Q1. Factors Affecting Pulse Rate

1. Age — Heart rate is higher in infants and children; it decreases progressively with age.
2. Autonomic Nervous System — Sympathetic stimulation increases HR; parasympathetic (vagal) stimulation decreases it.
3. Physical Activity & Exercise — Exercise increases HR proportionally to metabolic demand.
4. Emotional State & Stress — Fear, anxiety, and pain activate the sympathetic system, raising HR.
5. Body Temperature — Fever/hyperthermia causes sinus tachycardia; hypothermia causes bradycardia (reduced metabolic demand).
6. Medications & Drugs — β-blockers, digitalis, and antidysrhythmics lower HR; cocaine, methamphetamine, and anticholinergic drugs increase it.
7. Posture & Position — Standing from supine causes a reflex increase in HR (see Q7).

Q2. Tachycardia & Bradycardia — Definitions and Causes

(a) Tachycardia

• Fever / infection / sepsis
• Exercise / physical activity
• Anxiety, fear, pain
• Hypovolemia / hemorrhage / shock
• Hyperthyroidism (thyrotoxicosis)
• Anemia
• Heart failure
• Drugs: sympathomimetics (cocaine, amphetamines), anticholinergics, caffeine
• Hypoxia
• Pulmonary embolism

(b) Bradycardia

• Athletic conditioning (physiological)
• Hypothyroidism (myxedema)
• Hypothermia
• Increased intracranial pressure (Cushing's reflex)
• Drugs: β-blockers, digitalis, calcium channel blockers, antidysrhythmics
• Sick sinus syndrome
• Complete heart block (AV block)
• Vasovagal syncope

Q3. Sinus Arrhythmia

• During quiet respiration: heart rate varies by only ~5%
• During deep respiration: heart rate may vary by up to 30%

Q4. Pulse Deficit — Definition and Causes

• Atrial fibrillation (most common) — irregular, variable stroke volumes
• Atrial flutter with variable block
• Frequent premature ventricular contractions (PVCs)
• Premature atrial contractions (PACs)
• Any arrhythmia causing beats with inadequate ventricular filling time and low stroke volume

"The apical pulse is frequently greater than the peripheral pulse because of inadequate filling time and stroke volume, with resultant non-transmitted beats. A greater pulse deficit generally reflects more severe disease." — Roberts and Hedges' Clinical Procedures in Emergency

Q5. Arterial Pulse Recording (Sphygmogram)

      /\
     /  \        <- Anacrotic limb (upstroke / systolic rise)
    /    \
   /      \  /\  <- Dicrotic notch + dicrotic wave
  /        \/  \
 /               \  <- Catacrotic limb (diastolic descent)

Q6. Effect of Exercise on Heart Rate

• Exercise causes an immediate increase in heart rate (chronotropy).
• The mechanism:
  • Anticipatory rise: Even before exercise begins, the cerebral cortex activates the sympathetic nervous system (central command).
  • During exercise: increased CO₂, decreased O₂, and acidosis stimulate chemoreceptors → further sympathetic activation.
  • Sympathetic stimulation releases norepinephrine → increases SA node firing rate.
  • Simultaneous withdrawal of vagal tone further increases HR.
• During maximal exercise, HR can reach 180–200 bpm.
• After exercise, HR gradually returns to baseline (recovery), faster in fit individuals.
• Well-trained athletes have lower resting HR (bradycardia at rest) due to increased vagal tone, but achieve higher maximum HR during exercise.

Q7. Effect of Standing from Supine Position on Heart Rate

1. Blood pools in the lower limbs and splanchnic circulation due to gravity → venous return to the heart decreases.
2. Decreased venous return → decreased stroke volume → decreased blood pressure.
3. Baroreceptors in the carotid sinus and aortic arch detect the fall in BP.
4. They send fewer inhibitory signals to the vasomotor center → sympathetic activity increases, vagal withdrawal occurs.
5. Result: Heart rate increases by ~10–20 bpm (reflex tachycardia / orthostatic response).

• An increase of >30 bpm on standing (without significant BP drop) is diagnostic of POTS (Postural Orthostatic Tachycardia Syndrome).