Module 3 - cardiovascular system Flashcards
myocardium
the heart muscle
heart muscle
homogenous form of striated muscle, with high capillary density and numerous mitochondria
what does the right side of the heart do?
1)receives returning blood and 2) pumps blood to the lungs for aeration through the ‘pulmonary circulation’
left side of the heart
1) receives oxygenated blood from the lungs and 2) pumps blood into the thick-walled, muscular aorta for distribution throughout the body in the ‘systemic circulation’
what separated the left side of the heart from the right?
thick, solid muscular wall or interventricular septum
atrioventricular valves
within the heart provide one-way blood flow
tricuspid valve
blood flows from the right atrium to the right ventricle through this valve
mitral (bicuspid) valve
blood flows from the left atrium to the left ventricle through this valve
Where are the semilunar valves located and what do they do?
in the arterial wall just outside the heart. They prevent blood flow from flowing back into the heart between contractions
how long do heart valves remain closed?
0.02 - 0.06s
isovolumetric contraction period
when heart volume and muscle fibre length remain unchanged
when does blood eject from the heart?
When ventricular pressure exceeds arterial pressure
arteries
compose the high-pressure tubing that propels O2 rich blood to the tissues
Systolic blood pressure (normal)
120 mm Hg
diastolic blood pressure (normal)
60 - 80 mm Hg
what are the 3 types of adaptations that exercise and inactivity do on the cardiovascular system?
Function, structural and electrophysiological adaptations
functional adaptations (in heart) relate to what equation?
Fick equation - VO2 = Q x (a-VO2) —> and Q = HR x SV
effect of bedrest and training on resting Q (cardiac output)
not changed by bedrest or training
effect of bedrest and training on maximal exercise Q
decreased with bedrest, increased with training
effect of bedrest and training on resting and max HR
rest: incr HR with inactivity, decr HR with training
max HR: unaffected
effect of bedrest and training on SV
Rest SV: decr with inactivity, incr with training
max SV: decr with inactivity, incr with training
In fit people, beats less but SV incr so more blood per beat
what happens to SV if you are unfit and exercising?
it plateaus
effect of bedrest and training on a-VO2 diff? and why?
no significant changes for bed rest and training (why? becuase ability to extract O2 from blood to muscles doesn’t change much with fitness, so more oxygen through incr amount of blood by SV)
what is the main variable contributing to the incr in Q?
athletes have incr Q response to exercise due to incr SV (max HR, a-VO2 diff doens’t change)
SV range (rest) untrained vs trained
untrained = 60-80ml
trained = 90-120ml
SV range (maximal exercise) untrained vs trained
untrained = 100-120ml
trained = >150ml
how do athletes incr SV?
from incr end-diastolic volume capacity
what drives incr in end diastolic volume?
incr in blood volume (more blood = more O2)
adaptations depend on…
age, type of sport, sex, size, ethnicity, genetics
blood is made up of…
plasma and red blood cells
how are red blood cells produced and how long does this take?
erythropoiesis - produced in bone marrow. 2-3 weeks.
how does blood volume incr end diastolic volume capacity?
Plasma volume incr straight away (drink water!), then after 2-3 wk training, red blood cell volume incr, so total blood volume (TBV) incr which incr EDV —> incr SV
how much training to get blood volume homeostasis and how much (%) incr in TBV?
2-3 weeks, incr 8-10% (need to drink water)
how does incr in TBV incr EDV?
incr ventricular compliance, incr internal ventricular dimensions, incr venous return, incr myocardial contractility
structural difference between athlete and non heart?
ahtletes - larger heart chambers, greater mass and wall thickness
when do structural changes occur in the heart?
1 week (both left and right chamber adapt)
what is the LV compliance in athletes
more compliant heart (like a soft balloon) that is able to expand and accomodate the blood volume
LV hypertrophy
an absolute increase in LV mass and can develop in parallel with or independently from, LV dilatation
what is the law of laplace
T = (P x r)/(2 x h)
T= tension or stress in the LV wall
P = LV pressure
r = radius of the chamber
h = LV wall thickness
adaptation of the heart depends on the type of stimulus: pressure vs. volume
explain pressure overload
P incr so r decr and h incr. This is concentric hypertrophy (resistance training)
explain volume overload
r incr, so h incr. this is eccentric hypertrophy (endurance training)
eccentric hypertrophy and athlete cardiac dimensions
endurance training
- the addition of sarcomeres in series, leads to a large ventricle chamber relative to wall thinning. volume overload (increased preload)
10-15% larger than normal
concentric hypertrophy and athlete cardiac dimensions
power athletes
- the addition of myocyte sarcomeres in parallel
-incr thickness of the LV wall more than it incr the volume of the LV capacity
- the LV M/V ratio incr during concentric remodelling
- pressure overload (increased afterload)
10-20% larger than normal
what is the grey area (4 things) between athlete and cardio-myopathy
1) Dilated cardiomyopathy - LV cavity: 56-70mm
2) HCM; ARVC - distinctly abnormal ECG (T - wave inversion)
3) myocarditis - frequent or complex ventricular arrhythmias
4) HCM - LV wall thickness: 13-15mm
what happens to the cardiac structure with inactivity?
