Functions of the

Cardiovascular System
Delivers vital oxygen and nutrients to cells
Removes waste products
Transports hormones
 Branches of the
Cardiovascular System
Systemic
Carries blood throughout the body to meet the
bodys needs and removes waste products
Includes arteries, veins, and capillaries
Works with the lymphatic system
Pulmonary
Carries blood to and from the lungs for gas
exchange
 Heart
Pericardium
Surrounds the heart to provide protection and support
Myocardium
Cardiac muscle
Endocardium
Inner structures, including the valves
Four chambers
Two atria: receiving chambers
Two ventricles: pumping chambers
Ventricular walls (esp. left ventricle)thicker than atrial walls
 Blood Flow Through the Heart
(1 of 2)

Deoxygenated blood from the systemic circulation

enters from the superior vena cava and the inferior
vena cava.
Blood empties directly into the right atrium.
From the right atrium, blood travels through the
tricuspid valve to the right ventricle.
The right ventricle pumps blood through the
pulmonic valve to the pulmonary arteries.
The pulmonary arteries carry blood to the lungs for
gas exchange.
 Blood Flow Through the Heart
(2 of 2)

Oxygenated blood from the pulmonary circulation

enters from the pulmonary veins.
Blood empties directly into the left atrium.
Blood leaves the left atrium through the mitral valve
to the left ventricle.
The left ventricle then pumps blood through the aortic
valve to the aorta.
From the aorta, the blood is carried the rest of the
body.
 Conduction System
Organizes electrical impulses in the cardiac
cells
Controls
Excitability: ability of the cells to respond to
electrical impulses
Conductivity: ability of the cells to conduct
electrical impulses
Automaticity: ability to generate an impulse to
contract with no external nerve stimulus
 Conduction Pathway
(1 of 2)

Impulses originate in the sinoatrial (SA) node high

in the right atrium at a rate of 60100 bpm.
Impulses travel through the right and left atria,
causing atrial contraction.
Impulses then travel to the atrioventricular (AV)
node, in the right atrium adjacent to the septum.
The AV node can initiate impulses if the SA node fails
(rate: 4060 bpm).
 Conduction Pathway
(2 of 2)

Impulses are delayed in the AV node to allow

for complete ventricular filling.
Impulses then move rapidly through the
bundle of His, right and left bundle
branches, and Purkinje network of fibers,
causing ventricular contraction.
The ventricles can initiate impulses if the SA and
AV nodes fail (rate: 2040 bpm, which may be
inadequate).
 Electrical Activity
(1 of 2)

Depolarization
Increase in electrical charge
Accomplished through cellular ion exchange
Generates cardiac contraction
Repolarization
Cellular recovery
Ions returning to the cell membrane in
preparation for depolarization
 Electrical Activity
(2 of 2)

Can be read by an electrocardiogram

P wave: atrial depolarization
QRS complex: ventricular depolarization
T wave: ventricular repolarization
Sinus rhythm
Electrical activity when impulses originate in the SA node
Dysrhythmias
Abnormal electrical activity
Can result from issues such as myocardial infarctions and
electrolyte imbalances
 Conduction Control
Electrolyte signals
Sodium, potassium, and calcium
Medulla monitoring
Autonomic nervous system, endocrine system,
chemoreceptors, and baroreceptors
Effects
Chronotropic: rate of contraction
Dromotropic: rate of electrical conduction
Inotropic: strength of contraction
 Blood Pressure
Force that blood exerts on the walls of blood vessels
Reflects how hard the heart is working
Represented as a fraction
Systolic: top number; cardiac work phase
Diastolic: bottom number; cardiac rest phase
Normal BP according to AHA: 120/80 mmHg
Pulse pressure (~40)difference between the two
numbers
Reflects force of each contraction
 Influences on Blood Pressure
(1 of 2)

BP = CO PVR
Cardiac output (CO)
CO = SV HR
Stroke volume (SV)
Heart rate (HR)
Peripheral vascular resistance (PVR)
Sympathetic nervous system
Parasympathetic nervous system
Arterial elasticity
 Influences on Blood Pressure
(2 of 2)

Afterload: pressure needed to eject the blood

Blood viscosity
PVR
Preload: amount of blood returning
Blood volume
Venous return
Hormones
Antidiuretic hormone
Reninangiotensinaldosterone system
 Blood Vessels
(1 of 2)

