Cardio fifth yr

Question 1

What is pericarditis + its causes?

Answer 1

Condition referring to inflammation of pericardial sac - lasting for less than 4-6 weeks

Aetiology = viral infections (Coxsackie), TB, uraemia, post MI (early - fibrinous pericarditis, late - autoimmune pericarditis (Dresslers)), radiotherapy, CTD (SLE, RA), hypothyroidism, malignancy (lung/breast), trauma

Question 2

Features of pericarditis?

Answer 2

Chest pain - can be pleuritic, relieved by sitting forwards

Non-productive cough

Dyspnoea

Flu-like Sx

Pericardial rub

Question 3

Ix and Tx for pericarditis?

Answer 3

ECG - global/widespread, saddle-shaped ST elevation, PR depression

Transthoracic ECHO

Bloods - inflammatory markers, troponin (30% of pt’s may have elevated troponin - indicates possible myopericarditis)

Outpatient, unless fever >39 or elevated troponin then inpatient

Treat underlying cause

Strenuous physical activity avoided until Sx resolution

Combination of NSAIDs and colchicine are first line with acute idiopathic or viral pericarditis - until Sx resolution and normalitistion of inflammatory markers, followed by tapering of dose

Question 4

RFs for infective endocarditis?

Answer 4

previous episode of endocarditis

previously normal valves - MV most commonly affected

rheumatic valve disease

prostethic valves

congenital heart defects

IVDUs - typically causing tricuspid lesion

recent piercings

Question 5

Causes of infective endocarditis?

Answer 5

Staph aureus - most common cause - particularly common in acute presentation and IVDUs

Strep viridian’s - most common in developing countries, linked with poor dental hygiene

Staph epidermidis - colonise indwelling lines, most common following prosthetic valve surgery, 2 months post-op spectrum of organisms returns to normal

Strep bovis - associated with colorectal cancer

Non-infective - SLE, malignancy (marantic endocarditis)

Culture negative causes - prior ABx therapy, Coxiella burnetti, Bartonella, Brucella, HACEK (haemophilis, actinobacillus, cardiobacterium, eikenella, kingella)

Question 6

Poor prognostic factors for infective endocarditis?

Answer 6

Staphylococcus aureus infection

prosthetic valve (especially ‘early’, acquired during surgery)

culture negative endocarditis

low complement levels

Question 7

What is infective endocarditis?

Answer 7

condition where the inner lining of the heart (the endocardium) becomes inflamed secondary to an infection.

M>F (2:1)

higher in multimorbid pt’s, elderly, internal cardiac devices, IVDU

mostly left-sided

divided into native or prosthetic valve

Question 8

Pathophysiology of infective endocarditis?

Answer 8

Transient bacteraemia

Damage to valvular tissue - aggregation of platelets and fibrin

Formation of vegetations - pathogens bind to platelet-fibrin matrix and proliferate causing vegetation

Vegetations can embolism causing further complications. Emboli from left side > cerebral infarcts or cerebral abscess. Right side - mycotic aneurysms, pulmonary infarcts, pulmonary abscesses

Deposition of immune complexes (type 3 hypersensitivity reaction) in skin, kidneys, eyes

Question 9

Sx of infective endocarditis?

Answer 9

Hx - systemic infection (fever, malaise, night sweats, anorexia), anaemia (fatigue, breathlessness)

O/E
fever, tachycardia
new or changing heart murmur
splinter haemorrhages
oslers nodes (tender in fingers)
Janeway lesions (painless on palms)
Roth spots - retinal haemorrhages, pale in centre
clubbing - late sign
mild splenomegaly
bi-basal lung crepitation

clinical features from emboli (e.g., weakness from stroke)

Question 10

Ix for infective endocarditis?

