypnoea** - Symptoms - **Dyspnoea** - **Poor feeding** - **Failure to thrive**

Answer 323

- **Watch and wait:** for small VSD as they can close spontaneously - **Surgical closure of VSD** - Trans-catheter closure - Open heart surgery - **Antibiotic prophylaxis:** should be considered due to increased risk of infective endocarditis

Answer 324

Atrial septal defect - opening in the heart between the right and left atria.

Answer 325

Significant increase in blood flow through the right heart and lungs - pulmonary flow murmur. Enlarged pulmonary arteries. Right heart dilatation. SOBOE. Increased chest infection. - **Mid-systolic, crescendo-decrescendo murmur** loudest at the upper left sternal border - **Splitting S2 sound:** due to pulmonary valve closing after the aortic valve

Answer 326

- **Watch and wait:** for small ASD as it may spontaneously resolve - **Surgical closure of ASD** - Trans-catheter closure - Open heart surgery - **Anticoagulants:** used to reduce the risk of clots and stroke in adults

Answer 327

Patent ductus arteriosus (PDA) describes the persistent opening of the ductus arteriosus, after birth

Answer 328

In a foetus, Bronchioles are filled with Fluid, and pulmonary vessels are constricted due to lack of O2 *(Foetus gets O2 from placenta, not lungs)* **Pulmonary Vasoconstriction means pressure on right heart is greater than pressure on left heart**, ergo flow is from RA => LA via foramen ovale and Pulmonary artery => Aorta via Ducuts arteriosis

Answer 329

At birth, there is an **increased oxygen tension in the blood, and a **reduced level of prostaglandins;** both of which allow the patent ductus arteriosus to close. If it remains open then there is an **abnormal left to right shunt** (aorta to pulmonary artery) and eventually means the **lung circulation is overloaded with pulmonary hypertension (leading to Eisenmenger’s syndrome)** and right sided cardiac failure (due to RV hypertrophy in response to increased afterload)

Answer 330

premature babies and cases of maternal rubella

Answer 331

Continuous “machinery” murmur If large, big heart, breathless Eisenmenger’s syndrome **Differential cyanosis (clubbed and blue toes, but pink not clubbed fingers)** Large: Torrential flow from the aorta to the pulmonary arteries in infancy Breathless, poor feeding, failure to thrive Small: Little flow from the aorta to Pulmonary arteries Usually asymptomatic Murmur found incidentally Endocarditis risk

Answer 332

- **Monitor with ECHO until 1 years of age:** may close spontaneously - **Indomethacin:** NSAID that inhibits prostaglandin E2 so PDA can close - **Trans-catheter closure of PDA** - **Surgical ligation of PDA**

Answer 333

Type of **widespread sudden failure of circulatory system** , ==> lack of oxygen reaching bodies cells leading to **insufficient blood flow to the tissues,** resulting in cellular damage and harm to multiple organs If left untreated, **can lead to multi organ failure**

Answer 334

Often defined by low BP (mean arterial pressure <65mmHg), evidence of tissue hypoperfusion, raised serum lactate.

Answer 335

Septic Anaphylactic – Neurogenic Hypovolaemic – Cardiogenic shock *Sheffield's, annoying, naughty children's hospital*

Answer 336

Hypovolaemic - loss of **>20% of body's fluid/fluid supply**, so body cant sufficiently pump enough blood around the body. Either HAEMORRHAGIC, OR NON HAEMORRHAGIC (due to fluid loss)

Answer 337

Trauma GI bleeding Fractures Ruptured aortic aneurysms

Answer 338

Cardiogenic (pump failure) – heart isn’t pumping Cardiac tamponade. Pulmonary embolism. Acute MI. Fluid overload.