Arteries: carry oxygenated blood away from

the heart
Veins: carry deoxygenated blood back to the
heart
Capillaries: site of exchange
 Blood Vessels
(2 of 2)

Three layers
Tunica intima: inner layer
Tunica media: middle muscular layer
Tunica adventitia: outer elastic layer
Exception
Pulmonary artery: carries deoxygenated blood
away from the heart
Pulmonary vein: carries oxygenated blood to the
heart
 Lymphatic System
Works to return excess interstitial fluid
(lymph) to the circulation
Plays a role in immunity
Includes lymph nodes, the spleen, the thymus,
and the tonsils
 Understanding Cardiovascular
Conditions
Alterations resulting in decreased cardiac output:
pericarditis, infective endocarditis, myocarditis,
valvular disorders, cardiomyopathy, electrical
alterations, heart failure, and congenital heart defects
Alterations resulting in altered tissue perfusion:
aneurysm, dyslipidemia, atherosclerosis, peripheral
vascular disease, coronary artery disease, thrombi and
emboli, varicose veins, lymphedema, and myocardial
infarction
Alterations resulting in both: hypertension and shock
 Pericarditis
(1 of 5)

Inflammation of the pericardium

Triggered by viral infection, thoracic trauma,
myocardial infarction, tuberculosis,
malignancy, and autoimmune conditions
Fluid accumulates in the space between
pericardial sac and heartpericardial effusion
Swollen tissue creates friction
 Pericarditis
(2 of 5)

Cardiac tamponade
Cardiac compression from excessive fluid
accumulation
Life-threatening
Manifestations: falling arterial pressures, rising
venous pressures, narrowing pulse pressure, and
muffled heart sounds
Complications: heart failure, shock, and death
 Pericarditis
(3 of 5)

Constrictive pericarditis
Loss of elasticity (i.e., thick and fibrous
pericardium)
Results from chronic inflammation
 Pericarditis
(4 of 5)

Manifestations:
Pericardial friction rub (grating sound heard when breath
is held)
Sharp, sudden, severe chest pain that increases with deep
inspiration and decreases when sitting up and leaning
forward
Dyspnea
Tachycardia
Palpitations
Edema
Flulike symptoms
 Pericarditis
(5 of 5)

Diagnosis: history, physical examination,

complete blood count, electrocardiogram,
chest X-ray, echocardiogram, computed
tomography, and magnetic resonance imaging
Treatment: identify and resolve the underlying
cause, nonsteroidal anti-inflammatory drugs,
glucocorticoid agents, analgesics, bed rest,
oxygen therapy, pericardiocentesis, and
pericardectomy
 Infective Endocarditis
(1 of 3)

Formally called bacterial endocarditis.

Infection of endocardium and heart valves.
Commonly caused by Streptococcus and
Staphylococcus infections.
Vegetation forms on internal structures and creates
small thrombi.
Thrombi can travel to other locationsembolism.
Embolism can create life-threatening complications
like myocardial infarction, stroke, and pulmonary
embolism.
 Infective Endocarditis
(2 of 3)

Microemboli occur as they are dislodged,

resulting in microhemorrhages.
Risk factors: intravenous drug use, valvular
disorders, prosthetic heart valves, implanted
cardiac devices, rheumatic heart disease,
coarctation of the aorta, congenital heart
defects, and Marfan syndrome.
 Infective Endocarditis
(3 of 3)

Manifestations: flulike symptoms, embolization, heart

murmur, petechiae, splinter hemorrhages under the nails,
hematuria, Oslers nodes, and edema.
Diagnosis: history, physical examination, blood cultures,
complete blood count, urinalysis, serum rheumatoid factor,
erythrocyte sedimentation rate, electrocardiogram, and
echocardiogram.
Treatment: identification of causative agent, long-term agent-
specific therapy, bed rest, oxygen therapy, antipyretics,
surgical valve repair, and prosthetic valve replacement.
If untreated, infective endocarditis is usually fatal.
 Myocarditis
(1 of 3)

Inflammation of the myocardium.

Uncommon; poorly understood.
Organisms, blood cells, toxins, and immune
substances invade and damage the muscle.
Complications: heart failure, cardiomyopathy,
dysrhythmias, and thrombus formation.
 Myocarditis
(2 of 3)

Manifestations
Patient may be asymptomatic.
Symptoms, when present, include flulike
symptoms, dyspnea, dysrhythmias, palpitations,
tachycardia, heart murmurs, chest discomfort,
cardiac enlargement, pale and cool extremities,
syncope, decreased urine output, and joint pain
and swelling.
 Myocarditis
(3 of 3)

Diagnosis: history, physical examination, blood

cultures, electrocardiogram, cardiac enzymes,
complete blood counts, erythrocyte sedimentation
rate, chest X-rays, echocardiogram, and myocardium
biopsy
Treatment: identify and resolve the underlying cause,
antipyretics, anticoagulants, antidysrhythmics,
diuretics, immunosuppressants, bed rest, activity
restriction, and fluid limitation
 Valvular Disorders
(1 of 3)

Disrupt blood flow through the heart

Stenosis: narrowing
Less blood can flow through the valve.
Causes decreased cardiac output, increased
cardiac workload, and hypertrophy.
Regurgitation: insufficient closure
Blood flows in both directions through the valve.
Causes decreased cardiac output, increased
cardiac workload, hypertrophy, and dilation.
 Valvular Disorders
(2 of 3)

Causes: congenital defects, infective

endocarditis, rheumatic fever, myocardial
infarction, cardiomyopathy, and heart failure
Manifestations:
Vary depending on valve involved
Reflect alteration in blood flow through the heart
 Valvular Disorders
(3 of 3)

Diagnosis: history, physical examination, heart

catheterization, chest X-rays, echocardiogram,
electrocardiogram, and magnetic resonance imaging
Treatment: diuretics, antidysrhythmics, vasodilators,
angiotension-converting enzyme inhibitors, beta-
adrenergic blockers, anticoagulants, oxygen therapy,
low-sodium diet, surgical valve repair, and prosthetic
valve replacement
 Cardiomyopathy
Conditions that weaken and enlarge the
myocardium
Can be acquired or inherited
Classified into three groups: dilated,
hypertrophic, and restrictive
 Dilated Cardiomyopathy
(1 of 3)

Most common type.

Cardiomegaly and ventricular dilation damage myocardium
muscle fibers, resulting in decreased cardiac output and blood
stagnation.
Risk higher with advancing age and in African American men.
Causes: chemotherapy, alcoholism, cocaine abuse, pregnancy,
infections, thyrotoxicosis, diabetes mellitus, neuromuscular
diseases, hypertension, coronary artery disease, and
hypersensitivity to medications
 Dilated Cardiomyopathy
(2 of 3)

Manifestations:
Appear as compensatory mechanisms fail
Include: dyspnea, fatigue, nonproductive cough,
orthopnea, paroxysmal nocturnal dyspnea,
dysrhythmias, angina, dizziness, activity
intolerance, blood pressure changes, tachycardia,
murmurs, abnormal lung sounds, tachypnea,
peripheral edema, ascites, weak pedal pulses, cool
and pale extremities, poor capillary refill,
hepatomegaly, and jugular vein distension
 Dilated Cardiomyopathy
(3 of 3)

Diagnosis: echocardiogram, electrocardiogram, chest

X-ray, heart catheterization, and nuclear studies
Treatment: angiotension-converting enzyme
inhibitors, diuretics, digoxin (Lanoxin), beta-
adrenergic blockers, antidysrhythmics, implantable
cardiac defibrillator, cardioversion, pacemaker,
valvular repair, heart transplant, low-fat and low-
sodium diet, tobacco cessation, physical activity, and
abstinence from alcohol
 Hypertrophic Cardiomyopathy
(1 of 2)

Mainly affects systolic function.

More common in men and those who are
sedentary.
Risk higher with hypertension, obstructive
valvular disease, and thyroid disease.
May be autosomal dominant.
Ventricle wall becomes stiff and unable to
relax.
 Hypertrophic Cardiomyopathy
(2 of 2)

Manifestations: dyspnea on exertion, fatigue,

syncope, orthopnea, angina, activity intolerance,
dysrhythmias, left ventricular failure, and myocardial
infarction
Diagnosis: similar to that of dilated cardiomyopathy
Treatment: beta-adrenergic blockers, calcium channel
blockers, surgical removal of excess myocardium,
antidysrhythmics, and strenuous activity avoidance
 Restrictive Cardiomyopathy
(1 of 3)

Common in South and Central America, India,

Asia, and Africa
Caused by rigidity of ventricles, leading to
diastolic dysfunction
Causes: amyloidosis, hemochromatosis,
radiation exposure to the chest, connective
tissue diseases, myocardial infarction,
sarcoidosis, and cardiac neoplasms
 Restrictive Cardiomyopathy
(2 of 3)

Manifestations
Many cases are asymptomatic.
Symptoms, when present, include fatigue,
dyspnea, orthopnea, abnormal lung sounds,
angina, hepatomegaly, jugular vein distension,
ascites, murmurs, peripheral cyanosis, and pallor.
 Restrictive Cardiomyopathy
(3 of 3)

Diagnosis: similar to that of dilated

cardiomyopathy
Treatment
Treating the underlying cause, dysrhythmias, and
heart failure
May need a heart transplant
Prognosis
Generally poor, death due to heart failure
 Electrical Alterations
(1 of 2)

Dysrthymias classified by origin

Can affect cardiac output and blood pressure
Causes: acidbase imbalances, hypoxia,
congenital heart defects, connective tissue
disorders, degeneration of conductive tissues,
drug toxicity, electrolyte imbalances, stress,
myocardial hypertrophy, and myocardial
ischemia or infarction
 Electrical Alterations
(2 of 2)

Manifestations
Vary depending on the specific dysrhythmia
May include palpitations, fluttering sensation, skipped
beats, fatigue, confusion, syncope, dyspnea, and abnormal
heart rate
Diagnosis: history, physical examination,
electrocardiogram, and invasive electrophysiologic
studies
Treatment: antidysrhythmics, internal cardiac
defibrillator, pacemaker, cardioversion, defibrillation,
ablation, and avoiding triggers
 Heart Failure
(1 of 2)

Inadequate pumping
Leads to decreased cardiac output, increased
preload, and increased afterload
Causes of heart failure: congenital heart
defects, myocardial infarction, heart valve
disease, dysrhythmias, thyroid disease
 Heart Failure
(2 of 2)

Compensatory mechanisms activated.

Activation of the sympathetic nervous system
Activation of the reninangiotensinaldosterone
system
Ventricular hypertrophy
The compensatory mechanisms help at first,
but create a vicious cycle (perpetuate heart
failure).
 Types of Heart Failure
(1 of 2)

Systolic dysfunction
Decreased contractility
Diastolic dysfunction
Decreased filling
Mixed dysfunction
Both
 Types of Heart Failure
(2 of 2)
Left-sided failure
Cardiac output falls.
Blood backs up to the
pulmonary circulation.
Causes: left ventricular
infarction, hypertension, and
aortic and mitral valve
stenosis.
Manifestations: pulmonary
congestion, dyspnea, and
activity intolerance.
Right-sided failure
Blood backs up to the
peripheral circulation.
Causes: pulmonary disease,
left-sided failure, and
pulmonic and tricuspid
valve stenosis.
Manifestations: edema and
weight gain.
 Heart Failure
(1 of 2)

May be acute or chronic

Manifestations
Depend on type
Fluctuate in severity
Appear as compensatory mechanisms fail
Include indications of systemic and pulmonary
fluid congestion
Grading of severity: IIV
 Heart Failure
(2 of 2)

Diagnosis: history, physical examination, chest X-ray,

arterial blood gases, echocardiogram,
electrocardiogram, and brain natriuretic peptide
Treatment
Identify and manage underlying cause
Includes lifestyle modification, angiotensin-converting
enzyme inhibitors, diuretics, beta-adrenergic blockers,
calcium channel blockers, biventricular pacemaker, intra-
aortic balloon pump, and heart transplant
 Congenital Heart Defects
(1 of 3)

Structural issues present at birth

Most common type of birth defect
Examples:
Septal defect
Patent ductus arteriosus
Valve disorders
Dextro-transposition of great arteries
Tetralogy of Fallot
 Congenital Heart Defects
(2 of 3)