Answer 10

Vitals

ECG - exclude AV block as may be seen in aortic root abscesses which is a rare complication of IE

urine dipstick - microscopic haematuria

blood cultures - 3 sets taken 30 mins apart

FBC - exclude anaemia, check WCC to check infection

CRP/ESR - inflammatory markers

U&E - baseline if starting on nephrotoxic ABx such as gentamicin

TTE - identify vegettions
TOE - more detail than TTE
CXR - part of infection screen if Dx unclear, or if HF suspected
CT - if root abscess present

Question 11

Modified Duke criteria for infective endocarditis?

Answer 11

Infective endocarditis diagnosed if
pathological criteria positive, or
2 major criteria, or
1 major and 3 minor criteria, or
5 minor criteria

Pathological criteria - Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)

Major criteria - positive blood cultures (2 positive BC’s showing typical organisms consistent with IE), evidence of endocardial involvement (positive ECHO, new valvular regurgitation)

Minor criteria - predisposing heart condition or IVDU, microbiological evidence doesn’t meet major criteria, fever >38, vascular phenomena (major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura), immunological phenomena (glomerulonephritis, Osler’s nodes, Roth spots)

Question 12

Management of infective endocarditis?

Answer 12

IV ABx for 2 weeks before switching to oral. Tx for at least 6 weeks in prosthetic valve, 2-6 weeks for native valve.

start of the antibiotic course is taken from the first day a negative set of blood cultures is obtained

choice of antibiotic regimen depends on multiple factors including previous antibiotic use, the type of valve affected (native vs prosthetic), the microorganism involved and the antibiotic sensitivity of the particular organism

initial blind - native (amoxicillin and consider low-dose gentamicin), pen allergic, MRSA or severe sepsis (vancomycin + low dose gentamicin), prosthetic valve (vancomycin, rifampicin, + low dose gentamicin)

Native caused by staph - flucloxacillin

Caused by streptococci - benzylpenicillin

Indications for surgery:
severe valvular incompetence
aortic abscess (^ PR interval)
infections resistant to ABx/fungal infectons
cardiac failure refractory to standard medical Tx
recurrent emboli after ABx Tx

Question 13

Complications of infective endocarditis?

Answer 13

Localised = valve destruction, HF, arrhythmias and conduction disorders, MI, pericarditis, aortic root abscess

Systemic = emboli, immune complex deposition, septicaemia, death

Question 14

Management of stable angina?

Answer 14

Lifestyle changes - smoking cessation, cut down alcohol intake, dietary modification, exercise, target BMI <25

Medication - all pt’s receive aspirin and a statin if no CI. Sublingual GTN to abort angina attacks. Beta-blocker or calcium-channel blocker first-line depending on comorbidities, CI’s and pt preference.

if Ca-channel blocker as mono therapy should be rate-limiting - so verapamil or diltiazem. If in combination with beta-blocker then longer-acting dihydropyridine (amlodipine, nifedipine).

If poor response to initial Tx, then increase to maximum tolerated dose.

If not tolerated, add BB or CCB depending on which mono therapy

If can’t tolerate addition of CCB or BB, consider: long-acting nitrate, ivabradine, nicorandil, ranolazine

if pt taking both BB and CCB, then only add third drug whilst awaiting PCI or CABG

if using nitrate - asymmetric dosing interval to minimise nitrate tolerance

Procedure/surgical intervention - PCI with coronary angioplasty (catheter, ballon dilatation, stent)

CABG - if severe stenosis, midline sternotomy scar, graft vein (usually great saphenous vein) and bypass stenosis,

Question 15

What is angina?

Answer 15

Constricting chest pain, due to increased demand of the heart (during exertion) but there is insufficient supply of blood to meet demand

due to narrowing of coronary arteries reducing blood flow to myocardium

stable as on exertion and relieved by rest or GTN

NICE define anginal pain as the following:
1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
2. precipitated by physical exertion
3. relieved by rest or GTN in about 5 minutes
patients with all 3 features have typical angina
patients with 2 of the above features have atypical angina
patients with 1 or none of the above features have non-anginal chest pain

Question 16

Ix for stable angina?

