Brainscape's Knowledge GenomeTM

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


See full index

1B Cardiorespiratory > Structural heart disease > Flashcards

Structural heart disease Flashcards

1
Q

what does a ventricular cell require for contraction?

A

calcium

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

what shape is a ventricular cell?

A

rod shaped- can be stimulated to contract

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

what is the basic process of a ventricular cell contraction?

A
  • Electrical event
  • Calcium Transient (the amount of calcium in the sarcoplasm has increased for a short period of time)
  • Contractile event
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the difference between skeletal and cardiac muscle in contraction?

A

THE HEART WILL NOT BEAT WITHOUT EXTERNAL CALCIUM

This is DIFFERENT to skeletal muscle, which can contract without external calcium

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

explain the process of excitation-contraction coupling in the heart

A
  • Important ion channel in a cardiomyocyte is the L-type calcium channel
  • Depolarisation is sensed by the L-type calcium channel and calcium from outside enters the cell
  • Some of this calcium can directly cause contraction
  • The rest of the calcium binds to Ryanodine Receptors = release of calcium from the sarcoplasmic reticulum
  • After it has had its effect, some of the calcium is taken back up into the SR by Ca ATPase channels
  • Same amount of calcium that came into the cell is effluxed by a Sodium-Calcium Exchanger
  • This does NOT need energy - it uses energy from the concentration gradient of sodium to expel calcium form the cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the relationship between force production and intracellular calcium concentration?

A
  • The force-calcium relationship is SIGMOIDAL
  • Around a 10 micromolar intracellular concentration of calcium is sufficient to produce maximum force
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how does cardiac muscle contract with different muscle length?

A
  • This is ISOMETRIC CONTRACTION so the muscle doesn’t shorten - it is just pulling on the force transducer
  • An increase in muscle length causes an increase in force
  • As you keep stretching the muscle, you get to a point where further stretching DOES NOT generate more force - this is because there is not enough overlap between the filaments to produce force
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the difference in length-tension relationship in cardiac and skeletal muscle?

A
  • If you overstretch the muscle you get a decrease in force - this is what happens in skeletal muscle when you pull a muscle
  • NOTE: passive force is based on the resistance to stretch of the muscle
  • Skeletal muscle has much less passive force produced but there is still a bell-shaped curve
  • Cardiac muscle is MUCH MORE RESILIENT TO STRETCH than skeletal muscle so exerts more passive force
  • It is more resistant to stretch due to the properties of its extracellular matrix and cytoskeleton
  • ONLY THE ASCENDING LIMB OF THE LENGTH-TENSION CURVE IS IMPORTANT IN PHYSIOLOGICAL CIRCUMSTANCES IN CARDIAC MUSCLE
  • The descending limb doesn’t happen in physiological conditions because the pericardium restricts the stretching
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the two forms of cardiac contraction?

A

isometric and isotonic

  • ISOMETRIC contraction resists the high pressure - there is NO CHANGE IN LENGTH but there is a change in tone
  • ISOTONIC contraction is the shortening of fibres (no change in tension) when blood is ejected from the ventricles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is pre-load?

A
  • weight that stretched the muscle BEFORE it is stimulated to contract (i.e. the filling of the ventricles with blood makes it stretch before it is stimulated to contract)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is afterload?

A

weight that is NOT APPARENT to the muscle in the resting state - only encountered ONCE MUSCLE HAS STARTED TO CONTRACT

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

how does the force-load graph change in preload and afterload?

A
  • Preload causes stretching and so the Force-Preload graph is the SAME as the Force-Length graph that we saw earlier
  • The more preload you have, the more you stretch the muscle so the MORE FORCE is produced
  • MORE PRELOAD = MORE FORCE (up to a certain point)
  • Afterload is the back pressure on the aortic valves (when considering the left ventricle)
  • The more afterload you have, the less shortening you get
  • MORE AFTERLOAD = LESS SHORTENING
  • NOTE: If you have the same afterload with a LARGER PRELOAD you can shorten the muscle more
  • There is a similar relationship with velocity of shortening
  • MORE AFTERLOAD = LOWER VELOCITY OF SHORTENING
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are some in-vivo correlates of preload?

