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2a Conditions- Cardio > Inflammation/ Infection > Flashcards

Inflammation/ Infection Flashcards

1
Q

Define pericarditis

A

Pericarditis is inflammation of the pericardium.

Peri (around ) card (heart) itis (inflamed)

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2
Q

What is inflammation of the pericardium?

A

Inflammation of the pericardium. The pericardium is a fibroserous, fluid-filled sack that surrounds the muscular body of the heart and the roots of the aorta, pulmonary vessels and the superior and inferior vena cava.

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3
Q

What is the aetiology of Acute pericarditis?

A
  • Idiopathic usually
  • Infection
    • Viral
      • Coxsackievirus → the most common causative pathogen.
      • Mumps
      • Epstein-Barr virus (EBV)
      • Cytomegalovirus (CMV)
      • Varicella-Zoster virus (VZV)
      • HIV
      • Echovirus
    • Bacterial – Tuberculosis
    • Fungal – Histoplasma spp.
  • Systemic autoimmune disorders (immune system attacking the pericardium)
    • Sjogren’s
    • RA rheumatoid arthritis
    • SLE
  • Trauma
  • Uraemia secondary to kidney disease
    • high levels of urea irritate the serous pericardium, making it secrete a thick pericardial fluid full of fibrin strands and white blood cells
  • Post-Myocardial Infarction
  • Dressler syndrome: post MI inflammation **
    • (inflammation of pericardium after MI damaging it)
  • Malignancy – breast, lung, leukaemia and lymphoma
  • Connective tissue dosorders
  • Full-thickness acute myocardial infarction causes pericarditis overlying the infarct
  • Certain medication e.g. penicillin, anticonvulsants
  • Other miscellaneous causes include severe renal failure, hypothyroidism, multisystem autoimmune diseases, cardiac surgery, radiotherapy, malignant infiltration, and some drugs
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4
Q

What is the pathophysiology of Acute pericarditis?

A
  • Pericardium becomes acutely inflamed, with pericardial vascularisation and infiltration with polymorphonuclear leukocytes
  • A fibrinous reaction frequently results in exudate and adhesions within the pericardial sac, and a serous or haemorrhagic effusion may develop
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5
Q

Missed detailed pathophysiology

A
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6
Q

What is the epidemiology of acute pericarditis?

A
  • Pericarditis accounts for up to 5% of presentations to the emergency department
  • In the UK, pericarditis is most commonly secondary to viral infection or MI
  • Occurs more in men
    • M>F
  • Most common 20-50 years of age
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7
Q

What are the clinical manifestations of acute pericarditis?

A

Acute pericarditis generally lasts just a few weeks, whereas chronic pericarditis lasts longer, usually more than 6 months.

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8
Q

What are the symptoms of acute pericarditis?

A

Most cases of pericarditis are self-limiting.

  • Central chest pain
    • Severe, Sudden onset, sharp, central and pleuritic
    • Sharp and pleuritic (without constricting crushing character of ischaemic pain)
    • Exacerbated by lying flat
    • Relief upon sitting up or leaning forward
    • Chest pain worse on inspiration and lying flat
      • Gets worse with heavy breathing
    • May last from hours to days
  • Prodromal viral illness: e.g. upper respiratory tract infection
  • Fever and myalgia
  • Dyspnoea - Shortness of breath
  • Peripheral oedema: suggests right-sided heart failure secondary to constrictive pericarditis
  • Hiccups – if phrenic involvement
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9
Q

What are the signs of acute pericarditis?

A
  • Pericardial friction rub (scratching sound) heard by auscultation
    • Heard at the left sternal edge as the patient leans forward
    • Extra heart sound of a to-and-fro character
    • High-pitched or squeaky
  • Tachycardia
  • Tachypnoea
  • May radiate to neck and shoulders
  • Raised JVP
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10
Q

What are the investigations of acute pericarditis?