Answer 16

For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes):

1st line: CT coronary angiography - gold standard
2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia) - MPS with sPECT, stress ECHO
3rd line: invasive coronary angiography

Baseline Ix:
examination - heart sounds, signs of HF, BMI
BP
ECG
FBC - check for anaemia
U&Es - prior to starting ACEi and other meds
LFTS - prior to statins
Lipid profile
TFTs - thyrotoxicosis can exacerbate angina
HbA1c and fasting glucose

Question 17

MOA of nitrates?

Answer 17

release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels

in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand

Question 18

Side effects of nitrates?

Answer 18

hypotension
tachycardia
headaches
flushing

nitrate tolerance - asymmetric dosing

Question 19

Why are beta-blockers not used concurrently with non-dihydropyridine calcium channel blockers such as verapamil?

Answer 19

risk of complete heart block

Question 20

What is heart failure?

Answer 20

defined as a clinical syndrome where the heart is unable to pump enough blood to meet the metabolic needs of the body

usually result of structural or functional heart disease, but the term is also sometimes used more broadly e.g. high-output heart failure

Question 21

How is heart failure classified?

Answer 21

By ejection fraction - can have normal or abnormal LVEF. Reduced LVEF is typically defined as < 35 to 40%. So HF-rEF or HF-pEF. HF-rEF patients typically have systolic dysfunction (impaired myocardial contraction during systole - ineffective pumping), whereas HF-pEF patients have diastolic dysfunction (impaired ventricular filling during diastole - ineffective filling)

By time - acute or chronic. Most urgent Sx are usually due to LVF causing pulmonary oedema.

By left/right - HF-rEF and HF-pEF typically develop left-sided heart failure - due to increase LV afterload (HTN or aortic stenosis) or increase LV preload (AR resulting in back flow to LV)
Right-sided heart failure is caused by either increased right ventricular afterload (e.g. pulmonary hypertension) or increased right ventricular preload (e.g. tricuspid regurgitation).

High-output HF - ituation where a ‘normal’ heart is unable to pump enough blood to meet the metabolic needs of the body. Causes = anaemia, AVM, Paget’s, pregnancy, thyrotoxicosis, thiamine deficiency

Question 22

Systolic vs diastolic dysfunction in heart failure?

Answer 22

Systolic:
Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Arrhythmias

Diastolic:
Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis

Question 23

Sx of heart failure?

Answer 23

Left ventricular failure typically results in:
pulmonary oedema
dyspnoea
orthopnoea
paroxysmal nocturnal dyspnoea
bibasal fine crackles
cardiac wheeze
cardiac cachexia - WL

Right ventricular failure typically results in:
peripheral oedema
ankle/sacral oedema
raised jugular venous pressure
hepatomegaly - right hypochondriac pain
weight gain due to fluid retention
anorexia (‘cardiac cachexia’)

Question 24

What is cardiac output?

Answer 24

stroke volume X HR

stroke volume - volume of blood pumped in 1 beat

Question 25

What is ejection fraction?

Answer 25

stroke volume / end diastolic volume normal 55-70%

Question 26

Causes of HFrEF?

Answer 26

decreased contractility - coronary artery disease, volume overload (valvular disease - MR/AR, and RAAS neurohormonal system) and dilated cardiomyopathy increased afterload - HTN, aortic stenosis - LV becomes hypertrophied, (increasing O2 demand, decreasing O2 supply)

Question 27

Causes of HFpEF?

Answer 27

stiff left ventricle left ventricular hypertrophy - doesn't stretch, doesn't fill during diastole restrictive cardiomyopathy myocardial fibrosis pericardial constriction

Question 28

RFs for HFrEF and HFpEF?

Answer 28

obesity HTN DM renal disease

Question 29

RFs for HFpEF?

Answer 29

elderly 2:1 F:M higher co-morbidity burden - HTN, AF, anaemia, COPD

Question 30

Dx of heart failure?

Answer 30

clinical diagnosis Hx O/E - bibasal crackles, peripheral oedema, raised JVP, additional heart sounds (S3 in dilated ventricle, S4 poor LV compliance)

Question 31

Ix for heart failure?