A
  • as blood fills the ventricles during diastole - it stretched the resting ventricular walls
  • This stretching/filling determines the PRELOAD on the ventricles before ejection
  • So preload is dependent upon venous return to the heart
  • Measures of Preload:
    • End-diastolic volume (EDV)
    • End-diastolic pressure (EDP)
    • Right atrial pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are some invivo correlates of afterload?

A
  • Definition of Afterload: the load against which the left ventricle ejects blood after opening of the aortic valve
  • So the afterload is basically blood pressure - the pressure that the heart must overcome to eject blood
  • So if you are hypertensive, the heart has to work harder to eject the blood and pump it around the body
  • Simple measure of afterload: DIASTOLIC ARTERIAL BLOOD PRESSURE
  • INCREASE AFTERLOAD = DECREASE SHORTENING + DECREASE VELOCITY OF SHORTENING
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does the heart respond to ventricular filling and aortic pressure?

A
  • INCREASE IN AORTIC PRESSURE (increased AFTERLOAD) = DECREASE IN SHORTENING
  • But the same aortic pressure with MORE VENTRICULAR FILLING will give an INCREASE IN SHORTENING
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the Frank-starling relationship? (Starling’s law)

A

Increased diastolic fibre length increases ventricular contraction

  • In other words: an increase in stretching leads to an increase in shortening and speed of shortening/increase in preload leads to an increase in shortening and speed of shortening
  • Consequence: when diastolic fibre length increases, ventricles pump a greater stroke volume so that, at equilibrium, cardiac output exactly balances the augmented venous return
  • In other words: the amount of blood coming in to the ventricles determines the strength of the ventricular contraction and hence determines the amount of blood leaving the ventricles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what factors is the frank-starling relationship due to?

A
  • Changes in the NUMBER OF MYOFILAMENT CROSS BRIDGES that interact
  • Changes in the CALCIUM SENSITIVITY OF THE MYOFILAMENTS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how do cross-bridge interaction change at different lengths?

A
  • At shorter lengths than optimal, the actin filaments overlap thus reducing the number of myosin cross bridges that can be made
  • The more you stretch the muscle, the more optimum interdigitation of the actin and myosin filaments you achieve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how does length affect myofilament sensitivity to calcium?

A

calcium sensitivity increases when myofilaments are stretched

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

what causes the sensitivity to change with myosin length?

A

2 possibilities:

Possibility 1:

  1. Troponin C is a thin filament protein that binds to Calcium
  2. TnC regulates the formation of cross bridges between actin and myosin
  3. At longer sarcomere lengths, the AFFINITY OF TROPONIN C FOR CALCIUM IS INCREASED due a conformational change in the protein
  4. So less calcium is needed for the same amount of force

Possibility 2:

  1. When stretched, the space between myosin and actin filaments DECREASES
  2. NOTE: the space between myosin and actin filaments is called lattice spacing
  3. With decreasing myofilament lattice spacing - the probability of forming strong binding cross bridges INCREASES
  4. This produces more force for the same amount of calcium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is stroke work?

A

= work done by the heart to eject blood under pressure into the aorta and pulmonary artery

This is the work done by the heart in one contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how do you calculate stroke work?

A
  • Volume of blood ejected during each stroke (SV) MULTIPLIED BY the pressure at which the blood is ejected (P)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is stroke volume affected by?

A

preload

afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the pressure at which blood is ejected affected by?

A

structure of heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the law of laplace?

A

When the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius.

  • INCREASE RADIUS = INCREASE TENSION
  • So when you increase the radius, the force around the sides increases
  • Force around the side is equal to pressure x radius
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is the equation for wall tension?

A

T= (PxR)/h

Wall tension= (internal pressure x radius)/ wall thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the physiological relevance of law of laplace?

