EFECTS OF

SMOKING ON
CARDIOVASCULAR
SYSTEM

BY
ZEESHAN
ALI KHAN
KHIZAR MALIK
SEHRISH LATIF
RIMSAH AHMAD
 Table of contents
INTRODUCTION

• EFFECT OF NICOTINE ON CARDIOVASCULAR SYSTEM

• EFFECT OF CARBON MONOXIDE ON CARDIOVASCULAR SYSTEM

• SMOKING AND VASCULAR FUNCTION

• LIPID METABOLISM

• SMOKING AND AUTONOMIC NERVOUS SYSTEM

• EFFECT OF CARCINOGENIC SMOKE ON HEART RATE

CARDIOVASCULAR DISEASES CAUSED BY SMOKING

• HYPERTENSION

• HEART ATTACK

• STROKE

• ANEURYSMS

• PERPHERAL ARTERY DISEASE

• ATHEROSCLEROSIS/ARTERIOSCLEROSIS

• ISCHEMIC HEART DISEASE

 SECOND HAND SMOKE RISKS

 QUITTING
• STRATEGIES TO QUIT SMOKING
Effects of smoking on cardiovascular system

c
Introduction
igarette smoke is a toxic mix of more than 7,000 chemicals 1 and,
when inhaled, can interfere with important processes in the body
that keep it functioning normally. One of these processes is the
delivery of oxygen-rich blood to your heart and the rest of your body. When
you breathe in air from the atmosphere, the lungs take in oxygen and
deliver it to the heart, which pumps this oxygen-rich blood to the rest of the
body through the blood vessels. But when you breathe in cigarette smoke,
the blood that is distributed to the rest of the body becomes contaminated
with the smoke’s chemicals. These chemicals can damage to your heart
and blood vessels, which can lead to cardiovascular disease (CVD).
CVD is a generic term referring to multiple conditions affecting the heart or
blood vessels. Some of these conditions include:

 coronary heart disease

 hypertension (high blood pressure)
 heart attack
 stroke
 aneurysms
 peripheral artery disease

Nicotine
Nicotine is the primary alkaloid derived from tobacco leaves, and is the
substance in tobacco responsible for the addictive properties of
smoking. However not primary cause of smoking related diseases.  
Nicotine is extracting from the leaves of tobacco by burning or heating
the leaves cause release of this chemical. Cigarettes contain 1–2 per
cent nicotine, or approximately 10–20 mg of nicotine.

Note
Addictive action of Nicotine
Once nicotine inhaled its takes matter of seconds to absorb into the blood
streams, where it travel directly to the brain. The addictive action of nicotine is
on the area of brain called reward pathway. Once nicotine reach to this area it
bind to specific receptors called nicotine receptor present on the surface of
Cardiovascular
neuron. Once nicotineeffects of nicotine
bind to nicotine receptor activate the reward pathway in
the brain releasing dopamine. ( the feel good chemical )
Cardiovascular effects of nicotine
Nicotine causes your blood vessels to constrict or narrow, which limits
the amount of blood that flows to your organs. Over time, the constant
constriction results in blood vessels that are stiff and less elastic.
Constricted blood vessels decrease the amount of oxygen and nutrients
your cells receive. To meet the need for more oxygen, your heart rate
may increase. An increased heart rate, an enlarged heart and stiffer and
less elastic blood vessels make it harder to pump blood and provide the
body with the needed oxygen and nutrients. These changes in the
structure and function of your blood vessels and heart increase your
risk of high blood pressure and cardiovascular disease.
Effects of carbon monoxide
Carbon monoxide is harmful when breathed because it displaces oxygen in
the blood and deprives the heart, brain and other vital organs of oxygen.
Large amounts of CO can overcome you in minutes without warning —
causing you to lose consciousness and suffocate. Besides tightness across
the chest, initial symptoms of CO poisoning may include headache, fatigue,
dizziness, drowsiness, or nausea. Sudden chest pain may occur in people
with angina. During prolonged or high exposures, symptoms may worsen
and include vomiting, confusion and collapse in addition to loss of
consciousness and muscle weakness. Symptoms can vary widely from
person to person. CO poisoning may occur sooner in those most
susceptible: young children, the elderly, people with lung or heart disease,
people at high altitudes, or those who already have elevated CO blood
levels, such as smokers. Also, CO poisoning poses a special risk to
fetuses. CO poisoning can be reversed if caught in time. But even if you
recover, acute poisoning may result in permanent damage to the parts of
your body that require a lot of oxygen such as the heart and brain.
Significant reproductive risk is also linked to CO.