Answer 31

NTproBNP - released from atria and ventricle during volume expansion and pressure overload - prognostic marker if high (>2000) - assessment within 2 wks if raised (400-2000) - assessment within 6 wks Imaging - CXR - pulmonary oedema, pleural effusion, upper flow distribution, cardiomegaly ECHO - valves, volume of chambers, EF

Question 32

Scoring systems for HF?

Answer 32

Framingham Boston

Question 33

Tx of HF?

Answer 33

reduce mortality and manage Sx loop diuretics don't reduce mortality - just Sx First-line - ACEi and BB. One at time. ACEi and BB have no effect on mortality in heart failure with preserved ejection fraction Second-line - aldosterone antagonist. Can cause hyperkalaemia (as well as ACEi) so monitor K+. SGLT-2 if HFrEF Third-line - initiated by specialist - ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy Surgical: Implantable cardiac defibrillators (if EF <35% due to risk of VT/VF) Cardiac resynchronisation therapy (if EF <35% and QRS>150 or LBBB, paces left and right ventricle together) Other treatments offer annual influenza vaccine offer one-off pneumococcal vaccine

Question 34

Classification of HF?

Answer 34

The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure: NYHA Class I no symptoms no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations NYHA Class II mild symptoms slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea NYHA Class III moderate symptoms marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms NYHA Class IV severe symptoms unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

Question 35

Factors affecting BNP levels?

Answer 35

Increased - LVH, ischaemic, tachycardia, RV overload, hypoxia (including PE), GFR <60ml/min, sepsis, COPD, DM, age>70, liver cirrhosis decreased - obesity, diuretics, ACEi, BB, ARB, aldosterone antagonists

Question 36

Criteria for ivabradine?

Answer 36

sinus rhythm > 75/min and a left ventricular fraction < 35%

Question 37

Criteria for sacubitril-valsartan?

Answer 37

criteria: left ventricular fraction < 35% is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs should be initiated following ACEi or ARB wash-out period

Question 38

Criteria for digoxin?

Answer 38

strongly indicated if there is coexistent atrial fibrillation Not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties

Question 39

Criteria for cardiac resynchronisation therapy?

Answer 39

widened QRS (e.g. left bundle branch block) complex on ECG

Question 40

Effects of BNP?

Answer 40

vasodilator diuretic and natriuretic suppresses both sympathetic tone and the renin-angiotensin-aldosterone system

Question 41

Summary of acute HF?

Answer 41

sudden onset or worsening of the symptoms of heart failure. Thus it may present with or without a background history of pre-existing heart failure causes T1RF Iatrogenic (e.g. aggressive IV fluids in frail elderly patient with impaired left ventricular function) Causes of de novo HF - ischaemia, Viral myopathy, Toxins, Valve dysfunction Causes of decompensated HF - Acute coronary syndrome, Hypertensive crisis, Acute arrhythmia, Valvular disease

Question 42

Features of acute HF?

Answer 42

Sx - SOB, reduced exercise tolerance, oedema, fatigue, cough (frothy white/pink sputum) Signs - cyanosis, tachycardia, elevated JVP, displaced apex beat, bibasal crackles, wheeze, S3

Question 43

Ix for acute HF?

Answer 43

Blood tests – this is to look for any underlying abnormality such as anaemia, abnormal electrolytes or infection. FBC, U&E, LFTs, CRP/ESR, BNP, TFT, cardiovascular bloods (lipid, HbA1c, glucose) Chest X-ray – findings include pulmonary venous congestion, interstitial oedema and cardiomegaly Echocardiogram – this will identify pericardial effusion and cardiac tamponade B-type natriuretic peptide – raised levels (>100mg/litre) indicate myocardial damage and are supportive of the diagnosis.

Question 44

Management of acute HF?

Answer 44

Pour away (stop) their IV fluids Sit up Oxygen Diuretics IV loop diuretics O2 vasodilators - if concomitant myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease if respiratory failure - CPAP if hypotension/cardiogenic shock - inotropic agents (e.g. dobutamine), vasopressors (e.g. norepinephrine), mechanical circulatory assistance (e.g. intra-aortic balloon counterpulsation or ventricular assist devices) Stop BB if patient has heart rate less than 50 beats per minute, second or third degree atrioventricular block, or shock IV opiates not recommended - act as vasodilators MDT approach - GP, cardiologisy, HF specialist nurses, OT, PT, social care

Question 45

Mechanism of PND?

Answer 45

fluid settling across a large surface area of their lungs as they sleep lying flat. As they stand up the fluid sinks to the lung bases and their upper lungs clear and can be used more effectively. during sleep the respiratory centre in the brain becomes less responsive so their respiratory rate and effort does not increase in response to reduced oxygen saturation like it normally would when awake. This allows the person to develop more significant pulmonary congestion and hypoxia before waking up and feeling very unwell. less adrenalin circulating during sleep. Less adrenalin means the myocardium is more relaxed and this worsens reduces the cardiac output.

Question 46

What are inotropes?

Answer 46

strengthen the force of heart contractions and improve heart failure, however they need close titration and monitoring, so by this point you would need to send the patient to the local coronary care unit / high dependency unit / intensive care unit.

Question 47

SE of ACEi?

Answer 47

cough angioedema: may occur up to a year after starting treatment hyperkalaemia first-dose hypotension: more common in patients taking diuretics

Question 48

SE of beta blockers?

Answer 48

bronchospasm cold peripheries fatigue sleep disturbances, including nightmares erectile dysfunction

Question 49

What is atrial fibrillation?

Answer 49

Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and irregularly. This due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node. This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles. This results in: Irregularly irregular ventricular contractions Tachycardia Heart failure due to poor filling of the ventricles during diastole Risk of stroke

Question 50

Features of AF?

Answer 50

Asymptomatic Palpitations SOB Syncope (dizziness/fainting) Symptoms of associated conditions - stroke, sepsis, thyrotoxicosis

Question 51

Differentials for irregularly irregular pulse?

Answer 51

Atrial fibrillation Ventricular ectopics These can be differentiated using an ECG. Ventricular ectopics disappear when the heart rate gets over a certain threshold. Therefore a regular heart rate during exercise suggests a diagnosis of ventricular ectopics.

Question 52

What is valvular AF?

Answer 52

Valvular AF is defined as patients with AF who also have moderate or severe mitral stenosis or a mechanical heart valve. AF without valve pathology or with other valve pathology such as mitral regurgitation or aortic stenosis is classed as non-valvular AF.

Question 53

Most common causes of AF?

Answer 53

Sepsis Mitral Valve Pathology (stenosis or regurgitation) Ischemic Heart Disease Thyrotoxicosis Hypertension

Question 54

AF findings on ECG?

Answer 54

Absent P waves Narrow QRS Complex Tachycardia Irregularly irregular ventricular rhythm

Question 55

Treatment of AF?

Answer 55

There are two principles to treating atrial fibrillation: Rate or rhythm control Anticoagulation to prevent stroke Rate control - The higher the heart rate, the less time is available for the ventricles to fill with blood, reducing the cardiac output. The aim is to get the heart rate below 100 to extend the time during diastole when the ventricles can fill with blood. NICE guidelines (2014) suggest all patients with AF should have rate control as first line unless: There is reversible cause for their AF Their AF is of new onset (within the last 48 hours) Their AF is causing heart failure They remain symptomatic despite being effectively rate controlled Then rhythm control used. Return to sinus rhythm. This can be achieved through a single “cardioversion” event that puts the patient back in to sinus rhythm or long term medical rhythm control that sustains a normal rhythm.

Question 56

Options for rate control in AF?

Answer 56

Beta blocker is first line (e.g. atenolol 50-100mg once daily) Calcium-channel blocker (e.g. diltiazem) (not preferable in heart failure) Digoxin (only in sedentary people, needs monitoring and risk of toxicity)

Question 57

Summary of cardioversion in AF?

