Exercise & CVS Flashcards

1
Q

What is hypertrophy?

A

= Cardiomyocytes (cells that do all the work in the heart) get bigger
o Because they divide very sparingly
o Very little division from when your heart is fully grown

  • Only way that cardiomyocytes can deal with increased workload is to get bigger
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2
Q

What is the formula for wall stress?

A

Wall stress = P(pressure) * r(radius of heart) / h (wall thickness)
{Pr/h}

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3
Q

What is the equation for elasticity?

A

Elastance = ∆P/∆V

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4
Q

How is increased workload defined?

A

Increased workload defined in 2 ways:
1. Increased Pressure: Myocytes thicken -> concentric left-ventricular hypertrophy (walls get thicker evenly, no shape change)
o Thicken by laying down sarcomeres in parallel (on top of each other)
2. Increased Volume: Myocytes lengthen -> eccentric left-ventricular hypertrophy (heart gets bigger)
o Lengthen by laying down sarcomeres in series

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5
Q

Athletes Heart physiology

A
  • Increased Heart Mass
  • Normal or increased Cardiac Function
  • Reversible – i.e. if people stop exercising it can be reversed
    o This is the difference between physiological and pathological
-	3 types:
	o	Endurance athlete: 
		•	Thickening of LV walls
		•	LV dilation
	o	Strength athlete:
		•	Thickening of LV walls
		•	Mild LV dilation
	o	Combination athlete:
		•	Gross thickening of LV walls
		•	LV dilation
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6
Q

What are the dimensions of an athletes heart?

A
  • Elite athletes have around 10-20% increase in LV wall thickness & cavity diameter
  • Small percentage have dimensions that overlap with cardiac disease dimensions
  • Most pronounced in cycling/rowing/X-country skiing
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7
Q

What is Fick’s Principle?

A
  • VO2 = CO(CaO2 – CvO2)
    o CO = Cardiac output
    o CaO2 = incoming blood in pulmonary vein, highly oxygenated
    o CvO2 = returning deoxygenated blood to the heart
    o CO is what changes when you exercise
  • CO = SV (stroke volume) x HR (heart rate)
  • Max Heart Rate = age dependent
  • Stroke volume = exercise dependent
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8
Q

What is the result of volume overload due to dynamic/endurance exercise?

A
  • Increase Atrial/ventricular inotropy (ability of heart to contract)
    o Increases sensitivity of B1-adrenergic receptors to norepinephrine
    o Means LV can eject more blood on each cycle
  • Increased Lusitropy – ability of heart to relax
  • Increased Peripheral vascular dilation
    o Reduces peripheral resistance so blood flows more easily
  • Increased Skeletal & abdominothoracic (respiratory) pump activity
  • Increased Venous constriction
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9
Q

What is the respiratory/abdominothoracic pump?

A

o In the interpleural cavity (inside your chest)
o Negative pressure inside
o Breathing in expands chest, diaphragm goes down -> pressure drops -> venous dilation -> more blood in right atrium

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10
Q

What is venous compliance?

A

o Sympathetic nerve activity increased during exercise -> venous constriction
o Results in amount of blood that can be held in venous system decreasing -> blood pushed out into rest of the system

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11
Q

What is the result of Pressure Overload due to static/strength exercise?

A
  • Minimal increase in CO
  • Decrease pump activity
    o No rhythmic activity
    o Valsalva manoeuvre
  • Increased Peripheral resistance
    o Mechanical compression
    o Muscle contraction around arterioles and capillaries -> blocks blood flow
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12
Q

What makes theCVS adaptations to exercise physiological and not pathological?

A
  1. Reversible
    o Somewhat related to signals that drive it – seems to be related to IGF
  2. Increased mitochondrial load as energy requirements increase – doesn’t happen in pathological
  3. Increased blood vessel supply – doesn’t happen in pathological
  4. Essentially the system is more balanced
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13
Q

What happens during physiological hypertrophy during pregnancy?

