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Physiology Flashcards

1
Q

Heart failure (HF)

A

Inability of the heart to pump blood out into the systemic
circulation (cardiac output) at a level proportional to the body’s metabolic needs.

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2
Q

Cardiac fatigue

A

A temporary decrease in the heart’s ability to maintain normal function during or after prolonged exercise. (Transient Myocardial Dysfunction)

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3
Q

Why does cardiac fatigue occur?

A
  1. Due to prolonged aerobic exercise
  2. Supra-physiological stress
    (homeostasis disturbance)
  3. Prolonged pressure & volume overload
  4. Substrate depletion
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4
Q

What is the other name used for acute heart failure?

A

De Novo Heart Failure

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5
Q

What are the possible pathophysiological causes of acute heart failure?

A
  1. Biomarkers increased (NT-proBNP)
  2. Structural underlying pathology (cardiomyopathy, valve problems) *
  3. Inflammation (Myocarditis)
  4. Cardiac overload (high blood pressure, heat + exercise, high hematocrit)
  5. Hyponatremia (low levels of sodium / higher amount of water in the body)
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6
Q

What are the main characteristics of left-sided heart failure?

A
  1. Weakened left ventricle that cannot eject the blood efficiently into systemic circulation.
  2. Decreased ejection fraction.
  3. Blood backing to pulmonary circulation.
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7
Q

What are the main characteristics of right-sided heart failure?

A
  1. Weakened right ventricle that cannot eject the blood efficiently into pulmonary circulation.
  2. Preserved or slightly increased ejection fraction.
  3. Blood backing to systemic circulation (body).
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8
Q

Common compensations of left and right-sided HF

A
  1. Tachycardia (increased heart rate).
  2. Pallor.
  3. Secondary polycythemia (overproduction of red blood cells, leading to increased viscosity of the blood).
  4. Daytime oliguria (low urinary output) due to reduced blood flow to the kidney.
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9
Q

Common backup effects of right-sided HF

A
  1. Peripheral oedema.
  2. Hepatomegaly (enlargement of the liver).
  3. Splenomegaly (enlargement of the spleen due to reduced blood flow).
  4. Ascites (accumulation of fluid in the abdomen area).
  5. Distended neck veins.
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10
Q

Common backup effects of left-sided HF

A
  1. Orthopnea (difficulty breathing lying flat).
  2. Cough producing white or pink tinged phlegm (due to the presence of blood, indicating that small blood vessels in the lungs may be leaking).
  3. Shortness of breath.
  4. Paroxysmal nocturnal dyspnea (sudden shortness of breath that awakens a person from sleep).
  5. Hemoptysis (coughing up blood).
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11
Q

What are the most important clinical signs of heart failure?

A
  1. Exercise intolerance.
  2. Dyspnea on exertion.
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12
Q

Explain the Class I NYHA

A
  • NO limitation of physical activity.
  • Ordinary physical activity DOES NOT cause undue fatigue, palpitation, dyspnea (shortness of breath).
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13
Q

Explain the Class II NYHA

A
  • SLIGHT limitation of physical activity.
  • Comfortable at rest.
  • Ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath).
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14
Q

Explain the Class III NYHA

A
  • MARKED limitation of physical activity.
  • Comfortable at rest.
  • Less than ordinary activity causes fatigue, palpitation, or dyspnea.
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15
Q

Explain the Class VI NYHA

A
  • UNABLE to carry on any physical activity without discomfort.
  • Symptoms of heart failure at rest.
  • If any physical activity is undertaken, discomfort increases.
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16
Q

Signs and symptoms HR

A
  • Change in fatigue level or dyspnea
  • Paroxysmal nocturnal dyspnea (severe shortness of breath and cough that usually occurs at night).
  • Orthopnea (dyspnea that occurs when lying flat).
  • Dyspnea with fluid retention in the form of peripheral oedema or significant weight gain.
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17
Q

DECOMPENSATION signs

A
  • Weight gain 1,5 -2 kg in 2-3 days.
  • Increase in shortness of breath.
  • Palpitations, tachycardia.
  • Cognitive impairment.
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18
Q

Decompensation

A

Occurs when the heart’s ability to compensate for its reduced pumping function is overwhelmed, leading to a worsening of symptoms and signs of heart failure.

