general

Question 1

what are the medical terms for 1) SOB lying flat 2) episodes of SOB at night?

Answer 1

1. orthopnoea

2. paroxysmal nocturnal dyspnoea (PND)

Question 2

define heart failure

Answer 2

clinical syndrome characterised by typical symptoms that may be accompanied by signs caused by structural and/or functional cardiac abnormality, resulting in reduced CO and/or elevated intracardiac pressures at rest or during stress

symptoms (may not have all and some may be predominant at times):

• dyspnoea on exertion and fatigue
• orthopnoea
• paroxysmal nocturnal dyspnoea
• fluid retention (may cause pulmonary or peripheral oedema)
• nocturnal cough (±pink frothy sputum) or wheeze
• light-headedness or syncope
• anorexia

Question 3

what signs would suggest HF?

Answer 3

typical signs:

• tachycardia at rest
• low systolic pressure (BP)
• displaced apex (LV dilation) or RV heave (pulmonary HTN)
• narrow pulse pressure or pulses alternates
• raised JVP
• gallop rhythm due to the presence of S3
• murmurs of mitral or aortic valve disease
• bilateral basal end-inspiratory crackles ± wheeze
• tachypnoea
• pleural effusions
• tender hepatomegaly - pulsatile in tricuspid regurgitation can be with ascites
• peripheral oedema
• in acute failure, the pt may look ill and exhausted and there may be cyanosis

Question 4

what initial med can you give to a pt presenting with HF symptoms while you are waiting for results from blood, CXR etc.?

Answer 4

furosemide 20mg tablets
-> start with one in the morning, increasing to 2 if feel the tablet is helping with swelling and breathlessness

(loop diuretic - act on the thick ascending limb. inhibit transport of the Na+, 2Cl- and K+. typically used in pulmonary oedema due to LV failure and in pt’s with chronic HF)

Question 5

the European Society of Cardiology guidelines require that there be symptoms, signs and objective evidence present before a diagnosis of HF can be made. list example for these 3 categories

Answer 5

1. typical symptoms:
   - ankle oedema
   - fatigue
   - breathlessness
2. typical signs:
   - tachycardia
   - peripheral oedema, hepatosplenomegaly
   - tachypnoea
   - pulmonary effusion
   - raised JVP
3. objective evidence of a structural or functional abnormality of the heart at rest:
   - raised natriuretic peptide concentration
   - cardiomegaly
   - echo abnormality
   - 3rd heart sound
   - cardiac murmurs

Question 6

what is the significance of the ECG in diagnosis HF?

Answer 6

• can be used firstly as a screening tool to assess the likelihood of HF and the need for subsequent echocardiography to confirm or refute a diagnosis
• normal ECG makes HF very unlikely
• the ECG abnormalities reported in HF are non-specific, and relatively common in older pts
• the ECG abnormalities in pt’s with HF include:
• > pathological Q waves
• > LBBB
• > LVH
• > AF
• > non-specific ST and/or T-wave changes

*ECG not only identifies potential etiological factors (e.g. MI or arrhythmias), but is also necessary for Tx decisions e.g. rate control and anticoagulation for AF or pacing for bradycardia

Question 7

what features of a CXR suggest HF?

Answer 7

• helps exclude other causes of SOB and look for supportive evidence for a possible Dx of HF
• can’t diagnose HF on its own
• > pulmonary venous redistribution with upper lobe blood diversion on has been shown to have 65% sensitivity for increased preload in pt’s with HF
• > cardiomegaly had 51% sensitivity for decreased ejection fraction in its with HF

Question 8

what is the diagnostic test for HF?

Answer 8

echocardiogram

Question 9

what lifestyle advise can you give to someone with HF?

