Cardiovascular Effects of Drug Use

Running head: CARDIOVASCULAR EFFECTS OF DRUG 1

Cardiovascular Effects of Drug Use:

Focusing on Recreational and Illicit Drugs

Daniel Jones

Skagit Valley College

CARDIOVASCULAR EFFECTS OF DRUG 2

Abstract

Statistics show that 1 in 4 myocardial infarctions (MI), also known as heart attacks, in

people between the ages of 18 and 45 can be linked to cocaine use (Qureshi, A., Suri, F.,

Guterman, L., & Hopkins, N., 2001). Cocaine is not the only illicit and recreational drug

to have adverse affects on the cardiovascular system. The primary sources of data used for

this study will be reports and studies completed in the health care field. The secondary

source of data will be statistical data from local hospitals regarding cardiac complications

in patients with documented drug use and history. This study should pull the various

pieces together of the many non-associated studies into the subject. The selection of

specific participants used in this study and the other studies examined are random. The

control group for the study will be the statistical information regarding cardiac

complications in individuals with no history of recreational drug use. The age group of the

study is individuals between the ages of 18 and 45. The individuals examined come from

all ethnic and socioeconomic groups. There is no disclosure of personal health care

information and all patient information is held at the highest confidentiality.


Cardiovascular Effects of Drug Use:

Focusing on Recreational and Illicit Drugs

I. Introduction

According to the National Survey on Drug Use and Health (NSDUH),

approximately 21.8 million Americans, ages 12 or older, in 2009 consumed illicit drugs

(“Health, United States,” 2010.) Of the 21.8 million illicit drug users, approximately 5.1

million in total used drugs other than marijuana (“Health, United States,” 2010). Statistics

show that 1 in 4 myocardial infarctions (MI), also known as heart attacks, in people

between the ages of 18 and 45 can be linked to cocaine use (Qureshi, A., Suri, F.,

Guterman, L., & Hopkins, N., 2001).

Recreational and illicit drug use has a profound effect on the central nervous

system but studies also show acute effects to the heart and circulation system. Drug-related

morbidity has a strong link to their cardiovascular effects due to their significant and

profound changes to the cardiovascular system. According to Paramedic Kelly Grayson

(2011), most, if not all, emergency medical technicians (EMT), paramedics, nurses and

physicians will likely encounter patients with cardiovascular complications related to illicit

and recreational drug use. Medical professionals are required to have an awareness of the

pathophysiological and pharmacological effects of these substances in order to diagnose the

complications that are originated form their use.

The purpose of the study is to show and educate the present and forthcoming

facts and evidence of the link between recreational drug use and their effects on the

cardiovascular system. The more that recreational drugs are used; therefore, recreational

drugs will be linked to cardiovascular complications and disease.


II. Methods

I carefully searched the MEDLINE, EMBASE, PROQUEST and EBSCOHOST

databases for all relevant articles, published until July 2011, using the following keywords:

‘marijuana’, ‘atrial fibrillation’, ‘arrhythmias’, ‘tachycardia’, ‘pcp’, ‘narcotic’, ‘inhalant’,

‘volatile substance’, ‘hallucinogen’, ‘palpitations’, 'recreational drug', 'cocaine', 'khat',

'MDMA', 'stimulants', 'barbiturates', 'illicit drug', 'myocardial infarction', ‘heart’ and

‘cardiovascular’. A manual search of reference lists from identified reports, to find

additional sources, was also performed. Finally, I identified all relevant articles dealing

with the cardiovascular effects and complications of recreational and illicit use.

III. Medical Effects

The majority of cardiovascular complications from drug use are from their

sympathetic nervous system activation (Ghuran, A., Nolan, J., 2000). Sympathetic nervous

system activation can cause vasoconstriction, tachycardia, arrhythmias and erratic and

unpredictable blood pressure changes (Ghuran et al., 2000). Due to spiking catecholamine

levels and sympathetic nervous system activation hypertension is very common, but

hypotension is also possible (Delvin, R., Henry, J., 2008). Amphetamines are primarily

responsible for myocardial infarction and ischemia, which is a result of increased oxygen

requirement, thrombus formation and platelet aggregation from elevated catecholamine

concentrations.

