EDAIC I MCQs from the ESAIC sample paper with simplified explanations. Weekly free uploads by targetedaic. (3)

A. anaemia B. a shift to the left of the oxyhemoglobin dissociation curve C. low cardiac output D. local vasoconstriction E. metabolic alkalosis

A. True B. True C. True D. True E. True

Explanation: Oxygen delivery to tissue (DO₂) = CaO₂ × CO = (arterial oxygen content) × cardiac output.

Anything that changes the delivered oxygen to tissues (hypoxemia) or makes the delivery difficult (leftward shift) can result in tissue hypoxia. Here, PaO2 (a reflection of the dissolved oxygen that exerts the partial pressure) is normal. Hence, the other two factors will come into play in causing tissue hypoxia.
Hypoxemic Hypoxia: Low oxygen tension in the arterial blood (PaO2); due to the inability of the lungs to properly oxygenate the blood. Causes include hypoventilation, impaired alveolar diffusion, and pulmonary shunting.
Circulatory Hypoxia: Due to pump failure (heart is unable to pump enough blood, and therefore oxygen delivery is impaired).

Anaemic Hypoxia: Decrease in oxygen-carrying capacity due to low haemoglobin leading to inadequate oxygen delivery. The ‘critical’ haemoglobin concentration below which tissue hypoxia occurs ∼50 g litre⁻¹ in healthy humans.

Histotoxic Hypoxia (Dysoxia): Cells are unable to utilize oxygen effectively, the best example for this is Cyanide poisoning; which inhibits the enzyme cytochrome C oxidase in the mitochondria, blocking the use of oxygen to make ATP.

The dissociation curve also undergoes a leftward shift in carbon monoxide poisoning. CO has a 240-fold greater affinity for haemoglobin than oxygen and will displace oxygen. This favours the retention of O2 (keeping haemoglobin in the tense state) on haemoglobin at peripheral tissues. Despite a greater proportion of saturated haemoglobin molecules, total O2 content is decreased because of the high affinity of CO for haemoglobin.

Alkalosis also causes a leftward shift in the dissociation curve.
Local vasoconstriction impairs the blood supply/oxygen delivery to tissues leading to tissue hypoxia.

A. the carotid bodies are sensitive to arterial blood pressure B. hypotension produces increased baroreceptor discharge C. increased plasma renin activity stimulates aldosterone production D. posture influences aldosterone production E. antidiuretic hormone secretion is increased in systemic hypotension

A. False B. False C. True D. True E. True

Explanation: The carotid bodies are sensory organs that detect the chemical composition of the arterial blood. The carotid body sensory activity increases in response to arterial hypoxemia and the ensuing chemoreflex regulate vital homeostatic functions.

At normal resting blood pressures, baroreceptors discharge with each heart beat. If blood pressure falls, such as on orthostatic hypotension or in hypovolaemic shock, baroreceptor firing rate decreases and baroreceptor reflexes act to help restore blood pressure by increasing heart rate

Renin cleaves the blood protein angiotensinogen to form angiotensin I, which is then converted by a second enzyme to angiotensin II. Angiotensin II causes blood vessels to constrict, and it stimulates aldosterone production. Overall, this raises blood pressure and keeps sodium and potassium at normal levels.

Aldosterone excretion is increased during 120 minutes of upright posture and correlates directly with the elevation in renin activity. Upright posture induces increased plasma renin activity regardless of the level of sodium intake in the preparatory diet.

If blood flow to the kidneys is too low, the kidneys release a chemical (renin that becomes angiotensin 2) that causes the release of ADH and aldosterone. These hormones serve to increase blood volume and blood pressure.

A. allows transitory storage of the major part of the stroke volume during the ejection phase B. contributes to the onward flow of blood during ventricular diastole C. minimises the effects of intrathoracic pressure upon aortic pressure D. contributes to conversion from intermittent to continuous blood flow E. maintains coronary perfusion

A. False B. True C. false D. True E. true

Explanation: The aorta, the pulmonary artery, and their major branches have a large amount of elastin in their walls, which makes these vessels highly distensible (i.e., compliant). This distensibility serves to dampen the pulsatile nature of blood flow that results from the heart pumping blood intermittently. When blood is ejected from the ventricles during systole, these vessels distend, and during diastole, they recoil back and propel the blood forward . Thus, the intermittent output of the heart is converted to a steady flow through the capillaries.

A. oxygen saturation of mixed venous blood remains above 70 per cent B. minute volume of ventilation may reach 130 litres C. pulmonary vascular resistance falls D. cardiac output may reach 50 litres/min E. core temperature may reach 40°C

A. False B. true C. True D. False E. True

Explanation: Normal mixed venous oxygen saturation is 70-75%, which decreases during strenuous exercise due to increased oxygen consumption. Values as low as 40% may be seen during strenuous exercise.

During exercise, ventilation might increase from resting values of around 5–6 litre min⁻¹ to >100 litre min⁻¹.

During exercise, cardiac output and pulmonary blood flow increases while pulmonary vascular resistance decreases. This increases the amount of the lung that is perfused which decreases physiologic dead space. These changes increase oxygen delivery to exercising tissues.

Cardiac output may increase up to 5 times normal (from 5l/min to 25l/min, and in well trained athletes 35l/min) during exercise.
Heat exhaustion is possible in sustained severe exercise, especially in hot and humid conditions where the heat loss capacity of the body is compromised.

A. after-load B. pre-load C. myocardial contractility D. ionized calcium concentration E. heart rate

A. True B. True C. True D. True E. True

Explanation: Dp/dt represents the ratio of pressure change in the ventricular cavity during the isovolumic contraction period. It is a measure of contractility of the ventricle. Contractility is the change in peak isometric force (isovolumic pressure) at a given initial fibre length (end-diastolic volume).

LV dP/dt is estimated by using time interval between 1 and 3 m/sec on MR velocity spectrum. Normal LV dp/dt is > 1200 mmHg/s).

RV dP/dt is estimated by using a time interval between 1 and 2 m/sec on the TR velocity spectrum.

1. Physiological determinants of contractility include:
   1. Preload:
      1. Increasing preload increases the force of contraction
      2. The rate of increase in the force of contraction per any given change in preload increases with higher contractility
      3. This is expressed as a change in the slope of the end-systolic pressure-volume relationship (ESPVR)
   2. Afterload (the Anrep effect):
      1. The increased afterload causes an increased end-systolic volume
      2. This increases the sarcomere stretch
      3. That leads to an increase in the force of contraction
      4. Paradoxically, Dp/dt is minimally affected by normal afterload unless it is pathologically low.
   3. Heart rate  (the Bowditch effect):
      1. With higher hear rates, the myocardium does not have time to expel intracellular calcium, so it accumulates, increasing the force of contraction.
2. Contractility is also dependent on:
   1. Myocyte intracellular calcium concentration
      1. Catecholamines: increase the intracellular calcium concentration by a cAMP-mediated mechanism, acting on slow voltage-gated calcium channels
      2. ATP availability (eg. ischaemia):  as calcium sequestration in the sarcolemma is an ATP-dependent process
      3. Extracellular calcium- availability of which is necessary for contraction
   2. Temperature: hypothermia decreases contractility, which is linked to the temperature dependence of myosin ATPase and the decreased affinity of catecholamine receptors for their ligands.

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