Answer 9

• reduce weight
• nutritional support
• avoid salt (2g/day)/ sodium restriction
• take care to avoid excessive dehydration
• monitor fluid retention by weighing themselves (sudden weight gain >2kg in 3days, advice should be sought)
• restrict alcohol intake

Question 10

heart failure can be divided into what two types based on ejection fraction (% of the blood in the left ventricle which is pumped out with each heartbeat)

Answer 10

1. heart failure with reduced ejection fraction (HFeEF)/ systolic ventricular dysfunction:
   - defined as heart failure with an ejection fraction <40% (normal 50-65%)
   - impaired cardiac contractibility
2. heart failure with preserved ejection fraction (HFpEF)/ diastolic ventricular dysfunction:
   - usually, relaxation rather than contraction of the LV is affected, and ejection fraction is normal or at least 40%
   - normal ejection fraction but impaired systolic ventricular relaxation and decreased filling

Question 11

what three mechanisms can influence the SV and how can they be modified?

Answer 11

1. contractibility
   - extrinsic mechanism
   - modify the heart so there Is the same EDV, but greater degree of blood ejected
   - the SNS acts on the entire heart: sympathetic nerves (noradrenaline) act on beta-1 receptors and alter Ca++ storage in SR
   (- +ve ionotropes = noradrenaline ^ and drugs such as dobutmine. -ve ionotropes = PNS (acetylcholine) + BB)
2. Preload
   - intrinsic mechanism
   - increased EDV (more blood in = more blood out)
   - due to properties of the heart. increase in preload triggers the Frank-Starling mechanism
   - increase myosin stretch increases force
   (- influenced by venous return, blood volume and atrial contraction)
3. after load
   - increased by HTN, atherosclerosis of vasoconstriction
   - also in terms of the ventricle itself

Question 12

define HF in physiological terms

Answer 12

a syndrome characterised by either or both pulmonary and systemic venous congestion and/or inadequate peripheral oxygen delivery, at rest or during stress, caused by cardiac dysfunction

Question 13

what conditions lead to heart failure?

Answer 13

1. those that damage cardiac muscle:
   - ischaemic heart disease
   - cardiomyopathies
   - myocarditis
2. those that increase the workload of the heart:
   - HTN
   - valvular disease
   - severe anaelmia
   - thyrotoxicosis
   - arteriovenous fistulas

**coronary heart disease and HTN are the most common causes of heart failure in the UK

Question 14

what conditions commonly result in systolic dysfunction?

Answer 14

those that affect:

1. contractibility - e.g. cardiomyopathy, ischaemic heart disease
2. volume overload - stretching the ventricle over time that leads to change in compliance of the vessel wall and subsequent ability to contract. e.g. MR, AR
3. dilated cardiomyopathies
4. . pressure overload - valvular stenosis, HTN

(result in increased EDV/preload (not able to move vol returning the heart forward) -> ventricular dilation -> increased ventricular wall tension)

Question 15

what conditions commonly result in diastolic dysfunction?

Answer 15

those that affect:

1. impedance of ventricular expansion expansion/ restrictive cardiomyopathy - constrictive pericarditis
2. increased wall thickness - hypertrophy
3. delayed diastolic relaxation - ageing, ischaemia
4. increase HR

Question 16

what are the 3 categories of cardiomyopathies?

Answer 16

1. dilated (85%)
   - cardiac muscle is weakened and chamber distends
   - no hypertrophy or remodelling
   - cannot pump effectively (can’t generate correct force)
   - > idiopathic, alcohol toxicity, viral myocarditis, permpartum, drugs (chemo)
2. hypertrophic (10%)
   - portion of heart becomes thickened (pattern varies, but tends to affect the septum)
   - maybe more force, but decreased volume within ventricle
   - eventual problem delivering blood to all the myocytes so risk ischaemic damage
   - can lead to dysfunction of valvular system
3. restrictive (5%)
   - not necessarily a change in thickness, a change in properties of the wall
   - may come infiltrated with fibrotic tissue, changing how that ventricle can contract and relax
   - > amyloidosis, enomyocardial fibrosis

Question 17

left heart failure often leads to right heart failure (but not necessarily the other way around). use mitral stenosis as an example of how this happens

Answer 17

change in ability for valve to open -> reduced flow -> LV not effectively filled (diastolic dysfunction) -> blood accumulates in LA ->right sided circulation wants to return blood to LA, but its now too difficult as P increased -> blood accumulates in pulmonary circulation -> increase P In the pulmonary circulation -> pulmonary HTN and oedema -> right sides hear now pumping on greater pressure -> strain on the heart and failure on the right side as a result