Recreational and illicit drugs interact with various central nervous system

neurotransmitters. A general understand of these neurotransmitters is required to

understand how each drug effects the body and can have an effect on the cardiovascular

system. The primary neurotransmitters are GABA, Glycine, Glutamate, Aspartate,


Acetylcholine, Catecholamines (Dopamine, Norepinephrine and Epinephrine) Serotonin,

Histamine, Vasopressin, Oxytocin, Tachykinins, CCK, NPY, Neurotensin, Opiod peptides,

Somatostatin and Purines (Goodman, L., Brunton, L., Chabner, B., Knollmann, B., 2008).

GABA (γ-‐amino butyric acid) is the primary and major neurotransmitter

with an inhibitory effect in the central nervous system (Goodman et al., 2008). GABA

facilitates inhibitory actions of interneurons in the brain and presynaptic inhibition

within the spinal cord (Goodman et al., 2008). GABA receptors are divided into 3

types, A, B and C. GABAA being the most important to this study as it is the most

prominent subtype (Goodman et al., 2008). GABAA is a ligand gated Cl-‐ ion channel,

which is an inotropic receptor that opens after release of GABA by presynaptic neurons

(Goodman et al., 2008). GABAA is the binding site of neuroactive drugs such as

barbiturates, benzodiazepines, ethanol (alcohol), volatile anesthetics and anesthetic steroids

(Goodman et al., 2008).

Catecholamines are fight or flight hormones that are released by the adrenal

glands (Goodman et al., 2008). There are three different hormones released by the adrenal

glands (Goodman et al., 2008). Norepinephrine, sometimes called Noradrenaline,

Epinephrine, also known as adrenaline, and dopamine all have strong links to stimulant use

and have great effect on the cardiovascular system (Goodman et al., 2008).

Dopamine is the most predominant catecholamine hormone constituting for

over half its content. Within the CNS Dopamine plays a large part in the limbic zones of

the cerebral cortex, which is responsible for controlling the autonomic nervous system and

gives the high associated with many recreational drugs (Goodman et al., 2008). Dopamine


receptors have been linked to the pathophysiology of schizophrenia and Parkinson’s

disease (Goodman et al., 2008).

Norepinephrine is mostly located in the hypothalamus and in specific zones of

the limbic system, which include the central nucleus of the amygdala and dentate gyrus of

the hippocampus. Norepinephrine has three different androgenic receptors (α1, α2 and β)

characterized by their pharmacologic properties and distribution (Goodman et al., 2008). β

adrenergic receptors are coupled to stimulation of adenylyl cyclase activity. α1 is primarily

associated with neurons, where α2 are more characterized with vascular and glial elements

and functions (Goodman et al., 2008).

Epinephrine is found in the medullary reticular formation. Epinephrine makes

connections on a restricted level to a few pontine and diencephalic nuclei. The

physiological properties have yet to be identified for epinephrine.

Serotonin (5-Hydroxytryptamine, 5-HT, 3-[β-aminoethyl]-5-hydroxyindole) is

found in enterochromaffin cells in the gastrointestinal (GI) tract, broadly throughout the

central nervous system and in storage granules in platelets (Goodman et al., 2008).

Serotonin, or 5-HT, is synthesized from tryptophan by a two-step process, which is then

actively transported to the brain (Goodman et al., 2008). Serotonin’s cardiovascular system

response is blood vessel contraction (Goodman et al., 2008). The blood vessel contraction

is primarily in the pulmonary, renal, splanchnic and cerebral vasculatures (Goodman et al.,

2008). Serotonin in increased levels can cause notable bradycardia and hypotension

(Goodman et al., 2008).