Reduction in LV mass.
Heart atrophies after bed rest and spaceflight, presumably in response to decr physiological loading
what happens to cardiac function with inactivity?
decr in LV end-diastolic volume (EDV) and SV
how fast do cardiac changes happen with inactivity?
within a week, and the longer you are inactive, the greater the reductions in function and structure
elastic arteries (e.g, Aorta) properties
- thick elastic walls (due to lots of pressure)
- collagen and elastin
- distensible (able to stretch) for more blood
- store energy in systole, recoil in diastole
arteriole (called resistance vessels) properties
- smooth muscle (walls)
- vasoconstrict/vasodilate
capillaries properties
- thin walls
- gas exchange
- huge cross-sectional area
- low flow velocity
Large veins properties
- thin walls compared to similar sized arteries
- small changes in pressure in response to large changes in volume
- capacitance vessels
- one-way valves
Who controls blood flows? and which 3 things do they receive information from?
vasomotor centre which receives information from
1) Baroreceptors (changes in pressure)
2) blood and muscle chemoreceptors (metabolites/change in O2, CO2)
3) Higher brain areas
What do the 3 receptor systems (of blood flow) do and who do they tell? What does this thing do?
communicate with the medulla oblongata, which sends a message to the sympathetic nervous system to either vasoconstrict or vasodilate vessels to reshift blood and homeostasis
what is the main gatekeeper of vasoconstriction/dilation? and why do we need to do this?
arterioles - in order to allow the pressure of the system to stay nice and steady as we don’t want high changes on the overall mean arterial pressure system
functional and structural adaptation of vessels to training (3 each)
structural
1) cross section area
2) lumen size
3) wall thickness
functional
1) exercise response
2) maximal exercise response
3) response to vasodilatory stimuli
components of MAP (mean arterial pressure) i.e, formula
MAP = Q x TPR (total peripheral resistance)
how do we maintain MAP? (considering formula)
exercise training reduced total peripheral resistance (TPR), therefore vessels must be changing
vasculature adaptations with chronic exercise
- increased arteriolar diameters and/or densities
- changes in the vasomotor reactivity of resistance arteries
difference between athletes and inactive in terms of vasculature
athletes have a greater vasculature dilatory response compared with inactive
describe the athlete artery
-larger lumen
- thinner walls
how does the athlete artery change?
incr Q, incr in blood flow leads to
1) shear stress incr (force of blood on the endothelial surface of the blood vessels (friction stress))
2) cyclic circumferential strain incr
3) transmural pressure incr
what changes first in vascular adaptation to exercise? function or structure?
1st function, then structure
what is angiogenesis? and the two ways this occurs
the physiological process of capillary growth.
sprouting and intussusception
what are myokines?
proteins and peptides released by muscles in response to contraction
what is the endothelium?
a single layer of cells that line your blood vessels and help them contract and relax
what does FITT stand for?
frequency, intensity, time, type
Vascular effects of frequency in aerobic and resistance training
+ association of training frequency with endothelial function in resistance training.
no associations of training frequency with endothelial function in aerobic training
effects of time on resistance and aerobic training
NO DATA about ass. of session duration with vascular adapt. to resistance training
+ dose-response relationship of session duration with vascular adaptations in moderate int. aerobic training
effects of intensity in aerobic and resistance training
+ ass. of higher intensities with acute oxidative stress (resistance)
+ ass of higher intensities with expression of anti-oxidative and anti-inflammatory metabolites (aerobic)
type effect on resistance and aerobic training
incr of local and systemic endothelial function: aerobic training > resistance training
incr of organ perfusion/microcirculation: + for both aerobic and resistance training
summary of END vs RES training on femoral artery
- END has greater impact then RES training on femoral artery diameter and FMD (flow mediated dilation) responses
- males showed beneficial impact in response to both END and RES, females responded primarily to END
- arterial adaptation to exercise might be influenced by exercise modality and sex
what is inactivity linked to in terms of the cardiovascular system?
