block 1-cardiovascular Flashcards

(40 cards)

1
Q

stroke volume

A

-volume of blood ejected from the heart during each cycle.

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2
Q

cardiac output-CHEAT SHEET DEFINITONS IF SPACE

A

-the total volume of blood pumped by the ventricle per minute
=SR x HR

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3
Q

ECG

A

-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

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4
Q

different intervals on a ECG-CHEAT SHEET

A
  • 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
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5
Q

changes in the ECG intervals during exercise

A

-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

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6
Q

control of heart rate-CHEAT SHEET

A

-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

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7
Q

heart transplant patients

A

-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

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8
Q

How do you work out maximum HR

A

220-age

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9
Q

stroke volume during exercise-CHEAT SHEET

A

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.

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10
Q

why do elite athletes have a higher cardiac output during exercise

A
  • stroke volume is increased during exercise and can continue to increase and high intensities
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11
Q

chronic adaptations to training-CHEAT SHEET

A
  • 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
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12
Q

V02 max-CHEAT SHEET UNITS

A

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

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13
Q

V02 max response in genetics

A

-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

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14
Q

atrial fibrillation in endurance athletes-CHEAT SHEET

A
  • 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
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15
Q

blood pressure

A

-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

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16
Q

intrinsic mechanisms for regulating blood flow- CHEAT SHEET . learn later

A

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.

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17
Q

Extrinsic mechanism for regulating blood flow- CHEAT SHEET or learn later

A

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.

18
Q

how does venous blood return to the heart

A

-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

19
Q

minute ventIlation= Ve-CHEAT SHEET

A

-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.

20
Q

Ve sensitivity to o2 and CO2

A

-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

21
Q

what happens to our breathing rate during exercise?-CHEAT SHEET

A

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.

22
Q

changes in ventilation and PCO2/P02 during light exercise

A

-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.