Gilman Manual of Pharmacology and Therapeutics (2008) (p. 193)

Aggregation triggers the release of 5-HT stored in platelets. Local actions of 5-HT include

feedback actions on platelets (shape change and accelerated aggregation) mediated by 5-HT2A

receptors, stimulation of Nitric Oxide production mediated by 5-HT1-like receptors on vascular

endothelium, and contraction of vascular smooth muscle mediated by 5-HT2A receptors. These

influences act in concert with many other mediators (not shown) to promote thrombus formation

and hemostasis (Goodman et al., 2008).

IV. Recreational and Illicit Drugs

The majority of recreational and illicit drugs have an effect on the

cardiovascular system (Ghuran et al., 2000). Sedatives (Benzodiazepines, benzodiazepine

agonists, barbiturates, alcohol, gammahydroxybutyrate, GBL, 1,4-butandiol), Stimulants

(Amphetamines and cocaine), Narcotics (Full opiod agonists, partial, selective or mixed

opiod agonists), Cannabis (delta-4-tetrahydrocannabinol and cannabidiol), Psychedelics

(Phenethylamines, tryptamine and ergolines), Dissociative anesthetics (Phencyclidine

(PCP), dextromethorphan and ketamine), Inhalants (Diethyl ether (starter fluid),

chloroform, toluene, gasoline, glue, paint, xenon, cyclopropane, Freon, halothane,


sevoflurane, nitrous oxide, nitrites, isoamyl nitrite, isobutyl nitrite and Other (Salvinorin A

(salvia divinorum), muscimol, nicotine, caffeine, methaqualone, khat, thalidomide,

meprobamate, carisoprodol, glutethimide, chloral hydrate, ethchlorvynol, methyprylon and

primidone) substances have direct (primary) and indirect (secondary) adverse effects on the

cardiovascular system (Fallows, Z., 2009).

i. Sedatives

Sedative abuse is

very common among

recreational drug users.

Medically, sedatives are

normally prescribed and

used to treat anxiety,

insomnia, muscle tension,

drug and alcohol withdraw,

seizures and sometimes

hypertension (high blood

pressure) (Goodman et al.,

2008). Sedatives, such as

benzodiazepines and

barbiturates, act at benzodiazepine receptors that are located closely to ϒ-aminobutyric

acid (GABA1) receptors (Goodman et al., 2008). When benzodiazepines bind to the

1 GABA receptors (GABAA, GABAB and GABAC) are located on chloride ion channels at the inhibitory synapses within the central nervous system (CNS), which includes the reticular activating system (RAS).

Ashton, H., from http://www.benzo.org.uk/manual/bzcha01.htm


receptors and the chloride channels open the chloride ions flow inward causing the

neuronal membrane to hyperpolarize (Goodman et al., 2008). This causes a reduction

in anxiety and wakefulness because benzodiazepines enhance the effects of GABA at

their receptors (Goodman et al., 2008). Benzodiazepines primarily target the CNS and

only have two effects that act on the peripheral nervous system (PNS) (Goodman et

al., 2008). Coronary vasodilation, causing hypotension, observed after intravenous use

and blockade of neuromuscular receptors, only seen in very high doses, are the only

two PNS actions known of benzodiazepines (Goodman et al., 2008).

Benzodiazepine, along with other narcotic analgesic and sedative,

intoxication and withdraw can cause hypotension and bradycardia (Goodman et al.,

2008). Adverse cardiovascular effects due to histamine release from mast cell

degranulation can also induce cardiac arrhythmias including premature ventricular and

atrial ectopic activity, idioventricular rhythms, atrial fibrillation and ventricular

tachyarrhythmias (Ghuran, A., Nolan, J., 2000). Many of the sedatives are commonly

taken intravenously which is known to cause cardiac complications such as bacterial

endocarditis, which is sometimes associated with pulmonary abscesses (Goodman et

al., 2008).