Smoking and vascular function

cigarette smoke change your blood chemistry and causing plaque a waxy
substance comprised of cholesterol, scar tissue, calcium, fat, and other
material to build up in the arteries, the major blood vessels that carry blood
from your heart to your body. This plaque buildup can lead to a disease
called atherosclerosis. When the chemicals in cigarette smoke cause
atherosclerosis and thickened blood in the arteries, it becomes more
difficult for blood cells to move through arteries and other blood vessels to
get to vital organs like the heart and brain. This can create blood clots and
ultimately lead to a heart attack or stroke, even death.

Effect of smoking related to lipid metabolism

Tobacco smoke, and specifically nicotine, has a significant effect on lipid
metabolism and the regulation of lipid levels in the blood. Cigarette smoke
promote atherosclerosis, via affecting lipid profile. Smoking is associated
with increase in total cholesterol and triglycerides concentration in serum.
Smoking affect the tendency for low density lipoprotein and very low
density lipoprotein. These changes affect level of cholesterol. So
cholesterol level be high in smokers raise risk for heart disease and stroke.
On the other hand, smoking lowers serum concentrations of high-density
lipoprotein ( cholesterol, a powerful protective factor against the
development of atherosclerosis. The difference is usually small, 5 mg/dl or
less, but this difference represents a 10% decrease and would be expected
to affect atherogenesis to a significant degree.

Effect of smoking on heart rate

Smokers had significantly higher resting HR values than non-smokers.
Both female and male smokers showed a significantly slower HR increase
during exercise. Female smokers failed to reach their age-predicted
maximum HR by 6.0 bpm and males by 3.6 bpm. The actual maximum HR
achieved (HRmax) was significantly lower for both female smokers (191.0
bpm vs.198.0 bpm) and male smokers (193.2 bpm vs.199.3 bpm),
compared to non-smokers. Heart rate reserve was also significantly lower
in female (114.6 bpm vs. 128.1 bpm) and male smokers (120.4 bpm vs.
133.0 bpm). During recovery, the HR decline was significantly attenuated,
but only in female smokers. Females had a higher resting HR and showed
a higher HR response during sub-maximal exercise compared to
males. Smoking was found to affect young smokers' HR, increasing HR at
rest, slowing HR increase during exercise and impairing their ability to
reach the age-predicted HRmax. In addition, smoking was associated with
an attenuated HR decline during recovery, but only in females.

Cardiovascular diseases caused by

smoking

ARTERIOSCLEROSIS
Arteriosclerosis occurs when the blood vessels that transport oxygen and
nutrients from your heart to the rest of your body (arteries) become dense
and rigid. Occasionally confining blood flow to your organs and tissues.
Well arteries are malleable and stretchy, but over time, the walls in your
arteries can solidify, a condition generally called hardening of the arteries.

ISCHEMIC HEART DISEASE

Ischemia is defined as insufficient blood circulation to a regional area due
to obstruction of the blood vessels providing the area. Ischemic means that
an organ (e.g., the heart) is not getting adequate blood and oxygen.
Ischemic heart disease, also called coronary heart disease (CHD) or
coronary artery disease. Smoking is a considerable risk component for
ischemic heart disease, a situation in which plaque accumulate inside the
coronary arteries. These arteries provide your heart muscle with oxygen-
rich blood. When plaque accumulate in the artery. Despite the fact that the
narrowing can be created by a blood clot or by tightning of the blood
vessel, most often it is caused by accumulation of plaque, known as
atherosclerosis. When the blood flow to the heart muscle is totally choked,
the heart muscle cells expired, which is termed a heart attack or myocardial
infarction (MI).
PERIPHERAL ARTERY DISEASE (PAD)
Peripheral arterial disease (PAD) in the legs or lower boundaries is the
narrowing or obstruction of the vessels that transfer blood from the heart to
the legs. It is firstly caused by the enlargement of fatty plaque in the
arteries, which is called atherosclerosis. PAD can happen in any blood
vessel, but it is more common in the legs than the arms .

WHAT ARE THE POSSIBLE COMPONENTS FOR PAD?

1- High blood pressure
2- Atherosclerosis
3- Diabetes
4- High cholesterol
Aneurysms
An aneurysm is a bulge in a blood vessel caused by a weakness in the
blood vessel wall, usually where it branches. As blood passes through the
weakened blood vessel, the blood pressure causes a small area to bulge
outwards like a balloon.

Aneurysms can develop in any blood vessel in the body, but the 2 most
common places are:

 the artery that transports blood away from the heart to the rest of the
body (the abdominal aorta)

 the brain

Smoking cause of aneurysms

The deadly effects of smoking have again been shown, this time linked with
causing cerebral aneurysms, a weakening of the wall of the brain's blood
vessels that can potentially rupture and cause stroke and often death.

