block 2 past papers

Question 1

what electrical event does each wave, segment, and interval of the ECG represent? (3.5 marks)

Answer 1

p wave: atrial depolarization

PR segment: impulse conduction through AV node, bundle of His, purkinje fibers

PR interval: time from start of atrial depolarization → start of ventricular depolarization

QRS complex: ventricular depolarization

ST segment: ventricles are fully depolarized

T wave: ventricular repolarization

QT interval: start of ventricular depolarization → end of ventricular repolarization

Question 2

outline types of atrioventricular heart blocks (1.5 marks)

Answer 2

First-degree AV block: atrial impulses are delayed but all impulses reach ventricles (no missed beats)
- PR interval prolonged (>0.20 s)
- often benign

Second-degree AV block: some atrial impulses don’t reach ventricles
- Mobitz Type I (Wenckebach): PR interval lengthens progressively → one beat is dropped
- Mobitz Type II: PR interval constant, but sudden dropped QRS complexes → more serious

Third-degree (complete) AV block:
no conduction from atria to ventricles
- atria and ventricles beat independently (ventricles use escape rhythm)
- needs pacemaker

Question 3

describe mechanisms of auto regulation of blood flow. how do local factors, such as changes in tissue metabolism and myogenic responses, contribute to regulation of blood flow in different organs?

Answer 3

autoregulation: ability of an organ to maintain relatively constant blood flow despite changes in arterial pressure

Metabolic (local chemical) mechanism:
↑ tissue metabolism or ↓ O₂ → accumulation of vasodilators
- skeletal muscle during exercise

myogenic mechanism:
- When arterial pressure rises → vessel wall is stretched → smooth muscle contracts → vessel diameter decreases → flow kept constant
- When arterial pressure falls → vessel relaxes → dilates → flow maintained
protects capillaries from high pressure & maintains steady flow

Question 4

what are the starling forces affecting fluid exchange across arterial & venous ends of a capillary? state the mean values and their effect on net fluid exchange. (5 marks)

Answer 4

arterial end:
Pc = 30 mm Hg
Pif = –3 mm Hg
πp = 28 mm Hg
πif = 8 mm Hg

venous end:
Pc = 10 mm Hg
Pif = –3 mm Hg
πp = 28 mm Hg
πif = 8 mm Hg

net fluid pressure:
- Arterial end: Positive NFP → filtration (fluid leaves capillary)
- Venous end: Negative NFP → reabsorption (fluid enters capillary)

Question 5

outline compensatory mechanisms the body employs in heart failure

how do these mechanisms contribute to the development of the decompensated heart failure?

Answer 5

Frank–Starling mechanism: ↑ end-diastolic volume stretches myocardium → ↑ force of contraction (works short-term)

Sympathetic activation: ↑ heart rate, ↑ contractility, vasoconstriction (maintains BP)

Renin–angiotensin–aldosterone system (RAAS): ↑ Na⁺ and water retention → ↑ blood volume

ADH release: Water retention → ↑ volume.
Ventricular hypertrophy: Heart muscle thickens to generate more force

Question 6

what are the stages of shock?

Answer 6

Nonprogressive (compensated) stage:
body compensations can restore BP & tissue perfusion
- mechanisms: baroreceptor reflex, RAAS, ADH, capillary fluid shift

Progressive stage: compensations fail → worsening circulation
Tissue hypoxia → lactic acidosis → vasodilation → more drop in BP

Irreversible stage: severe cell damage → organ failure → death, even if BP restored

Question 7

outline pathophysiology of hemorrhagic shock.

Answer 7

loss of blood volume (whole blood loss thorough hemorrhage or plasma loss through burns & dehydration)
↓
↓ Mean Systemic Filling Pressure (MSFP): pressure that drives venous return, low blood volume = less pressure pushing blood back to heart
↓
↓ Venous Return: less blood returning to heart through veins
↓
↓ Central Venous Pressure (CVP): CVP reflects pressure in right atrium, less venous return = CVP drops
↓
↓ End-Diastolic Volume (EDV): less blood coming into heart = lower preload
↓
↓ Stroke Volume (SV): stroke volume depends on preload, less stretch = weaker contraction (frank starling law)
↓
↓ Cardiac Output (CO): even if HR decreases, if stroke volume is too low then CO decreases (*CO = SV x HR**)
↓
↓ Mean Arterial Pressure (MAP): pressure driving blood into tissues, when CO drops = MAP falls = hypotension
↓
↓ Tissue Perfusion: organs like brain, kidneys, heart dont get enough enough (called hypoperfusion)
↓
results in CIRCULATORY SHOCK

Question 8

short-term and long-term benefits/consequences of body’s compensatory mechanisms during heart failure

Answer 8

Short-term benefits:
- Maintain cardiac output and BP
- Maintain perfusion to vital organs

Long-term consequences:
- fluid retention → congestion, edema
- Vasoconstriction → ↑ afterload → harder for heart to pump
- Hypertrophy → stiff heart → ↓ filling
- Sympathetic overdrive → arrhythmias, myocardial oxygen demand ↑

Question 9

explain the mechanism of generation of pacemaker potential in the heart’s natural pacemaker (5 marks)

Answer 9

Phase 4: Slow diastolic depolarization (pacemaker potential)
- funny Na⁺ channels (If): ppen when the membrane is hyperpolarized at the end of the previous AP → slow Na⁺ influx starts depolarization
- T-type Ca²⁺ channels: open briefly as membrane potential rises → Ca²⁺ influx continues depolarization toward threshold.
- K⁺ channels closing: Outward K⁺ current decreases, helping depolarization

Phase 0: Depolarization
- L-type Ca²⁺ channels open at threshold → large Ca²⁺ influx → upstroke of AP.
Note: In SA node, Ca²⁺ (not Na⁺) causes the AP upstroke.