Barbiturates, derivatives of 2,4,6-trioxohexahydropyrimidine, reversibly

reduce the activity of all excitable tissues (Goodman et al., 2008). The action of

barbiturates takes place by decreasing nerve impulses traveling to the cerebral cortex

by potentiating gamma-aminobutyric acid (Lisanti, P., 1998). The mechanisms in

which barbiturates act on GABAA receptors are markedly distinct from GABA or

benzodiazepines (Goodman et al., 2008). Barbiturates promote with the binding of


benzodiazepines to GABAA receptors and potentiate GABA induced chloride by

lengthening periods where bursts of channel opening occur instead of making bursts

more frequent as of benzodiazepines (Goodman et al., 2008). Also, α and β subunits

of the channel are required for barbiturate action unlike benzodiazepines (Goodman et

al., 2008). Because of these actions, barbiturates produce depression of the CNS

varying from mild sedation to anesthesia clinically (Goodman et al., 2008).

Barbiturates normally cause bradycardia and hypotension due to their

depression of the CNS (Goodman et al., 2008). In cases of barbiturate abuse and

intoxication, mixed with alcohol, and overdose have caused cardiovascular collapse

from extreme CNS depression (Goodman et al., 2008). Intravenous use of barbiturates

has an increased incidence of ventricular arrhythmias, particularly, but not required,

when epinephrine and halothane2 are present (Goodman et al., 2008). Serious and

sometimes-extreme deficits in cardiovascular functions occur after acute barbiturate

intoxication, which is why barbiturates have mostly been replaced by somewhat safer

benzodiazepines (Goodman et al., 2008).

ii. Stimulants

Stimulant use is among the top of the list in recreational and illicit drug users.

Most stimulants commonly abused have analogous adverse effects on the

cardiovascular system (Ghuran et al., 2000). The majority of adverse effects of

stimulants are related to sympathetic nervous system activation (Ghuran et al., 2000).

Cocaine inhibits reuptake of norepinephrine and dopamine at sympathetic nervous

2 Volatile liquid anaesthetic that has growing levels of abuse as many barbiturates and benzodiazepines are increasing more difficult to obtain due to tighter drug control regulations.


system terminals as well as stimulating release of norepinephrine from the adrenal

medulla oblongata (Goodman et al., 2008). Amphetamines, including

methylenedioxymethamphetamine (MDMA), cause indirect activation of the

sympathetic nervous system by releasing dopamine, norepinephrine and serotonin from

central and autonomic nervous system (ANS) terminals (Goodman et al., 2008). The

toxicity of amphetamines is exemplified when administered with alcohol (Ghuran et al.,

2000). The sympathetic activation by both cocaine and amphetamines causes

vasoconstriction, tachycardia, hypertension, hypotension and cardiac arrhythmias

(Ghuran et al., 2000). Cocaine is also commonly known for causing myocardial

infarction (Aslibekyan, S., Levitan, E., Mittleman, M., 2008).

Cocaine can raise catecholamine levels as high as five times their normal

level (Ghuran et al., 2000). At extremely high doses, cocaine impairs myocyte

electrical activity as well as blocking fast sodium and potassium channels and

inhibiting the entry of calcium into myocytes (Goodman et al., 2008). The serum half-

life of cocaine is relatively short, being approximately 30-80 minutes (Goodman et al.,

2008). Ninety percent of cocaine is metabolized and excreted in urine within two

weeks (Goodman et al., 2008). The period of excretion provides a means of diagnosing

recent ingestion in the hospital environment (Goodman et al., 2008). When cocaine is

consumed alongside alcohol, a metabolite is formed called cocaethylene (Goodman et

al., 2008). Cocaethylene is an extremely cardiotoxic metabolite that is much more

toxic than its parent, cocaine (Goodman et al., 2008). A study also revealed that

marijuana use with cocaine increases plasma cocaine levels and concentrations of the

drug (Goodman et al., 2008).


