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brs (phase 1b) > (cardioresp) valvular disease and heart failure > Flashcards

(cardioresp) valvular disease and heart failure Flashcards

1
Q

how do you calculate cardiac output?

A

CO = HR x SV

where HR = heart rate and SV = stroke volume

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2
Q

how do you calculate stroke volume?

A

SV = EDV - ESV

where EDV = end diastolic volume and ESV = end systolic volume

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3
Q

what is cardiac output?

A

the volume of blood pumped out by the heart per minute (litres/min but can also be cm3/min)

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4
Q

what are the units for cardiac output?

A

litres per minute OR cm3 per minute

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5
Q

how do you calculate ejection fraction?

A

EF = (SV/EDV) x 100

where SV = stroke volume and EDV = end diastolic volume

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6
Q

what is ejection fraction?

A

the volumetric fraction of blood that is ejected by the ventricles with each contraction

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7
Q

how is ejection fraction given?

A

usually as a a percentage (as SV/EDV is multiplied by 100)

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8
Q

how do you calculate mean arterial pressure?

A

MAP = (CO x SVR) + CVP

where CO = cardiac output, SVR = systemic vascular resistance and CVP = central venous pressure

OR (ONLY if at normal resting heart rates)

MAP = 1/3 SBP + 2/3 DBP

where SBP = systolic blood pressure and DBP = diastolic blood pressure

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9
Q

what is the mean arterial pressure?

A

an average of arterial blood pressure throughout a single cardiac cycle of systole and diastole

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10
Q

what is an alternative equation for mean arterial pressure?

A

MAP = 1/3 SBP + 2/3 DBP

where SBP = systolic blood pressure and DBP = diastolic blood pressure

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11
Q

what is the desired range for mean arterial pressure?

A

should be >65mmHg as this represents the pressure necessary to adequately perfuse the body organs

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12
Q

what are the units of mean arterial pressure?

A

mmHg

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13
Q

why is it important that the mean arterial pressure is greater than 65mmHg at all times?

A

as this is the desired MAP that allows sufficient perfusion of the body’s organs

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14
Q

how does the mean arterial pressure vary during exertion?

A

usually during exertion the MAP moves more closely towards an average of SP and DP instead of the usual equation (1/3 SBP + 2/3 DBP)

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15
Q

what is systolic blood pressure?

A

the pressure in the arteries during ventricular contraction (i.e. during systole)

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16
Q

what is diastolic blood pressure?

A

the pressure in the arteries during ventricular relaxation (i.e. during diastole)

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17
Q

what is pulse pressure?

A

the difference between the systolic and the diastolic blood pressures

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18
Q

what is the desired pulse pressure?

A

should be between 30-40 mmHg (along with desired systolic and diastolic blood pressures)

higher = wide pulse pressure
lower = narrow pulse pressure
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19
Q

what does a narrow pulse pressure suggest (in hypotension)?

A

that there is not sufficient blood in the arteries to exert normal pressure on the artery walls

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20
Q

what does a narrow pulse pressure suggest (in hypotension)?

A

that there is not sufficient blood in the arteries to exert normal pressure on the artery walls

(may be due to severe blood loss)

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21
Q

what does a wide pulse pressure suggest?

A

that the heart has to work harder to pump sufficient amounts of blood around the body

may be due to a change in structure or function of the heart

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22
Q

what does a narrow pulse pressure suggest (in hypotension)?

A

that there is not sufficient blood in the arteries to exert normal pressure on the artery walls

(can be due to severe blood loss)

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23
Q

what does a wide pulse pressure suggest?

A

that the heart has to work harder to pump sufficient amounts of blood around the body

can be due to a change in structure or function of the heart

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24
Q

what is stroke volume?

A

the volume of blood that is pumped out of the left ventricle with each systolic contraction

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25
Q

what is pyrexia?

A

raised body temperature (i.e. fever)

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26
Q

what is infective endocarditis?

A

inflammation of the endocardium, vascular endothelium or valves of the heart caused by viral or bacterial infection

endo (inner lining), card (heart), itis (inflammation)

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27
Q

what causes infective endocarditis?

A

viral or bacterial infection

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28
Q

what does infective endocarditis usually affect?

