LP #110 Understanding The Mechanics Of Heart Fxn & Coronary Circulation Flashcards

1
Q

Measures difference b/w the volume of blood in one ventricle at the end diastolic volume (EDV) & end systolic volume (ESV)

A

Stroke volume

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

3 frank-starling law of the heart

A
  1. preload
  2. contractility
  3. after load
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  • degreee of heart m stretch before m contracts
  • determined by EDV
  • critical factor controlling SV
  • stretch: at rest: myocardial cells shorter than optimal length for contraction
  • stretch applied to heart (diastole):
  • myofibres lengthen
  • decrease overlap of actin & myosin (optimizes force of contraction)
A

Preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  • ability of myocardial cells shorten & compress ventricle
  • independent of stretch & EDV
  • affected by CA+ released from IF & SR
  • increase influx of ca2+= increase contraction force= increase SV & CO
A

Contractibility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  • increase of stretch on myocardial cells= increase force of contraction= increase bald ejected
  • excessive increase BVol in ventricles stretches myocardial cells beyond capacity= ineffective SV & decrease blood ejected -occurs in hypertension
A

Preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  • P exerted by bold (aorta or pulmonary trunk) against a SL valve
  • valve closes- allows P from incoming atrial blood to build in ventricle
  • stretch’s ventricle
  • ventricular P must overcome after load to open SL valves & eject blood from heart
A

After load

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  • w/normal BP:
  • afterloadis not major factor or SV
  • but it is important in increase BP
  • w/increase BP:
  • increase after load= increase ventricular effort to overcome resistance & open Sl valve
  • if afterload cannot be overcome:
  • decrease SV & increase ESV
  • compensatory effects increase workload= cardiac hypertrophy
A

Afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  • supplies myocardium
  • body’s shortest vascular circuit
  • begins w/ L & R coronary aa
  • branches envelope & invade myocardium
  • cardiac vv drain bled into coronary sinus, which drains into R atrium
A

Coronary circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  • group of disorders affecting myocardium
  • 1’ (idiopathic), or
  • 2’ to CV disease
A

Cardiomyopathies

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

3 types of 1* cardiomyopathies

A
  • dilated or congestive myopathies
  • hypertrophic myopathies
  • restrictive myopathies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

-fibrosis & atrophy of moycardial cells; dilation of heart chambers

A

Dilated or congestive myopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  • hypertrophy of one or both ventricles
  • L ventricular hypertrophy is more common
  • enlarged ventricle leads to decrease chamber volume= decrease SV
A

Hypertrophy myopathies

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

-decrease ventricular filling d/t increase ridge Ty of ventricular wall

A

Restrictive myopathies

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

In all myopathies cases s/s are

A
  • dyspnea
  • fatigue
  • chest pn on exertion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Structural changes in mardiomyopathies d/t

A

Hearts excessive workload

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

4 structural changes in cardiomyopathies

A
  1. sclerosis of valve faps
  2. reduced cardiac reserve
  3. myocardial scar tissue (fibrosis)
  4. atherosclerosis
17
Q
  • leads to valvular stenosis & regurgitation

- more common w/ mitral & SL valves

A

Sclerosis of valve flaps

18
Q

-d/t decrease CO2, heart is less able to meet increase demand in a short period of time/during intense activity

A

Reduced cardiac reserve

19
Q
  • fibrosis of heart tissue leads to decrease myocardial elasticity
  • results in decrease preload & decrease contraction force
A

Myocardial scar tissue (fibrosis)

20
Q
  • fat deposits & plaque formation
  • may restrict/ obstruct BF
  • BF obstruction result in:
  • reduce BF > ischemia & hypoxia > death of myocardial cells
  • may lead to heart failure & strokes (CVAs)
A

Atherosclerosis

21
Q

Risk factors (plaque formation)

A

1.hypertension: effect of increase BP- stress on walls of already damaged aa (may lead to ulcers & scar tissue)

  1. DM (diabetes mellitus): effects predisposes hyperlipidemia & increase plaque deposit in aa
    - onset is associated w/ middle age & obesity