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MD3001 > pathophysiology of heart failure > Flashcards

pathophysiology of heart failure Flashcards

1
Q

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

A

1- contractility and pre load
2- after load

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2
Q

cardiac output?

A

HR x SV

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3
Q

preload?

A

determined by venous return, End diastolic volume

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4
Q

afterload?

A

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

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5
Q

what may excessive after load impair?

A

it may impair ventricular ejection and increase wall tension

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6
Q

ionotropy?

A

myocardial contractility

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7
Q

what is contractility dependant on?

A

(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

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8
Q

how man classes of heart failure are there?

A

4

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9
Q

class 1 heart failure?

A
  • no limitation of physical activity
  • ordinary physical activity does not cause undue fatigue, palpitation, dyspnea
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10
Q

class 2 heart failure?

A
  • slight limitation of physical activity
  • comfortable at rest
  • ordinary physical activity results in fatigue, palpitation, dyspnea
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11
Q

class 3 heart failure?

A
  • marked limitation of physical activity
  • comfortable at rest
  • less than ordinary activity causes fatigue, palpitation or dyspnea
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12
Q

class 4 heart failure?

A
  • unable to do any physical activity without discomfort
  • symptoms of heart failure at rest
  • if any physical activity is undertaken, discomfort increases.
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13
Q

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

A

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

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14
Q

systolic ventricular dysfunction?

A
  • impaired cardiac contractility
  • decreased ejection fraction
    (<40% is bad but around 50-65% is normal)
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15
Q

diastolic ventricular dysfunction?

A
  • normal ejection fraction but impaired diastolic ventricular relaxation and decreased filling
  • decrease in stroke volume and cardiac output
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16
Q

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

A

1- contractility
2- volume overload
3- pressure overload

  • results in increased end diastolic volume 9preload), ventricular dilation, increased ventricular wall tension
17
Q

causes of diastolic dysfunction?

A

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

18
Q

what 3 things (diseases) can cause impaired contractility?

how will these effect the ejection fraction?

A

(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
19
Q

2 causes of increased after load?

what effect does this have on the ejection fraction?

A

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

  • reduced ejection fraction
  • can lead to heart failure
20
Q

5 causes of impaired diastolic filling?

how does the effect the ejection fraction?

A

(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
21
Q

what is right vs left ventricular dysfunction classified according to?

A

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.

22
Q

causes of right ventricular dysfunction?

A

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

23
Q

left ventricular dysfunction causes?

A
  • 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)
24
Q

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

A

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.

25
Q

problems with compensatory mechanisms: Frank Starling?

A
  • this mechanism causes an increase in vascular volume leading to increased end diastolic volume
  • increase in muscle stretch and oxygen consumption
26
Q

problems with compensatory mechanisms: sympathetic activity?

A

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)

27
Q

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

A

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.

28
Q

problems with compensatory mechanisms: renin angiotensin?

A
  • 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)
29
Q

what is angiotensin 2 and aldosterone also involved in?

A

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.

30
Q

what are the strategies for treatment for heart failure?

A
  • 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)
31
Q

What is the ejection fraction?

How does ejection fraction differ in systolic vs diastolic ventricular dysfunction?

What is impaired in diastolic dysfunction?

A
  • 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)
32
Q

What is the difference between oedema and ascites?

What is the difference between PND and orthopnoea?

A
  • 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
33
Q

Where else are these compensatory mechanisms seen?

Why is this?

A
  • 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
34
Q

What are the 3 compensatory mechanisms seen during cardiac failure?

A
  • 3 compensatory mechanisms seen during cardiac failure:
    1) Frank-Starling mechanism
    2) Sympathetic activity
    3) RAAS system – Renin-angiotensin-aldosterone system
35
Q

How is the Frank Starling triggered?

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

A
  • 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
36
Q

What changes in receptor sensitivity do we see in long term sympathetic activity?

How does this contribute to the worsening of heart failure?

A
  • 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
37
Q

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

A
  • 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,
38
Q

what is contractility influenced by?

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

MD3001 (56 decks)

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