Decompensated heart failure is often characterized by a sudden deterioration in the patient’s clinical status.

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19
Q

What are the signs of ISCHEMIA during exercise?

A
  1. Drop of blood pressure (cave: not always, sometimes extreme hypertension occurs).
  2. Fatigue not matching the effort.
  3. Shortness of breath not matching the effort.
  4. Chest pain.
  5. Fast heart rate, weak pulse, increasing irregularities.
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20
Q

BNP levels

A
  • BNP levels (>100 mg/dL can be a sensitive index of decompensated HF).
  • Protein in the blood that tells hows hard the heart is working.
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21
Q

What are the 2 main pathophysiological causes of heart failure?

A
  1. Structural abnormalities.
  2. Failure of the compensatory mechanisms.
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22
Q

Explain the negative effect on CO:
Muscle loss ➔ Contractility ➔ Ejection fraction

A

After a heart attack, a portion of the heart muscle may be damaged or lost (infarcted). The affected area may not contract normally, leading to a decrease in contractility. The reduction in contractility contributes to a decrease in ejection fraction, which is the percentage of blood ejected from the heart with each contraction. A lower ejection fraction means the heart pumps out less blood per beat.

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23
Q

Explain the negative effect on CO:
Scar tissue ➔ Stiffness ➔ Ejection fraction

A

Scar tissue forms in the area of the infarction as part of the healing process. Scar tissue is less elastic and more rigid than healthy heart muscle.
The stiffness of the scar tissue affects the heart’s ability to contract and relax properly, leading to reduced compliance. This stiffness contributes to a decrease in ejection fraction, as the heart has difficulty pumping blood effectively.

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24
Q

Explain the negative effect on CO:
Conduction system

A

The electrical conduction system of the heart may be affected by the infarction. Damaged or compromised conduction pathways can lead to arrhythmias (abnormal heart rhythms) that further impact the coordination of heart contractions.
Arrhythmias can disrupt the synchronised pumping of the heart chambers, affecting cardiac output.

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25
Q

Explain the negative effect on CO:
Dyskinesia ventricular wall during contraction

A

Dyskinesia refers to abnormal movement. In the context of a heart attack, the affected portion of the ventricular wall may exhibit abnormal contractions during systole (contraction phase).
Dyskinesia can lead to inefficient pumping and a decrease in the overall effectiveness of the heart’s contractions, contributing to a reduction in cardiac output.

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26
Q

Explain the negative effect on CO:
Damage papillary muscle ➔ Valve leakage

A

The papillary muscles are responsible for anchoring the heart valves (particularly the mitral valve). If these muscles are damaged during a heart attack, the valves may not close properly.
Valve leakage, known as regurgitation, can occur, allowing blood to flow backward during the cardiac cycle. This leads to a decrease in forward blood flow and a reduction in cardiac output.

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27
Q

Explain the negative effect on CO:
Dilation ➔ Valve leakage

A

Dilation refers to the enlargement of the heart chambers, often as a compensatory response to reduced contractility or increased workload.
As the heart chambers dilate, the valve leaflets may not come together properly, leading to valve leakage and regurgitation.

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28
Q

What are the 3 causes of cardiomyopathy?

A
  1. Genetic.
  2. Ischemic.
  3. Enduring pressure or volume overload.
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29
Q

How does enduring pressure or volume overload lead to cardiomyopathy?

A

Due to years of hypertension or valve leakage or extreme volume aerobic exercise, ‘adverse remodelling’ takes place (hypertrophy and/or dilation).

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30
Q

How do genetic mutations lead to cardiomyopathy?

A

Gene mutations cause morphological and structural abnormalities that eventually lead to heart failure.

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31
Q

How does ischemia lead to cardiomyopathy?

A

Insufficient oxygen and nutrients initiate changes at the cellular level that cause the heart muscle to weaken and eventually dilate. This is an ischemic cardiomyopathy.

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32
Q

What are the normal values of EDL, ESV, EF and SV?