A
  • VO2 increases 33%
  • Blood volume increases 40%
  • CO increases 50%
  • Total peripheral resistance falls
  • Reversible (Because physiology)
    o Some women don’t go back to due issues in angiogenesis (vessel supply to cardiomyocytes)
    o Results in peripartum-cardiomyopathy
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14
Q

What is heart failure?

A

Inability of the heart to produce sufficient CO to profuse the body sufficiently for it to function

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15
Q

What are the 2 types of heart failure?

A
  1. Forward failure: Decreased CO = heart overflowing
  2. Backwards failure: Increased venous pressure
    o Results in edema (fluid leaking out of circulatory system into tissue)
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16
Q

What are the acute causes of heart failure?

A

Myocardial infarction (heart attack):
- Caused by sudden & complete blockage of a cardiac artery
- Unstable plaque ruptures exposing blood to thrombotic surface due to removal of endothelial surface which causes sudden and catastrophic blockage by thrombosis and fibrin forming fibrinogen clot
- Zone of perfusion becomes ischemic (doesn’t get blood supply)
- Zone of perfusion immediately becomes compliant (unable to contract)
o Compliant means increased P -> increased stretching
- Cardiomyocytes start to die within 2hrs
- If blockage isn’t removed, zone of necrosis (dying cells) grows – starting on endocardial side
o Very thin layer of safe tissue on endocardial side due to diffusion of highly oxygenated blood in the left ventricle
- Increased P after systole -> Dyskinesis -> decreased SV -> volume overload
o Initially compensatory mechanisms acts via increased preload (V of blood in heart at end of diastole)
o Places increased workload on surviving cardiomyocytes

17
Q

What is the zone of perfusion?

A

Area that would have been supplied by the now blocked vessel in the endothelium
o Area of risk during myocardial infarction

18
Q

What are the chronic causes of heart failure?

A
  • Valvular disease
  • Cardiomyopathies
    o Bacterial, viral
    o Alcohol
    o Idiopathic
  • Myocarditis (inflammation)
  • Hypertension (leading to increased pressure)
  • Increased body demands
19
Q

What is preload?

A
  • The initial stretching of cardiomyocytes prior to contraction ( in diastole)
  • Increase in preload -> more rapid generation of tension = contracts to same final length over same period of time
  • EDV (end-diastolic volume)
20
Q

What is afterload?

A
  • The load against which a heart must contract to eject

- Combination of Blood pressure & Wall stress

21
Q

What is inotropy?

A

Cardiomyocyte contractility

22
Q

What is the effect of inotropy on a Pressure-Volume loop?

A
  • Increased inotropy = Shift to left & steeper curve - i.e. higher P at any loading V
  • Decreased inotropy = Shift to right & lower curve - i.e. Decreased P
23
Q

Characteristics of chronic heart failure due to systolic dysfunction

A
  • ↓inotropy: likely due to impaired excitation-contraction coupling
  • ↓ ESPVR
  • Increased ESV -> increased EDV
  • EDV increases less than ESV
  • EDP can rise causing increased pulmonary venous P
  • Edema
  • Decrease in Ejection Factor (EF) is a marker of a poor prognosis
24
Q

Characteristics of chronic heart failure due to diastolic dysfunction

A
  • Impaired filling
    o Hypertension; hypertrophic cardiomyopathy, old age
    o Thickened wall, scarred wall
  • EDPVR shift up and to left
  • Reduction in SV
  • If EDP increases too much results in edema
25
What is an edema?
Puffiness caused by excess fluid trapped in the body's tissues
26
What is the systemic response to heart failure?
- Baroreceptors sense CO drop - Sympathetic tone increases: o Norepinephrine, resulting in: • Increase HR, inotropy, lusitropy • Via B1 adrenoreceptors o Long term increased workload/O2 consumption - RAAS (slower response) o AngII (potent vasoconstrictor) increases MAP (mean arterial pressure) and preload o Aldosterone/vasopressin o Increased fluid retention o Compensatory mechanisms o Long term increased workload/O2 consumption o Edema