Amphetamine and MDMA both produce indirect sympathetic activation by

releasing norepinephrine, serotonin and dopamine from CNS and ANS terminals

(Ghuran et al., 2000). Compared to cocaine, amphetamine inhibits monoamine oxidase

and does not contain a local anaesthetic effect (Goodman et al., 2008). Alcohol

potentiates amphetamine when taken concurrently with each other (Goodman et al.,

2008). Ecstasy and amphetamine plasma half-life are similar, as ecstasy is a derivative

of amphetamine (Goodman et al., 2008).

iii. Narcotics (Opioid Analgesics)

Opiod is a term that refers to all compounds that have a relation to opium,

which is a derivative of the poppy (Goodman et al., 2008). The drugs that are derived

from opium are opiates that include morphine, thebaine, codeine and a large amount of

semi- and synthetic derivatives (Goodman et al., 2008). Opiates work by mimicking

endogenous opiod peptides, also known as endorphins that are the naturally occurring

ligands for opiod receptors (Goodman et al., 2008). Opiod receptors, or endogenous

opiod receptors, have the known sensory role, which is inhibiting painful response from

painful stimuli (Goodman et al., 2008).

Opioids primarily act through three different receptor types. The three

receptor types are the µ, δ and κ, which have been studied thoroughly (Goodman et al.,

2008). Similar to morphine, the majority of clinical used opioids select µ receptors

(Goodman et al., 2008). High doses possibly change the pharmacological profile of the

opioid taken and become especially true when doses are increased to overcome

tolerance, which is very common with recreational opioid use (Goodman et al., 2008).


Tolerance occurs when a decrease in effectiveness of a drug due to repeated

administration (Goodman et al., 2008).

Clinically used opiates exert themselves through the µ receptors affecting

numerous systems (Goodman et al., 2008). The effects most commonly seen are

alterations of respiratory, gastrointestinal, neuroendocrine and cardiovascular system

function (Goodman et al., 2008). Morphine-like opioids produce many CNS effects as

well (Goodman et al., 2008). The effects most likely encountered are drowsiness,

analgesia, mental clouding and mood changes (Goodman et al., 2008). In addition to

these effects, euphoria is commonly reported which is one of the factors that make

opioids a commonly abused recreational and illicit drug (Goodman et al., 2008). As

doses increase the effects of the drugs increase including respiratory and cardiovascular

depression (Goodman et al., 2008).

The specific cardiovascular effects of opioids vary according to the dose

taken. When a patient or user is supine, the majority of cardiovascular effects of

opioids are negligible (Rea, R., Thames, M., 1993). Orthostatic hypotension and

fainting generally occur when a supine patient assumes the upright position (Rea et al.,

1993). Much of these effects are provoked by the concurrent release of histamine when

taking opioids (Rea et al., 1993).

Goodman & Gilman’s Manual of Pharmacology and Therapeutics (2008) shows that:

Effects on the myocardium are not significant in normal individuals. In patients

with coronary artery disease but no acute medical problems, 8–15 mg morphine

administered intravenously produces a decrease in oxygen consumption, left

ventricular end-diastolic pressure, and cardiac work; effects on cardiac index


usually are slight. In patients with acute myocardial infarction, the

cardiovascular responses to morphine may be more variable than in normal

subjects, and hypotension may be more pronounced.

Morphine may exert its well-known therapeutic effect in the treatment of

angina pectoris and acute myocardial infarction by decreasing preload, inotropy,

and chronotropy, thus favorably altering determinants of myocardial O2

consumption and helping to relieve ischemia. Morphine can mimic the

phenomenon of ischemic preconditioning, where a short ischemic episode

paradoxically protects the heart against further ischemia. This effect appears to

be mediated by d receptor modulation of a mitochondrial ATP-sensitive K+

channel in cardiac myocytes.

Morphine-like opioids should be used with caution in patients who have a

decreased blood volume because the drugs can aggravate hypovolemic shock.

Morphine should be used with great care in patients with cor pulmonale because

deaths after ordinary therapeutic doses have been reported. The concurrent use of

certain phenothiazines may increase the risk of morphine-induced hypotension.