A
  • End-diastolic volume (EDV): 120 mL.
  • End-systolic volume (ESV): 55 mL.
  • Ejection fraction (EF): 65 mL.
  • Stroke volume (SV): 55%
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33
Q

What is the EF found in HFrEF patients?

A

Ejection fraction (EF) of 30%.

34
Q

Why is there is an increase in LV mass, with end-diastolic and end-systolic volumes increase in systolic failure patients?

A

Systolic failure is characterized by the heart’s inability to contract effectively during systole. This results in reduced ejection fraction (the percentage of blood pumped out of the left ventricle with each contraction).

The increase in LV mass and volumes, along with dilation, is a compensatory mechanism that aims to maintain cardiac output despite impaired contractility.

35
Q

Why is there is an increase in LV mass, with end-diastolic and end-systolic volumes decrease in diastolic failure patients?

A

Diastolic failure ➜ Impaired ventricular filling during diastole ➜ Less compliance (stiffer)➜ Unable to relax and fill adequately.

Diastolic heart failure can be associated with an increase in LV mass, but the key feature is the impairment in diastolic function.

36
Q

How does blood doping improves VO2 max?

A
  1. Increase in Hb concentration and blood volume.
  2. Increase in HR and SV (max CO).
  3. Max O2 extraction
  4. Increases O2 carrying capacity.
37
Q

What is the the difference between EPO and Blood Doping?

A

EPO can be detected .
Re-infusion cannot be detected

38
Q

By what percentage does re-infusion enhance VO2 max?

A

4 - 9%

39
Q

By what percentage does increased hematrocit becomes dangerous?

A

From 60%

40
Q

What are the adverse effects of blood doping?

A
  • Increased viscosity (thrombosis; embolism).
  • Increased risk of cardiac arrest.
  • Sepsis (blood poisoning).
  • Infectious diseases.
41
Q

How does endurance training impact blood volume?

A
  • Increase in blood volume (plasma).
  • Increase in red blood cells.
  • Decrease in hematrocit (= % formed elements / total blood volume).
  • Increase in total Hb mass.
42
Q

How do steroids lead to an improvement in performance?

A
  • Increased protein synthesis.
  • Reduces muscle wasting (block cortisol).
  • Shorten recovery time.
  • Reduce body fat.
43
Q

How is respiration controlled in the human body?

A

5% “conscious” via (Neo) Cortex.
95% “unconscious” via Brainstem and Limbic system (can override).

44
Q

What is the role of the central chemoreceptors in the control of respiration?

A
  • Sense pH changes, O2 and CO2 concentrations, in the central nervous system.
  • Chemoreceptors, in turn, respond to pH changes as they become more acidic and send sensory input to the brain to stimulate hyperventilation.
45
Q

What is the role of the mechanoreceptors in the control of respiration?

A
  • Found in the airways, trachea, lung, and pulmonary vessels.
  • Provide sensory information with regards to lung volume, airway stretch, and vascular congestion.
  • Adapting stretch spindles (conveys only volume information) and rapid adapting irritant receptors.
  • The mechanoreceptors transmit information to the respiratory center via cranial nerve X (the vagus nerve) to increase the breathing rate, the volume of breathing, or to stimulate cough.
46
Q

What is the role of the peripheral chemoreceptors in the control of respiration?

A
  • Found in the carotid and aortic bodies.
  • Sense the arterial O2 levels in the blood.
  • Responds to hypercapnia or acidosis (higher levels on CO2 in the blood).
47
Q

Name the lung volumes

A

Tidal volume.
Vital capacity.
Total lung capacity.
Functional residual volume.
Residual volume.

48
Q

What are the common clinical signs of EIB?

A
  1. Dyspnea.
  2. Fatigue.
  3. Poor performance in sports.
  4. Cough.
  5. Wheezing.
49
Q

What are the common causes of EIB?

A
  1. Air pollution.
  2. Allergens.
  3. Cold dry air.
  4. Breathing air containing chloramines.
  5. Asthma.
50
Q

A transient (reversible) airway narrowing occurring during physical exertion. It is caused by an acute large increase in the amount of air entering the airways that require heating and humidifying.

