Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SEM2 BIOSCIENCE > Case 4 > Flashcards

Case 4 Flashcards

1
Q

What is isovolumetric contraction?

A

The transient increase in pressure when the ventricle contracts but aortic valve is not open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is isovolumetric relaxation?

A

The transient decrease in pressure when the ventricle relaxes but the mitral valve is not open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is the pressure/volume relationship altered in a patient with heart failure?

A

Stroke volume decreases
Total LV volume increases
LV pressure decreases (due to LV dilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define stroke volume

A

Volume of blood ejected from the ventricles in each beat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define cardiac output (2 equations)

A 
CO = SV x HR
CO= MAP / TPR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is cardiac reserve?

A

Difference between resting CO and CO upon exertion

Average increase is around 5 times

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the four determinants of cardiac output?

A

Preload
Afterload
HR
Contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is preload?

A

The notion that a greater stretch on muscle fibres prior to contraction increases forces of contraction (Starling’s law)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is afterload?

A

The pressure that has to be overcome in order for the semilunar valves to open

Increased aortic/pulmonary pressures decrease cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the two molecular factors that effect force of cardiac contraction?

A

Intracellular Ca2+ levels

Contractile machinery sensitivity to Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Starlings law?

A

Increased venous return increases blood flow into the ventricles. Increasing ventricular volume stretches cardiac muscle fibres, leading to increased force of contraction.

This mechanism hence couples venous return and cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What three mechanisms ensure that venous return is maintained?

A

Pressure difference between venules and RA
Skeletal pumping
Respiratory pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is skeletal muscle pumping?

A

Muscle contraction forces blood through veins, aided by valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does respiration effect venous return?

A

Inspiration decreases thoracic pressure and increases abdominal pressure –> abdo IVC squeezed and thoracic IVC dilated –> blood moves upwards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What valves are responsible for the S1 heart sound? What does this indicate?

A

Closure of tricuspid and mitral valve

End of diastole and start of systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What valves are responsible for the S2 heart sound? What does this indicate?

A

Closure of aortic and pulmonary valves

End of systole and start of diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the physiological splitting of S2?

A

Inspiration can split the S2 sound in two as the due to the pulmonary valve closing just after the aortic valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How are heart murmurs produced?

A

Produced by turbulent blood flow through the heart valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Mitral regurgitation is most likely to be auscultated as a murmur during which phase of the cardiac cycle?

A

Systolic murmur

Retrograde leakage of blood during ventricular contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Mitral stenosis is most likely to be auscultated as a murmur during which phase of the cardiac cycle?

A

Diastolic murmur

Turbulence of flow through narrowed valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the symptoms of left heart failure?

A

Dyspnoea
Orthopnoea
Paraoxysmal nocturnal dyspnoea

22
Q

How is severity of heart failure categorised?

A

New york heart association scale

NYHA1 –> asymptomatic
NYHA 4 –> severe limitations of activity, symptoms when resting

23
Q

What findings would you expect when examining a patient with heart failure?

A

Bilateral basal chest crackles caused by pulmonary oedema
Pitting peripheral oedema (only in severe cases with RHF too)
Cyanosis
Raised JVP
Displaced apex beat (due to LV hypertrophy)
Heart murmurs
S3 gallop
Dullness on percussion
Tachycardia

24
Q

Why do patients with heart failure often present with tachycardia?

A

HF leads to decreased blood pressure. This is sensed by baroreceptors in carotid and aortic bodies which raise HR in response to decreased cardiac output

25
Q

What are the main causes of heart failure?

A

Pump failure
Arrhythmia
Obstruction to flow (mitral stenosis)
Flow regurgitation (mitral regurgitation)

26
Q

What are the most common causes of failure of the pumping function of the heart?

A 
Ischaemic disease post MI
Hypertensive heart disease
Diabetes melitis
Infective endocarditis
Endocrine causes
Drugs and toxins
27
Q

How do urea/electrolyte tests indicate heart failure status?