Answer 57

There are two options for cardioversion: Pharmacological cardioversion Electrical cardioversion Pharmacological Cardioversion: NICE guidelines (2014) say for pharmacological cardioversion first line is: Flecanide Amiodarone (the drug of choice in patients with structural heart disease) Electrical Cardioversion: The aim of electrical cardioversion is to rapidly shock the heart back into sinus rhythm. This involves sedation or a general anaesthetic and using a cardiac defibrillator machine to deliver controlled shocks in an attempt to restore sinus rhythm.

Question 58

Long Term Medical Rhythm Control in AF?

Answer 58

Beta blockers are first line for rhythm control Dronedarone is second line for maintaining normal rhythm where patients have had successful cardioversion Amiodarone is useful in patients with heart failure or left ventricular dysfunction

Question 59

What is paroxysmal atrial fibrillation?

Answer 59

when the AF comes and goes in episodes, usually not lasting more than 48 hours. anti coagulated based on CHADVASc score may be appropriate for a “pill in the pocket” approach. This is where they take a pill to terminate their atrial fibrillation only when they feel the symptoms of AF starting. To be appropriate for a pill in the pocket approach they need to have infrequent episodes without any underlying structural heart disease. - this uses flecanide

Question 60

Summary of anticoagulation in AF?

Answer 60

uncontrolled and unorganised movement of the atria leads to blood stagnating in the left atrium, particularly in the atrial appendage. Can lead to thrombus, and if mobilises becomes embolus. Can cause ischaemic stroke. Anticoagulation based on CHADVASC - reduces risk by 2/3 HASBLED/ORBIT score

Question 61

Summary of CHA2DS2-VASc

Answer 61

List of RFs. The higher the score the higher the risk of developing a stroke or TIA and the greater the benefit from anticoagulation. Score: 0: no anticoagulation 1: consider anticoagulation >1: offer anticoagulation C – Congestive heart failure H – Hypertension A2 – Age >75 (Scores 2) D – Diabetes S2 – Stroke or TIA previously (Scores 2) V – Vascular disease A – Age 65-74 S – Sex (female)

Question 62

Summary of ORBIT tool?

Answer 62

ORBIT tool for assessing a patient’s risk of major bleeding whilst on anticoagulation. It is scored based on: Low haemoglobin or haematocrit Age (75 or above) Previous bleeding (gastrointestinal or intracranial) Renal function (GFR less than 60) Antiplatelet medications

Question 63

Summary of HASBLED tool?

Answer 63

H – Hypertension A – Abnormal renal and liver function S – Stroke B – Bleeding L – Labile INRs (whilst on warfarin) E – Elderly D – Drugs or alcohol

Question 64

DOACs vs Warfarin?

Answer 64

DOAC - more expensive, no monitoring, no major interaction problems Warfarin - cost of monitoring, restrictions for patient,

Question 65

What is S1?

Answer 65

Closure of AV valves - tricuspid and mitral Start of systolic contraction of ventricles

Question 66

What is S2?

Answer 66

Closure of semilunar valves - pulmonary and aortic valves Once systolic contraction is complete

Question 67

What is S3?

Answer 67

heard roughly 0.1 seconds after the second heart sound rapid ventricular filling causing chord tendineae to pull to their full length and then twang like a guitar string normal in young healthy people - as ventricles allow rapid filling Older people = indicates heart failure - as ventricles and chord are stiff and weak so reach limit much faster than normal.

Question 68

What is S4?

Answer 68

Heard before S1 Always abnormal and relatively rare to hear Stiff or hypertrophic ventricle - turbulent flow from atria contracting against a non-compliant ventricle

Question 69

What is Erbs point?

Answer 69

Third intercostal space of left sternal border - best area for listening to heart sounds (S1 and S2)

Question 70

Special manoeuvres to emphasise murmurs?

Answer 70

Patient on left hand side - mitral stenosis Patient sat up, leaning forward and holding exhalation - aortic regurgitation

Question 71

How to assess a murmur?

