Date: 25/05/2025
Prepared by: Mohamadkaif Rafik Yelavikar
PHYSIOLOGICAL EFFECT OF NICOTINE ON CARDIOVASCULAR
SYSTEM
Introduction
The primary addictive substance that causes
cigarette dependency is nicotine, a strong
alkaloid found naturally in tobacco. Through
direct processes like stimulating nicotinic
acetylcholine receptors and indirect mechanisms
like inducing the release of catecholamine,
which raise blood pressure and heart rate, it
affects the cardiovascular system. The
absorption of nicotine into the body, its precise
mechanism of action, its acute and long-term
effect on the cardiovascular system, and its
therapeutic relevance – particularly with regard
to patient management and cardiovascular
health risk will be covered in this presentation.
Nicotine Absorption and
Pharmacokinetics
The body absorbs nicotine through a variety of routes,
including the lungs, oral mucosa, gastrointestinal tract,
and transdermal application (e.g., patches). The most
effective route is inhalation, as nicotine reaches peak
plasma levels within 10 to 15 minutes of smoking.
Because nicotine is lipid-soluble, it can easily cross cell
membranes and the blood-brain barrier, affecting the
central nervous system quickly. Once absorbed, nicotine
is widely distributed throughout body tissues, and its
half-life is relatively short-acting, requiring repeated use
to maintain its effects. The liver is the primary site of
metabolism, where the enzyme CYP2A6 converts
nicotine into cotinine, the primary metabolite used to
measure nicotine exposure in clinical and research
settings.
Mechanism Of Action
Nicotinic acetylcholine receptors (nAChRs), which are found in the autonomic
ganglia and central nervous system, are the site of nicotine binding. Widespread
physiological effects result from this interaction's stimulation of the sympathetic
nervous system. One important result is the activation of the adrenal medulla,
which causes catecholamines, especially norepinephrine and adrenaline, to be
released into the bloodstream. The typical cardiovascular reactions associated
with nicotine use, including raised blood pressure, vasoconstriction, and an
accelerated heartbeat, are caused by these catecholamines. Further adding to its
general stimulatory effects on the body, nicotine also encourages metabolic
alterations by raising the amounts of glucose and free fatty acids in the blood.
Nicotine's addictive qualities and effects on cardiovascular health are mostly due
to these coupled actions.
Acute Cardiovascular Effect
Acute nicotine intake has a variety of cardiovascular
consequences. It raises blood pressure by producing
vasoconstriction, predominantly through alpha-adrenergic
receptor activation, and increases heart rate through a
chronotropic action. Nicotine also improves myocardial
contractility, an inotropic effect that increases the force of
cardiac contractions. These alterations cause an increase in
cardiac output and oxygen demand by the heart muscle.
Additionally, nicotine causes peripheral vasoconstriction,
which can result in cold extremities and a reduction in skin
temperature. Together, these acute effects put additional
burden on the cardiovascular system, increasing the hazards
associated with nicotine use.
Chronic Cardiovascular Effect
Chronic nicotine exposure causes persistent stimulation of
the sympathetic nervous system, putting the cardiovascular
system under constant stress. It promotes endothelial
dysfunction by decreasing nitric oxide-mediated
vasodilation, which reduces blood vessel relaxation. Over
time, nicotine increases arterial stiffness and structural
remodeling of blood arteries, making them less flexible.
These alterations contribute to the progression of
atherosclerotic plaques, which constrict and stiffen the
arteries. As a result, long-term nicotine use increases the
incidence of major cardiovascular events such as
myocardial infarction (heart attack) and ischemic stroke,
emphasizing the negative influence on cardiovascular
health.
Effects on Heart
and Rhythm
Nicotine alters heart rate and rhythm by altering the autonomic nervous
system equilibrium. It lowers heart rate variability, which is a major
indicator of autonomic function and indicates poor rhythm control. This
imbalance raises the chance of developing arrhythmias such as atrial
fibrillation, which is characterized by an irregular pulse, and ventricular
ectopy, which are premature beats that originate in the ventricles. These
irregular rhythms can induce symptoms like palpitations and dizziness,
which can develop to more serious problems. Nicotine's effect on heart
rhythm is particularly dangerous in persons who already have heart
problems, as it increases the risk of sudden cardiac death. Overall,
nicotine increases the occurrence of cardiac rhythm abnormalities,
highlighting its negative impact on cardiovascular health.
Effects on Blood Vessels
Nicotine directly constricts the coronary arteries,
reducing blood flow to the heart muscle. This
narrowing of the arteries reduces oxygen delivery
while raising the heart's oxygen demand, resulting
in an imbalance that strains the myocardium. The
combination of diminished oxygen delivery and
increased demand can cause myocardial ischemia.
Nicotine can also cause coronary vasospasm, which
is a quick, temporary constriction of the coronary
arteries that can lead to angina or chest pain. These
vascular effects add greatly to the cardiovascular
hazards associated with nicotine use, raising the risk
of heart attacks and other ischemic heart diseases.
Effects on Platelet Function and
Coagulation
Nicotine interferes with platelet function and
coagulation by increasing platelet activation and
aggregation, promoting blood clot formation. It
also elevates fibrinogen levels, a critical protein
involved in clotting, which increases the blood's
ability to clot. These alterations raise the risk of
acute thrombotic events like heart attacks and
strokes, since excessive clot formation can block
blood vessels and disrupt blood flow. Overall,
nicotine's influence on coagulation contributes to
its negative effects on cardiovascular health by
encouraging circumstances that might result in
life-threatening arterial blockages.
Cardiovascular Disease Risk
Nicotine greatly raises the risk of acquiring cardiovascular
disease. It contributes to the initiation or progression of
hypertension by increasing blood pressure via sympathetic
activation and vasoconstriction. Nicotine also hastens the
evolution of atherosclerosis and coronary artery disease by
increasing plaque formation and vascular inflammation. Aside
from the heart, it raises the risk of peripheral artery disease
(PAD), which impairs blood flow to the extremities, and
cerebrovascular illness, such as ischemic stroke. Additionally,
nicotine use has been associated to an increased risk of
abdominal aortic aneurysm, a hazardous disorder characterized
by the weakening and potential rupture of the primary blood
vessel delivering blood to the abdomen and lower body.
Overall, nicotine's effects are linked to a wide range of
cardiovascular problems.
Clinical Implication and Smoking
Cessation
Nicotine replacement treatment (NRT), such as
patches and gums, delivers controlled, lower
amounts of nicotine while posing a considerably
reduced cardiovascular risk than smoking. Quitting
smoking significantly reduces cardiovascular risk
in months to years, improving heart and artery
health over time. Tobacco product taxes, warning
labels, and easily available cessation programs are
all important public health interventions for
encouraging smokers to quit. Educating patients
on the cardiovascular dangers of nicotine and
smoking is critical for encouraging behavior
change and facilitating successful cessation,
thereby lowering the burden of cardiovascular
disease associated with tobacco use.
Summary
To summarize, nicotine has a major effect on
cardiovascular physiology, both acutely and
chronically. It causes an abrupt increase in heart
rate, blood pressure, and myocardial oxygen
demand, putting the heart under stress. Chronic
nicotine use contributes to the development of
atherosclerosis, increases thrombosis, and
induces endothelial damage, all of which
increase the risk of major cardiovascular events.
Importantly, quitting smoking remains an
important strategy for improving cardiovascular
health, lowering both short-term and long-term
hazards, and increasing overall outcomes for
people who stop using nicotine.
References
Benowitz NL. Nicotine pharmacology: addiction, smoking-related
diseases, and treatments. Annu Rev Pharmacol Toxicol, 2009.
World Health Organization (WHO). Tobacco info sheet.
Centers for Disease Control and Prevention (CDC). Smoking is
linked to cardiovascular disease.

PHYSIOLOGICAL EFFECT OF NICOTINE ON CARDIOVASCULAR SYSTEM.pptx

  • 1.
    Date: 25/05/2025 Prepared by:Mohamadkaif Rafik Yelavikar PHYSIOLOGICAL EFFECT OF NICOTINE ON CARDIOVASCULAR SYSTEM
  • 2.
    Introduction The primary addictivesubstance that causes cigarette dependency is nicotine, a strong alkaloid found naturally in tobacco. Through direct processes like stimulating nicotinic acetylcholine receptors and indirect mechanisms like inducing the release of catecholamine, which raise blood pressure and heart rate, it affects the cardiovascular system. The absorption of nicotine into the body, its precise mechanism of action, its acute and long-term effect on the cardiovascular system, and its therapeutic relevance – particularly with regard to patient management and cardiovascular health risk will be covered in this presentation.
  • 3.
    Nicotine Absorption and Pharmacokinetics Thebody absorbs nicotine through a variety of routes, including the lungs, oral mucosa, gastrointestinal tract, and transdermal application (e.g., patches). The most effective route is inhalation, as nicotine reaches peak plasma levels within 10 to 15 minutes of smoking. Because nicotine is lipid-soluble, it can easily cross cell membranes and the blood-brain barrier, affecting the central nervous system quickly. Once absorbed, nicotine is widely distributed throughout body tissues, and its half-life is relatively short-acting, requiring repeated use to maintain its effects. The liver is the primary site of metabolism, where the enzyme CYP2A6 converts nicotine into cotinine, the primary metabolite used to measure nicotine exposure in clinical and research settings.
  • 4.
    Mechanism Of Action Nicotinicacetylcholine receptors (nAChRs), which are found in the autonomic ganglia and central nervous system, are the site of nicotine binding. Widespread physiological effects result from this interaction's stimulation of the sympathetic nervous system. One important result is the activation of the adrenal medulla, which causes catecholamines, especially norepinephrine and adrenaline, to be released into the bloodstream. The typical cardiovascular reactions associated with nicotine use, including raised blood pressure, vasoconstriction, and an accelerated heartbeat, are caused by these catecholamines. Further adding to its general stimulatory effects on the body, nicotine also encourages metabolic alterations by raising the amounts of glucose and free fatty acids in the blood. Nicotine's addictive qualities and effects on cardiovascular health are mostly due to these coupled actions.
  • 5.
    Acute Cardiovascular Effect Acutenicotine intake has a variety of cardiovascular consequences. It raises blood pressure by producing vasoconstriction, predominantly through alpha-adrenergic receptor activation, and increases heart rate through a chronotropic action. Nicotine also improves myocardial contractility, an inotropic effect that increases the force of cardiac contractions. These alterations cause an increase in cardiac output and oxygen demand by the heart muscle. Additionally, nicotine causes peripheral vasoconstriction, which can result in cold extremities and a reduction in skin temperature. Together, these acute effects put additional burden on the cardiovascular system, increasing the hazards associated with nicotine use.
  • 6.
    Chronic Cardiovascular Effect Chronicnicotine exposure causes persistent stimulation of the sympathetic nervous system, putting the cardiovascular system under constant stress. It promotes endothelial dysfunction by decreasing nitric oxide-mediated vasodilation, which reduces blood vessel relaxation. Over time, nicotine increases arterial stiffness and structural remodeling of blood arteries, making them less flexible. These alterations contribute to the progression of atherosclerotic plaques, which constrict and stiffen the arteries. As a result, long-term nicotine use increases the incidence of major cardiovascular events such as myocardial infarction (heart attack) and ischemic stroke, emphasizing the negative influence on cardiovascular health.
  • 7.
    Effects on Heart andRhythm Nicotine alters heart rate and rhythm by altering the autonomic nervous system equilibrium. It lowers heart rate variability, which is a major indicator of autonomic function and indicates poor rhythm control. This imbalance raises the chance of developing arrhythmias such as atrial fibrillation, which is characterized by an irregular pulse, and ventricular ectopy, which are premature beats that originate in the ventricles. These irregular rhythms can induce symptoms like palpitations and dizziness, which can develop to more serious problems. Nicotine's effect on heart rhythm is particularly dangerous in persons who already have heart problems, as it increases the risk of sudden cardiac death. Overall, nicotine increases the occurrence of cardiac rhythm abnormalities, highlighting its negative impact on cardiovascular health.
  • 8.
    Effects on BloodVessels Nicotine directly constricts the coronary arteries, reducing blood flow to the heart muscle. This narrowing of the arteries reduces oxygen delivery while raising the heart's oxygen demand, resulting in an imbalance that strains the myocardium. The combination of diminished oxygen delivery and increased demand can cause myocardial ischemia. Nicotine can also cause coronary vasospasm, which is a quick, temporary constriction of the coronary arteries that can lead to angina or chest pain. These vascular effects add greatly to the cardiovascular hazards associated with nicotine use, raising the risk of heart attacks and other ischemic heart diseases.
  • 9.
    Effects on PlateletFunction and Coagulation Nicotine interferes with platelet function and coagulation by increasing platelet activation and aggregation, promoting blood clot formation. It also elevates fibrinogen levels, a critical protein involved in clotting, which increases the blood's ability to clot. These alterations raise the risk of acute thrombotic events like heart attacks and strokes, since excessive clot formation can block blood vessels and disrupt blood flow. Overall, nicotine's influence on coagulation contributes to its negative effects on cardiovascular health by encouraging circumstances that might result in life-threatening arterial blockages.
  • 10.
    Cardiovascular Disease Risk Nicotinegreatly raises the risk of acquiring cardiovascular disease. It contributes to the initiation or progression of hypertension by increasing blood pressure via sympathetic activation and vasoconstriction. Nicotine also hastens the evolution of atherosclerosis and coronary artery disease by increasing plaque formation and vascular inflammation. Aside from the heart, it raises the risk of peripheral artery disease (PAD), which impairs blood flow to the extremities, and cerebrovascular illness, such as ischemic stroke. Additionally, nicotine use has been associated to an increased risk of abdominal aortic aneurysm, a hazardous disorder characterized by the weakening and potential rupture of the primary blood vessel delivering blood to the abdomen and lower body. Overall, nicotine's effects are linked to a wide range of cardiovascular problems.
  • 11.
    Clinical Implication andSmoking Cessation Nicotine replacement treatment (NRT), such as patches and gums, delivers controlled, lower amounts of nicotine while posing a considerably reduced cardiovascular risk than smoking. Quitting smoking significantly reduces cardiovascular risk in months to years, improving heart and artery health over time. Tobacco product taxes, warning labels, and easily available cessation programs are all important public health interventions for encouraging smokers to quit. Educating patients on the cardiovascular dangers of nicotine and smoking is critical for encouraging behavior change and facilitating successful cessation, thereby lowering the burden of cardiovascular disease associated with tobacco use.
  • 12.
    Summary To summarize, nicotinehas a major effect on cardiovascular physiology, both acutely and chronically. It causes an abrupt increase in heart rate, blood pressure, and myocardial oxygen demand, putting the heart under stress. Chronic nicotine use contributes to the development of atherosclerosis, increases thrombosis, and induces endothelial damage, all of which increase the risk of major cardiovascular events. Importantly, quitting smoking remains an important strategy for improving cardiovascular health, lowering both short-term and long-term hazards, and increasing overall outcomes for people who stop using nicotine.
  • 13.
    References Benowitz NL. Nicotinepharmacology: addiction, smoking-related diseases, and treatments. Annu Rev Pharmacol Toxicol, 2009. World Health Organization (WHO). Tobacco info sheet. Centers for Disease Control and Prevention (CDC). Smoking is linked to cardiovascular disease.