CVS AND HEART FAILURE Flashcards
what does an athletes heart look like
- increased left ventricular dilation
- thickening of the left ventricular wall
- increased heart mass
- increased cardiac function
what is ficks principle
CO=VO2/Ca-Cv
what changes to the heart occur with endurance/isotonic exercise
this leads to VOLUME OVERLOAD which with healthy exercise is good
1. increased lusitropy
2. increased inotropy
3. increased frank starling effect ie; stroke volume
4. peripheral vascular dilation- increase blood flow to the periphery
5. venous constriction ie; increased venous compliance to promote venous return to the heart
6. increased skeletal muscle and abdominothoracic pumps
what changes to the heart occur with isometric/strength training
leads to PRESSURE OVERLOAD
1. minimal increase in cardiac output
2. decrease in pump activity
3. increased peripheral resistance
define heart failure
the heart has the inability to produce a sufficient cardiac output
what is the main cause of heart failure
myocardial infarction ie; heart attack which damages the heart leading to heart failure
explain how a myocardial infarction occurs
- plaque builds up in the coronary arteries
- this forms a blockage as it thickens
- so part of the heart no longer receives blood
- call this the perfusion area
- if this area remains without blood for long enough then necrosis/tissue death is going to occur which leads to an infarct
in the diagram of the heart why where some areas near the perfusion area protected/ still receiving blood
because these myocytes lie close to the left ventricle and so they are still receiving blood from this area via diffusion
what can a myocardial infarction lead to
dyskinesis
what is dyskinesis
this is when the heart structure changes in response to damage
- so in the case of an infarct forming(area of dead tissue); this causes dyskinesis to occur
-dyskinesis is where the damaged area will bulge outwards upon contraction; causing the blood to pool in this bulge instead of being pumped out of the heart
-thus; dyskinesis results in a decreased stroke volume
what compensatory mechanism does the heart use to counteract the decline in stroke volume caused by the damage to myocytes
so the damage caused decreasing pumping capacity of the heart right and so increased preload occurs to try and compensate for the decline in stroke volume from the heart upon damage to the heart
-but this then puts increased workload on the surviving myocytes so although it is a compensatory mechanism against the decline in cardiac output; it inevitably leads to heart failure
what are other causes of heart failure
- valvular disease
- cardiomyopathies
- myocarditis
- hypertension
explain the pressure volume loop
pressure on the y axis and volume on the x axis
A= ESV
A-B= ventricular filling so mitral valves must open at A
B=EDV and slight increase in pressure to force the mitral valves close
B-C= then pressure rapidly increases to open the aortic valves
C-D= the blood leaves the heart and so volume drops
D= the aortic valves close as pressure drops slightly
D-A= large drop in pressure so the mitral valves can open
what is preload
initial stretching of the cardiomyocytes prior to contraction thus; the more blood present at EDV the more they are going to stretch
-the more they stretch the greater the tension they generate in systole
- it is an initial compensatory mechanism to try and increase the stroke volume in heart damage
how does preload change the pressure volume loop
EDV will be greater but all the rest will be the same
-thus SV will increase
what is afterload
load against which cardiomyocytes must contract to eject blood
what are the 2 main contributors to afterload
- wall stress
- blood pressure outside the heart
-an example of afterload is hypertension
how does increased afterload influence the heart
the greater the afterload; the shorter the myocytes become ie; their contractility declines and so does the tension they generate and thus; decreases stroke volume
- so the heart works harder to maintain cardiac output which can lead to hypertrophy and thus heart failure
how does afterload influence the pressure volume loop
it causes the ESV to increase because less blood can be pumped out
- also see increase in the height of loop ie; increased arterial pressure
define inotropy
cardiomyocyte contractility
how does inotropy influence the the pressure volume loop
- increased inotropy means the ESV is going to be less
- decreased inotropy means the ESV is going to be more
what are the 3 types of heart failure
- systolic dysfunction
2.diastolic dysfunction
3.systolic and diastolic dysfunction
explain what systolic dysfunction is
- decrease inotropy
2.increased ESV
3.increased EDV but by less than the ESV so SV declines - increased EDP
- increased venous pressure
- edema
explain what diastolic dysfunction is
impaired filling of the ventricles
-can be caused by hypertension(hypertrophy)
- cardiomyopathies
1.decreased venous compliance
2. decreased SV
3. Increased EDP
4. decreased EDV and increased ESV
diastolic and systolic dysfunction
-result of a large heart attack because the heart attack can cause hypertrophy of the surviving myocytes that are working extra hard
-and they cause loss of inotropy
what is the bodies systemic response to heart failure
- the baroreceptors will sense the drop in cardiac output and secrete norepinephrine to do the following:
a. increase inotropy
b. increase lusitropy
c. increase heart rate
d. increase preload and mean arterial pressure
e. increase workload of the heart
f. then later the RAAS kicks in to firther increase preload and mean arterial pressure and to retain fluid from the kidneys to increase the volume of the blood
what are therapeutics used in heart failure
- diuretics to reduce edema
- vasodilators
- B blockers
how can volume overload lead to pathological hypertrophy
it can cause eccentric hypertrophy where the cardiac walls thin ie; enlarged ventricular chamber
