block 1-cardiovascular Flashcards
(40 cards)
stroke volume
-volume of blood ejected from the heart during each cycle.
cardiac output-CHEAT SHEET DEFINITONS IF SPACE
-the total volume of blood pumped by the ventricle per minute
=SR x HR
ECG
-only detects rapidly changing electrical activity in a large mass of tissue
-P=atrial depolarisation
-atrial repolarisation isn’t seen on the ECG it’s hidden by ventricular depolarisation as it occurs at the same time
-QRS= ventricular depolarisation
-T=ventricular repolarisation
different intervals on a ECG-CHEAT SHEET
- R-R interval gives the heart beat duration
-Q-T = shows the time taken for the ventricles to depolarise and then repolarise. almost important for measuring the duration of a heart beat
-long Q-T durations=arrthymogenic= sudden death sometimes
-P-R (basically p-q interval is measured from the beginning of the upstroke of the p wave to the beginning of the QRS wave.
-shows the onset of atrial depolarisation to theonsent of ventricular depolarisation therefore is the length for electrical conduction to pass from the atria to the ventricles.
-see image document on goodnotes
changes in the ECG intervals during exercise
-shortening of the R-R interval = because of the increased HR
-a slight increase in the p wave amplitude= increase in atrial contraction
-shortening of the P-R and Q-T interval
-S-T segment depression
-T-wave amplitude may flattern
control of heart rate-CHEAT SHEET
-SAN have a natural rhythm of 100bpm
- resting HR is around 60-70bpm due to the vagus nerve being activated. release ACHT induces a “breaking” effect on the HR (parasympathetic activity)
-during exercise, the vagus nerve isn’t stimulated so the HR returns to 100bpm usually during early/light exercise such as walking
-vigorous exercise activates the sympathetic nervous system via two ways: sympathetic nerve innervation= nerves innervates the heart to release more adrenaline= increased HR
or = increase in circulating adrenaline and noradrenaline= increase HR
heart transplant patients
-demonstrates the control of HR
-during transplantation nerves are cut so there is no sympathetic or parasympathetic activity
-HR is increased via circulating adrenaline released from the adrenal glands
-therefore, it takes longer for the HR to increase during exercise and decrease following exercise.have higher testing HR 90-100 bpm
How do you work out maximum HR
220-age
stroke volume during exercise-CHEAT SHEET
During exercise, stroke volume increases due to three main factors:
Increased End-Diastolic Volume (Preload):
More blood returns to the heart (↑ venous return) due to muscle contractions and respiratory pump.
This stretches the ventricular walls more (Frank–Starling mechanism).
More stretch = stronger contraction = greater stroke volume.
Decreased Afterload (Arterial Pressure):
Exercise causes vasodilation in active muscles.
This reduces systemic vascular resistance (↓ aortic/pulmonary pressure the heart must pump against).
Lower afterload makes it easier for the heart to eject blood = increased stroke volume.
Increased Contractility (Sympathetic Activation):
Exercise triggers release of adrenaline (epinephrine) and noradrenaline (norepinephrine).
These increase calcium availability in heart muscle cells.
More calcium = stronger contractions = higher stroke volume.
why do elite athletes have a higher cardiac output during exercise
- stroke volume is increased during exercise and can continue to increase and high intensities
chronic adaptations to training-CHEAT SHEET
- heart size= hypertrophy mostly in the left ventricle
-stroke volume= increased end-diastolic volume
-heart rate decreased resting HR = bradycardia= max doesn’t change
-Recovery of HR more rapid after exercise
-cardiac output= increases during exercise same at rest
-V02 max increases
V02 max-CHEAT SHEET UNITS
the max amount of oxygen that can be taken in,transported and utilised in 1 minute.
-measured in L/min or mL/kg/min
- for men 30-49mL/kg/min for women 25-35
V02 max response in genetics
-genetics play a role. the Heritage family study found about 47% of the variation of V02 max response to training was attributed the genetic factors
atrial fibrillation in endurance athletes-CHEAT SHEET
- irregular heart rhythm which causes the upper chambers of the heart to fibrillate instead of beat regularly.
- blood doesn’t leave the atrium efficiently and can pool in the chamber= blood clot= strokes
-not fully understood why the occurs in athletes may be due to the increased vagal tone or the enlargement of the atrium
-of stimulants/ energy drinks
-electrolyte abnormalities as a result of dehydration
blood pressure
-pressure exerted by the blood on the walls of the vasculature
-values depend on where and when its measured
-systolic bp= occurs during ventricular contractions= increases substantiality during exercise
-diastolic blood pressure= represent arterial pressure between contractions= no increase during excersize= dependent of vascular resistance which is reduced during exercise
intrinsic mechanisms for regulating blood flow- CHEAT SHEET . learn later
Blood Flow and Metabolic Demand:
Blood flow is tightly linked to the metabolic activity of tissues.