Smoking and stroke

Cigarette smoking is a well-established risk factor for all forms of stroke.
While both the general public and the global healthcare system are aware
of the vascular risks associated with smoking, the prevalence of tobacco
use has remained largely unchanged over the last quarter of a century.
Approximately one in five US adults are classified as regular smokers, with
the initiation of smoking typically occurring during the teenage years.
Although the increased risk of stroke associated with smoking is generally
acknowledged, it is less well recognized that considerable scientific
evidence implicates a strong dose–response relationship between smoking
and stroke risk. In this article, we summarize the literature regarding
smoking-related stroke risk, the dose–response relationship, and the costs
of this detrimental habit to both the individual and society as a whole .

Smoking and hypertention

Cigarette smoking is a powerful cardiovascular risk factor and smoking
cessation is the single most effective lifestyle measure for the prevention of
a large number of cardiovascular diseases. Impairment of endothelial
function, arterial stiffness, inflammation, lipid modification as well as an
alteration of antithrombotic and prothrombotic factors are smoking-related
major determinants of initiation, and acceleration of the atherothrombotic
process, leading to cardiovascular events. Cigarette smoking acutely exerts
an hypertensive effect, mainly through the stimulation of the sympathetic
nervous system. As concern the impact of chronic smoking on blood
pressure, available data do not put clearly in evidence a direct causal
relationship between these two cardiovascular risk factors, a concept
supported by the evidence that no lower blood pressure values have been
observed after chronic smoking cessation. Nevertheless, smoking, affecting
arterial stiffness and wave reflection might have greater detrimental effect
on central blood pressure, which is more closely related to target organ
damage than brachial blood pressure. Hypertensive smokers are more
likely to develop severe forms of hypertension, including malignant and
renovascular hypertension, an effect likely due to an accelerated
atherosclerosis.

Smoking and heart attack

Considerable evidence supports the premise that higher levels of
education lead to enhanced health, including protective health
behaviors. This paper focuses on how education affects one health
behavior known to lead to enhanced health: the cessation of smoking. In
particular, the authors examine the extent to which education influences
the decision by middle-aged adults to quit smoking following a heart
attack, a potentially life- threatening health event. We first hypothesize
that middle-aged adults with more formal education will stop smoking
more readily than people with less formal education following the
experience of a heart attack. Second, we ask what other factors might
underlie and explain that hypothesized effect. Using longitudinal data,
the authors track changes in individual smoking behaviors after a heart
attack among preretirement-age Americans. We control for documented
correlates of smoking and heart attack plus other factors associated with
education, heart attack, and smoking that may also influence whether a
person quits smoking. In addition to confirming evidence on the
education-health association as well as the documented connection
between heart attack and smoking cessation, this study provides a
surprising twist on those links: Our results show that the move to quit
smoking following the experience of a heart attack among middle-aged
adults is significantly and dramatically moderated by their level of
educational attainment.

SECOND HAND SMOKE RISKS

Secondhand smoke is the amalgamation of smoke from the blazing end
of a cigarette and the smoke exhaled out by smokers. Secondhand
smoke consist of more than 7,000 chemicals. Hundreds are toxic and
about 70 can cause cancer. Subjection to secondhand smoke has
instant unfavourable effects on the cardiovascular system and can
cause coronary heart disease and stroke.

Secondhand smoke causes virtually 34,000 untimely deaths from heart

disease each year in the United States among nonsmokers.

1. Nonsmokers who are revealed to secondhand smoke at home or

at work enlarged their risk of advancing heart disease by 25–30%.

2. Secondhand smoke enlarged the risk for stroke by 20−30%.

3. Secondhand smoke exposure cause more than 8,000 deaths from

stroke yearly.

Breathing secondhand smoke can have instant unfavourable effects on

your blood and blood vessels, increasing the probability of having a
heart attack.Breathing secondhand smoke involves with the usual
functioning of the heart, blood, and vascular systems in ways that
increase the possiblity of having a heart attack.Even short exposure to
secondhand smoke can harm the lining of blood vessels and cause your
blood platelets to become adhesive. These substitute can cause a fata
heart attack.
STRATEGIES TO QUIT SMOKING

Smoking tobacco is both a bodily weakness and a mental habit. The nicotine
from cigarettes give a temporary and addictive high. Removing that systematic
fix of nicotine causes your body to encounter physical withdrawal symptoms
and longings. As a result of nicotine’s “feel good” effect on the brain, you may
turn to cigarettes as a fast and dependable way to boost your point of view,
alleviate stress, and unwind. Smoking can also be a way of coping with
depression, anxiety, or even boredom. Leaving means finding unlike,
beneficial ways to cope with those feelings.

1. Set a quit date.

2. Tell family, friends, and co-workers that you plan to quit.

3. Predict and proposal for the challenges you’ll face while quitting.
4. Detach cigarettes and other tobacco products from your home,
car, and work.

5. Talk to your doctor about getting help to quit.