A
  • Radius of curvature of the LV is LESS than the RV
  • This allows the left ventricle to generate HIGH PRESSURES with similar wall stress (tension)
  • Giraffe - wall stress is kept low in giraffe by the long, narrow, thick-walled ventricle - it has a small radius so it can generate high pressure
  • Frog - pressures are low so the ventricles are almost spherical - large radius so low pressure
  • Failing Hearts (Dilated Cardiomyopathy) - hearts become dilated which increases wall stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what phases is normal cardiac physiology divided into?

A

diastole and systome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is diastole?

A
  • ventricular relaxation during which the ventricles fill with blood
    • Split into FOUR sub-phases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is systole?

A
  • ventricular contraction when the blood is pumped into the arteries
    • Split into TWO sub-phases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how do you calculate ejection fraction (EF)?

A

EF= SV/ EDV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

how do you calculate stroke volume?

A

SV= end diastolic volume- end-systolic volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are the different stages of the cardiac cycle?

A
  1. Atrial Systole
  2. Isovolumic Contraction
  3. Rapid Ejection
  4. Reduced Ejection
  5. Isovolumic Relaxation
  6. Rapid Ventricular Filling
  7. Reduced Ventricular Filling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

draw the time pressure diagram during a cardiac cycle

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what occurs during atrial systole?

A
  • Just before atrial systole, the blood will flow PASSIVELY through the open AV valves into the ventricles
  • Atrial Systole tops off the volume of blood in the ventricles
  • ECG - atrial systole is seen as a P wave - indicates atrial excitation
  • atrial pressure shows a small increase due to contraction
  • at this point there is very little change in aorta and ventricles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

when does S4 occur?

A
  • S4 is usually caused by valve incompetency (valves don’t shut properly making the blood flow become turbulent)
  • S4 occurs with:
    • Pulmonary Embolism
    • Congestive Heart Failure
    • Tricuspid Incompetence
  • S4 can occur during atrial systole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

when can the jugular pulse be felt?

A

during atrial systole- pulse in jugular due to atrial contraction pushing blood back up the jugular vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is the P-wave on an ECG?

A

atrial depolarisation

39
Q

what is isovolumic contraction?

A
  • This happens in between the AV valves closing and the semi-lunar valves opening
  • The ventricles are completely sealed off during this period
  • The ventricles start to contract AGAINST CLOSED VALVES
  • So the ventricles contract with NO CHANGE IN VOLUME hence it is isovolumic
  • This contraction against closed valves leads to a rapid increase in pressure
  • ECG - seen as the QRS complex = signified ventricular excitation
  • The first heart sound occurs during this period - caused by the closing of the AV valves
  • S1 is the first heart sound - caused by the closing of the AV valves (this is the ‘lub’)
  • The ventricles are contracting ISOMETRICALLY so the muscle fibres ARE NOT CHANGING IN LENGTH but they are generating force and the pressure increases
  • You reach a point at which the ventricular pressure EXCEEDS aortic pressure (afterload) and at this point the aortic valve opens and blood starts to be ejected from the ventricles
  • Once blood begins to be ejected, isovolumic contraction ends
40
Q

what is the QRS complex?

A

ventricular depolarisation

41
Q

what happens during rapid ejection?

A
  • Aortic and pulmonary valves open marking the start of rapid ejection
  • As the ventricles contract in the closed ventricular chamber the ventricular pressure rapidly increases until it exceeds the pressure in the aorta and pulmonary arteries (afterload)
  • At this point the semi-lunar valves open and the ventricular volume decreases
  • The ‘c wave’ seen in the atrial pressure is caused by the right ventricular contraction pushing the tricuspid valve into the atrium and creating a small wave into the jugular vein
  • Once the valves are open, aortic pressure increases in line with the ventricular pressure
  • ECG - as the excitation process has happened, there is NO ELECTRICAL ACTIVITY on the ECG and there are NO HEART SOUNDS because no valves are closing
42
Q

what wave is seen during rapid ejection?