A

Dearrangement implies poor renal perfusion, caused by heart failure induced hypotension and fluid retention

28
Q

How is thyroid function related to heart failure? (2 mechanisms)

A

Hypothyroidism prevents proper relaxation of vascular smooth muscle. Increasing peripheral resistance decreases cardiac output.

RAAS system inhibited due to increase in diastolic BP. This decreases blood volume and preload.

29
Q

What is brain natriuretic peptide?

A

Peptide secreted by ventricles in response to stretch or pressure overload. It binds its receptor to;

Decrease vascular resistance
Decrease central venous pressure
Increase in natriuresis

30
Q

How can an ECG diagnose heart failure?

A

AF
Branch block identification (HF secondary to MI)
S3 gallop
No early R waves

31
Q

How can a CXR indicate heart failure?

A

Enlargement of cardiothoracic ratio
LA enlargement
Kerley B lines show pulmonary oedema

32
Q

What is trans-oesophageal ECHO used to image?

A

To image LA and mitral valve disease

33
Q

What is trans-thoracic ECHO?

A

Provision of real time ultrasound images of heart functioning
Ventricular functions can be calculated
Severity and type of valvular regurgitation can be calculated

34
Q

What does cardiac MRI show in patients with heart failure?

A

Provides detailed images on the contractibility of cardiac muscle, diagnosing cardiomyopathies and ischaemic disease post MI

35
Q

What is left ventricular ejection fraction?

A

A measurement of how much blood is be pumped from the LV with each contraction

55-70% = normal

36
Q

Outline the pathophysiology of mitral stenosis

A

Decrease in valve diameter –> LA:LV pressure gradient increases –> LA enlarges –> Decreased LVEDV due to narrowed valves –> Pressure gradient causes retrograde congestion, pulmonary oedema, pulmonary hypertension and eventual right sided heart failure

37
Q

What is the difference between primary and secondary mitral regurgitation?

A

Primary —> problem with the valve itself

Secondary –> problem with the ventricular tissue that impacts on valve function

38
Q

What valvular disease is most likely associated with atrial fibrillation?

A

Mitral stenosis

39
Q

What valvular disease is most likely associated with LV dilation and hypertrophy?

A

Mitral regurgitation

40
Q

What is one of the main causes of mitral stenosis?

A

Rheumatic heart disease

41
Q

What is rheumatic heart disease?

A

Autoimmune disease due to molecular mimicry leading to prelonged inflammation of the valve leaflets with fibrinous repair

42
Q

What is molecular mimicry?

A

Cross activation of T/B cells by a host antigen that is similar in structure to a pathogenic antigen

43
Q

What is the most common causative agent of rheumatic heart disease?

A

Streptococci infection during childhood

44
Q

How does streptococcus infection play a part in the pathogenesis of mitral stenosis?

A

Vavular tissue is misrecognised as Streptococcal M protein (bacterial antigen). This causes activation of t cell responses, leading to valve inflammation, damage and fibrosis

There is some genetic predisposition as to the likelihood of developing rheumatic heart disease post strep infection

45
Q

What surgical intervention can be used to treat mitral regurgitation?

A

Mitraclip catherisation

46
Q

What surgical intervention can be used to treat mild mitral stenosis? Explain the process

A

Percutaneous transvenous mitral commissurotomy (PTMC)

Catheter inserted into femoral vein, passed into RA, through septum into LA. Mitral valve opened using a balloon catheter

47
Q

What surgical intervention can be used to treat moderate/severe mitral stenosis? Explain the process

A

Mitral valve replacement

Uses prothesis (ball and cage or discs) or animal valves

48
Q

How does sympathetic activation effect the pacemaker potential of the cells of the SA node?

A

Noradrenaline release

Shortens pacemaker potential via action of cGMP

49
Q

What is the effect of sympathetic activation on the AV node?

A

Speeds conduction through the AV node

50
Q

How does parasympathetic activation effect the pacemaker potential of cells of the SA node?

A

Acetylcholine release

K+ channel opening increases pacemaker potential os SA node to slow the heart down

SEM2 BIOSCIENCE (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions