What can increase heart rate?

What Can Increase Heart Rate

Heart rate increases primarily through decreased vagal (parasympathetic) tone followed by increased sympathetic nervous system activity, with the most potent physiological triggers being exercise, emotional stress, and pharmacological agents like atropine.

Physiological Mechanisms

Exercise and Physical Activity

• Exercise is the most powerful physiological stimulus for heart rate elevation, causing a linear increase with workload at approximately 10 bpm per metabolic equivalent (MET) 1.
• The immediate cardiovascular response to exercise involves decreased vagal tone, followed by increased sympathetic outflow 1.
• During dynamic exercise, heart rate can increase 2- to 3-fold above resting values, with maximal heart rate heavily influenced by age (predicted as 220 minus age in years, though with ±10-15 bpm variability) 1, 2.
• Dynamic exercise increases heart rate more than isometric or resistance exercise 1.

Autonomic Nervous System Factors

• Sympathetic activation directly increases heart rate through β-1 adrenergic receptor stimulation, while parasympathetic (vagal) withdrawal removes the heart's natural brake 1.
• Emotional factors including anger, anxiety, and fear increase sympathetic output and elevate heart rate 3.
• Mental stress can amplify heart rate responses 1.

Pharmacological Agents

Atropine (Antimuscarinic Agent)

• Atropine increases heart rate by blocking muscarinic receptors and inhibiting vagal control of the heart 4.
• Adult dosing for antisialagogue or antivagal effects: initial single dose of 0.5 to 1 mg intravenously 4.
• For bradyasystolic cardiac arrest: 1 mg dose, repeated every 3 to 5 minutes if asystole persists 4.
• Atropine-induced parasympathetic inhibition may be preceded by transient bradycardia with small doses before characteristic tachycardia develops 4.
• Effects on heart rate are delayed by 7 to 8 minutes after intravenous administration and are non-linearly related to drug levels 4.

Dobutamine (β-Adrenergic Agonist)

• Dobutamine acts directly on β-1 adrenergic receptors, producing substantial increases in heart rate (2- to 3-fold) and contractility 1.
• Heart rate increases are less than with exercise but still clinically significant 1.

Pathological and Clinical Conditions

Conditions Causing Elevated Resting Heart Rate

• Prolonged bed rest causes accelerated heart rate response to submaximal workloads, indicating deconditioning 1.
• Anemia, variable vascular volume, peripheral resistance changes, or ventricular dysfunction can accelerate heart rate responses 1.
• Heart failure patients exhibit elevated resting heart rates with blunted heart rate reserve despite achieving lower maximal heart rates 1.

Myocardial Ischemia and Stress

• Myocardial ischemia can increase heart rate variability and T-wave alternans magnitude, particularly at lower heart rate thresholds than in normal hearts 1.
• Coronary artery occlusion and reperfusion amplify heart rate responses 1.
• Adrenergic stimulation increases heart rate more than pacing alone at comparable rates 1.

Environmental and Lifestyle Factors

Alcohol and Substance Use

• Heavy alcohol intake, especially binge drinking, increases heart rate and risk of sudden cardiac death 1.
• Moderate alcohol consumption shows protective effects, but excessive intake causes QT prolongation and tachycardia 1.

Physical Deconditioning

• Lack of regular physical activity results in higher resting heart rates and exaggerated heart rate responses to submaximal exercise 1.

Clinical Significance and Risk Implications

Elevated Heart Rate as Risk Factor

• Increased heart rate is an independent risk factor for sudden cardiac death and cardiovascular mortality in both healthy individuals and those with cardiac disease 1, 5, 6, 7.
• The risk associated with heart rate elevation is comparable to that of elevated blood pressure, with each 10 bpm increase associated with at least 20% increase in cardiac death risk 7.
• This relationship remains significant after controlling for other cardiovascular risk factors, suggesting a direct pathogenic role 5, 6.

Important Clinical Caveats

• Beta-blockers and other cardiovascular medications lower both incremental heart rate rise and maximal heart rate, limiting interpretation of cardiac responses to exercise 1, 2.
• Body position, type of exercise, physical conditioning, blood volume, sinus node function, and environmental conditions all influence heart rate responses 1.
• In patients with coronary artery disease, limit total atropine dose to 0.03-0.04 mg/kg to avoid excessive tachycardia 4.
• Rapid heart rate increase at exercise onset (>12 bpm in first minute) predicts adverse cardiac events in coronary artery disease patients with hazard ratio of 5.0 8.