A

NONE

no electrical activity

43
Q

what happens during reduced ejection

A
  • This phase marks the end of systole
  • Blood leaves the ventricles and ventricular pressure begins to fall, eventually aortic and pulmonary pressure will exceed the ventricular pressure and so the VALVES WILL BEGIN TO CLOSE
  • ECG - cardiac cells begin to REPOLARISE (action potential went very positive and is now returning to resting potential) - this is seen as a T wave
  • NO heart sounds because no valves are shutting
44
Q

what wave happens during ventricular repolarisation?

A

T- Wave

45
Q

what happens during isovolumic relaxation?

A
  • Beginning of diastole
  • Aortic and pulmonary valves have shut and the AV valves remain shut
  • As the AV valves are closed there is NO CHANGE IN VENTRICULAR VOLUME hence it is isovolumic relaxation
  • Atria fill but the AV valves are shut hence there is an increase in atrial pressure
  • ‘v wave’ in the atrial pressure is caused by blood pushing the tricuspid valve and giving a second jugular pulse
  • DICHROTIC NOTCH - small, sharp increase in aortic pressure due to the rebound pressure against the aortic valve as the distended aortic wall relaxes
  • SECOND HEART SOUND is heard when the aortic and pulmonary valves close
46
Q

what happens during rapid ventricular filling?

A
  • AV valves open again and the blood flows rapidly from the atria in to the ventricles
  • Ventricular Volume INCREASES
  • Atrial Pressure DECREASES
  • REMEMBER: This filling of the ventricles is PASSIVE as it is not due to atrial systole
47
Q

what is S3 heart sound?

A

During isovolumic relaxation you may hear a THIRD HEART SOUND (S3) which is ABNORMAL and can signify turbulent ventricular filling

S3 can be due to severe hypertension or mitral incompetence

S3 is often referred to as VENTRICULAR GALLOP

48
Q

what happens during reduced ventricular filling?

A
  • This slow filling of the ventricles is also called DIASTASIS
  • Ventricular volume increases more slowly
  • There are NO changes in the ECG and there are NO heart sounds
49
Q

how can the information be shown on a wiggers diagram?

A
50
Q

what is the difference in pressure changes in right and left side heart?

A

same pattern of pressure changes

right side = lower pressures

but: right side ejects same volume of blood

51
Q

what are the blood pressure values for systemic and pulmonary?

A
  • SYSTEMIC = 120/80 mmHg
  • Pulmonary = 25/5 mmHg
52
Q

how can you measure pressure changes?

A
  • A catheter can be inserted into a large vein and worked up into the right atrium and the right ventricle and you can have a pressure tip on it which allows you to measure changes in pressure
53
Q

what is the pulmonary artery wedge pressure (PAWP)?

A
  • In the pulmonary artery, as you have the valve closing, the diastolic pressure rises in the pulmonary artery
  • You can insert a catheter with a balloon on the end into the pulmonary artery and inflate the balloon so that no blood can go past it
  • Distal to the balloon, you can measure pressure changes further up the pulmonary system which is linked to the left atrium
  • So by measuring on the right side of the heart, you can measure the preload on the LEFT side of the heart
54
Q

what can the PAWP show?

A

if elevated= problems on left side of heart (particularly left atrium) or problems with mitral valve

55
Q

what do the points show on a pressure-volume loop?

A
  • You plot VENTRICULAR PRESSURE against VENTRICULAR VOLUME
  • Point 1 = End Diastolic Volume (EDV) - the ventricle has a large volume but hasn’t generated any pressure yet
  • Point 2 = Isovolumic Contraction - the volume in the ventricle hasn’t changed but there is a large increase in pressure
    • At this point, the ventricular pressure has got to the same point as the aortic pressure (afterload) and is just about to overcome it
  • Between Point 2 and Point 3 = the ventricle starts to expel blood so the volume of blood in the ventricle fall and the ventricular pressure rises then falls
  • This ends on Point 3 which is the End Systolic Volume (ESV)
  • THE DIFFERENCE BETWEEN POINT 3 and POINT 2 IS THE STROKE VOLUME
  • Pressure falls in the ventricles due to Isovolumic Relaxation but the volume stays the same so there is a straight line downwards between Point 3 and Point 4
56
Q

how do preload and afterload affect the pressure-volume loop?

