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Factors Affecting Pulse Rate

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1. Age

• Neonates: 120–160 bpm
• Children: 80–120 bpm
• Adults: 60–100 bpm (normal range)
• Elderly: Resting rate may decrease slightly; maximum achievable heart rate declines (~220 − age)

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2. Autonomic Nervous System (ANS)

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3. Physical Activity & Exercise

• Exercise increases sympathetic drive and decreases vagal tone → HR rises
• Trained athletes have lower resting HR (sometimes 40–50 bpm) due to increased vagal tone and cardiac hypertrophy (athletic bradycardia)

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4. Emotional State & Stress

• Anxiety, fear, excitement, and pain activate the sympathoadrenal axis → elevated HR
• Deep relaxation and meditation increase vagal tone → lower HR

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5. Body Temperature

• Fever/hyperthermia: Each 1°C rise in core temperature increases HR by approximately 10–15 bpm (direct effect on SA node automaticity)
• Hypothermia: Decreases HR; extreme hypothermia can cause bradycardia and cardiac arrest

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6. Medications & Drugs

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7. Blood Pressure & Hemodynamic Status

• Hypotension/hemorrhage/dehydration: Triggers baroreceptor reflex → sympathetic activation → tachycardia (compensatory)
• Hypertension: Can stimulate baroreceptors → reflex bradycardia

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8. Respiratory Cycle (Sinus Arrhythmia)

• HR increases during inspiration (inhibition of vagal tone) and decreases during expiration
• This respiratory sinus arrhythmia is normal and more pronounced in children and athletes

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9. Hormonal Factors

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10. Posture & Position

• Moving from lying → sitting → standing activates orthostatic reflexes → slight HR increase (sympathetic activation to maintain BP)
• Orthostatic tachycardia is pronounced in POTS (Postural Orthostatic Tachycardia Syndrome)

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11. Pathological Conditions

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12. Sex

• Women tend to have a slightly higher resting HR than men on average, partly due to smaller heart size and hormonal differences

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13. Pain

• Acute pain typically causes tachycardia via sympathetic activation
• Severe visceral pain (e.g., inferior MI, vasovagal syncope) can cause bradycardia via vagal activation

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14. Blood Gas & Metabolic Factors

• Hypoxia: ↑ HR (peripheral chemoreceptor stimulation)
• Hypercapnia: Initially ↑ HR; severe hypercapnia → bradycardia
• Acidosis: Can depress SA node function → bradycardia
• Electrolyte imbalances (e.g., hyperkalemia): Bradycardia; hypokalemia → tachyarrhythmias

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Summary Table

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Q6. Effect of Exercise on Heart Rate

1. Anticipatory rise — even before exercise begins, HR increases due to cortical stimulation of the sympathetic nervous system
2. During exercise: Increased muscle activity → rise in CO₂ and lactic acid → stimulation of chemoreceptors → sympathetic activation → HR increases significantly
3. Circulating epinephrine from adrenal medulla further increases HR
4. Withdrawal of vagal (parasympathetic) tone contributes to rise
5. Rise in body temperature during exercise directly stimulates the SA node

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Q7. Effect of Standing from Supine Position on Heart Rate

1. ~500–700 mL of blood pools in the lower limb veins due to gravity
2. Venous return to the heart decreases → cardiac output falls → blood pressure drops transiently
3. Baroreceptors in the aortic arch and carotid sinus detect the drop in BP
4. Baroreceptor reflex is activated → sympathetic stimulation increases, vagal tone decreases
5. Result: Heart rate increases by 10–20 bpm to compensate and maintain BP and cardiac output

In POTS (Postural Orthostatic Tachycardia Syndrome), HR rises by >30 bpm upon standing without an adequate BP response.