A
  • ECG - diagnostic
    • Concave (saddle-shaped) ST segment elevation in all leads (global ST elevation) (highly sensitive)
    • PR segment depression (highly specific)
    • Followed by T-wave flattening and eventual T-wave inversion.
    • PeRicardiTiS
  • CXR
    • Bottle-water shaped silhouette
      • Should be performed in all patients may demonstrate an associated pericardial effusion; “water-bottle heart”.
    • Pneumonia common with bacterial
    • May show cardiomegaly in cases of effusion
  • Transthoracic echocardiogram
    • Should be performed in all patients to exclude a pericardial effusion or tamponade.
  • Bloods
    • ESR and CRP:elevated secondary to inflammation
    • Cardiac enzymes
      • Troponin:elevated in 35-50% of patients.
        • Troponin will be raised if there is an element of concomitant myocarditis (myopericarditis)
        • Additionally, acute coronary syndrome is a differential diagnosis and serialtroponins must be performed if acute coronary syndromeis suspected
    • FBC - Modest increase in WCC, mild lymphocytosis
    • Urea:elevated levels indicate a uraemic cause
  • friction rub sound —> thickened layers of pericarditis rub against each other and create friction rub sound
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11
Q

What is the management of acute/viral pericarditis?

A
  • NSAIDS and gastric protection (proton pump inhibitor e.g. lansoprazole)
    • Systemic corticosteroids used when resistant to NSAIDs
    • Acute idiopathic or viral pericarditis
      • 1st line: NSAIDsandcolchicine are often both used together
      • 2nd line: NSAIDs, colchicineandlow-dose prednisolone
      Colchicine: down regulation of multiple inflammatory pathways and modulation of innate immunity
      • Colchicine – inhibits migrations of neutrophils to site of inflammation to reduce risk of occurrence
  • Rest until symptoms resolve
  • Treat underlying cause if there is one e.g. steroid for autoimmune causes
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12
Q

What is the management of bacterial pericarditis?

A
  • Bacterial pericarditis
    • IV antibiotics and pericardiocentesis (removal of fluid) with washout, culture and sensitivities
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13
Q

What is the management for cardiac tamponade?

A

Urgent therapeutic pericardiocentesis

  • Pericardiocentesis – drainage of fluid if there is cardiac tamponade or symptomatic pericardial effusion
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14
Q

What is the management for refractory pericarditis?

A

Pericardectomy may be considered for refractory cases of pericarditis unresponsive to medical therapy

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15
Q

What is the differential diagnosis for acute pericarditis?

A

Pneumonia
• Pleurisy —> is a condition in which the pleura — two large, thin layers of tissue that separate your lungs from your chest wall —becomes inflamed.
• Pulmonary Embolus
• Chostocondritis
• Gastro-oesophageal reflux
• Myocardial ischaemia/infarction
• Aortic dissection

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16
Q

What are the complications for acute pericarditis?

A
  • Pericardial effusion
    • Accumulation of fluid in the pericardial sac secondary to pericardial inflammation. Perform urgent pericardiocentesis if there is evidence ofcardiac tamponade, such as a raised JVP and hypotension, as this is potentially life-threatening.
  • Myocarditis: inflammation of the myocardium. Patients may require steroids initially, whilst chronic cases of myocarditis can result in heart failure.
  • 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
    • A thickened, fibrotic pericardium limits the heart’s ability to function normally, potentially resulting in congestive heart failure, and is most commonly associated with tuberculosis. Complete resection of pericardium may be required.
  • 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
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17
Q

What are the risk factors for acute pericarditis?

A
  • Male gender
  • 20-50 years of age
  • Previous Myocardial Infarction
  • Viral or bacterial infection
  • Systemic autoimmune disorders
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18
Q

What is the prognosis for acute pericarditis?

A
  • The majority of cases of idiopathic and viral pericarditis are self-limiting, whereas bacterial (purulent) pericarditis can be fatal if untreated.
  • Factors associated with a poor prognosis include a pericardial effusion, high fever, a sub-acute course and resistance to NSAIDs.
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19
Q

What is chronic (constrictive) pericarditis?

A

If the inflammation persists for weeks to months, the process is called chronic pericarditis.

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20
Q

What is the aetiology of chronic pericarditis?

A
  • Certain causes of pericarditis such as tuberculosis, bacterial infection and rheumatic heart disease result in the pericardium becoming thick, fibrous and calcified.
  • Can occur after any form of pericarditis.
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21
Q

What is the Pathophysiology of chronic pericarditis?

A

In chronic pericarditis, immune cells initiate fibrosis of the serous pericardium which produces an inelastic shell around the heart making it hard for the ventricles to expand.

Over time, it becomes harder for the heart to relax or expand, and the stroke volume decreases. To compensate, the heart rate increases.