A

point 1 is proportional to preload (blood filling the ventricles and stretching ventricular muscle)

increasing preload moves point 1 and 2 right

afterload is just after point 2 - when left ventricles encounter aortic pressure when the aortic valve begins

increasing afterload shifts 2 and 3 up

57
Q

how does the frank-starling relationship change in vivo?

A
  • Instead of force we have pressure and instead of length we have volume - these are the in vivo correlates in the Frank-Starling Relationship
  • Point 3 is the End Systolic Volume so the active force curve at this point represents the End-Systolic PV Line
  • Just remember how the pressure-volume loop fits into the Frank-Starling Relationship
58
Q

how does preload change stroke volume?

A

increasing preload= increasing stroke volume

  • If we increase the amount of blood flowing back to the heart and hence increase the stretch on the muscle we would move from the smaller PV loop to the bigger one
  • Point 1 and 2 move further to the right because there is more volume returning to the heart and hence the preload increases and End Diastolic Volume increases
  • Greater preload allows us to produce more contraction and therefore more stroke volume
  • The increase in stroke volume is shown by an increase in the distance between point 3 and point 2
59
Q

how does increasing afterload affect stroke volume?

A

increasing afterload decreases stroke volume

  • When you increase the afterload you decrease the amount of shortening
  • So if you have high blood pressure, the afterload is increased so the ventricular muscle has to work harder to eject the blood against the higher pressure
  • Therefore, when we increase the afterload, more pressure is needed to open the aortic valve so Point 2 moves in a positive y direction
  • Point 1 remains the same because the End Diastolic Volume is the same
  • The increase in afterload also means that less shortening can occur and so the stroke volume decreases
60
Q

how do you calculate cardiac output?

A

CO= HR x SV

SV determined by preload, afterload, and contractility

cardiac output can be changed by altering contractility of heart (e.g adrenaline)

61
Q

what is cardiac contractility?

A

contractile capability (or strength of contraction) of the heart

a simple measure of cardiac contractility= Ejection fraction

contractility can be increased by sympathetic stimulation

62
Q

how does contracility change stroke volume and pressure-volume loop?

A
  • Increase in contractility means that more blood is pumped out hence the stroke volume increases and Point 3 moves further to the left
63
Q

how does pressure-volume loop change during exercise?

A
  • During exercise contractility is INCREASED due to increased sympathetic activity
  • Changes in peripheral circulation (e.g. venoconstriction and muscle pump) means that more blood is returned to the heart and so End Diastolic Volume INCREASES
  • So the increase in End Diastolic Volume (EDV) means that point 1 and 2 are pushed further right
  • And the increase in contractility means that point 3 and 4 are pushed further to the left
  • Thus there is an INCREASE in stroke volume
64
Q

what are stenotic lesions?

A

narrowing of the valves

65
Q

what valves can be affected by stenotic lesions?

A

all 4 valves can become narrowed (pulmonary, tricuspid, aortic and mitral)

66
Q

what lesions are more signigicant?

A

left sided valvular lesions (aortic and mitral)

  • Affect chambers which supply blood to whole body
  • Increased afterload on left ventricle
  • Contractions less effective
  • Remodelling hypertrophy
67
Q

what are the causes of aortic stenosis?

A
  • Bicuspid aortic valve
  • elderly degeneration of valve
  • Rheumatic heart disease
  • Infective endocarditis
  • Hyperuricaemia
68
Q

when is aortic stenosis classified as severe?

A

<1cm prescribed

  • Transthoracic echocardiogram to calculate severity by determining speed of blood flow; severe> 4m/s
69
Q

what happens in mitral stenosis?

A

narrowing mitral valve causes increase pressure on left atrium (dilation) and causing irregular rhythm

rarer

70
Q

what are the causes of mitral stenosis?

A
  • Rheumatic fever
  • Congenital
  • Rheumatic arthritis
  • Systemic lupus erythematosus
  • Whipples disease
71
Q

what is a regurgitation lesion?

A

Dilation of valves causing regurgitation

72
Q

what are the causes of mitral regurguation?