*most common underlying cause of mitral stenos is prior rheumatic fever

Question 18

compare acute and chronic mitral regurgitation

Answer 18

acute:

• no problem with wall properties, but blood being pushed back -> higher LA P
• get same problem as Mitral Stenosis with pulmonary HTN + oedema

chronic:

• changes occur in the ventricle
• dilated cardiomyopathy driven by the MR
• chronic insidious increase in EDV
• exacerbating systolic dysfunction

Question 19

how can hypertrophy trigger valvular problems?

Answer 19

• IV septum changes angle of which blood flows from LV -> aorta
• mitral valve prone to forces that can push it open –> regurgitation + narrow passage for blood to get into aorta
• anterior leaflet can obstruct any outflow and get almost complete MR occurring

Question 20

what are the clinical signs and symptoms associated with left and right HF?

Answer 20

right:

• not dealing with the venous return from systemic circulation -> accumulates blood in the vv. -> increasing pressure -> change in Starling forces (lose more fluid in the capillaries) -> oedema and ascites
• GIT congestion -> changes in exchange of nutrients and normal GI functions -> anorexia, GI distress and w.loss
• lose ability for liver to detoxify things -> accumulation

left:

• decreased CO -> don’t meet oxygen demands of myocardium itself of other tissues -> decreased activity tolerance -> cyanosis, and signs of hypoxia
• because we can’t deal with blood returning to the left side of the hear -> pulmonary congestion -> pulmonary oedema, orthopnea, cough, PND
• pulmonary congestion and HTN state increases after load that the right side of the heart needs to push against -> greater stressing/remodelling -> RSHF

Question 21

what are the causes of RV dysfunction?

Answer 21

conditions impeding flow into the lungs:

• pulmonary HTN
• valve damage/stenoso/incompetence

pumping ability of right ventricle:

• cardiomyopathy
• infarction

Left ventricular failure

congenital heart defects

Question 22

what is the pathophysiology of RV failure?

Answer 22

increased after load e.g. pulmonary HTN -> prolonged isovolumetric. contraction (contracting when both valves in/out of ventricle are shut, building up the pressure to move that blood forward) -> increased myocardial wall stress (increasing energy consumption and leading to hypertrophy) -> RV hypertrophy -> shift of IV septum -> strain on LV region (MR issue) -> RV ischaemia (because less LV output into aorta to wither ventricle) -> RV failure

Question 23

To explain the issues with the compensatory mechanisms that are initiated to deal with low cardiac output and predict how these may worsen the underlying issue in heart failure

Answer 23

• in the early stages, compensatory mechanisms (i.e. those involved in hypovolemia) maintain CO
• longer term, they contribute to worsening of the condition

1. ADH
   - decrease in CO -> decrease in MABP. this is detected by baroreceptors which trigger responses to restore blood volume (ADH).
   - > increasing the blood volume would add more stress + worsen condition
2. SNS
   - can initially be helpful by increasing contractibility but long term tachycardia (can precipitate arrhythmias), vasoconstriction, decrease perfusion of tissues –> increase workload of the heart, ischaemia, arrhythmia, damage to myocytes, decrease contractility
   - will vasoconstrict vessels to change the total peripheral resistance and try increase MABP. will actually increase after load
   - increases contractibility of the heart -> increasing workload and stress
   - also increase blood volume vis RAAS
3. RAAS
   - decrease in blood flow stimulates release of renin
   - stimulates angiotensin II formation - vasoconstriction, plus stimulated aldosterone
   - sodium and water reabsorption
   - angiotensin + aldosterone are also involved in inflammatory responses leading to deposition of fibroblasts + collagen in the ventricles. therefore, increase the stiffness and decrease contractility of the heart, leading to myocardial remodelling and progressive dysfunction

Question 24

why is the frank-staring mechanism inappropriate in HF?