Answer 71

SCRIPT S – Site: where is the murmur loudest? C – Character: soft / blowing / crescendo (getting louder) / decrescendo (getting quieter) / crescendo-decrescendo (louder then quieter) R – Radiation: can you hear the murmur over the carotids (AS) or left axilla (MR)? I – Intensity: what grade is the murmur? 1 - Difficult to hear 2 - Quiet 3 - Easy to hear 4 - Easy to hear with a palpable thrill 5 - Can hear with stethoscope barely touching chest 6 - Can hear with stethoscope off the chest P – Pitch: is it high pitched or low and grumbling? Pitch indicates velocity. T – Timing: is it systolic or diastolic?

Question 72

How does valvular heart disease cause hypertrophy/dilatation?

Answer 72

Hypertrophy - thickening both outwards and into the chamber Dilatation - thinning and expanding - balloon! Stenosis = pushing against stenotic valve so muscle has to try harder = hypertrophy MS = left atrial hypertrophy AS - LV hypertrophy Regurgitation = leaky valve allows blood to flow back into chamber and hence stretches muscle = dilatation MR = left atrial dilatation AR - left ventricular dilatation

Question 73

Summary of mitral stenosis?

Answer 73

Causes = rheumatic heart disease, infective endocarditis Mid-diastolic, low pitched "rumbling" - due to low velocity of blood flow Loud S1 = due to requiring large systolic force to shut, and then shutting suddenly Associated with: Malar flush - due to back-pressure of blood into pulmonary system, caused a rise in CO2 and vasodilation AF - caused by LA struggling to push blood through stenotic valve causing strain, electrical disruption and resulting fibrillation

Question 74

Summary of mitral regurgitation?

Answer 74

When incompetent mitral valve allows blood to leak back through during systolic contraction of left ventricle Results in congestive cardiac failure as causes reduced ejection fraction, and backlog of blood waiting to be pumped through left side of the heart Pan-systolic, high-pitched 'whistling' murmur due to high velocity blood flow through the leaky valve. Radiates to left axilla. May hear S3 Causes = idiopathic weakening of valve with age, IHD, IE, rheumatic heart disease, CTD (EDS and Marfan)

Question 75

Summary of aortic stenosis?

Answer 75

Most common valve disease Ejection-systolic, high pitched. Crescendo-decresendo - due to speed of blood flow across valve during different parts of systole. Radiates to carotids Slow rising pulse and narrow pulse pressure Exertional syncope Causes = idiopathic age related calcification, rheumatic heart disease

Question 76

Summary of aortic regurgitation?

Answer 76

early diastolic, soft murmur Corrigans pulse (collapsing pulse) Results in heart failure due to a back pressure of blood waiting to get through the left side of the heart. Can cause Austin-Flint murmur. Heard at the apex and is an early diastolic “rumbling” murmur. This is caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate. Causes = idiopathic aged related weakness, CTD (EDS, Marfan syndrome)

Question 77

Use of adrenaline in ALS?

Answer 77

1mg ASAP for non-shockable rhythms In VF/VT - 1mg after 3rd shock Repeat adrenaline 1mg every 3-5 minutes whilst ALS continues

Question 78

Use of amiodarone in ALS?

Answer 78

amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered Further dose of 150mg after 5 shocks Lidocaine as alternative if amiodarone not available

Question 79

Reversible causes of cardiac arrest?

Answer 79

H's Hypoxia Hypovolaemia Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acideaemia and other metabolic Hypothermia T's Thrombosis (coronary or pulmonary) Tension pneumothorax Tamponade Toxins

Question 80

Summary of coarctation of the aorta?

Answer 80

Congenital narrowing of descending aorta More common in males SX: HF in infancy HTN in adult Radio-femoral delay Mid systolic murmur Apical click from aortic valve Notching of inferior border of ribs Associations - Turners, biscuspid aortic valve, berry aneurysms, neurofibromatosis

Question 81

Signs of hypothermia on ECG?

Answer 81

Bradycardia J wave First degree heart block Long QT Partial and ventricular arrhythmias