endothelial dysfunction plays an important role in the pathogeneses of cardiovascular diseases, and impaired endothelium dependant dilation (condition where blood vessels ability to dilate in response to signals from the endothelium is compromised) is directly linked with cardiovascular morbidity and mortality
how fast to functional and structural adaptations happen?
functional - within days
structural - 2-3 weeks (structural remodelling of the vessel wall is completed) - note, same amount of time to decrease and by about 25%
training vs inactivity affect on artery diameter and wall thickness
artery diameter - incr with trianing, decr with inactivity
wall thickness - decr with training, incr with inactivity
the 6 issues that can impact the rhythm of the heart
Sinus bradycardia
Sinus tachycardia
Atrial fibrillation
AV blocks
Ventricular Tachycardia
Ventricular Ectopic
Sinus Rhythm vs Sinus Arrhythmias (what are the two types of sinus arrhythmias and what is the HR) and who might have them?
sinus rhythm - regular rhythm derived from the SA node (60-100 bpm)
Sinus Bradycardia: HR <60 bpm (common in athletes)
Sinus Tachycardia: HR >100 bpm (happens when we exercise)
Sinus Bradycardia (explain key points)
HR: <60 bpm
Rhythm: regular
P wave: present before each QRS
PR interval: 0.12-0.20s
QRS: <0.12s
Sinus Tachycardia (key points)
HR: > 100 bpm
Rhythm: regular
P wave: present before each QRS
PR interval: 0.12-0.2s
QRS: < 0.12s
Atrial Fibrillation (key points)
- Irregular and accelerated rhythm
- No obvious P wave
- common arrhythmia
- increased risk for stroke
- caused by abnormal electrical signals within the atria, leading to a rapid and chaotic beating pattern
AV blocks (definition and 3 degrees explained)
Is a conduction block within the AV node that impairs impulse conduction from atria to ventricle.
1st degree block:
- all normal P waves are followed by QRS complexes, but the PR interval is longer than normal (>0.20s)
2nd degree block:
- some P waves are followed by QRS complexes, while others are not. 3 diff categories of 2nd degree block
3rd degree block:
- Complete block. No relationship between P waves and QRS complexes
Ventricular Tachycardia (key points)
- abnormal electrical signals generated at the ventricle
- widened QRS
- Rates of 100-200 bpm
- Life threatening
- ECG looks like big zig-zags
Ventricular Ectopic (or PVC - premature ventricular complexes) (key points)
- wider than normal QRS: > 0.12
- preceding P wave is absent
- no PR interval
- cell that randomly contracts and is fairly common
why do we do exercise ECG test?
majority of the issues we have in the heart occur during exercise
why do athletes have a larger QRS?
thicker muscle, so more voltage to get electric pathway through muscle
Common ECG patterns in athletes and why?
- sinus bradycardia (most common)
- sinus arrhythmia
- 1st degree atrioventricular block (AV)
- QRS voltage criteria (LV hypertrophy)
These 4 common ECG patterns are mostly due to increased vagal tone and incr chamber size due to physiologic remodelling account for ECG patterns seen in highly trained athletes
what is vagal tone?
activity and strength of the vagus nerve, a key component of the PNS
sudden cardiac death summary
hereditary, structural or electrical cardiac disorders are associated with SCD in young athletes, the majority of which can be identified or suggested by abnormalities on a resting and exercise 12-lead ECG
ventricular implications
athletes with ventricular arrhythmias are at high risk
- repeated insults may lead to irreversible damage to RV
- the dose of exercise required for this effect is probably >20h/week for >20 yrs
but then…
- 114 olympic endurance athletes did not show any deterioration in cardiac function
- tour de france athletes live longer than untrained
Heart rate variability
HRV is the variation in the time interval between consecutive heartbeats in milliseconds. There is constant variation.
Higher HRV - associated with a healthy SNS/PNS
Higher fitness levels - associated incr HRV
the more variation (to a point) shows how responsive you autonomic system is
what are autorhythmic cells?
self-excitable; they are able to generate an action potential without nerve stimulation
Do all parts of the heart contract at once?