Answer 24

• stretch increases force of contraction, but force means greater O2/energy demand. so, even if it initially increases the CO, it still comes with a cost of energy to an already failing system
• the curve also changes in HF: we dont get the same return in output for increase in stretch

Question 25

identify risk factors for artherosclerosis

Answer 25

• age
• sex (M>F)
• genetics
• hyperlipidaemia
• hypertension
• smoking
• diabetes

Question 26

explain the pathogenesis of artherosclerosis

Answer 26

• endothelial dysfunction with high amounts go LDLs, haemodynamic disturbances, HTN, smoking, toxins, viruses etc
• LDLs deposit in tunica intima and oxidise
• oxidised LDLs activate endothelial cells to express receptors for WBCs/ leukocytes
• adhesion of of leukocytes activated movement of monocytes into tunica intima where they become macrophages
• macrophages take up the oxidised LDLs and become foam cells
• foam cells are key in A/S: promote migration of smooth muscle cells from tunica media -> intima and promote their proliferation
• increase in sac proliferation heightens collagen synthesis -> hardening plaque
• during this whole process, foam cells die and release their lipid contents -> help growth of plaque
• as plaque grows and build up pressure it can –> rupture -> thrombosis -> coagulation occurs -> thrombus -> impede blood flow

Question 27

identify and explain the morphology of artheroma

Answer 27

• raised local plaque within intima. yellow
• core which is rich in lipid (cholesterol and cholesterol esters)
• fibrous cap formed from proliferating smooth muscle cells
• fatty streaks may be precursor

Question 28

discuss clinical features and prevention of artherosclerosis

Answer 28

CFS:

• only if complications
• thrombosis
• calcification
• aneurysmal dilation
• ischaemic events (heart, brain, lower extremities + other organs)

primary prevention:

• stop smoking
• control HTN
• weight reduction
• lowering LDL
• reduce calories intake

secondary prevention:

• prevent complication
• anti platelet drugs in thrombosis
• lower blood lipid levels

Question 29

what is the impact HF can have on pts/family/carers?

Answer 29

complex disease:

• impact on social, financial, family e.g. changing roles, strain and burden, loss of previous relationships
• feeling of uncertainty e.g illness timeline, managing changes in symptoms, medications etc
• associated poor prognosis and high morbidity e.g quality of life
• accounts for a high number of unplanned hospital admissions

Question 30

describe the different models the can help understand pt and carer/family experience

Answer 30

1. biological disruption:
   - onset of problems and recognition; initially there is symptoms but behaviours dont response until these symptoms progress and dont resolve
   - emerging disability and uncertainty; re-adjusting perspective of their own biography. uncertainty about how they will manage
   - chronic illness and mobilisation of resources; they have adjusted. information about the symptoms etc. realise how their biography has changed and how they will deal with it
2. common sense model of illness perception:
   - how pt’s view their illness
   - formulation of its perceptions which then guide coping and influence choices made
   - how pt identifies their illness; timeline; causes; consequences; controllability
3. coping mechanisms
   - involves the pt’s environment and the relationship between the 2
   - this contributes to adaption
4. health related quality of life
   - extent of which one’s usual or expected physical, emotional and social well-being are affected by a medical condition or its treatment

Question 31

identify the complexities related to self management programmes in relation to HF

Answer 31

• burden of care
• emotions - fear, anger, stress
• depression and anxiety
• complexities of health care information
• family dynamics with health care team

important to check:

• do they understand the diagnosis?
• do they have impact from HCPs to help
• motivational interviewing o help adapt to lifestyle changes

Question 32

how can we apply knowledge of pt experience to medical practice?

Answer 32

HCPs understanding illness experience means:

• more appropriate care delivered
• processes and impact that can happen to help improve QoL e.g. management of crisis, control symptoms, adherence to medical regimes, prevent living in isolation, adjusting to disease change, finance, addressing psychological/marital/social/family role changes

Question 33

describe the pathophisiology of infective endocarditis (inflammation of the structures lining the inside of the heart)

Answer 33

1. bacterial entry (or other pathogens) - e.g. from mouth via trauma or dental treatment, long-term and multiple IV access points (i.e. dialysis), bowel tumour gut translocation and spread through your bloodstream
2. bacterial adherence to damage endothelium and microthrombi
3. bacterial proliferation, neutrophil and macrophage infiltration
4. vegetation formation - inflammatory or infective material on the heart valve