As these changes are chronic, allowing the body time to compensate, this condition is not as immediately life-threatening as cardiac tamponade.

In the later stages of constrictive pericarditis, the sub-endocardial layers of the myocardium may undergo fibrosis, atrophy and calcification

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22
Q

What are the clinical manifestations of chronic pericarditis?

A
  • Kussmaul’s sign: rise in jugular venous pressure and increased neck vein distension during inspiration
  • Pulsus paradoxus: an exaggeration in the normal variation in pulse pressure seen with inspiration, such that there is a drop in systolic blood pressure
  • Diffuse heart sounds
  • Right heart failure signs
  • Ascites
  • Oedema
  • Atrial dilatation
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23
Q

What are the investigations of chronic pericarditis?

A
  • CXR: small heart with/without pericardial calcification
  • ECG: low voltage QRS
  • ECHO: thickened calcified pericardium restricting the heart’s movement; small ventricular cavities
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24
Q

What is the management for chronic pericarditis?

A

May require complete resection of the pericardium

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25
Q

What are the complications of chronic pericarditis?

A

Congestive heart failure

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26
Q

What is cardiac tamponade?

A

Cardiac tamponade describes a reduction in cardiac output due to a raised intrapericardial pressure secondary to a pericardial effusion.

27
Q

What is the epidemiology of a cardiac tamponade?

A

Cardiac tamponade is a rare condition

28
Q

What is the aetiology of cardiac tamponade?

A
  • Caused by the accumulation of blood, fluid, pus, clots, or gas in the pericardial space, resulting in reduced ventricular filling and subsequent haemodynamic compromise.

Aetiology

  • Idiopathic: Unknown cause of effusion
  • Pericarditis e.g. due to
    • Infectious: viral, TB
    • Uraemia: renal failure
    • Autoimmune (e.g., dressler’s syndrome: post MI inflammation) less commonly progresses to tamponade
  • Iatrogenic
    • Interventional cardiac procedures
    • Cardiothoracic surgery
  • Malignancy
    • Lung
    • Breast
    • Haematological
  • Trauma
    • e.g. thoracic knife wound
  • Aortic dissection
    • Type A dissection: blood pools in the wall of the aorta, this can rupture and spill into the pericardium
  • Rheumatological
    • SLE
    • Rheumatoid arthritis
    • Scleroderma
29
Q

What is the pathophysiology of cardiac tamponade?

A
  • A potential complication of pericardial effusion is cardiac tamponade.
  • In this condition,the excess fluid within the pericardium puts pressure on the heart.
  • The strain prevents the heart chambers from filling completely with blood.
30
Q

Missed pathophysiology detail

A
31
Q

What are the symptoms of cardiac tamponade?

A
  • Dyspnoea
  • Chest discomfort
  • Peripheral oedema: heart failure
  • Confusion: decreased CNS perfusion
  • Coughing
  • Lightheadedness: if large effusion
32
Q

What are the signs of cardiac tamponade?

A
  • Beck’s triad:
    • Hypotension: due to reduced cardiac output
      • Falling Blood Pressure
    • Kussmaul’s sign: raised JVP (heart failure) & distended jugular veins
    • Muffled heart sounds (pericardial fluid muffles sound transmission)
  • Tachycardia: compensatory mechanism
  • Pulsus paradoxus: systolic blood pressure reduction of >10mmHg on inspiration
  • Prolonged capillary refill time
  • Cool peripheries
33
Q

What is kussmaul’s sign?

A

The atria can’t distend enough to accommodate the venous blood returning to the heart. That blood will have nowhere to go but back into the veins, causing distended jugular veins.

34
Q

What is pulsus paradoxus?

A

Normally, inspiration creates a negative pressure which pulls blood into the heart, momentarily increasing systemic venous return. When that happens, the right heart volumes increases, and the right ventricle expands into the pericardial space, so it doesn’t affect the left heart volume at all.

During inspiration in someone with cardiac tamponade, the right ventricle can’t move into the pericardial space, so the extra volume pushes the interventricular septum leftwards. This leads to a reduction in left ventricular diastolic volume, a lower stroke volume, and a drop in systolic blood pressure during inspiration.

35
Q

What are the primary investigations for cardiac tamponade?