(p. 355)

iv. Ethanol (Alcohol)

Ethanol is a sedative and CNS depressant but has a different structure and

action than the pharmacological sedatives listed earlier (Goodman et al., 2008).

Ethanol is the only legal, non-prescription recreational drug that is as widely accepted

and as much of a societal problem as it is. The disturbance between the inhibitory and

excitatory influences in the brain causing disinhibition, sedation and ataxia are some of


the adverse effects of ethanol (Goodman et al., 2008). Unlike most drugs, exceedingly

large amounts of ethanol are required to cause physiological effects (Goodman et al.,

2008).

Studies regarding the epidemiology of alcohol consumption show that 20-30

grams ethanol/day confers a cardioprotective effect (Goodman et al., 2008).

Paradoxically consumption of larger amounts of alcohol daily infer a much greater and

increased risk of cardiovascular failure including, cardiomyopathy, arrhythmias and

stroke (hemorrhagic) (Whicker, S., Sayer, G., Saltman, D., 2006). Large amounts of

alcohol use can cause hypertension by raising diastolic and systolic blood pressure

(Goodman et al., 2008). Ethanol causes numerous effects pharmacologically on cardiac

conduction, which includes sympathetic stimulation and ventricular repolarization

(Goodman et al., 2008). The ventricular repolarization is indicated by a prolonged QT

interval (Goodman et al., 2008).

Goodman & Gilman’s Manual of Pharmacology and Therapeutics (2008) shows that:

Atrial arrhythmias associated with chronic alcohol use include

supraventricular tachycardia, atrial fibrillation, and atrial flutter. Some

15–20% of idiopathic cases of atrial fibrillation may be induced by

chronic ethanol use. Ventricular tachycardia may be responsible for the

increased risk of unexplained sudden death that has been observed in

persons who are alcohol-dependent. During continued alcohol use,

treatment of these arrhythmias may be more resistant to cardioversion,

digoxin, or Ca2+-channel blocking agents. (p. 376)


Alcohol is known to cause cardiomyopathy by having a toxic dose-related

effect on cardiac and skeletal muscles (Goodman et al., 2008). Various studies show

the depression of cardiac contractility by alcohol, which leads to cardiomyopathy

(Goodman et al., 2008). Statistics show that half or more of patients with idiopathic

cardiomyopathy are alcohol dependent (Goodman et al., 2008). 40-50% of all patients

with cardiomyopathy that is ethanol/alcohol induced will die within 3-5 years as an

effect of their alcohol dependence (Goodman et al., 2008).

v. Cannabis and Khat

Cannabis, also known as Marijuana, is the 2nd most used drug in America

right behind ethanol (Health, United States, CDC, 2010). Δ-9-tetrahydrocannabinol

(THC) is the primary psychoactive chemical in cannabis. (Ghuran et al., 2000) THC is

only one of 61 cannabinoids and approximately 340 other chemical compounds in

cannabis not including the same carbon monoxide, tars, carcinogens and irritants found

in tobacco smoke (Hall, W., Solowij, N., 1998).

The action of THC is on at least two types of cannabinoid receptors, CB1 and

CB2. CB1 receptors are primarily present in the cognitive, memory, reward, anxiety,

pain, endocrine function, sensory perception and motor co-ordination regions of the

brain (Goodman et al., 2008). CB2 can be found in the spleen and other tissues and can

possibly but culprit for the immunosuppressive activities of cannabis (Goodman et al.,

2008). Outside of the psychoactive effects of cannabis it also has cardiovascular and

respiratory effects that can be notable (Hall, W., Solowij, N., 1998). The

cardiovascular effects of cannabis have a biphasic effect based off of dose taken

(Ghuran et al., 2000). Cannabis in acute doses is responsible for tachycardia and


vasodilation resulting in hypotension and increased core temperature (Ghuran et al.,