23
Q

changes in ventilation and PC02/PC02 during moderate exercise

A

-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

24
Q

ventilation threshold

A
  • the point where our ventilation rate increases inproportionally to Vo2 and VCo2.
25
ventilation and pCO2/pCo2 during high intensity exercise-CHEAT SHEET
- VE increase. -passes the ventilation threshold(ventilation increases faster than VO₂,) so changes are due to our anaerobic system -3. Lactate Threshold This is the point where lactate starts to accumulate faster than the body can clear it. It usually occurs around 1 mmol/L above resting levels, though this varies. 4. OBLA (Onset of Blood Lactate Accumulation) Defined as when blood lactate concentration reaches 4 mmol/L. It's a practical marker of when fatigue rises sharply and ventilation spikes. 5. pCO₂ (Partial Pressure of CO₂) At first, pCO₂ may increase slightly, but during intense effort: Hyperventilation (↑ VE) lowers pCO₂ because you exhale more CO₂. This is part of the body's attempt to buffer the blood and control pH.
26
heat affect on ventilation rate-CHEAT SHEET
-Exercising in hot conditions increases ventilation rate (𝑉̇E), primarily to aid heat loss through increased breathing. This elevated ventilation is not driven by CO₂ levels, so it can lead to a decrease in arterial PCO₂ (partial pressure of carbon dioxide). -see graph
27
effects of endurance training on ventilation during exercise
Endurance training reduces ventilation at a given workload (by ~30–40%) because trained muscles produce less CO₂. Trained individuals also reach their ventilation threshold later (around 75% of VO₂ max vs. 50% in untrained), and show a delayed drop in blood pH. Arterial PO₂ typically remains stable, but in elite athletes, PO₂ can drop significantly due to high cardiac output reducing oxygen loading time in the lungs (exercise-induced hypoxemia).
28
use of nasal strips from athletes
- some people beleive that nasal stripes= reduce vascular resistance =but it may be a placebo effect
29
transport of oxygen in the blood.
-Oxygen Binding in the Lungs: In the alveoli of the lungs, oxygen diffuses into the blood and binds to hemoglobin molecules in red blood cells. Each hemoglobin molecule has four heme groups, each capable of binding one oxygen molecule (O₂), forming oxyhemoglobin. -Transport Through the Bloodstream: The oxygen-rich blood is carried through arteries to tissues and organs. Hemoglobin helps maintain a high concentration of oxygen in the blood, ensuring efficient transport. -Oxygen Release in Tissues: In tissues with low oxygen levels, hemoglobin releases oxygen due to the lower partial pressure of oxygen and changes in hemoglobin's affinity for oxygen (influenced by pH, CO₂ levels, and temperature). The oxygen then diffuses into the cells where it is needed for metabolic processes. -Return to the Lungs: Hemoglobin, now less saturated with oxygen, returns to the lungs via veins, ready to bind more oxygen and repeat the cycle
30
effect of exercise on O2 dissociation curve
-with exercise shifts to the right -due to increased heat,lactate and H+ in working tissue -more unloading of O2 in working tissue
31
Co2 transport
1.60–70% as bicarbonate ions (HCO₃⁻) — formed when CO₂ reacts with water: CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻ This reversible reaction happens in red blood cells. 2.In the lungs (low PCO₂), the reaction reverses to release CO₂ for exhalation. 7–10% is dissolved directly in plasma. 3. 20% binds to hemoglobin (as carbaminohemoglobin), especially in tissues with high CO₂ levels.
32
How does gaseous exchange occur in muscle tissue?
Oxygen (O₂) diffuses from the blood into the muscle down its partial pressure (pO₂) gradient — from high (in blood) to low (in muscle tissue). This gradient becomes steeper during exercise because muscles use more oxygen, increasing the demand. Carbon dioxide (CO₂) moves out of muscle cells into the blood down its own partial pressure (pCO₂) gradient, as CO₂ accumulates from cellular respiration.
33
o2 transport within the muscle
-once dissociated from haemoglobin binds to myoglobin which is a muscle-specific oxygen carrier. has a high affinity for oxygen and oxygen is delivered in conditions with very low partial pressure. the curve is shifted to the left
34
the effect on oxygen transport at higher altitudes
According to Henry’s Law, the amount of oxygen that dissolves in the blood is directly proportional to the partial pressure of oxygen (pO₂) in the alveoli. At higher altitudes, atmospheric pressure (and therefore alveolar pO₂) is lower, so less oxygen enters the blood. This reduced oxygen availability impairs oxygen transport to tissues, making it harder for the body to meet metabolic demands — especially during exercise.
35
what physiological changes occur at high amplitudes-CHEAT SHEAT
-increased EPO which stimulates the bone marrow to have an increased production of red blood cells -increased in vascularisation= increased in blood supply -a right shift of oxyhaemoglobin dissociation curve= unloading and dissociation -hyperventilation=increases blood ph(The body compensates for reduced oxygen by breathing more rapidly (hyperventilation), which helps increase blood pH and reduces the buildup of CO₂.)
36
EPOC stand for
Excess Post Exercise Oxygen Consumption
37
oxygen deficit-MAYBE CHEAT SHEET
When exercise begins, the demand for ATP increases. Initially, the aerobic system cannot produce ATP quickly enough to meet this demand, so the body relies on anaerobic energy stores (like phosphocreatine and glycogen) to provide ATP. This creates an oxygen deficit, which is the difference between the total amount of oxygen consumed during exercise and the amount that would be consumed if the body reached steady-state aerobic metabolism immediately.
38
steady state
-we are able to produce atp ant the rate required by the muscle -primarily use our aerobic stores to provide atp
39
the fast component of EPOC(Excess Post-exercise Oxygen Consumption)
Occurs in the first few minutes after exercise. The body uses oxygen to: Re-saturate hemoglobin and myoglobin with oxygen. Restore ATP and phosphocreatine (PCr) levels in muscle cells. This phase is all about quick recovery of immediate energy systems and oxygen stores.
40
the slow component of EPOC-CHEAT SHEET
-can be from 30 minutes to even 24 hours after exercise -remove any lactic acid produced during exercise -can do transported to the liver or can be excreted to sweat and urine . -reduces body temperature and so increased blood flow and so we need a higher oxygen consumption to support higher heart rate and higher blood flow -repair damage tissues = need an increase in blood flow -restore equilibrium of ions= so ATP is needed to restore ion pumps -hormone released by the sympathetic nerve system can have long lasting effects on our oxygen consumption several hours after exercise has finished