Respiratory Disease and Heart Failure Flashcards

1
Q

What is atrial systole?

A

Atrial contraction

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2
Q

What happens in ventricular systole?

A
  1. Isovolumic / isovolumetric contraction
  2. Ventricular contraction
  3. Ventricular ejection
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3
Q

What happens in atrial diastole?

A
  1. Isovolumic / isovolumetric relaxation

2. Ventricular filling

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4
Q

How do you calculate stroke volume?

A

EDV - ESV

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5
Q

How do you calculate cardiac output?

A

SV x HR

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6
Q

How do you calculate ejection fraction?

A

(SV/EDV) x 100

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7
Q

How do you calculate mean arterial blood pressure?

A

(CO x SVR) + CVP

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8
Q

Why do you calculate ejection fraction like that?

A

Ejection fraction is the volumetric fraction of blood ejected by the ventricle with each contraction. It is commonly given as a percentage (hence multiplication by 100)

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9
Q

How can mean arterial pressure be estimated at normal resting heart rates?

A

MAP = DP + 1/3(SP-DP).

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10
Q

What is infective endocarditis?

A
  • infection of the endocardium or vascular endothelium of the heart
  • ENDO (inner lining), CARD (heart) ITIS (inflammation
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11
Q

What is the pathophysiology of infective endocarditis?

A
  • affects the heart valves
    1. bacteria entering the blood stream and forming ”a vegetation”
    2. (a bacterial infection surrounded by a layer of platelets and fibrin) in the endocardium
    3. Streptococci (20-40 % of cases) are the most common infection
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12
Q

what are common symptoms

of infective endocarditis?

A
  • Fever
  • malaise
  • sweats
  • unexplained weight loss
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13
Q

what may be found in investigation of infective endocarditis?

A

-new heart murmur on examination

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14
Q

what may be found in blood of infective endocarditis patient?

A
  • anaemia
  • raised markers of infection
  • blood cultures may isolate a microorganism
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15
Q

What would the echocardigam of infective endocarditis show?

A
  1. vegetation, abscess, valve perforation and/or new dehiscence of prosthetic valve
  2. regurgitation of the affected valve
  3. Transoesophageal echo has higher sensitivity compared with transthoracic
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16
Q

What is Duke’s criteria?

A

set of criteria to determine the likelihood of an individual having infective endocarditis

17
Q

What are the major criteria in duke’s?

A
  1. Persistently +ve blood culture for typical organisms
  2. ECHO: vegetation, dehiscence of prosthetic valve, abscess
  3. New valvular regurgitation murmur
  4. Coxiella burnetti infection
18
Q

What is the minor criteria in duke’s?

A
  1. Predisposing heart condition or IV drug use
  2. Fever greater than 38 C
  3. Vascular: emboli to organs, brain
  4. Immunologic: glomerulonephritis, Oslers nodes, Roth spots
  5. Positive blood cultures that do not meet specific criteria
19
Q

What is definitive endocarditis according to duke’s?

A

-2 major clinical criteria
1 major and any 3 minor clinical criteria
-5 minor criteria
+ ve gram stain or culture from surgery or autopsy

20
Q

What is possible endocarditis according to duke’s?

A
  • 1 major and >1 minor clinical criteria

- 3 minor criteria

21
Q

What is rejected endocarditis according to duke’s?

A
  • Resolution after less than 4 days antibiotic treatment
  • No evidence of infection after surgery
  • Definite or possible criteria not met
22
Q

What features of heart decompensation would you look for in endocarditis?

A

Cardiac decompensation
•hortness of breath, frequent coughing, swelling of the legs and abdomen, fatigue
• raised JVP, lung crackles and oedema

23
Q

What are the other complications of endocarditis?

A
  1. Vascular and embolic phenomena
  2. (stroke, Janeway lesions, splinter/ conjunctival haemorrhages)
  3. Immunological phenomena
  4. (Osler’s nodes, Roth spots)
24
Q

What is decompensation?

A

inability of the heart to maintain adequate circulation

25
Q

What part of the heart does infective endocarditis affect?

A

endocardium, especially the valves of the heart

26
Q

Which valve is mostly affected in endocarditis?

A

aortic > mitral > right-sided valves

27
Q

Why is it the aortic valve that is most common affected in endocarditis?

A
  1. formation of a vegetation at the valves of the heart either results in changes to their thickness or a failure in their ability open and close appropriates
  2. more common for bacteria to attach to the endocardium if underlying damage is present
  3. This occurs more frequently at sites of turbulent blood flow such as the valves of the heart
28
Q

How is infective endocarditis risk different for IV drugs users?

A

increased risk of infective endocarditis due to repeated injection – potentially exposing their bloodstream to bacteria on the surface of the skin or use of non-sterile needles

29
Q

Why can IV drug users get infective endocarditis?

A
  1. Entry of bacteria into the blood stream is first and critical step in infective endocarditis
  2. Increased risk of infective endocarditis is therefore seen in I.V. drug users, but also a complication of routine surgeries such as dental surgery
  3. also more common in individuals that are immunosuppressed or have congenital heart defects leading to damaged endocardium
30
Q

What is dilated cardiomyopathy?

A

characterised by dilated and thin-walled cardiac chambers with reduced contractility

31
Q

Why does dilated cardiomyopathy affect contractility?

A
  1. Dilation of the chambers leads to reduced contractility
  2. . Echo shows a dilated left ventricle with reduced systolic function (ejection fraction) and typically global hypokinesis
32
Q

What are the commonest cause of dilated cardiomyopathy?

A

Idiopathic, genetic, toxins (alcohol, cardiotoxic chemotherapy), pregnancy (peripartum cardiomyopathy), viral infections (myocarditis), tachycardia-related cardiomyopathy, thyroid disease, muscular dystrophies

33
Q

What genes have been implicated in the diagnosis of dilated cardiomyopathy?

A

Mutations in genes encoding cardiac cytoskeletal proteins e.g. Titin, Lamin, Phospholamban, cardiac myosin binding protein C, myosin heavy chain

34
Q

Why do these gene mutations affect dilated cardiomyopathy?

A
  1. A number of genes have been identified to associate with dilated cardiomyopathy
  2. Frequently in genes essential for the formation or effective contraction of heart chambers thus either affect myofibril or cellular structure
35
Q

How is dilated cardiomyopathy managed?

A
  1. Medical heart failure therapy - ACE inhibitors, beta-blockers, mineralocorticoid receptor antagonists
  2. Diuretics for fluid overload
  3. Anticoagulation for atrial fibrillation
  4. Cardiac devices – cardiac resynchronisation therapy and/or implantable cardioverter defibrillator
  5. Transplant
36
Q

How can dilated cardiomyopathy matter in the future?

A

at risk of heart failure hospitalization, cardiac arrhythmias, sudden cardiac death due to ventricular arrhythmia, and reduced survival