A

the heart valves

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29
Q

what is the most common infection in infective endocarditis?

A

Streptococci (20-40% of cases)

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30
Q

how does a bacterial infection lead to infective endocarditis?

A

bacteria enter the bloodstream and form a vegetation (a bacterial infection surrounded by a layer of platelets and fibrin)

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31
Q

what tests would be done to investigate infective endocarditis?

A

FBC (esp markers of infection and inflammation)

blood culture

ECG

transoesophageal echocardiogram

32
Q

what symptoms do people with infective endocarditis present with?

A

fever, malaise, sweats and unexplained weight loss

33
Q

why is a full blood count done for an infective endocarditis patient?

A

to test for anaemia and markers of infection or inflammation

34
Q

why is a blood culture done for an infective endocarditis patient?

A

to isolate the causative organism of infective endocarditis

35
Q

why is an ECG done for an infective endocarditis patient?

A

to show a vegetation, abscess, valve perforation or dehiscence of a prosthetic valve

36
Q

what is the dehiscence of a prosthetic valve?

A

breakdown of sutures leading to partial or complete detachment of the prosthesis from annulus

uncommon complication of valve replacement surgery

37
Q

what type of echocardiogram is performed on suspected infective endocarditis patients and why?

A

transoesophageal echo > transthoracic echo as transoesophageal has higher sensitivity

38
Q

what is cardiac decompensation?

A

inability of the heart to maintain adequate circulation

39
Q

what symptomatic features of cardiac decompensation?

A

shortness of breath, frequent coughing, swelling of the legs and abdomen, fatigue

40
Q

what are the clinical features of cardiac decompensation?

A

raised JVP (jugular venous pressure), lung crackles, oedema

41
Q

what are the possible complications of cardiac decompensation?

A

vascular and embolic phenomena (stroke, Janeway lesions, splinter/conjunctival haemorrhages)

immunological phenomena (Osler’s nodes, Roth sports)

42
Q

what part of the heart does infective endocarditis affect?

A

affects the endocardium (especially the heart valves)

aortic > mitral > right-sided valves

43
Q

which heart valve is most commonly affected in infective endocarditis?

A

aortic > mitral > right-sided valves

44
Q

what is the impact of vegetation formation at the valves of the heart?

A

1) changes in valve thickness

2) impaired ability of the valves to open/close appropriately

45
Q

how do bacteria interact with endocardium that has underlying damage in infective endocarditis?

A

more common for bacteria to attach to the endocardium if underlying damage is present

46
Q

where does vegetation formation occur most commonly?

A

at sites of turbulent blood flow (i.e. heart valves)

  • exacerbated if endocardium has underlying damage
47
Q

how does the risk of infective endocarditis vary for drug users?

A

increased risk of IE for IV drug users due to needle exposure as there are more opportunities for infection introduction into the body

1) exposed to bacteria on skin surface
2) exposed to bacteria on non-sterile needles

48
Q

why are IV drug users at a higher risk of infective endocarditis?

A

increased needle exposure SO more opportunities to introduce pathogens directly into the bloodstream by

1) use of non-sterile needles
2) repeat injection forming skin wounds by which bacteria on skin surface can enter

49
Q

what is the first and critical step of infective endocarditis?

A

entry of bacteria into the bloodstream

50
Q

besides IV drug users, where else can infective endocarditis be seen?

A
  • as a possible complication of routine surgeries such as dental surgery
  • the immunocompromised OR immunosuppressed
  • those w congenital heart defects leading to a damaged endocardium
51
Q

which individuals are at a greater risk of infective endocarditis?

A
  • IV drug users
  • the immunosuppressed/immunocompromised
  • those w congenital heart diseases that lead to a damaged endocardium
52
Q

what is hypokinesia?

A

abnormally diminished motor activity

i.e. typical habitual moments are reduced in frequency

53
Q

what is atrial fibrilllation?

A

irregular arrhythmia of the heart that can lead to clot formation

54
Q

what is dilated cardiomyopathy?

A

dilated cardiomyopathy is characterised by dilated, thin-walled cardiac chambers with reduced contractility

55
Q

describe the thickness of the cardiac walls in dilated cardiomyopathy

A

thin-walled cardiac chambers (due to dilation)

56
Q

what impact does dilated cardiomyopathy have on the heart?

A

dilation + thin walled chambers

= reduced contractility of LV
= reduced ejection fraction and stroke volume
= inadequate perfusion of the organs
= typically resulting in global hypokinesis (insufficient motor activity)

57
Q

why are the ejection fraction and stroke volume in a patient with dilated cardiomyopathy reduced?

A

reduced due to the thin-walled nature of the cardiac chambers

= cannot contract with sufficient force to enable efficient perfusion of the arteries

58
Q

describe the systolic function in a patient with dilated cardiomyopathy

A

reduced

reduced contractility due to thinner walls

59
Q

what are the most common causes of dilated cardiomyopathy?

A

idiopathic
genetics

toxins (alcohol, cardiotoxic chemo)
viral infections (myocarditis)

pregnancy (peripartum cardiomyopathy)

tachycardia-related cardiomyopathy,
thyroid disease,
muscular dystrophies

60
Q

how is dilated cardiomyopathy managed?

A

medical heart failure therapy - ACE inhibitors, beta-blockers, mineralocorticoid receptor antagonists, diuretics for fluid overload (ABCD)

anticoagulation for atrial fibrillation

cardiac devices - cardiac resynchronisation therapy/implantable cardioverter defibrillation

transplant

61
Q

what kind of cardiac devices are used to correct dilated cardiomyopathy?

A

implantable cardioverter defibrillator

cardiac resychronisation therapy

62
Q

why are diuretics given in dilated cardiomyopathy?

A

to correct fluid overload

63
Q

why is anticoagulation given in dilated cardiomyopathy?

A

preventative measure in case atrial fibrillation occurs

64
Q

what is the implication of dilated cardiomyopathy on patients in the future?

A

increased risk of heart failure hospitalisation

cardiac arrhythmias

sudden cardiac death due to ventricular arrhythmias

reduced survival

65
Q

what is the value of central venous pressure usually?

A

negligible

66
Q

what is Duke’s criteria?

A

set of clinical criteria for the diagnosis of infective endocarditis

used to diagnose definitive, possible or rejected endocarditis (three types)

67
Q

how many cases of dilated cardiomyopathy are attributed to idiopathic caused?

A

over 50%

68
Q

what is the most common cause of dilated cardiomyopathy?

A

most of the time - unknown cause (idiopathic) but there can be underlying reasons

69
Q

how is the fluid intake managed in patients with dilated cardiomyopathy?

A

can drink to thirst

70
Q

what is Duke’s criteria for definite endocarditis?

A

1) 2 major
2) 1 major and 3 minor (1-3) criteria
3) 5 minor criteria (5)

+ gram stain/culture from sugery

71
Q

what is Duke’s criteria for possible endocarditis?

A

1) 1 major AND > 1 minor clinical criteria

2) 3 minor

72
Q

what is Duke’s criteria for rejected endocarditis?

A

resolution after less than 4 days of antibiotic treatment

no evidence of infection after surgery

definite or possible endocarditis criteria not met = ruled out

73
Q

what are the major symptoms for Duke’s criteria?

A

(BE)

B = (consistently positive) blood cultures
E = positive echocardiogram (abscess, dehiscence, vegetation, or new regurg murmur)
74
Q

what are the minor symptoms for Duke’s criteria?

A

F = fever (greater than 38)

I = immunological phenomena (Osler’s nodes, Ruth spots)

V = vascular phenomenon (emboli organs)

E = echo/positive blood cultures not meeting major criteria

R = risk factor present (IV drug use or predisposing heart condition)

75
Q

which genes are implicated in the development of dilated cardiomyopathy?

A

mutations in genes encoding the cardiac cytoskeletal proteins
(Titin, Lamin, myosin heavy chain, Phospholamban, cardiac myosin binding protein C)

76
Q

explain how genetic mutations can lead to the development of dilated cardiomyopathy

A

genetic mutations

= impaired cardiac cytoskeleton proteins
= impaired myofibril formation and myocyte function
= thinner, weaker cardiac muscle
= ineffective contraction of the walls (as a sufficiently high force cannot be generated)

brs (phase 1b) (71 decks)

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