A
  • Rheumatic fever
  • Mitral valve prolapse
  • Infective endocarditis
  • Functional
    • Left ventricle dilates too much
73
Q

what can be heart during mitral regurgitation?

A

systolic murmur (hear when heart contracting)

74
Q

what happens during mitral regurgitation?

A
  • Regurgitation of blood when LV contraction = less cardiac output in to aorta = decreased volume blood reaching rest of body
75
Q

what treatment is required for mitral regurgitation?

A

require diuretics

76
Q

what can be heard during an aortic regurgitation lesion?

A

diastolic murmur (hear when heart relaxing)

77
Q

what are the causes of aortic regurgitation lesion?

A
  • Bicuspid
  • Marfan syndrome
  • High BP
  • Rheumatic fever
  • Infection – infective endocarditis in an acute manner
78
Q

what can aortic regurgitation lesion cause?

A
  • Can cause volume overload of left ventricle
79
Q

what is the treatment for aortic regurgitation lesion?

A

replacement required if decompensated

fluid build up

80
Q

what are the different types of cardiomyopathies?

A
  • Dilated Cardiomyopathy (DCM) - specific or idiopathic
  • Hypertrophic Cardiomyopathy
    • (HCM or HOCM or ASH)
    • hypertrophic obstructive cardiomyopathy
    • asymmetrical septal hypertrophy
  • Restrictive Cardiomyopathy
  • Arrhythmic Right Ventricular Cardiomyopathy (ARVC)
81
Q

what can cause heart failure?

A
  1. hypertension
  2. drugs

(overdosing beta-blockers can decrease HR so much that get heart failure type syndrome)

all the anti- arrhythmias can cause dysfunction

calcium antagonists

82
Q

how does myocardial remodeling occur?

A
83
Q

what is cardiomyopathy?

A
  • Cardiomyopathy is heart disease in the absence of a known cause
  • This occurs in about 5% of heart failure in a population
  • The different types of cardiomyopathy were mentioned earlier
  • Hypertrophic cardiomyopathy is the most common cause of young athletes dropping dead
84
Q

what are the causes of dilated cardiomyopaathy?

A
85
Q

what are the causes of restrictive cardiomyopathy?

A
86
Q

what is restrictive cardiomyopathy?

A

the heart is restricted so cant dilate the way usually does

  • Patients with restrictive cardiomyopathy can preserve the ejection fraction so it pumps ok but there is diastolic dysfunction so it’s very slow in relaxing
  • It is associated with other diseases such as hypertrophy and scleroderma

Patients can be very short of breath because relaxation is impaired

87
Q

what is the difference in arrhythmic right ventricular cardiomyopathy than other cardiomyopathies?

A

may not be symptomatic in ARVC but high cause ventricular tachycardia- sudden cardiac death

88
Q

when are valve replacements required?

A

valve degeneration will continue to get worse and require treatment- required before decompensation

89
Q

what are the types of valve replacements?

A
  1. metallic- in younger population, ensure durability
    1. lifetime biological replacement= 2 years
    2. patients required to be on warfarin with valve replacements
  2. prosthetics
    1. increasing emphasis especially with aortic
    2. TAVR- transaortic valve replacement
      1. minimally invasive using catheters via arteries in groin
90
Q

which valve is harder to replace?

A

mitral valve more complicated

anatomically built to withstand pressures

repair if possible rather than replace

mitral clip can improve function

91
Q

what is cardiogenic shock?

A

impairment of cardiac systolic function resulting in reduced CO causing end-organ dysfunction

92
Q

what is cardiogenic shock usually due to?

A

MI

93
Q

what is the treatment for cardiogenic shock?

A
  • Treatment different to other types of shock
    • Do NOT give more fluids
      • This may cause decompensation further as heart cannot deal with further fluids
      • Transthoracic echo to determine
  1. early coronary angiography- visualise narrowing
  2. PCI- using stents to open arteries that are causing the MI
  3. reassess haemodynamics/ tissue perfusion
  4. if still in shock= inotropes then mechanical support devices

1B Cardiorespiratory (15 decks)

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