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MD3001 > Pathophysiology of Cardiac Failure > Flashcards

Pathophysiology of Cardiac Failure Flashcards

1
Q

How is CO calculated?

A

HR x SV

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2
Q

What two factors is preload determined by?

A

EDV

Venous return

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3
Q

Define afterload.

A

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

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4
Q

What two factors determine afterload?

A

Vascular resistance
Ventricular wall tension

(think…T = PR, therefore P is going to be determined by T & R)

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5
Q

What is inotropy (for the purposes of the CVS)?

A

Myocardial contractility

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6
Q

Define myocardial contractility.

A

The sympathetic mediated change of cardiac muscle

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7
Q

What direct effect does increased myocardial contractility have?

A

Increases CO

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8
Q

Does myocardial contractility refer to the speed of contraction of the force at which the contraction is generated?

A

Force

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9
Q

Which ion influences myocardial contractility?

A

Ca2+

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10
Q

What chemical mediator is L-type Ca2+ channel opening facilitated by?

A

cAMP

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11
Q

What inhibits Na+/Ca2+ exchange?

A

Cardiac glycosides, e.g. digoxin

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12
Q

Outline the New York Heart Association Classification of Heart Failure.

A

Classes 1 - 4
Class 1 = no limitation of physical activity; no fatigue, dyspnea (shortness of breath) or palpitations
Class 2 = slight limitation of physical activity; ordinary activity results in fatigue, dyspnea or palpitations
Class 3 = marked limitation of physical activity; less than ordinary activity results in fatigue, dyspnea or palpitations
Class 4 = unable to carry out any physical activity without discomfort; fatigue, dyspnea or palpitations at rest

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13
Q

What is the difference between systolic and diastolic dysfunction with regard to ejection fraction and EDV (and hence SV)?

A

Systolic: ejection fraction @ 40% as opposed to normal 50-65%
Diastolic: no change in ejection fraction
Systolic: EDV only increases if volume overload affecting conditions; if caused by contractility or pressure overload affecting conditions, same EDV
Diastolic: EDV decreases due to decreased filling, leading to decreased SV and decreased CO
Systolic: impaired contraction
Diastolic: impaired relaxation

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14
Q

What does systolic dysfunction result from?

A

Conditions that affect:

  • Contractility
  • Volume overload
  • Pressure overload
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15
Q

What causes diastolic dysfunction?

A

Impedance of ventricular expansion
Increased wall thickness
Delayed diastolic reaction
Increased HR

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16
Q

How is SV calculated?

A

EDV - ESV

17
Q

What is ascites?

A

An accumulation of fluid in the abdominal cavity

18
Q

What can be an issue in heart failure patients when going from a standing position to a supine lying position?

A

Blood redistributed from the lower limbs can backup and cause congestion in the lungs

19
Q

What can left heart failure cause?

A

Congestion in the lungs

Decreased cardiac output

20
Q

Bearing in mind what left heart failure causes, what are some signs and symptoms of this condition?

A 
Orthopnea
Cough with frothy sputum
Paroxysmal nocturnal dyspnea
Cyanosis
Hypoxia
21
Q

What can right heart failure cause?

A

Congestion in the peripheral tissues
Liver congestion
GI tract congestion

22
Q

Bearing in mind what right heart failure causes, what are some signs and symptoms of this condition?

A 
Impaired liver function
Anorexia
GI distress
Weight loss
Oedema
Ascites
23
Q

What are some causes of right ventricular dysfunction?

A 
Pulmonary hypertension
Valve damage/stenosis/incompetence
Cardiomyopathy
Infarction
Left ventricular failure
Congenital heart defects
24
Q

How can left ventricular failure lead to right heart dysfunction (failure)?

A

Since afterload of right ventricle is significantly increased due to congestion in the lungs, pressure required for right ventricle to pump blood to the pulmonary system is also significantly increased –> increased pulmonary pressure, so right heart failure is very possible

25
Q

What are some causes of left ventricular dysfunction (failure)?

A

Hypertension (TPR increase)
Acute MI
Aortic or mitral valve stenosis or regurgitation

26
Q

What is the function of cardiac failure compensatory mechanisms?

A

Involved in hypovolaemia

27
Q

What is the chain of events that makes the Frank-Starling compensatory mechanism problematic?

A

Increased vascular volume

  • -> increased EDV
  • -> increase in muscle stretch & O2 consumption
  • -> change in preload (length - tension curve)
  • -> sarcomere beyond optimal length and SV decrease
28
Q

What is the chain of events that makes the Sympathetic Activity compensatory mechanism problematic?

A

Tachycardia, vasoconstriction and decreased perfusion of non-essential tissues

  • -> blood directed towards tissues that it is essential to oxygenate
  • -> increased TPR & renin release
  • -> increased workload of the heart
  • -> damage to myocytes & ischaemia
  • -> decreased contractility
  • -> desensitisation of Beta (but not Alpha) receptors
29
Q

Where are beta receptors predominantly situated?

A

The heart

30
Q

Where are alpha adrenoreceptors predominantly situated?

A

The vasculature

31
Q

What is the chain of events that makes the Renin-Angiotensin compensatory mechanism problematic?

A

Focus on blood volume:
Decrease in renal blood flow
–> renin release
–> increased angiotensin II formation
–> increased vasoconstriction & aldosterone release
–> increased Na+ & water reabsorption
–> oedema & increased congestion

32
Q

Why can fibroblasts and collagen deposits sometimes be found in the ventricles in cardiac failure patients?

A

Angiotensin II and aldosterone are involved in inflammatory responses leading to deposition of collagen and fibroblasts in the ventricles

33
Q

What is the result of deposition of collagen and fibroblasts in the ventricles?

A

Increased stiffness
Decreased contractility
–> Myocardial remodelling and progressing dysfunction

34
Q

What 4 physiological CV parameters need to be targeted in cardiac failure treatment and what change needs to take place to each?

A

Increase CONTRACTILITY
Decrease PRELOAD and/or AFTERLOAD –> decrease CARDIAC WORKLOAD
- by relaxing vascular smooth muscle
- by reducing blood volume
Inhibit Renin Angiotensin Aldosterone System (RAAS)
Prevent inappropriate increase in HR

MD3001 (63 decks)

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