Question 34

outline the diagnostic criteria for infective endocarditis

Answer 34

major criteria:

(1) blood cultures positive for IE:
- typical micro-organism consistent with IE from 2 separate blood cultures
- viridans streptococci, streptococcus gallolyticus, staphacoccus aureus or enterococcus
(2) echocardiograph (TTE then TOE) positive for vegetation; abscess; valvular perforation or in prothetic valve descant/detached

minor criteria:

(1) predisposition such as predisposing heart condition, or IVDU
(2) fever >38C
(3) vascular phenomena e.g major arterial emboli, septic pulmonary infarcts, intracranial haemorrhage, Janeway lesions
(4) immunological phenomena: glomerlonephritis, Oslers nodes, Roths spots, rheumatic factor
(5) microbiological evidence: blood cultures but doesn’t meet major criteria

criteria =
2 major criteria or
1 major and 3 minor or
5 minor

(eponymous signs = Osler nodes (painful, erythematous nodules on the tips of fingers and toes); Janeway lesions (non painful, erythematous macule on the palms of hands and soles of feet); Roth spots (retinal haemorrhages with pale centres)

Question 35

describe the management of infective endocarditis

Answer 35

mainstay = antibiotic therapy

• high conc for long time usually required IV for 2 weeks
• further oral Abs for 2-4weeks

Question 36

outline some of the complications that can occur as a result of infective endocarditis

Answer 36

• embolization from vegetation
• perforated valve leaflets
• cavities communicate via fistula
• mobile or slightly detached prosthetic
• metastic abscess formation in the brain, kidney, spleen

Question 37

describe the pathogenesis of myocarditis (inflammation of the myocardium)

Answer 37

-usually caused by viral infection (particularly coxsackie, but also diphtheria, rheumatic fever)
- anti-viral immune response from cytokines and either of the following happens:
1. viral elimination and then healed inflammation. can be no/minor myocardial injury or damaged myocytes and subsequent dilated cardiomyopathy
or;
2. viral elimination but persistent inflammatory process –> inflammatory cardiomyopathy
or;
3. chronic viral infection with/without inflammation –> viral heart disease

Question 38

describe the clinical features of myocarditis

Answer 38

• presents with acute illness characterised by fever and varying degrees of biventricular failure
• chest pain
• ECG changes (non-specific T-waves and ST changes and arrhythmias)
• troponin rise
• Hx of viral illness or serum viral titres

Question 39

outline the management of myocarditis

Answer 39

supportive car:

• bed rest
• analgesia
• HF treatment
• immunomodulation
• mechanical support

Question 40

what is the likely diagnosis if someone presents complaining of fever, malaise, night sweats and on auscultation you discover a new heart murmur?

Answer 40

infective endocarditis

Question 41

what is the name given to a form of nonbacterial endocarditis that is seen in association with systemic lupus erythematosus?

Answer 41

Libman-Sacks endocarditis

fibrin
neutrophils
lymphocytes
histocytes
deposit on the valve

Question 42

what are the strategies for Tx of chronic HF?

Answer 42

*true right sided HF is fluid managed

non-pharma

1. lifestyle factors - as per all CVD conditions
2. device therapy:
   - pacing
   - cardiac resynchronisation therapy
   - implantable cardiac defibrillators
   - coronary revascularisation
   - heart transplant

pharma
Step 1. “DAB” - (diuretic if fluid retention… start with loop), ACEi or ARB and BB

Step 2. add aldosterone antagonist e.g. spironolactone

• add if ACEi/ARB + BB and diuretic and still symptoms
• in NYHA class II-IV failure

Step 3. Sacubitril-Valsartan combination

• neprilysin inhibitor and ARB
• neprilysin inhibitor increase bioavailability of natriuretic peptides, bradykinin and substance P, resulting in vasodilatory and anti-proliferative effects
• Ivabradine = specialist use only reduced HR

other options if concurrent:

• persistent sodium/water retention -> additional diuretics (thiazides like metolazone)
• co-existing angina -> oral nitrates, amlodipine
• AF -> digoxin
• flexible dosing for DABs, may need to up and down totrate
• review BP - may be low but is pt symptomatic?
• bradycardia - if symptomatic may need to stop BB

Question 43

what are the strategies for Tx of acute (decompensated) HFpEF?

