(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
what is pyrexia?
raised body temperature (i.e. fever)
26
what is infective endocarditis?
inflammation of the endocardium, vascular endothelium or valves of the heart caused by viral or bacterial infection endo (inner lining), card (heart), itis (inflammation)
27
what causes infective endocarditis?
viral or bacterial infection
28
what does infective endocarditis usually affect?
the heart valves
29
what is the most common infection in infective endocarditis?
Streptococci (20-40% of cases)
30
how does a bacterial infection lead to infective endocarditis?
bacteria enter the bloodstream and form a vegetation (a bacterial infection surrounded by a layer of platelets and fibrin)
31
what tests would be done to investigate infective endocarditis?
FBC (esp markers of infection and inflammation) blood culture ECG transoesophageal echocardiogram
32
what symptoms do people with infective endocarditis present with?
fever, malaise, sweats and unexplained weight loss
33
why is a full blood count done for an infective endocarditis patient?
to test for anaemia and markers of infection or inflammation
34
why is a blood culture done for an infective endocarditis patient?
to isolate the causative organism of infective endocarditis
35
why is an ECG done for an infective endocarditis patient?
to show a vegetation, abscess, valve perforation or dehiscence of a prosthetic valve
36
what is the dehiscence of a prosthetic valve?
breakdown of sutures leading to partial or complete detachment of the prosthesis from annulus uncommon complication of valve replacement surgery
37
what type of echocardiogram is performed on suspected infective endocarditis patients and why?
transoesophageal echo > transthoracic echo as transoesophageal has higher sensitivity
38
what is cardiac decompensation?
inability of the heart to maintain adequate circulation
39
what symptomatic features of cardiac decompensation?
shortness of breath, frequent coughing, swelling of the legs and abdomen, fatigue
40
what are the clinical features of cardiac decompensation?
raised JVP (jugular venous pressure), lung crackles, oedema
41
what are the possible complications of cardiac decompensation?
vascular and embolic phenomena (stroke, Janeway lesions, splinter/conjunctival haemorrhages) immunological phenomena (Osler's nodes, Roth sports)
42
what part of the heart does infective endocarditis affect?
affects the endocardium (especially the heart valves) aortic > mitral > right-sided valves
43
which heart valve is most commonly affected in infective endocarditis?
aortic > mitral > right-sided valves
44
what is the impact of vegetation formation at the valves of the heart?
1) changes in valve thickness | 2) impaired ability of the valves to open/close appropriately
45
how do bacteria interact with endocardium that has underlying damage in infective endocarditis?
more common for bacteria to attach to the endocardium if underlying damage is present
46
where does vegetation formation occur most commonly?
at sites of turbulent blood flow (i.e. heart valves) - exacerbated if endocardium has underlying damage
47
how does the risk of infective endocarditis vary for drug users?
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
why are IV drug users at a higher risk of infective endocarditis?
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
what is the first and critical step of infective endocarditis?
entry of bacteria into the bloodstream
50
besides IV drug users, where else can infective endocarditis be seen?
- 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
which individuals are at a greater risk of infective endocarditis?
- IV drug users - the immunosuppressed/immunocompromised - those w congenital heart diseases that lead to a damaged endocardium
52
what is hypokinesia?
abnormally diminished motor activity | i.e. typical habitual moments are reduced in frequency
53
what is atrial fibrilllation?
irregular arrhythmia of the heart that can lead to clot formation
54
what is dilated cardiomyopathy?
dilated cardiomyopathy is characterised by dilated, thin-walled cardiac chambers with reduced contractility
55
describe the thickness of the cardiac walls in dilated cardiomyopathy
thin-walled cardiac chambers (due to dilation)
56
what impact does dilated cardiomyopathy have on the heart?
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
why are the ejection fraction and stroke volume in a patient with dilated cardiomyopathy reduced?
reduced due to the thin-walled nature of the cardiac chambers = cannot contract with sufficient force to enable efficient perfusion of the arteries
58
describe the systolic function in a patient with dilated cardiomyopathy
reduced | reduced contractility due to thinner walls
59
what are the most common causes of dilated cardiomyopathy?
idiopathic genetics ``` toxins (alcohol, cardiotoxic chemo) viral infections (myocarditis) ``` pregnancy (peripartum cardiomyopathy) tachycardia-related cardiomyopathy, thyroid disease, muscular dystrophies
60
how is dilated cardiomyopathy managed?
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
what kind of cardiac devices are used to correct dilated cardiomyopathy?
implantable cardioverter defibrillator cardiac resychronisation therapy
62
why are diuretics given in dilated cardiomyopathy?
to correct fluid overload
63
why is anticoagulation given in dilated cardiomyopathy?
preventative measure in case atrial fibrillation occurs
64
what is the implication of dilated cardiomyopathy on patients in the future?
increased risk of heart failure hospitalisation cardiac arrhythmias sudden cardiac death due to ventricular arrhythmias reduced survival
65
what is the value of central venous pressure usually?
negligible
66
what is Duke's criteria?
set of clinical criteria for the diagnosis of infective endocarditis used to diagnose definitive, possible or rejected endocarditis (three types)
67
how many cases of dilated cardiomyopathy are attributed to idiopathic caused?
over 50%
68
what is the most common cause of dilated cardiomyopathy?
most of the time - unknown cause (idiopathic) but there can be underlying reasons
69
how is the fluid intake managed in patients with dilated cardiomyopathy?
can drink to thirst
70
what is Duke's criteria for definite endocarditis?
1) 2 major 2) 1 major and 3 minor (1-3) criteria 3) 5 minor criteria (5) + gram stain/culture from sugery
71
what is Duke's criteria for possible endocarditis?
1) 1 major AND > 1 minor clinical criteria | 2) 3 minor
72
what is Duke's criteria for rejected endocarditis?
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
what are the major symptoms for Duke's criteria?
(BE) ``` B = (consistently positive) blood cultures E = positive echocardiogram (abscess, dehiscence, vegetation, or new regurg murmur) ```
74
what are the minor symptoms for Duke's criteria?
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
which genes are implicated in the development of dilated cardiomyopathy?
mutations in genes encoding the cardiac cytoskeletal proteins (Titin, Lamin, myosin heavy chain, Phospholamban, cardiac myosin binding protein C)
76
explain how genetic mutations can lead to the development of dilated cardiomyopathy
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)