No, the atria contract first, then the ventricles contract. This sequence of contraction allows the ventricle to fill with blood before they contract
what generates an electrical potential in the heart? and where does this signal go?
autorhythmic cells. The signal travels along a conduction pathway, to ensure coordinated contraction of the heart.
what is an electrical signal? and what does it do?
it is a cardiac action potential. It involves a rapid and short-lasting rise in electrical potential, then a fall in the electrical potential. This is the result of opening and closing of channels in the membrane, which acutely change the membrane permeability to different ions.
where is the pacemaker action potential initiated from?
sinoatrial node (SA)
what is the heart’s electrical conduction pathway composed of? (4 things)
- Atrioventricular (AV) node
- Bundle of His
- Left and right bundle branches
- Purkinje fibres
what are purkinje fibres?
terminal branches of the bundle branches become Purkinje fibres, cardia muscle fibres that have special structural modifications.
These modifications allow action potentials to travel more rapidly than they would in cardiac muscle tissue.
where are purkinje fibres found?
towards the endocardial surface (endo = within), electrical activity travels outwards towards the epicardial surface (epi = near)
which component of the electrical conduction system is the ‘pacemaker’?
SA node - generates cardiac action potentials at a greater frequency than any other cardiac muscle cells
what does an ECG measure?
the collective electrical activity of the heart
what do ECG electrodes record?
The overall direction and magnitude of electrical activity in the heart.
what do deflections in the ECG trace indicate? and what are they followed by?
an electrical event in the heart. They are followed by an associated mechanical event.
what could cause atrial flutter? first describe what is normal
Normally, the SA node conducts the electrical signal across the atria to the AV node.
In atrial flutter, the signal from the SA node travels rapidly in a continuous loop around the atria. The AV node does not conduct every signal to the ventricles, so although HR is usually incr, it is not as rapid as the atrial waves of depolarisation.
For e.g, the atria might be contracting at 300 bpm, but the AV node (gatekeeper) might only allow 150 bpm to reach the ventricles otherwise it would be dangerous
describe a “Standard limb Lead II setup”
+ve electrode is on the left foot, the -ve electrode is on the right arm and the earth electrode on the right foot.
P waves represents…?
atrial depolarisation
QRS complex represents…?
Ventricular depolarisation
T wave represents…?
ventricular repolarisation
approximate durations for 60 bpm of
P wave
PR interval
QRS complex
T wave
QT interval
P wave - 0.1s
PR interval - 0.2s
QRS complex - 0.08s
T wave - 0.16s
QT interval - 0.4s
isoelectric
when there is no net electrical charge or electrical potential difference. (ECG flat)
first negative defection is what wave?
Q wave
first positive deflection is what wave?
R wave
upward deflection that returns the negative potential to the isoelectric point name of wave?
S wave
if someone was experiencing atrial flutter, what component of the ECG would look abnormal and why?
P wave - as it represents atrial depolarisation
how does electrical activity arise in the heart, and what pathway does it follow?
Autorhythmic cells of the SA node in the right atrium of the heart generate an electrical signal (action potential) which travels along a conduction pathway composed of the following:
- AV node
- Bundle of His
- Left and right bundle branches
- purkinje fibres
how are the electrical events of the heart recorded on an ECG?
An ECG provides a visual representation of the spread of electrical events through the heart. This is detected on the surface of the body using electrodes, which record positive or negative deflections depending on the direction of the summed electrical activity relative to the axis of the lead:
- an electrical vector that moves toward a +ve electrode (i.e. away from a negative electrode) produces a positive deflection.
- an electrical vector that moves away from a positive electrode (i.e, toward a negative electrode) produces a negative deflection.
- an electrical vector at right angles to the axis of a lead produces no deflection.
ischemia and can it be diagnosed by ECG?
acute impairment of blood flow to the heart
myocardial infarction (MI) and can it be diagnosed by ECG?
blood flow to part of the heart stops, which causes damage to the heart muscle
arrhythmia and can it be diagnosed by ECG?
abnormally fast, slow or irregular heart rhythms
can aberrant (abnormal) conduction of electrical activity through the heart be diagnosed by ECG?
yes
diagnosis of ischemia and infarction can be done by examining what parts of ECG?
ST segment, T wave and Q wave
term for when a single HB occurs earlier than normal
premature contraction
3 examples of atrial tachycardias and premature atrial contractions
atrial fibrillation
atrial flutter
paroxysmal atrial tachycardia
what ventricular arrhythmia commonly causes death? and why?
Ventricular fibrillation (VF)
as ventricles can no longer contract in a coordinated fashion, and therefore cannot pump blood.
what are the 3 ventricular arrhythmias?
premature ventricular complexes, ventricular fibrillation, ventricular tachycardia
