Cardiac Muscle Flashcards

1
Q

Define CV disease and outline common types

A

Disease affecting the heart or blood vessels
CV disease- flow of blood to the heart is reduced/ stopped putting increased strain on heart–> angina–> heart attach (blood supply suddenly stopped- myocardial infarction)–> heart failure (unable to pump blood efficiently) and irreversible cell death of cardiac muscle
Stroke/ TIA (transient ischaemic attack)- blood floe to brain blocked- FAST
Diseases of arteries, arterioles or capillaries e.g. peripheral arterial disease, aortic disease (e.g. aortic aneurism)
Hypertrophic cardiomyopathy- congenital disease- thickening heart walls

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

Why is the heart called a dual circuit peristaltic pump?

A

Dual circuit= pipes of R and L contiguous (common border/ touching)
Peristaltic= operates in squeezing motion

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

What types of images can be achieved with an MRI

A
  • Short axis- mis-ventricular section
  • Long axis- oblique sagittal (through midline) plane
  • Sinai magnetic resonance imaging- photos taken in quick succession to form video
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain what structures can be seen from MRI

A
  • Dominated by muscular wall of the left ventricle
  • within left ventricle 2 black dots - papillary muscles
  • Connected to the chordae tendineae and to the mitral valves
  • Assist opening and closing of the mitral valve (left atrium to ventricle) in cardiac contraction
  • White areas= blood so MRI distinguishes between fluid and solid masses (myocardium)
  • Surrounding the 2nd white are= thinner myocardium of the right ventricle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define terms inotropy and chronotropy

A

Inotropy- increased force of contraction

Chronotropy- increased frequency of contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Outline structure cardiac tissue

A
  • Mononucleated
  • Branched and connected via intercalated discs
  • Fibres organised to max. electrical propagation through heart
  • Fibres more vertical in inside and more transverse on outside
  • Helical arrangement causes wringing motion of heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How are cardiac cells adapted for synchronous electrical activity

A
  • intercalated dics- desmosomes holding scaffolding of heart together and low resistance gap junctions improving electrical conductivity of heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Explain what type of twitches are utilised in cardiac muscle

A
  • synchronous, single twitches
  • Electrical impulse form SAN- AVN, Purkinje fibres and other adaptations maximising and ensure simultaneous contraction
  • Twitch contractions- due to a single electrical event the cell decreases In length
  • Duration of twitch contraction similar to vesicular contraction
  • These twitches summate in heart at a single point in time causing an increase in function i.e. causing contraction of heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain how the action potential is propagated into the myocyte

A
  • Cardiac AP propagated along the sarcolemma into the T- tubules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain differences in the twitches in cardiac and skeletal muscle and what causes this

A
  • Cardiac muscle- depolarisation caused by single twitch,
  • Further twitches prevented by plateau of action potential before full repolarisation
  • Skeletal muscle- we gave a summation of twitches, more frequent so they fuse forming smooth tetanus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain how membrane potential changes in cardiac and skeletal muscle tissue? Why?

A
  • Cardiac tissue: depolarisation (Na), then there is a platau (Ca), then repolarisation occurs (K)
  • The plateau is due to an influx of Ca ions
  • Due to opening of L- type Ca channels (long type Ca channels), which open more slowly than the Na channels
  • Therefore there is a plateau as Ca enters cell
  • Therefore cardiac action potentials are much longer than in muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain how Ca handling regulates cardiac contraction

A
  • Some Ca channels on surface of cardiac tissue
  • Open in response to an action potential
  • Accounts for only 10-25% contraction
  • Or Ca- induced Ca release
  • T tubules are associated with structures called a diad- consist of L type Ca channels, ryanodine receptors and the terminal cisternae of the sarcoplasmic reticulum
  • Action potential causes opening of L-type Ca channels causing Ca to flow into the cell down its concentration gradient
  • The extracellular Ca binds to ryanodine receptors in induces endings of sarcoplasmic reticulum to release more Ca
  • ATPase pumps more Ca into SR (75-90%) or expelled from cell via Na- Ca exchange (10-25%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Outline differences in Ca handling between skeletal and cardiac muscle

A
  • Skeletal muscle: Triads- 1 t-tubule has terminal cisternae on either side aka terminal cisternae- t-tubule- terminal cisternae
    • More SR
    • T-tubules: less lacier
  • VS Cardiac- Diad- t-tubule associated with 1 terminal cisternae
    • Less SR
    • More lacier t-tubules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Explain how the Ca transient is key to many drug actions and give an example of a positive and negative inotrope

A
  • Positive inotrope- increases force of contraction
  • caffeine- acts on Ca release channels of sarcoplasmic reticulum
  • more Ca release allows for more actin- myosin cross bridges to for so greater strength of contraction
  • Negative inotrope- decreases force of contraction
  • L-type Ca blockers- Verapamil
  • Insufficiency of coronary flow caused by stenosis on coronary artery (narrowing of blood vessel): muscle contracting while producing too mush lactate (anaerobic respiration)–> angina (heart pain)
  • Beneficial in angina (chest pain) as reduces energy demand reducing ischaemia and therefore chest pain
  • Also blood pressure drug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does digitalis work

A
  • positive inotrope- like caffeine allows for more free cytosolic Ca being released from SR so more force
  • Relieves symptoms of congestive heart failure
  • Yet small therapeutic window as safe dose close to lethal dose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Does cardiac muscle have a high demand for ATP- why and where does it get this from. What happens if obstruction in coronary artery?

A
  • Many mitochondria in cardiac muscle as tissue never really at rest
  • Most from oxidised fat (70%), some form oxidation of glucose (20%), other sources such as glycolysis, lactate and ketones (10%- in starvation)
  • ATP needed to re-energise myosin head- returning it to its original position
  • Infarct is a zone of ischaemic dying tissue- happen quickly
  • Caused by acute obstruction in coronary artery (not getting O2 for ATP production)- needs to be fixed via stent
17
Q

Explain the 2 types of cardiac muscle mitochondria

A
  • Continuous reticulum of mitochondria throughout cardiomyocyte
  • Interfibrillar mitochondria- providing ATP for muscular contraction

Subsarcolemmal mitochondria- suppling ATP for ATP-depended action potential processes e.g. Pumps within SR (????- we don’t really know)

18
Q

What happens in concentric cardiac hypertrophy?

A
  • Increase in resistance against left ventricle (increasing cardiac afterload)
  • Causes hypertrophy (increase in muscle mass just like effect on exercise in Sk muscle)
  • Effect seen due to hypertension (high blood pressure) or athletic heart- as heart pumps harder in response to doing more exercise
  • Muscle gets fatter and lumen gets bigger
  • The heart gets steadily larger and longer when afterload persists- compensated hypertrophy
19
Q

What happens in decompensation?

A
  • In extreme cases leads to de-compensation
  • Hypertrophy stops and heart becomes baggier and muscle begins to fall apart
  • We see the left and right ventricle become enlarged and inefficient ejection of blood (reduced ejection fracture)
  • Ejaculation fracture not only measure of quality of life as although it can effect peripheral perfusion and not be well may still able to preform simple tasks
  • Makes tasks such as walking up stairs difficult
20
Q

Why is LV much bigger than RV?

A
  • Left ventricle very muscular dominates muscle mass (2/3) VS right ventricle (1/3 muscle mass)
  • As pumping against peripheral resistance- from series of organs
  • Right Ventricle: pumping against much lower resistance of lungs