A
  • Primary investigations
    • ECGTachycardia andelectrical alternans
      • Shows tachycardia, low QRS complex voltage andelectrical alternans (QRS complex varies in amplitude as the heart moves in the fluid)
      • shows low voltage complexes with sinus tachycardia
      • Alternation of QRS complex amplitude between beats is known as electrical alternans and occurs due to movement of the heart within the pericardial fluid. As the heart moves closer to the chest wall, more electrical activity is detected and therefore a greater QRS complex amplitude, with the opposite occurring on movement away from the chest wall.
    • Bloods
      • Inflammatory markers:if raised may suggest underlying pericarditis
      • Troponin:myocardial infarction can cause ventricular rupture and subsequent tamponade
    • Imaging
      • Transthoracic echocardiogram: diagnostic and allows for visualisation of the effusion and the effect on cardiac function. Shows a ‘dancing’ heart as it moves in the fluid.
      • Chest X-Ray:enlarged cardiac silhouette
36
Q

What are other investigations to consider for cardiac tamponade?

A

Pericardial fluid analysis: this is obtained through pericardiocentesis, which is a therapeutic procedure, and may reveal the underlying aetiology

37
Q

What is the management for Pericardial effusion with no evidence of tamponade?

A
  • Conservative management:repeat echocardiograms and monitor blood pressure
    • NSAIDsorcolchicineif the underlying cause is suspected pericarditis
    • Pericardiocentesis:may be required for larger effusions
38
Q

What is the management for Pericardial effusion with evidence of tamponade?

A
  • Urgent pericardiocentesis:a needle is inserted between the xiphisternum and left costal margin and directed towards the left shoulder. This can be done under ultrasound guidance. Pericardial fluid can be aspirated to relieve intrapericardial pressure
  • Urgent surgicaldrainage is usually indicated in cases related to neoplasia, a purulent effusion, or haemopericardium (e.g. trauma)
39
Q

What are the complications for cardiac tamponade?

A
  • Cardiac arrest:increased intrapericardial pressures may eventually lead to a significantly reduced cardiac output and cardiac arrest
  • Constrictive pericarditis:a small proportion of patients with a pericardial effusion will go on to develop constrictive pericarditis once the effusion is treated
40
Q

What are the risk factors for cardiac tamponade?

A
  • Risk factors
    • Cancer
    • Autoimmune disorders
    Risk factors depend upon the underlying cause of the pericardial effusion.
41
Q

What is the prognosis for cardiac tamponade?

A
  • There is a risk of haemodynamic instability and cardiac arrest.
  • The prognosis of idiopathic pericardial effusions is usually good.
  • However, if the pericardial effusion is caused by malignancy, the prognosis is poor.
42
Q

What is infective endocarditis?

A

Infective endocarditis (IE) is an infection of the endocardium (including the valvular structures, the chordae tendineae, sites of septal defects etc).

Endocarditis typically affects valves - native valves or prosthetic valves.

43
Q

What does infective endocarditis involve?

A

Infective endocarditis is an infection involving the endocardial surface of the heart, including the valvular structures, the chordae tendineae, sites of septal defects, or the mural endocardium.

44
Q

What is the aetiology of infective endocarditis?

A
  • Staphylococcus aureus
    • Most common cause
  • Viridans group streptococci
    • Dental problems - gram positive, alpha haemolytic and optochin resistance
  • Pseudomonas aeruginosa
  • Enterococci
  • Bacterial
  • May be fungal
  • May be non-bacterial thrombotic endocarditis
    • Malignancy
    • SLE
45
Q

What are the common bacteria organisms that can cause infective endocarditis?

A

Common organisms:

  1. staphyloccus aureus: the most common cause overall, associated with IV drug use and prosthetic heart valves; has a high mortality
  2. Staphylococcus epidermidis: associated with indwelling lines and prosthetic valves
  3. Streptococcus bovid: associated with colon cancer; the subtype streptococcus gallolyticus is most associated with colon cancer
  4. Viridans streptococci: cause subacute endocarditis and second most common overall; usually affects a native valve
  5. Streptococcus mites and sanguinis (viridans streptococci) : associated with poor dental hygiene and infection after a dental procedure
46
Q

What is HACEK?

A

Rare causes of subcutaneous disease and are usually culture negative

H - haemophilus
A - aggregatibacter
C - cardiobacterium
E - eikenella
K - kingella

47
Q

What are other culture negative causes of infective endocarditis?