Risk factors: heredity, genetic disorders (Downs

syndrome), fetal exposure to tobacco and certain
medications, maternal health status (e.g., diabetes
mellitus, obesity).
Manifestations
Can be asymptomatic.
Symptoms, when present, include heart murmurs,
dyspnea, tachypnea, cyanosis, fatigue, chest pain or
discomfort, difficulty gaining weight.
Heart failure can develop due to increased cardiac
workload.
 Congenital Heart Defects
(3 of 3)

Diagnosis: history (including mothers

history), physical examination, fetal
ultrasound, echocardiogram, EKG, chest X-ray
Treatment: heart catheterization or surgery,
heart transplant, medications (diuretics,
antihypertensives, antidysrhythmics)
 Aneurysms
(1 of 4)

Weakening of an artery
Common in the abdominal aorta, thoracic aorta,
and cerebral, femoral, and popliteal arteries
Can rupture: exsanguination
Risk factors: congenital defect, atherosclerosis,
hypertension, dyslipidemia, diabetes mellitus,
tobacco use, advanced age, trauma, and
infection
 Aneurysms
(2 of 4)

True aneurysms: affect all three vessel layers

Saccular aneurysm: bulge on the side
Fusiform aneurysm: affects the entire
circumference
False aneurysms: do not affect all three layers
of the vessel
Dissecting aneurysms: occurs in the inner layers
 Aneurysms
(3 of 4)

Manifestations
Depend on location and size
May be asymptomatic
May include pulsating mass, pain, respiratory
difficulty, and neurologic decline
 Aneurysms
(4 of 4)

Diagnosis: physical examination, X-ray,

echocardiogram, computed tomography,
magnetic resonance imaging, and
arteriograph
Treatment: eliminating or managing cause and
surgery
 Dyslipidemia
(1 of 4)

High levels of lipids in the blood.

Increases risk for many chronic diseases.
Lipids come from dietary sources and are
produced by the liver.
Dietary sources
Cholesterol: animal products
Triglycerides: saturated fats
 Dyslipidemia
(2 of 4)

Classified based on density, which is based on

the amount of triglycerides (low density) and
protein (high density)
Very-low-density lipoproteins
Low-density lipoproteinsAKA bad
cholesterol
High-density lipoproteinsAKA good
cholesterol
 Dyslipidemia
(3 of 4)

LDL
Most serum cholesterol is LDL.
More invasive.
To decrease LDL level: lifestyle modification.
HDL
Helps remove cholesterol from bloodstream
To increase HDL level: lifestyle modification
 Dyslipidemia
(4 of 4)

Manifestations: asymptomatic until it develops

into other diseases
Diagnosis: cholesterol screening and lipid
panels
Treatment: dietary changes, weight reduction,
routine exercise, tobacco cessation, lipid-
lowering agents, and complication
management
 Atherosclerosis
(1 of 3)

Chronic inflammatory disease characterized by

thickening and hardening of the arterial wall.
Inflammatory process is triggered by a vessel
wall injury.
Lesions develop on the vessel wall and calcify
over time.
 Atherosclerosis
(2 of 3)

Leads to vessel obstruction, platelet

aggregation, and vasoconstriction
Complications: peripheral vascular disease,
coronary artery disease, thrombi, hypertension,
and stroke
Manifestations: asymptomatic until
complications develop
 Atherosclerosis
(3 of 3)

Diagnosis: identify contributing factors and

complications
Treatment: similar to dyslipidemia with the
addition of angioplasty, bypass, laser
procedures, and artherectomy
 Peripheral Vascular Disease
(1 of 2)

Narrowing of the peripheral vessels

Causes: atherosclerosis, thrombus, inflammation, and
vasospasms
Thromboangiitis obliterans: an inflammatory
condition of the arteries
Raynauds disease: vasospasms of arteries, usually in
the hands, because of sympathetic stimulation
Raynauds phenomenon: associated with an autoimmune
condition
 Peripheral Vascular Disease
(2 of 2)

Manifestations: pain, intermittent claudication, numbness,

burning, nonhealing wounds, skin color changes, hair loss, and
impotency
Diagnosis: history, physical examination, ankle/brachial index,
treadmill exercise test, angiography, ultrasound, and magnetic
resonance imaging
Treatment: reducing contributing factors, angioplasty, bypass
procedures, laser procedures, atherectomy, antiplatelet agents,
anticoagulants, thrombolytics, and lipid-lowering agents
 Coronary Artery Disease
(1 of 4)

