Heart rate and it's factors

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Heart Rate and Its Factors

What is Heart Rate?

Heart rate (HR) is the number of times the heart beats per minute. It is an intrinsic function of the sinoatrial (SA) node - the heart's primary pacemaker - which spontaneously depolarizes via the "funny current" (I_f, an inward Na⁺ current) during phase 4 of the pacemaker action potential. The normal intrinsic SA node rate in young adults is approximately 90-100 beats/min, and it decreases with age according to the formula:

Intrinsic HR = 118 beats/min - (0.57 × Age)

Normal resting heart rate is 60-100 beats/min in adults (the difference from intrinsic rate reflects constant vagal tone at rest).

Morgan and Mikhail's Clinical Anesthesiology, 7e
Costanzo Physiology, 7th Edition

Factors Affecting Heart Rate

Heart rate is modified by autonomic, humoral, local, and physiological factors. Below is a systematic breakdown:

1. Autonomic Nervous System (Most Important)

Sympathetic (Positive Chronotropy - ↑ HR)

Norepinephrine released from sympathetic fibers activates β₁-adrenergic receptors (mainly) and β₂ receptors on the SA node
Via Gs protein → adenylyl cyclase activation → ↑ cAMP → increases I_f (increases rate of phase 4 depolarization)
Also increases I_Ca, which lowers threshold potential (SA node reaches threshold more quickly)
Net effect: SA node fires more action potentials per unit time → tachycardia

Parasympathetic (Negative Chronotropy - ↓ HR)

Acetylcholine released from vagal fibers activates M2 muscarinic receptors on the SA node
Via Gk protein → inhibits adenylyl cyclase → ↓ I_f (slows phase 4 depolarization)
Also activates K⁺-ACh channels → ↑ outward K⁺ current (I_KAch) → hyperpolarizes the maximum diastolic potential (cell moves further from threshold)
Decreases I_Ca → raises threshold potential
Three-pronged mechanism → SA node fires less frequently → bradycardia

At rest, vagal tone predominates, keeping resting HR below the intrinsic SA node rate of 90-100 bpm.

Costanzo Physiology, 7th Edition, p. 147

2. Baroreceptor Reflexes

Stimulus	Heart Rate Effect
↑ Arterial pressure (baroreceptor activation)	↓ HR (reflex bradycardia)
↓ Arterial pressure (baroreceptor inhibition)	↑ HR (reflex tachycardia)
Atrial stretch receptor activation (↑ venous return)	↑ HR (Bainbridge reflex)

Baroreceptors in the carotid sinus and aortic arch send afferents via CN IX and X to the nucleus tractus solitarius (NTS) → CVLM → RVLM → modulate both sympathetic outflow and vagal cardiac motor neurons.

Ganong's Review of Medical Physiology, 26th Edition

3. Respiratory Influence (Respiratory Sinus Arrhythmia)

Inspiration → ↑ HR (decreased vagal tone due to medullary respiratory center "spillover" to vasomotor center)
Expiration → ↓ HR
During quiet breathing: HR varies ~5%; during deep breathing: HR varies up to 30%
Guyton and Hall Textbook of Medical Physiology

4. Temperature

Heart rate increases approximately 10 beats/min per °F (or 18 beats/min per °C) rise in body temperature
Mechanism: elevated temperature increases the metabolic rate of SA node cells, directly increasing spontaneous depolarization rate
Beyond ~105°F (40.5°C): HR may paradoxically fall due to myocardial depression
Guyton and Hall Textbook of Medical Physiology

5. Exercise

HR rises due to: withdrawal of vagal tone (early), sympathetic activation (sustained), circulating catecholamines, increased temperature, decreased blood CO₂/increased O₂ demand
In well-trained athletes: resting bradycardia (HR often <60 bpm) occurs due to enhanced vagal tone, larger stroke volume (Frank-Starling), and downregulation of SA node funny current (I_f) ion channels from training adaptations

6. Hormonal/Humoral Factors

Substance	Effect on HR	Mechanism
Epinephrine (adrenaline)	↑ HR	β₁/β₂ agonist
Thyroid hormones (T3/T4)	↑ HR	Upregulate β-receptors, increase SA node automaticity
Glucagon	↑ HR	Direct chronotropic effect
Acetylcholine	↓ HR	M2 receptor activation
Adenosine	↓ HR	A1 receptor, hyperpolarization

7. Emotional and Central Nervous System Factors

Ganong's Table 32-3 summarizes these clearly:

Factors that accelerate heart rate:

Excitement, anger, most painful stimuli
Hypoxia
Exercise
Fever
Thyroid hormones
Inspiration
Decreased arterial baroreceptor activity
Increased atrial stretch receptor activity

Factors that slow heart rate:

Fear, grief
Stimulation of trigeminal pain fibers
Increased intracranial pressure (Cushing reflex - hypertension + bradycardia)
Expiration
Increased arterial baroreceptor activity
Ganong's Review of Medical Physiology, 26th Edition

8. Age

Neonates: ~120-160 bpm (normal)
Children: ~80-120 bpm
Adults: 60-100 bpm
Elderly: intrinsic SA node rate declines; β-receptor sensitivity also decreases with age

9. Pathological Factors

Tachycardia (>100 bpm) causes:

Fever, infections
Hypovolemia/blood loss (sympathetic reflexes)
Anemia
Heart failure (compensatory)
Hyperthyroidism
Pain, anxiety
Drugs (atropine, sympathomimetics, caffeine)

Bradycardia (<60 bpm) causes:

Vagal stimulation (carotid sinus pressure, Valsalva)
Hypothyroidism
Increased intracranial pressure
SA node disease (sick sinus syndrome)
AV block
Drugs (beta-blockers, digoxin, calcium channel blockers)
Athletic training
Guyton and Hall Textbook of Medical Physiology

Summary Diagram

SA Node (intrinsic rate ~90-100 bpm)
         |
    _____|_____
   |           |
Sympathetic  Parasympathetic (vagus)
(β₁ receptors)  (M2 receptors)
↑ I_f, ↓ threshold  ↓ I_f, ↑ K⁺ outflow
   ↑ HR             ↓ HR
         |
Other modifiers:
• Baroreceptors • Temperature
• Hormones (T3, epi) • Respiration
• Exercise • Emotion • Age • Drugs

The SA node sets the intrinsic rhythm, but in health, vagal tone dominates at rest, and the interplay of all the above factors continuously fine-tunes HR to meet the body's metabolic demands moment to moment.

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