What is hypertrophy?
= 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
What is the formula for wall stress?
Wall stress = P(pressure) * r(radius of heart) / h (wall thickness)
{Pr/h}
What is the equation for elasticity?
Elastance = ∆P/∆V
How is increased workload defined?
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
Athletes Heart physiology
- 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
What are the dimensions of an athletes heart?
- 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
What is Fick’s Principle?
- 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
What is the result of volume overload due to dynamic/endurance exercise?
- 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
What is the respiratory/abdominothoracic pump?
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
What is venous compliance?
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
What is the result of Pressure Overload due to static/strength exercise?
- 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
What makes theCVS adaptations to exercise physiological and not pathological?
- Reversible
o Somewhat related to signals that drive it – seems to be related to IGF - Increased mitochondrial load as energy requirements increase – doesn’t happen in pathological
- Increased blood vessel supply – doesn’t happen in pathological
- Essentially the system is more balanced
What happens during physiological hypertrophy during pregnancy?
- 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
What is heart failure?
Inability of the heart to produce sufficient CO to profuse the body sufficiently for it to function
What are the 2 types of heart failure?
- Forward failure: Decreased CO = heart overflowing
- Backwards failure: Increased venous pressure
o Results in edema (fluid leaking out of circulatory system into tissue)
What are the acute causes of heart failure?
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
What is the zone of perfusion?
Area that would have been supplied by the now blocked vessel in the endothelium
o Area of risk during myocardial infarction
What are the chronic causes of heart failure?
- Valvular disease
- Cardiomyopathies
o Bacterial, viral
o Alcohol
o Idiopathic - Myocarditis (inflammation)
- Hypertension (leading to increased pressure)
- Increased body demands
What is preload?
- 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)
What is afterload?
- The load against which a heart must contract to eject
- Combination of Blood pressure & Wall stress
What is inotropy?
Cardiomyocyte contractility
What is the effect of inotropy on a Pressure-Volume loop?
- 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
Characteristics of chronic heart failure due to systolic dysfunction
- ↓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
Characteristics of chronic heart failure due to diastolic dysfunction
- 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