Phase 3 – Repolarization
K⁺ channels open → K⁺ efflux → membrane becomes negative again → cycle repeats.

Question 10

give the function of the aortic valve and how aortic valve stenosis affects ventricular pressure & cardiac output.

Answer 10

located b/w left ventricle and aorta
- opens during ventricular systole → allows ejection of blood into the aorta
- closes during diastole → prevents backflow from aorta to ventricle

Aortic valve stenosis: narrowed opening → ventricle must generate higher pressure to overcome resistance

Effects:
- ↑ left ventricular systolic pressure
- ↓ stroke volume & cardiac output (especially during exercise)
LV hypertrophy develops due to chronic pressure overload

Question 11

give the role of mitral valve and how mitral valve regurgitation affects atrial pressure and cardiac output.

Answer 11

located b/w left atrium and left ventricle
- opens during diastole → allows LV filling
- closes during systole → prevents backflow into LA

Mitral valve regurgitation: valve doesn’t close properly → blood leaks back into LA during ventricular systole

Effects:
- ↑ left atrial pressure during systole → LA dilates over time
- part of the stroke volume goes backward → ↓ forward cardiac output.
- chronic volume overload → LV dilatation + LA enlargement.
Can cause pulmonary congestion → dyspnea

Question 12

Give the role of chemoreceptors in regulation of respiration.

Answer 12

Central chemoreceptors:
- Location: Ventral medulla.
- Stimulus: ↑ PaCO₂ (via ↑ H⁺ in CSF, because CO₂ diffuses across BBB and forms carbonic acid)
- Response: Strong drive to increase ventilation
- Slow to respond (~20–30 sec) but most powerful long-term driver

Peripheral chemoreceptors:
- Location: Carotid bodies (CN IX) & aortic bodies (CN X)
- Stimulus:
- ↓ PaO₂ (< 60 mmHg) — most sensitive stimulus here
- ↑ PaCO₂ (less sensitive than central)
- ↑ H⁺ (metabolic acidosis)

• Response: Increase ventilation via medullary centers
• Fast response (< 1 sec) — important for rapid changes

Question 13

Explain the following respiratory concepts:

a. Haldane effect
b. cheyne-stokes breathing
c. high altitude pulmonary edema (HAPE).
d. HACE
e. Bohr effect

Answer 13

a. Haldane effect: oxygenation of hemoglobin in lungs reduces its ability to carry CO₂
- opposite in tissues: deoxygenated Hb carries more CO2

b. cheyne-stokes breathing: cycles of gradual ↑ then ↓ tidal volume, followed by apnea
- delay in feedback between lungs & respiratory centers

c. high altitude pulmonary edema: rapid ascent to high altitude decreases PaO2
- hypoxic pulmonary vasoconstriction (HPV) → uneven constriction of blood vessels which leads to increased capillary pressure and leakage of fluid into alveoli

d. high altitude cerebral edema (HACE): hypoxia causes cerebral vasodilation = ↑ capillary permeability → fluid accumulation in the brain

e. Bohr effect: ↑ CO₂ or ↑ H⁺ in blood → Hb’s affinity for O₂ decreases
- in tissues with high metabolism, causes enhanced unloading of O2
- in lungs, has the reverse effect and in low CO2, O2 binds more easily

Question 14

Pre-Bötzinger complex

Answer 14

generates rhythm

Question 15

decompression sickness (aka bends)

Answer 15

condition caused by nitrogen forming bubbles in the body’s tissues during rapid pressure changes

symptoms: joint pain, skin problems, neurological issues (numbness, weakness, paralysis), fatigue, difficulty breathing, loss of consciousness

treatment: come up slowly, hyperbaric oxygen therapy

Question 16

what causes O2-hemoglobin dissociation curve to shift right/left?

Answer 16

left shift (increased affinity for O2): will release less O2
↓ PCO2
↓ [H+]
↓ 2,3-DPG
↓ Temp

right shift (decreased affinity for O2): will release more O2
↑ PCO2
↑[H+] (decreased pH)
↑ 2,3-DPG
↑ Temp

basically think going right everything increasing except for pH which is doing the opposite

Question 17

high altitude acclimization

Answer 17

1. increased ventilation
2. increased RBC production (can take weeks)
3. increased 2,3-bisphosphoglycerate (binds to hemoglobin & decreases its affinity for O2)
4. hypoxic pulmonary vasoconstriction
5. increased mitochondria # & oxidative enzymes
6. increased heart rate & cardiac output

Question 18

acute mountain sickness

Answer 18

Step 1 — Hypoxia stimulates peripheral chemoreceptors

Step 2 — Hyperventilation → Respiratory alkalosis

Step 3 — Cerebral vasodilation from hypoxia

Step 4 — Fluid shifts and pressure changes