2000). The cardiac output due to the effects of cannabis has been noted to increase as

high as 30%, which is normally accompanied by and increased cardiac work and O2

demand (Goodman et al., 2008). At higher doses the actions of cannabis reverse

commonly causing bradycardia and hypotension (Caldicott, D., Holmes, J., Roberts-

Thompson, K., Mahar, L., 2005). Along with these higher dose effects there have been

ECG abnormalities affecting the P & T waves as well as the ST segment (Goodman et

al., 2008). The onset of the physiological effects of cannabis is seen very shortly after

absorption (Hall, W., Solowij, N., 1998). The plasma half-life of cannabis is between

20-30 hours (Goodman et al., 2008).

Catha edulis, also known more commonly as khat, is one of the more

common and popular drugs in the Arabian Peninsula and horn of Africa (Al-Motarreb,

A., Al-Kebsi, M., Al-Adhi, B., Broadley, K., 2002). It is estimated that there are

between 5-10 million khat users in the world (Al-Motarreb et al., 2002). Khat has

various pharmacologically active constituents but S-(-)-Cathinone [S-(-)-α-

aminopropiophenone] is the most significant (Widler, P., Mathys, K., Brenneisen, R.,

Kalix, P., Fisch, H., 1994). Cathinone is an alkaloid that is closely related to

amphetamines, which raises concern for cardiovascular complications (Wilder et al.,

1994). Much of these complications are caused by marked hypertension due to

cathinone metabolizing into norephedrine and norpseudoephedrine (Apps, A., Matloob,

S., Dahdal, M., Dubrey, S., 2011). There have been reported cases of khat use linked

with myocardial infarction and ischemia (Al-Motarreb et al., 2002).

vi. Psychedelics


Lysergic acid diethylamide (LSD) and psilocybin (Shrooms) are the primary

recreationally used psychedelics (Ghuran et al., 2000). Both LSD and psilocybin

chemically resemble serotonin so their actions are similar (Ghuran et al., 2000). LSD is

an ergot alkaloid that is a nonselective 5-HT agonist (Goodman et al., 2008). LSD

primarily acts through the 5-HT2 receptors inhibiting the firing of raphe neurons (5-HT)

(Goodman et al., 2008). The cardiovascular effects of LSD can include increased pulse

and hypertension (Ghuran et al., 2000). Serotonin abnormalities may result in atypical

clotting and reduced clot retraction (Goodman et al., 2008). Although rare, myocardial

infarction and supraventricular tachyarrhythmias have occurred as a result of LSD use

(Ghuran et al., 2000).

vii. Dissociative anesthetics

Phencyclidine (PCP) and Ketamine and are the primary dissociate anesthetics

abused (Goodman et al., 2008). Ketamine clinically is used for conscious sedation and

anesthesia and has some very unique properties (Goodman et al., 2008). Ketamine is in

the same drug class as phencyclidine (PCP) and is water-soluble (Goodman et al.,

2008). Administration and induction of ketamine normally causes hypertension,

tachycardia and an increase in cardiac output (Goodman et al., 2008). These

cardiovascular effects are most likely due to the inhibition of central and peripheral

catecholamine reuptake making this an indirect effect (Goodman et al., 2008).

Ketamine does have direct adverse cardiovascular effects including inotropic and

vasodilation activity (Goodman et al., 2008). Ketamine also increases myocardial O2

consumption that can cause severe cardiac complications in users with myocardial

ischemia (Goodman et al., 2008).


viii. Inhalants or Volatile Substances

Recreationally used inhaled substances are common among adolescents and

non-selective drug seekers (Ghuran et al., 2000). These volatile substances are

normally cheap, legal and can easily be obtained which make this very concerning and

hard to control (Ghuran et al., 2000). Varied and extremely detrimental cardiovascular

effects can occur from inhalant use, including sudden death (Ghuran et al., 2000).