Answer 43

• sudden worsening of signs and symptoms of HF as a result of severe congestion of multiple organs
• increased dyspnoea, oedema
• causes: MI, infection, anaemia, thyroid dysfunction, arrhythmia, uncontrolled HTN

first-line TX = LMNOP:

• IV loop diuretics (cause ventilation and diuresis; reduce preload)
• IV opiates/ morphine (reduce anxiety; vasodilates, reducing preload; reduces sympathetic drive)
• IV, buccal or sublingual nitrates (GTN) (reduce preload and after load; vasodilator)
• Oxygen (maintains O2 sats)
• Positioning (keep pt upright and prevent pooling of blood)

2nd line = use isotopic agents
- increase contractibility will increase SV and CO –> increase clearance of pooled blood in ventricles
- as CO increases, baroreceptors sense change in MABP and decrease sympathetic drive and so decrease HR and TPR
(see another card)

3. milrinone
   - phosphodiester 3 inhibitor
   - increases intracellular Ca causing vasodilation and increase myocardial contractility
   - works to increase the heart’s contractility and decrease pulmonary vascular resistance

Question 44

how does the apparently paradoxical use of BB actually offer benefit in HF Tx?

Answer 44

.. may slow HR, which could decrease CO

BUT

• allows ventricle to fill more completely during diastole
• some BB (carvedilol) cause vasodilation through blockage of alpha-receptors and so decrease after load
• reduce renin release by kidney

(*start if reduced ejection fraction but stable NYHA class II-IV)

SEs:

• bradycardia
• fatigue
• bronchoconstiction/ SOB
• dizziness, cold peripheries, decreased libido

CI:

• obstructive lung disease
• PVD

Question 45

describe the MoA and uses of drugs which inhibit the RAAS system

Answer 45

ACEi:

• e.g. ramipril, lisinopril
• inhibit conversion of angiotensin I -> angiotensin II

ARB:

• e.g. candesartan, valsartan
• prevent angiotensin II binding to its cell receptors

effects of both:

• decrease sympathetic activity
• decrease vasoconstriction
• prevent stimulation of aldosterone

SEs:

• dizziness
• headache
• nausea
• ACEi= dry cough, angioedema
• ARB= back pain

CI:

• pregnancy (tetrogenic)
• bilateral renal artery stenosis

Question 46

what is the MoA of digoxin and how can it increase myocardial contractability

Answer 46

• cardiac glycoside
• in HF increases force of myocardial contraction: inhibits Na/K ATPase pump, thus affecting Na/Ca exchanger, elevating intracellular calcium levels in SR
• in AF: increase vagal efferent activity to the heart. decrease SAN firing rate (decrease HR) and decrease conduction velocity in the AV node

SEs:

• GI upset
• dizziness
• conduction abnormalities
• blurred or yellow vision

Question 47

what is the MoA and uses of inotropes (ICU)

Answer 47

• catecholamines that act on sympathomimetic system to increase myocardial contractility
• maintain CO and BP

1. dobumine (beta 1 agonist > beta 2) - use in its with Cardiogenic shock to maintain BP. increase contractility and heart rate
2. dopamine (DA > beta > alpha…. this means dose dependant) - increase renal person at low doses, can increase BP at high doses
3. isopenaline - used in emergency situations to stimulate HR
4. adrenaline (beta>alpha)
5. noradrenaline (alpha > beta) - vasopressor, cause vasoconstriction, raise BP, used in severe septic shock

Question 48

what is the initial investigation for someone presenting with HF symptoms?

Answer 48

ECG

- if normal, HF is slim

Question 49

how is HF diagnosed?