A

Coxiella Burnetii
Bartonella
Brucella
Previous antibiotic therapy

48
Q

What are other miscellaneous bacterial aetiology of infective endocarditis?

A

Group B streptococci: acute disease with high mortality usually requiring valve replacement, most commonly associated with pregnancy

Candida albicans: causes server infective endocarditis

49
Q

What is the pathophysiology of infective endocarditis?

A
  • This condition typically develops on the valvular surface of the heart, which have sustained endothelial damage secondary to turbulent blood flow.
  • As a result platelets and fibrin adhere to the underlying collagen surface and create a prothrombotic milieu.

Bacteraemia leads to colonisation of the thrombus and perpetuates further fibrin deposition and platelet aggregation, which develops into a mature infected vegetations.

50
Q

Missed detailed pathophysiology

A
51
Q

What is the epidemiology of infective endocarditis?

A
  • IE is a rare disease. Between 2009-2010, there were 3,969 episodes of acute and subacute endocarditis in the UK
  • Endocarditis used to be a disease of the young affected by rheumatic heart disease.
  • Now it is a disease of:
    • The elderly (in an ageing population)
    • Young IV drug abusers
    • Young congenital heart disease
    • Anyone with prosthetic heart valves or pacemakers
    • Poor dental hygiene
  • More common in males
    • M>F
  • More common in developing countries
  • The mitral valve is most commonly affected overall
  • The tricuspid valve is most associated with IV drug use
52
Q

What are the symptoms of infective endocarditis?

A
  • General
    • Headache
    • Fever or chills
    • Malaise (Faintness)
    • Fatigue
    • Weight loss
    • Confusion
    • Night sweats
    • Dyspnoea - Shortness of breath
  • Joint pain: may be due to septic emboli
  • Fever plus
    • Prosthetic material in heart
    • Risk factors of infective endocarditis e.g. IVDU
    • Newly developed ventricular arrhythmias or conduction disturbances
53
Q

What are the signs of infective endocarditis?

A
  • Heart murmur: due to turbulent blood flow; +/- evidence of heart failure
  • Splinter haemorrhages: red-plum lines under the nails due to microemboli deposition
    • On nail beds of fingers
  • Roth spots - retinal haemorrhages with white or clear centres on fundoscopy
    • White centred retinal haemorrhages due to immune complex deposition
  • Janeway lesions - haemorrhages and nodules in fingers
    • Painless plaques on palms and soles due to septic microemboli deposition
  • Osler nodes - tender nodules in fingers
    • Painful nodules on fingers or toes due to immune complex deposition
  • Mild splenomegaly
  • Clubbing
  • Signs of glomerulonephritis: due to immune complex deposition in kidneys
54
Q

What is the modified duke criteria?

A

The Modified Duke Criteria requires 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria for a diagnosis of infective endocarditis.

A possible diagnosis meets one major and one minor criteria, or three minor criteria.

55
Q

What is the major criteria for modified duke criteria?

A

Two positive blood cultures
Endocardial involvement on echo:
- endocardial vegetation
- perivalvular abscess
- new partial dehiscence of prosthetic valve
- new valvular regurgitation

56
Q

What are the minor criteria for modified duke criteria?

A
  • predisposing heart condition or IVDU
  • fever > 38.C
  • immunological phenomenon
    Glomerulonephritis
    Osler nodes
    Roth’s spots
    Rheumatoid factor
  • microbiological evidence
    Positive blood cultures not meeting major criteria
  • vascular abnormalities
    Arterial emboli
    Septic emboli
    Pulmonary infarct
    Intracranial haemorrhage
57
Q

What are the investigations of infective endocarditis?

A
  • Inflammatory markers:raised WCC often with neutrophilia, as well as raised CRP and ESR
  • Blood cultures:3 sets of blood cultures, 1 hour apart, ideally before initiating antibiotic therapy
    • Some organisms cause culture negative endocarditis as they are hard to culture. Serology or PCR may be used for these.
    • Other patients may have culture negative endocarditis as they had taken antibiotics prior to blood culture.
  • Echocardiogram (echo): confirms diagnosis. Used to visualise the heart and look for vegetations or the way the valve’s move etc
    • Atransthoracicecho is first-line but if this is negative and clinical suspicion remains, atransoesophagealecho should be performed, which has a higher sensitivity for endocarditis
  • Transthoracic Echo (TTE) - 1st line
    • Safe
    • Non invasive
    • No discomfort
    • Often poor images so slower sensitivity
  • Transesophageal Echo (TOE) - Diagnostic
    • Diagnostic
    • Generally safe but risk of perforation or aspiration
    • Easiest if ventilated (but never ventilate just for TOE)
  • Chest X-ray: to screen for other causes of dyspnoea, and to detect evidence of heart failure e.g. pulmonary congestion
    • Cardiomegaly - enlarged heart
  • 12-lead ECG: disease progression is associated with conduction defects. Perform daily to detect complications, such as aortic root abscess (prolonged PR interval).
  • Urinalysis:glomerulonephritis secondary to septic emboli may cause haematuria
58
Q

