pathophysiology of heart failure

Question 1

1- what 2 things will increase stroke volume?
2- what will decrease stroke volume?

Answer 1

1- contractility and pre load
2- after load

Question 2

cardiac output?

Answer 2

HR x SV

Question 3

preload?

Answer 3

determined by venous return, End diastolic volume

Question 4

afterload?

Answer 4

the force the contracting heart must generate to eject blood from the heart

Question 5

what may excessive after load impair?

Answer 5

it may impair ventricular ejection and increase wall tension

Question 6

ionotropy?

Answer 6

myocardial contractility

Question 7

what is contractility dependant on?

Answer 7

(increased contractility increases cardiac output independent of preload and after load)

it is influenced by Calcium movement.
- L type channels = opening will be facilitated by cAMP
- Na/Ca exchange = inhibited indirectly by cardiac glycosides

Question 8

how man classes of heart failure are there?

Answer 8

4

Question 9

class 1 heart failure?

Answer 9

• no limitation of physical activity
• ordinary physical activity does not cause undue fatigue, palpitation, dyspnea

Question 10

class 2 heart failure?

Answer 10

• slight limitation of physical activity
• comfortable at rest
• ordinary physical activity results in fatigue, palpitation, dyspnea

Question 11

class 3 heart failure?

Answer 11

• marked limitation of physical activity
• comfortable at rest
• less than ordinary activity causes fatigue, palpitation or dyspnea

Question 12

class 4 heart failure?

Answer 12

• unable to do any physical activity without discomfort
• symptoms of heart failure at rest
• if any physical activity is undertaken, discomfort increases.

Question 13

what way can you classify heart failure and what is this classification based on?

Answer 13

systolic vs diastolic dysfunction
- this is based non the ejection fraction.

Question 14

systolic ventricular dysfunction?

Answer 14

• impaired cardiac contractility
• decreased ejection fraction
  (<40% is bad but around 50-65% is normal)

Question 15

diastolic ventricular dysfunction?

Answer 15

• normal ejection fraction but impaired diastolic ventricular relaxation and decreased filling
• decrease in stroke volume and cardiac output

Question 16

what does systolic dysfunction commonly result from conditions that effect what?
what do they result in?

Answer 16

1- contractility
2- volume overload
3- pressure overload

• results in increased end diastolic volume 9preload), ventricular dilation, increased ventricular wall tension

Question 17

causes of diastolic dysfunction?

Answer 17

1- impedance of ventricular expansion
2- increased wall thickness
3- delayed diastolic relaxation (aging, ischeamia)
4- increased hr

Question 18

what 3 things (diseases) can cause impaired contractility?

how will these effect the ejection fraction?

Answer 18

(systolic dysfunction)
1- coronary artery disease (MI, ischamia)
2- chronic volume overload (mitral regurgitation, aortic regurgitation)
3- dilated cardiomyopathy

• reduced ejection fraction
• can lead to heart failure

Question 19

2 causes of increased after load?

what effect does this have on the ejection fraction?

Answer 19

(systolic dysfunction)
1- advanced aortic stenosis
2- uncontrolled severe hypertension

• reduced ejection fraction
• can lead to heart failure

Question 20

5 causes of impaired diastolic filling?

how does the effect the ejection fraction?

Answer 20

(diastolic dysfunction)
1- left ventricular hypertrophy
2- restrictive cardiomyopathy
3- myocardial fibrosis
4- transient myocardial ischamei
5- pericardial contraction or tamponade

• persevered ejection fraction
• can lead to heart failure

Question 21

what is right vs left ventricular dysfunction classified according to?

Answer 21

according to the side of the heart that is primarily effected
- if long term, it will usually be both sides
- majority will be left sided heart failure.

Question 22

causes of right ventricular dysfunction?

Answer 22

1- conditions impeding flow into lungs (pulmonary hypertension, valave damage/stenosis/incompetance)
2- pumping ability of right ventricle (cardiomyopathy, infarction)
3- left ventricular failure
4- congenital heart defects

Question 23

left ventricular dysfunction causes?

Answer 23

• hypertension (increased TPR)
• acute myocardial infarction
• aortic or mitral valve stenosis or regurgitation
• increase in pulmonary pressure can lead to right ventricular failure (blood is backing up into the RV)

Question 24

describe how the heart compensates in the early stages of heart failure?

Answer 24

it will try to maintain cardiac output, but by doing so, it only increases the stress on. the heart.
- longer term the condition will worsen.

Question 25

problems with compensatory mechanisms: Frank Starling?

Answer 25

- this mechanism causes an increase in vascular volume leading to increased end diastolic volume - increase in muscle stretch and oxygen consumption

Question 26

problems with compensatory mechanisms: sympathetic activity?