A

Exercise-induced bronchoconstriction (EIB)

51
Q

When is EIB diagnosed?

A

A positive bronchodilation test (reversibility of 16%): Test two times, before and after medication. If there is an increase of 16% in FEV1 when using the medication, the test is considered positive, reversible obstruction.

52
Q

What are the 3 factors that make someone prone to EIB?

A
  1. Increased levels of exhaled nitric oxide (elevated NO levels are associated with inflammation).
  2. Increase levels of leukotrienes (inflammatory mediators).
  3. Increased airway epithelial shedding.
53
Q

Explain EILO

A
  • Inappropriate closing of the vocal cords during exercise.
  • Dyspnea originates from the larynx.
  • Happens fast.
  • Symptoms peak at peak exercise.
  • Symptoms stop or reduce within 1-5 minutes after exercise.
  • Take up to 10 minutes to complete recover from all the symptoms, depending on the O2 deficit.
54
Q

Explain EIB

A
  • Exercise induced bronchoconstriction, due to air pollution, allergens, cold dry air, breathing air containing chloramines or asthma.
  • Takes longer to happens than EILO.
  • Symptoms peak after exercise.
  • Symptoms stop or reduce within 3-15 minutes after exercise.
  • Can also star during exercise.
55
Q

LOW ENERGY AVAILABILITY (LEA)

A

Mismatch between the dietary energy intake and the energy expenditure, leading to inadequate energy to maintain body functions.

56
Q

What are the 2 factors that lead to LOW ENERGY AVAILABILITY (LEA)?

A

(A) Dietary intake is too low.
(B) Energy expenditure is too high.

57
Q

What is the formula used to calculate ENERGY AVAILABILITY?

A

EA = Dietary energy intake (kcal) - Energy expenditure (kcal) / Fat free mass (kg)

58
Q

Overtraining Syndrome (OTS)

A
  1. Acute fatigue (normal in athletes).
  2. Inadequate recovery of acute fatigue.
  3. Short-terms decrements in sports:
    a. Functional overreaching (NFOR).
    b. Non-functional overreaching (NFOR).
  4. Overtraining Syndrome.

“Accumulation of training and/or non-training stress resulting in long term decrements in performance capacity.”

59
Q

Explain the difference between NON-FUNCTIONAL and FUNCTIONAL OVERREACHING (FOR)

A

When the there is an inadequate recovery from acute fatigue, the performance decrements can range in a continuum from:
(A) FUNCTIONAL OVERREACHING (FOR): Sort-term decrements (planned).
(B) NON-FUNCTIONAL OVERREACHING (NFOR): Unplanned fatigue and decrements.

60
Q

Explain the TRIAD in sports

A

The negative health outcomes of low energy availability (LEA) on reproductive and bone health.

61
Q

RED-S

A

RELATIVE ENERGY DEFICIT IN SPORTS
RED-S is a complex syndrome caused by LEA, resulting in impaired physiological function, negatively impacting aspects of health and performance.

62
Q

What are the physiological impairments caused by RED-S?

A
  • Metabolic rate.
  • Menstrual function.
  • Bone health.
  • Immunity.
  • Protein synthesis.
  • Cardiovascular health.
63
Q

What are the effects of RED-S on the endocrine system?

A

IN FEMALES:
- Disruption of the hypothalamic-pituitary-gonodal axis, leading to amenorrhea.
- Thyroid function alterations.
- Appetite regulation hormones changes (reduced liptin).
- Decreased insulin.
- Increased growth hormone resistance.
- Cortisol elevation.
- MALES: Reduction in testosterone.

64
Q

What are the effects of RED-S on the menstrual function?

A

Functional hypothalamic amenorrhoea (FHA)

65
Q

What are the effects of RED-S on bone health

A
  • Oestradiol sensitivity: Increased osteoclasts and decreased osteoblasts.
  • Altered microarchitecture.
  • Bone turnover. markers are decreased.
  • Decreased bone strength.
  • Increase risk of bone stress fractures.
66
Q

What are the effects of RED-S on the metabolic function?