Tachyarrhythmias from sympathetic nervous system activation are a common

occurrence from volatile substance use (Ghuran et al., 2000). Myocardial sensitivity to

circulating catecholamines may also cause lethal tachyarrhythmias (Ghuran et al.,

2000). Some of the notable cardiovascular complications from volatile substances

include bradyarrhythmias, supraventricular arrhythmias, ventricular arrhythmias,

hypotension, cardiac ischemia and cardiomyopathy (Ghuran et al., 2000).

ix. Synthetics and Analogues

Spice, K2 and bath salts are among the top of the list of the most popular

“legal” drugs available on the street (“HDAP,” 2011; “Office of,” 2011). Spice and K2

are synthetic cannabinoids, which belong in the same drug class as cannabis (“HDAP,”

2011). Bath Salts are a stimulant being sold as a legal cocaine and ecstasy substitute

that contains Methylenedioxypyrovalerone (MPDV), which is also known as

mephedrone (Wehman, J., 2011; O’Malley, P., 2011). MPDV has no known clinical

medical value therefore information is extremely limited on it’s pharmacodynamic,

pharmokinetic and pharmacological properties (O’Malley, P., 2011).

Spice being like cannabis has many similar effects. One frightening

difference between spice and cannabis is that the potency has been found to be upwards


of 5 times more potent than the strongest marijuana (“HDAP,” 2011). The effects of

the synthetic cannabinoids have not been fully tested yet but many adverse effects have

been seen. Spice has been associated with adverse effects such as heart palpitations,

respiratory complications, paranoia and aggression (“HDAP,” 2011).

V. Statistics

Drug use and abuse is growing in massive proportions from year to year and is causing

an overwhelming and increasing workload on emergency rooms and prehospital providers

around the globe. The Drug Abuse Warning Network (DAWN) monitors drug-related

emergency room/department visits and deaths as a public health surveillance system in order to

track the impact of drug use in the United States. Each year data is compiled from hospitals

across the country about drug-related emergency department visits and death and made available

to the public.

According to the National Survey on Drug Use and Health (NSDUH), approximately

21.8 million Americans, ages 12 or older, in 2009 consumed illicit drugs (“Health, United

1,619,054 1,616,311 1,742,887 1,883,272 1,999,861 2,070,439

0

500,000

1,000,000

1,500,000

2,000,000

2,500,000

Annual Estimated Visits

Total ED Visits

DAWN Drug Related ED Visits

Estimates 2004 Estimates 2005 Estimates 2006

Estimates 2007 Estimates 2008 Estimates 2009

CARDIOVASCULAR EFFECTS OF DRUG 21 States,” 2010.) Of the 21.8 million illicit drug users, approximately 5.1 million in total used

drugs other than marijuana (“Health, United States,” 2010). Between 2004 and 2009 there have

been a staggering 10,931,824 drug-related ED visits (DAWN, 2009). Not all of these drug-

related have cardiovascular complications associated with them. Of these 10.9 million visits 3.7

million can alone be contributed to alcohol consumption, which is commonly in combination

with other recreational drugs (DAWN, 2009). Statistics show that 1 in 4 myocardial infarctions

(MI), also known as heart attacks, in people between the ages of 18 and 45 can be linked to

cocaine use (Qureshi, A., Suri, F., Guterman, L., & Hopkins, N., 2001). A total of 2.966,511

visits can be attributed to cocaine use that means nearly 741,627 of those cocaine related visits

had a non-fatal myocardial infarction (DAWN, 2009). Dependence of the various recreational

and illicit drugs is a contributing factor to cardiovascular complications (DAWN, 2009).

Goodman and Gilman’s 2008

VI. Conclusion


Recreational and illicit drug use across the board has some varying effect on the

cardiovascular system. More information and studies are required to find definitive links to

some drugs and their cardiovascular effects, such as marijuana, but evidence does exist that even

the drugs viewed as harmless are far from it. Every year there is an increasing number of pre-

hospital and emergency room cases showing and linking cardiovascular complications to drug

use. Cardiovascular effects are not the only concern of recreational and illicit drugs but ranks

high on the list.


References

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