Local vasodilators are produced in response to imbalances, such as low oxygen availability and increased levels of metabolic by-products (e.g., CO₂, lactate, H⁺).
These vasodilators help match blood flow to the tissue’s metabolic needs.
Endothelium-Derived Vasodilators:
The endothelium plays a key role in regulating blood vessel tone by releasing vasodilators, including:
Nitric oxide (NO): Promotes smooth muscle relaxation.
Prostaglandins: Lipid compounds that contribute to vasodilation.
Endothelium-derived hyperpolarizing factor (EDHF): Causes hyperpolarization of vascular smooth muscle, leading to relaxation.
Importance During Exercise:
In skeletal muscle, these intrinsic mechanisms are particularly critical during exercise.
They ensure a robust increase in local blood flow to meet the high oxygen and nutrient demands of the working muscles.
Extrinsic mechanism for regulating blood flow- CHEAT SHEET or learn later
Extrinsic Neural Regulation of Blood Flow
Sympathetic Nervous System Control:
Blood flow to most vascular beds is regulated by the sympathetic nervous system.
Sympathetic nerves innervate the smooth muscle of blood vessels, controlling vasoconstriction and blood flow.
Resting Vasoconstriction:
At rest, there is a high level of vasoconstriction in arterioles within skeletal muscle, reducing blood flow.
Sympathetic Activity During Exercise:
During exercise, sympathetic stimulation increases, and the adrenal medulla releases adrenaline.
In most tissues, noradrenaline (NA) and adrenaline cause vasoconstriction, reducing blood flow (e.g., in the kidneys and liver).
Functional Sympatholysis in Exercising Muscle:
In skeletal muscle, locally released vasoactive substances counteract or reverse sympathetic vasoconstriction.
This mechanism ensures high blood flow to meet the demands of active muscles.
This phenomenon is termed functional sympatholysis.
Complex Mechanisms:
Regulation involves intricate compensatory mechanisms, cross-linking signaling pathways, and redundancies to ensure adequate blood flow adjustments.
how does venous blood return to the heart
-blood is at low pressure in the veins
-muscle and respiratory contractions pump the blood back to the heart more activity during exercise
-values in the blood prevents the blood from flowing back
-also aided by vasoconstriction stimulated by sympathetic imputs.= reduces the ability of the veins to store blood
minute ventIlation= Ve-CHEAT SHEET
-the amount or volume of air inspired or expired in one minute
* Measured in l/min
* Product of both tidal volume and breathing frequency
* Ve = Vt (Tidal vol)x breathing rate
* Well matched to oxygen consumption at steady-state exercise
and has a linear relationship, but at higher workloads this
the relationship becomes non-linear.
Ve sensitivity to o2 and CO2
-insensitive to changes in o2 concentration
-sensitive to changes in co2 concentration
-small changes to co2 can have a large impact on breathing rate but this ain’t the case for o2 as its always changing
what happens to our breathing rate during exercise?-CHEAT SHEET
When you start exercising, your breathing rate (ventilation) doesn’t just slowly rise — it follows a specific pattern with three distinct phases:
Phase 1: Rapid Increase (First ~15 seconds)
This is an immediate jump in breathing rate.
It’s mainly driven by neural input — your brain instantly tells your respiratory muscles to increase breathing as you start moving.
It happens before there’s even a big change in CO₂ or O₂ levels in the blood.
Phase 2: Gradual Increase (~15 seconds to ~4 minutes)
Breathing continues to rise, but more gradually and smoothly.
This follows a single exponential curve.
It’s now driven by actual chemical changes in the blood (e.g., ↑ CO₂, ↓ O₂, ↓ pH).
It continues until it reaches a steady state, depending on how intense the exercise is.
Phase 3: Steady-State (or Slight Hyperventilation if Intense)
If exercise is below the anaerobic threshold (AT):
→ Breathing reaches a steady state (you breathe more, but consistently).
If exercise is above the AT:
→ You might start to hyperventilate slightly, as lactate builds up and your body tries to clear CO₂ faster.
changes in ventilation and PCO2/P02 during light exercise
-During steady-state exercise, ventilation increases in direct proportion to VO₂ and CO₂ production. Early in exercise, PO₂ and PCO₂ may shift, but they stabilize once your body finds a balance — no further major changes occur unless exercise intensity increases.
changes in ventilation and PC02/PC02 during moderate exercise
-increase in Ve rate still in proportion to vo2 and vCo2 (oxidative phosphorylation increases in both moderate and light)
-relies more on our anaerobic metabolism to provide atp during glycolysis.
-increase in pco2
ventilation threshold
- the point where our ventilation rate increases inproportionally to Vo2 and VCo2.