LP #110 Understanding The Mechanics Of Heart Fxn & Coronary Circulation Flashcards
Measures difference b/w the volume of blood in one ventricle at the end diastolic volume (EDV) & end systolic volume (ESV)
Stroke volume
3 frank-starling law of the heart
- preload
- contractility
- after load
- 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)
Preload
- 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
Contractibility
- 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
Preload
- 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
After load
- 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
Afterload
- 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
Coronary circulation
- group of disorders affecting myocardium
- 1’ (idiopathic), or
- 2’ to CV disease
Cardiomyopathies
3 types of 1* cardiomyopathies
- dilated or congestive myopathies
- hypertrophic myopathies
- restrictive myopathies
-fibrosis & atrophy of moycardial cells; dilation of heart chambers
Dilated or congestive myopathies
- hypertrophy of one or both ventricles
- L ventricular hypertrophy is more common
- enlarged ventricle leads to decrease chamber volume= decrease SV
Hypertrophy myopathies
-decrease ventricular filling d/t increase ridge Ty of ventricular wall
Restrictive myopathies
In all myopathies cases s/s are
- dyspnea
- fatigue
- chest pn on exertion
Structural changes in mardiomyopathies d/t
Hearts excessive workload
4 structural changes in cardiomyopathies
- sclerosis of valve faps
- reduced cardiac reserve
- myocardial scar tissue (fibrosis)
- atherosclerosis
- leads to valvular stenosis & regurgitation
- more common w/ mitral & SL valves
Sclerosis of valve flaps
-d/t decrease CO2, heart is less able to meet increase demand in a short period of time/during intense activity
Reduced cardiac reserve
- fibrosis of heart tissue leads to decrease myocardial elasticity
- results in decrease preload & decrease contraction force
Myocardial scar tissue (fibrosis)
- 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)
Atherosclerosis
Risk factors (plaque formation)
1.hypertension: effect of increase BP- stress on walls of already damaged aa (may lead to ulcers & scar tissue)
- DM (diabetes mellitus): effects predisposes hyperlipidemia & increase plaque deposit in aa
- onset is associated w/ middle age & obesity