Atherosclerotic changes of the coronary

arteries
Impairs myocardial tissue perfusion
Angina: chest pain resulting from myocardium
ischemia
Infarction: necrotic damage to the myocardium
Causes: atherosclerosis, vasospasms,
thrombus, and cardiomyopathy
 Coronary Artery Disease
(2 of 4)

Angina: intermittent chest pain resulting from

myocardium ischemia
Stable: goes away with demand reduction
Unstable: increased intensity or frequency, does
not go away with demand reduction, or occurs at
rest
Infarction: permanent necrotic damage to the
myocardium
 Coronary Artery Disease
(3 of 4)

Complications: myocardial infarction, heart

failure, dysrhythmias, and sudden death
Manifestations: angina, indigestion-like
sensation, nausea, vomiting, clammy
extremities, diaphoresis, and fatigue
 Coronary Artery Disease
(4 of 4)

Diagnosis: history, physical examination,

identify contributing factors, exercise stress
test, echocardiogram, and electrocardiogram
Treatment: similar to those used to treat
dyslipidemia and atherosclerosis with the
addition of nitrates, beta-adrenergic blockers,
calcium channel blockers, and oxygen
 Thrombus
(1 of 2)

Stationary blood clot consisting of platelets,

fibrin, erythrocytes, and leukocytes
Virchows triad: endothelial injury, sluggish
blood flow, and increased coagulopathy
Emboli: traveling body
May be a thrombus, air, fat, tissue, bacteria,
amniotic fluid, tumor cells, or foreign substances
Can become lodged in places like the lungs,
brain, and heart
 Thrombus
(2 of 2)

Manifestations: depend on location

Diagnosis: arteriography, ultrasound,
echocardiogram, and magnetic resonance imaging
Prevention: increasing mobility, hydration,
antiembolism hosiery, sequential compression
devices, antiplatelet agents, and anticoagulants
Treatment: thrombolytic agents and embolectomy
 Varicose Veins
(1 of 4)

Engorged veins resulting from valve incompetency.

Most common in the legs.
May also occur as esophageal varices and hemorrhoids.
Increased venous pressure and blood pooling lead to vein
enlargement and valve stretching.
Valves become incompetent, leading to reversal of blood flow
and increased distension.
Capillary pressure increases, which leads to fluid leak,
resulting in edema and skin discoloration.
 Varicose Veins
(2 of 4)

Can cause stasis pigmentation, subcutaneous

induration, dermatitis, and thrombophlebitis
Risk factors: genetic predisposition,
pregnancy, obesity, prolonged sitting or
standing, alcohol abuse and liver disorders
(esophageal varices), and constipation
(hemorrhoids)
 Varicose Veins
(3 of 4)

Manifestations:
Irregular, purplish, bulging veins
Pedal edema
Fatigue
Aching in the legs
Shiny, pigmented, hairless skin on the legs and
feet
Skin ulcer formation
 Varicose Veins
(4 of 4)

Diagnosis: physical examination, Doppler

ultrasound, and venogram
Treatment: rest with affected leg elevated,
compression stockings, avoid prolonged
periods of standing or sitting, exercise,
sclerotherapy, and surgical removal
 Lymphedema
(1 of 2)

Swelling due to a lymph obstruction

Primary lymphedema
Rare, usually congenital
Secondary lymphedema
Causes: surgery, radiation, cancer, infection, and
injury
Additional manifestations: hyperpigmentation,
ulcerations, and thickening of the skin
 Lymphedema
(2 of 2)

Diagnosis: physical examination, magnetic

resonance imaging, computed tomography,
Doppler ultrasound, and nuclear imaging
Treatment: sequential compression devices,
compression stockings, exercise, massage
therapy, antibiotics, benzopyrone agents,
diuretics, and surgery
 Myocardial Infarction
(1 of 3)

Death of the myocardium.