A
  • Reduced RESTING ENERGY EXPENDITURE (REE).
  • Lower leptin and insulin levels.
67
Q

How much of the TOTAL DAILY ENERGY EXPENDITURE does RESTING ENERGY EXPENDITURE corresponds to?

A

RRE corresponds to 60-70% of the TDEE.

68
Q

What are the effects of RED-S on the haematological function?

A
  • Iron deficiency contributes to energy deficiency.
  • Impaired metabolic function.
69
Q

What are the effects of RED-S on the cardiovascular function?

A
  • Early atherosclerosis.
  • Endothelial dysfunction.
  • Unfavourable lipid profile.

in severe cases with anorexia nervosa:
- Valve abnormalities.
- Pericardial dysfunction.
- Severe bradycardia.
- Hypotension.
- Arrhythmias.

70
Q

What are the effects of RED-S on performance?

A
  • Decreased glycogen stores.
  • Decreased muscle strength.
  • Decrease endurance performance.
  • Decreased training response.
  • Impaired judgement.
  • Decreased coordination.
  • Decreased concentration..
  • Irritability.
  • Depression.
  • Lower bone health.
  • Stiffness of connective tissue.
71
Q

What is considered a healthy Energy Availability (EA) for females?

(A) 35 kcal/kg FFM/day
(B) 40 kcal/kg FFM/day
(C) 45 kcal/kg FFM/day

A

(C) 45 kcal/kg FFM/day

72
Q

What is considered a healthy Energy Availability (EA) for males?

(A) 35 kcal/kg FFM/day
(B) 40 kcal/kg FFM/day
(C) 45 kcal/kg FFM/day

A

(B) 40 kcal/kg FFM/day

73
Q

What is considered a reduced Energy Availability (EA)?

(A) 30 - 45 kcal/kg FFM/day
(B) 20 - 30 kcal/kg FFM/day
(C) 25 - 30 kcal/kg FFM/day

A

(A) 30 - 45 kcal/kg FFM/day

74
Q

How many days does it typically take for severe health consequences to manifest when Energy Availability (EA) is between 25 and 30 kcal/kg of Fat-Free Mass (FFM) per day?

(A) 4 days.
(B) 5 days.
(C) 6 days.

A

(B) 5 days.

75
Q

What is considered a critical Energy Availability (EA)?

(A) < 20 kcal/kg FFM/day
(B) < 25 kcal/kg FFM/day
(C) < 30 kcal/kg FFM/day

A

(B) < 25 kcal/kg FFM/day

76
Q

What are common reasons for the development of Low Energy Availability (LEA)?

A
  • Body dissatisfaction.
  • Beliefs, misconceptions and myths in sports.
  • Type os sport.
  • Focus on leanness in sports (dancing, figure skating).
  • Weight-performance ration (cycling, running).
  • Selection criteria in sports.
  • Dieting behavior.
  • Eating disorders.
  • Unintentional (lack of knowledge, cooking skills, financial reasons, increased training volume, illness).
  • Coach and team pressure.
  • Social media.
  • Gradual shifting to unhealthy behaviours.
77
Q

What psychological elements could contribute to the development of Relative Energy Deficiency in Sport (RED-S)?

A
  • Drive for thinness.
  • Perfectionism.
  • Self-confidence levels.
  • Sport identity.
  • Disordered eating.
78
Q

What are the consequences of consuming a diet low in carbohydrates?

A
  • Lower glycogen stores, suggesting that there is less storage form of glucose available in the body.
  • Increased lipolysis.
  • Decreased rate of glycolysis (the breakdown of glucose for energy), which is consistent with the reduced availability of glucose from glycogen stores.
  • There is an increase in free fatty acids (FFA), glycerol, cholesterol, and β-hydroxybutyrate, indicating a shift to fat as a primary energy source due to low availability of glucose.
79
Q

How is LEA impact healing?

A
  • Slowed healing process.
  • Healing can require 15-50% more energy.
  • Exacerbates muscles loss, down regulation of muscle protein.
80
Q

Body composition of $% total body fat mass results in:

A
  • Reduced muscle mass.
  • Loss of strength.
  • Endocrine dysfunction.
  • Mood disturbances.

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