Answer 49

Ix:

• ECG
• CXR (enlarged heart)
• FBC (anaemia, check ferritin, U+Es, GFR, LFTs, TFTs, HbA1c, NT ProBMP)
• Echo (shows LV function/ valve problems)
• cardiac CT
• cardiac MRI

Question 50

what is NT ProBMP?

Answer 50

hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume

Question 51

what is the aim of treating HF?

Answer 51

• relieve symptoms
• increase exercise tolerance
• reduce incidence of acute exacerbation
• reduce mortality
• improve end of life experience for both pt’s and carers

acute aims:

• normalise ventricular filling pressure
• restore adequate tissue perfusion

Question 52

outline some of the main causes of acute pericarditis

Answer 52

• in the UK acute inflammation of the pericardium is most commonly secondary to viral infection (coxsackie, echovirus, HIV)
• other causes = uraemia (i.e. in advanced kidney disease), autoimmune rheumatic disease, trauma, infection (bacterial, tuberculosis, fungal) and malignancy (breast, lung, leukaemia and lymphoma)

Question 53

describe the clinical features, investigation and management of acute pericarditis

Answer 53

CF:

• sharp retrosternal chest pain which is characteristically relieved by leaning forward
• pain may be worse on inspiration and radiate to the neck and shoulders
• pericardial friction rub

Ix:

• ECG is diagnostic: concave (saddle-shaped) ST elevation and PR depression
• bloods (FBC, ESR, U+ES, cardiac enzymes e.g. troponin may be raised if associated myocarditis)
• CXR (cardiomegaly in cases with effusion)
• CT and CMR may be helpful in cases with thickens or inflamed pericardium

Mx:

• treat underlying disorder + NSAID (+gastric protection) for 1-2 weeks
• aspirin is the drug of choice for pt’s with recent MI
• rest
• if not improving prescribe steroids

Question 54

describe the aetiology, clinical features, Ix and management of pericardial effusion

Answer 54

aetiology:

• accumulation of fluid in the pericardial sac which may result from any of the cause of pericarditis
• commonly accompanies pericarditis
• other causes = aortic dissection, malignancy, myocardial rupture (e.g. surgical, stab wound)

CF:

• effusion obscures the apex beat and the heart sounds are soft/ muffled
• dyponea
• chest pain
• signs of local structures being compressed e.g. hiccups (phrenic nerve)
• signs of cardiac tamponade as effusion worsens

Ix:

• CXR (large globular or pear shaped heart)
• ECG (shows low voltage QRS complexes with sinus tachycardia)
• echo is diagnostic (shows echo-free zone surrounding the heart)
• invade tests to establish the cause may be necessary if persistent - pericardiocentesis, pericardial biopsy and culture or PCR

Mx:

• sought and Tx cause
• most resolve spontaneously
• BUT tamponade results if the effusion collects rapidly. pericardial fluid it drained percutaneously
• but it is re-accumulates (most commonly due to malignancy) may require pericardial fenestration

Question 55

describe what is meant by cardiac tamponade

Answer 55

• pericardial effusion that raises intrapericardial pressure, reducing ventricular filling and thus dropping CO
• can rapidly lead to cardiac arrest
• signs = tachycardia, hypotensive, raised JVP (Kussmaul’s sign), pulses paradoxus (a fall in BP of >10mmHg on inspiration)
• this is a result of increased venous return to the right side of the heart during inspiration. the increased right ventricular volume thus occupies more space within the rigid pericardium and impairs left ventricular filling

Question 56

Describe the aetiology, clinical presentation, investigation and management of constrictive pericarditis

Answer 56

heart is incased in a rigid pericardium

aetiology:
-in the UK, most cases are idiopathic in origin or result from intrapericardial haemorrhage during heart surgery

CF:

• prevents adequate diastolic filling of the ventricles
• CFs resemble those of right-sided heart failure with raised JVP (Kussmaul’s sign- JVP rises paradoxically with inspiration)
• pulses parasoxus, AF

Ix:

• CXR (normal heart with pericardial calcification)
• ECG shows low voltage qrs complex with generalises t-wave flattening
• diagnosis made on CT or MRI, which shows pericardial thickening and calcification

Mx:
- surgical excision of the pericardium