Coronary artery blood flow is blocked due to
atherosclerosis, thrombus, or vasospasms.
Risk factors are the same as for
atherosclerosis.
 Myocardial Infarction
(2 of 3)

Manifestations
Some are asymptomaticsilent MI.
Symptoms, when present, include angina, fatigue,
nausea, vomiting, shortness of breath,
diaphoresis, indigestion, elevation in cardiac
biomarkers, electrocardiogram changes,
dysrhythmias, anxiety, syncope, and dizziness.
Complications: heart failure, dysrhythmias,
cardiac shock, thrombosis, and death
 Myocardial Infarction
(3 of 3)

Diagnosis: history, physical examination,

electrocardiogram, cardiac biomarkers, stress
testing, nuclear imaging, and angiography
Treatment
Varies depending on timing of treatment.
Immediately: morphine, oxygen, nitrate, aspirin;
thrombolytics can also be administered.
Post-MI: similar to those for atherosclerosis.
 Hypertension
(1 of 7)

Prolonged elevation in blood pressure.

Excessive cardiac workload due to
vasoconstriction, which leads to increased
afterload.
Vasoconstriction decreases renal blood flow,
leading to inappropriate activation of the
reninangiotensinaldosterone system.
 Hypertension
(2 of 7)

Risk factors: advancing age, ethnicity, family

history, being overweight or obese, physical
inactivity, tobacco use, high-sodium diet, low-
potassium diet, high vitamin D intake,
excessive alcohol intake, and stress
 Hypertension
(3 of 7)

Primary hypertension
Most common form
Develops gradually over time
Secondary hypertension
Tends to be more sudden and severe
Causes: renal disease, adrenal gland tumors,
certain congenital heart defects, certain
medications, and illegal drugs
 Hypertension
(4 of 7)

Malignant hypertension
Especially intense form
Does not respond well to treatment
Hypertension can be classified into systolic or
diastolic based on which measure is elevated.
 Hypertension
(5 of 7)

Pregnancy-induced hypertension
Hypertension first seen in pregnancy
Indicators: high blood pressure, proteinuria, and edema
Risk factors: history of pregnancy-induced hypertension,
renal disease, diabetes mellitus, multiple fetuses, and
maternal age less than 20 years or greater than 40 years
Complications: seizures, miscarriages, poor fetal
development, and placental abruption
Treatment: bed rest and magnesium sulfate
 Hypertension
(6 of 7)

Manifestations
Silent killer
Symptoms, when present, include fatigue,
headache, malaise, and dizziness
Complications: atherosclerosis, aneurysms,
heart failure, stroke, hypertensive crisis, renal
damage, vision loss, metabolic syndrome, and
memory problems
 Hypertension
(7 of 7)

Diagnosis: history, physical examination,

multiple blood pressure readings at varying
times of the day, electrocardiogram, and
laboratory tests to determine the presence of
complications
Treatment:
Based on JNC8 standards.
Early detection and management are essential to
prevent complications.
 Shock
Decreased blood volume or circulatory
stagnation resulting in inadequate tissue and
organ perfusion
 Stages of Shock
Compensatory
Sympathetic nervous system and reninangiotensin
aldosterone system are activated.
Progressive
Compensatory mechanisms fail.
Tissues become hypoxic, cells switch to anaerobic
metabolism, lactic acid builds up, and metabolic acidosis
develops.
Irreversible
Organ damage occurs.
 Types of Shock
(1 of 2)

Distributive shock
Neurogenic shock
Loss of vascular sympathetic tone and autonomic
function lead to massive vasodilatation.
Septic shock
Bacterial endotoxins activate an immune reaction.
Anaphylactic shock
Excessive allergic reaction
 Types of Shock
(2 of 2)

Cardiogenic shock
Left ventricle cannot maintain adequate cardiac
output.
Hypovolemic shock
Venous return reduces because of external blood
volume losses.
 Shock
(1 of 2)

Manifestations
Vary depending on type
Include thirst, tachycardia, restlessness, irritability,
tachypnea progressing to Cheyne-Stokes respiration, cool
and pale skin, hypotension, cyanosis, and decreasing
urinary output
Complications: acute respiratory distress syndrome,
renal failure, disseminated intravascular coagulation,
cerebral hypoxia, and death
 Shock
(2 of 2)

Diagnosis: complete blood counts, cultures,

coagulation studies, cardiac biomarkers,
arterial blood gases, chest X-ray,
hemodynamic monitoring, electrocardiogram,
and echocardiogram
Treatment: identification and treatment of
underlying cause, maintaining respiratory
status, cardiac monitoring, and rapid fluid
replacement