What is the 1st line of management for IE?

A
  • IV antibiotics:
  • Generally for 4-6 weeks → generally continued for four weeks, which is often extended to at least six weeks in patients with a prosthetic valve
    • Choice of agents based on culture sensitivities
    • Patients usually require a central line or peripherally inserted central catheter (PICC)
      • Streptococci , use penicillin - benzylpenicillin and gentamicin
      • If staphylococcus, use vancomycin and rifampicin
    • Local guidelines should be followed
  • Treat complications
59
Q

What are the local guidelines?

A

DO I NEED TO KNOW THEM????

60
Q

What is the second line of management for iE?

A
  • Surgery:aim to remove infected tissue and repair or replace affected valves
    • Indicationsinclude: decompensated heart failure, resistance to antibiotic therapy, severe sepsis, perivalvular abscess, intracardiac fistulae, prosthetic valve endocarditis
61
Q

What is another management for IE?

A

NICEdo not
generally recommend antibiotic prophylaxis for infective endocarditis, although this remains controversial.

- Prophylaxis is**NOT**recommended for:
    - Dental procedures
    - Genitourinary (GU), gynaecological or obstetric procedures (including childbirth)
    - Upper and lower gastrointestinal (GI) tract procedures
    - Upper and lower respiratory tract procedures (including bronchoscopy and ENT)

But **Important considerations:**

- If a personat riskof infective endocarditisis receiving antibiotics for a GI or GU tract procedureat a site where there isa suspected infection, theyshouldbe offered antibiotics that covers organisms that cause infective endocarditis
- Any episodes of infection that occur in people at risk of infective endocarditis should beinvestigatedandtreatedurgentlyto reduce the risk of endocarditis
- Chlorhexidine mouthwash**should NOT be offered**as prophylaxis against infective endocarditis to people at risk of infective endocarditis undergoing dental procedures
- Be aware that the European Society of Cardiology and American Heart Association**do still advocate antibiotic prophylaxis**for patients at high risk of infective endocarditis undergoing dental procedures
62
Q

What are the complications of IE?

A
  • Congestive heart failure:heart failure has the greatest impact on prognosis
  • Septic embolisation:occurs in up to 50% of cases and may involve the lungs, spleen, joints, brain and coronary arteries.
    • Embolisation to the brain may result in a stroke
  • Aortic root abscess: should be suspected in patients with aortic valve endocarditis that fails to improve within 72 hours of appropriate antibiotics; prolonged PR interval on ECG
  • Valvular rupture or fistula:mostly involves patients with prosthetic valves or staphylococcus aureus infection
  • Regurgitation: as heart valves are damaged due to microbes
  • Arrhythmia
  • Heart block
  • Stroke rehab
  • Abscess drainage
63
Q

What are the risk factors for IE?

A
  • Older age
  • Male gender:men are 2.5 times more prone to endocarditis than women
  • Previous infective endocarditis
  • Prosthetic heart valves (Artificial heart valve) **or implantable cardiac device
  • Damaged heart valves
  • Congenital heart disease esp affecting the valves
  • Rheumatic heart disease causing damage to the valves
  • Intravenous drug use (IVDU) typically affects tricuspid valve
    • Injecting illicit intravenous drugs with a needle contaminated with bacteria or fungi.
  • Scarring caused by heart valve damage, which allows bacteria to grow
  • Poor dental hygiene/ dental treatment: a way of microbes entering
  • Intravenous catheter
  • Immunosuppression
64
Q

What is the prognosis of IE?

A

Death is mainly due to congestive heart failure. However, after one year, the main prognostic factor is age.

2a Conditions- Cardio (9 decks)

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