Answer 26

initially, sympathetic activity can be helpful but long term it is not. - tachycardia, vasoconstriction, decreased perfusion of tissue, cardiac arrhythmias, renin release - all of which will increase the workload of the heart causing ischaemia, damage to myocytes and a decrease in contractility - there will be desensitisation of b receptors (but not alpha ones)

Question 27

what does renin do and how does it effect blood volume?

Answer 27

Renin (released from kidneys) will act in several steps to make angiotensin 2. -accompanied with aldosterone -angiotensin will narrow blood vessels -aldosterone causes your kidneys to retain water and salt. -increasing the amount of fluid in body and raises blood pressure.

Question 28

problems with compensatory mechanisms: renin angiotensin?

Answer 28

- decrease in renal blood flow stimulates release of renin - increase in renin release therefore increase in angiotensin 2 formation THIS WILL CAUSE VASOCONTRICTION and stimulate aldosterone release - therefore sodium and water reabsorption is increasing both directly (decreased flow rate through the kidney and directly via aldosterone)

Question 29

what is angiotensin 2 and aldosterone also involved in?

Answer 29

they are also involved in inflammatory responses leading to deposition of fibroblasts and collagen in the ventricles - therefore there is increased stiffness and a decrease in the contractility of the heart - this causes myocardial remodelling and progressing dysfunction.

Question 30

what are the strategies for treatment for heart failure?

Answer 30

- increase contractility (you have to be able to match the oxygen consumption of the heart) - decrease preload and/or after load to decrease cardiac work demand (this is done by relaxing vascular sooth muscle and by reducing blood volume) - inhibit RAAS - prevent inappropriate increase in heart rate. - remove volume of fluid by diuretics - angina methods (relax vascular smooth muscle)

Question 31

What is the ejection fraction? How does ejection fraction differ in systolic vs diastolic ventricular dysfunction? What is impaired in diastolic dysfunction?

Answer 31

* The ejection fraction is a measurement, expressed as a % of how much blood is pumped out of the ventricle with each contraction * In systolic ventricular dysfunction, there is impaired cardiac contractility, meaning the ejection fraction decreases (from the normal 50-65% to less than 40%) * In diastolic ventricular dysfunction, the ejection fraction is normal, but there is impaired ventricular relaxation and decreased filling, leading to a decreases in stroke volume (SV) and therefore cardiac output (CO)

Question 32

What is the difference between oedema and ascites? What is the difference between PND and orthopnoea?

Answer 32

* Ascites is fluid build-up in the abdomen while oedema is the swelling and puffiness in the different parts of the body * PND and orthopnoea are both caused by fluid build-up in the lungs, but PND can take a few hours to occur

Question 33

Where else are these compensatory mechanisms seen? Why is this?

Answer 33

* These compensatory mechanisms are also seen in hypovolaemia (decrease in blood volume due to blood loss) * The body does not sense the drop in volume from hypovolaemia or drop in cardiac output from cardiac failure, only the drop in MABP which is sensed by arterial baroreceptors in both cases * This leads to the same compensatory mechanisms being used for hypovolaemia and heart failure

Question 34

What are the 3 compensatory mechanisms seen during cardiac failure?

Answer 34

* 3 compensatory mechanisms seen during cardiac failure: 1) Frank-Starling mechanism 2) Sympathetic activity 3) RAAS system – Renin-angiotensin-aldosterone system

Question 35

How is the Frank Starling triggered? What are problems with the Frank Starling mechanisms as compensatory mechanism in cardiac failure?

Answer 35

* The Frank Starling mechanism is triggered by an increase in vascular return * This leads to an increase in EDV, which triggers an increase in muscle stretch and O2 consumption * This triggers an increase in contractility through a greater overlap between actin and myosin in the sarcomeres

Question 36

What changes in receptor sensitivity do we see in long term sympathetic activity? How does this contribute to the worsening of heart failure?

Answer 36

* Sympathetic innervation will cause the Desensitisation of β but not α receptors * With β-receptor desensitisation, this decreases the ability of the sympathetics to increase HR and contractility * With the α receptor sensitivity staying the same, sympathetic mediated vasoconstriction can still stay in place, meaning resistance in the vessels will stay high * These changes will all ↑ the workload of the heart, leading to ischaemia, damage to myocytes, and ↓ contractility, leading to worsening of heart failure

Question 37

What can occur if the heart stretches too far? Frank Starling mechanism

Answer 37

* Problems with the Frank Starling mechanisms as compensatory mechanism in cardiac failure: * When EDV starts to become too high, this can stretch the overlap of actin and myosin too far, decreasing the ability of the ventricle to generate force, causing ventricular dysfunction * This will mean the Frank Starling mechanism won't contribute a huge amount of ability towards heart contraction * If the heart stretches too far, this can lead to dilated cardiomyopathies,

Question 38

what is contractility influenced by?

Answer 38

- L type channels (opening is facilitated by cAMP) - Na/Ca exchange (inhibited indirectly by cardiac glycosides)