Answer 339

Neurogenic – nervous system damaged so can’t control BP Classically see **hypotension** (secondary to massive vasodilation from loss of sympathetic tone), **bradycardia and a flushed appearance** (again secondary to vasodilation). Typically caused by a spinal cord injury above T6

Answer 340

Sepsis is a condition where the body launches a large immune response to an infection that causes systemic inflammation and affects the functioning of the organs of the body.

Answer 341

Septic shock is defined when arterial blood pressure drops and results in organ hypo-perfusion

Answer 342

Endotoxins *(most commonly found on Gram negative bacteria)* get recognised by *Macrophages, lymphocytes, mast cells etc* and releases various **Cytokines, TNF, interleukins,** that activate other parts of the immune system, leading to the further release of **nitrous oxide and other vasodilators** This causes **endothelium of blood vessels to become more permeable**, leading to oedema, and **decreased intravascular volume**

Answer 343

The oedema around the blood vessels **decreases the amount of oxygen that reaches the tissues.** In addition coagulation system starts depositing **fibrin throughout circulation**, which also decreases the perfusion of O2 to organs

Answer 344

It also leads to consumption of platelets and clotting factors as they are being used up to form the clots within the circulatory system. This leads to thrombocytopenia, haemorrhages and an inability to form clots and stop bleeding. This is called disseminated intravascular coagulopathy (DIC).

Answer 345

Blood lactate rises due to hypoperfusion of tissues that starves the tissues of oxygen causing them to switch to anaerobic respiration. A waste product of anaerobic respiration is lactate.

Answer 346

Any condition that impacts the immune system or makes the patient more frail or prone to infection is a risk factor for developing sepsis: Very young or old patients (under 1 or over 75 years) Chronic conditions such as COPD and diabetes Chemotherapy, immunosuppressants or steroids Surgery or recent trauma or burns Pregnancy or peripartum Indwelling medical devices such as catheters or central lines

Answer 347

High Temp High Resp rate O2 sats decreased Low BP, despite fluids Reduced urine output cyanosis Rigors *Elderly patients often present with confusion or drowsiness or simply “off legs” Neutropenic or immunosuppressed patients may have normal observations and temperature despite being life threatening unwell*

Answer 348

Arrange blood tests for patients with suspected sepsis: Full blood count to assess cell count including white cells and neutrophils U&Es to assess kidney function and for acute kidney injury LFTs to assess liver function and for possible source of infection CRP to assess inflammation Clotting to assess for disseminated intravascular coagulopathy (DIC) Blood cultures to assess for bacteraemia Blood gas to assess lactate, pH and glucose Additional investigations can be helpful in locating the source of the infection: Urine dipstick and culture Chest xray CT scan if intra-abdominal infection or abscess is suspected Lumbar puncture for meningitis or encephalitis

Answer 349

Patients should be assessed and treatment initiated within 1 hour of presenting with suspected sepsis. This involves performing the sepsis six. This involves three tests and three treatments. BUFALO Blood Culture Urine - measure output - Fluids - get some in Antibiotics Lactate - measure Oxygen - give ***measuring urine output will indicate how well the kidneys are perfused - which can indicate perfusion for the rest of the body***

Answer 350

An INR (international normalized ratio) is a type of **calculation based on PT test results.** A prothrombin time (PT) test measures how long it takes for a clot to form in a blood sample. A PT/INR test is most often used to: **See how well warfarin is working.** Find out the reason for abnormal blood clots Find out the reason for unusual bleeding Check clotting function before surgery Check for liver problems

Answer 351

The INR goal for people who take warfarin is **usually from 2 to 3.5.** INR levels that are too low may mean you are at risk for dangerous blood clots. INR levels that are too high may mean you are at risk for dangerous bleeding.

Answer 352

Primary prevention prevents the condition developing altogether (eg no smoking, eliminate risk factors before the condn develops) Secondary prevention aims to tackle a disease that is diagnosed but has not become complicated yet (i.e to manage the disease conservatively before symptoms ensue) Tertiary prevention is essentially preventing complications of the condition eg surgical procedures, medications