Patho Cardiovascular Study Guide

Front 1

Differentiate between structural alterations in blood vessels and blood vessel obstructions and their potential effect on blood flow. p 361

Back 1

valvular incompetence, arteriosclerosis / atherosclerosis, aneurysms, arteriovenous fistulas

Front 2

valvular incompetence

Back 2

damage to the intimal folds of veins, interfering with the effective flow of blood through a portion of the venous system

Front 3

arteriosclerosis / atherosclerosis

Back 3

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Front 4

aneurysms

Back 4

a dilation of an arterial wall...represents a wekened area in the artery that may eventually rupture

Front 5

arteriovenous fistulas

Back 5

abnormal communication between arteries and veins
usually congenital in origin but may result from traumatic injury
provide a “shortcut” between the two vascular systems
can result in alterations in oxygenation to the involved tissues and systemic heodynamic changes
one type is AVM (arteriovenous malformation)

Front 6

Describe the development of arteriosclerosis. (intima picture pg43 Figure 18-2).

Back 6

Abnormal thickening & hardening of the vessel wall
· Smooth muscle cells & collagen fibers migrate into the tunica intima causing it to stiffing and thicken.
· Gradually, the arterial lumen narrows and decreases their ability to dilate.

Front 7

Describe the development of atherosclerosis. How does it differ from #2?

Back 7

A form of arteriosclerosis. “Plaque”: Deposits of fatty substances, cellular waste products, calcium and other substances build up in the inner lining of an artery
...The difference between the two are: Arteriosclerosis= hardening of the vessel walls. Atherosclerosis= plaque build- up inside the lumen (vessel).
see p364 Figure 15 -19


(Slide 7: Athersclerosis- Pathogenesis) and (p.364: writing under fig. 15.9)
-Damage to the innermost layer of the artery- endothelial surface of the intima
-fats, cholesterol, platelets, cellular waste products, calcium and other substances are deposited in the damaged artery wall
-artery wall cells are stimulated to produce other substances that result in further buildup of cells
-These cells and surrounding material thicken the endothelium significantly. The artery's diameter shrinks and blood flow decreases, reducing the oxygen supply

Front 8

Identify possible etiologies of an aneurysm (slide # 9, textbook pg. 367-368).

Back 8

Aneurysms are localized arterial dilations
The arterial wall deteriorates until it is weakened sufficiently to bulge outward
The underlying causes for aneurysm may be:
· Atherosclerotic changes in the vessel
· Congenital weakness
· Weakening induced due to infection, Inflammation, or traumatic injury

-HTN= (high blood pressure) produces more tension and enlargement within the artery (Iggy, p.811)
-Hyperlidemia and cigarette factors are other contributing factors
(Iggy, p.811)

Front 9

Explain why a dissecting aneurysm is so serious.

Back 9

Dissecting aneurysm is a serious condition in which a tear develops in the arterial wall creating a channel for blood flow.

· As more blood escapes into the spaces between intima and media or between media and adventitia, the layers are separated from one another and as the vessel becomes weaker, it may rupture.

· As the radius of the wall increases, the tension in the wall increases, rupture of major vessel such as aorta is highly fatal in less than one hour.

When dissecting aneurysms occur, the aneurysm enlarges, blood is lost, and blood flow to organs is diminished. (Iggy: p.811)

Front 10

Explain the etiology of varicose veins and identify associated risk factors.
See vascular incompetence
Cardiovascular slide 14

Back 10

Varicose veins:
· The vascular incompetence of the superficial veins causes by overstretching of the valves from excessive venous pressure.
Risk factors:
· Pregnancy
· Obesity
· Crossing legs
· Right heart failure
· Prolonged standing

Front 11

Understand the pathogenesis of venous stasis ulcers (slide # 16, pg. 370)

Back 11

Venous stasis ulcer is a chronic disorder where the flow of blood is slowed down or halted causing ischemia to the extremities and ulcer formation
· Previous deep vein thrombosis is a risk factor.

Valvular incompetence involves the deep veins (superficialo femoral, anterior and posterior tibial, peroneal) of the legs.
Communicating or perforating veins provide direct access between the superficial and deep veins.
As the pressure in the superficial veins remains elevated for a prolonged period, the deep veins are eventually affected.
Venous stasis ulcers also develop as superficial veins rupture with the increased pressures associated with activity.
The skin pigmentation becomes brown as small veins rupture, leaking red blood ceels, which are eventually broken down.
Defining characteristics of Chronic venous insufficiency p370 Box 15 - 4

Front 12

Describe the pathophysiology of Lymphedema (Pg. 371)

Back 12

Lymphedema occurs when the normal flow of lymph is obstructed or altered in some fashion.
· This results in the collection of lymphatic fluid in the interstitium, initiating an inflammatory response, hypertrophy of subcutaneous adipose tissue, and fibrotic changes

Obstruction of lymph flow is most commonly the result of surgical removal of, or radiation damage to, lymphatic vessels during treatment of cancer. Manifestations of lymphatic obstruction include regional edema and thickened subcutaneous tissue.

Front 13

Primary lymphedema

Back 13

r/t a congenital anomaly or dysfunction of the lymphatic system

Front 14

Secondary lymphedema

Back 14

develops in associtaion with a disease process or is iatrogenic ( a consequece of medical intervention)

secondary lymphedema is most commonly caused by an infection by filarial worms that come to rest in the nodes of the lymphatic system, producing an obstruction of flow.

in the U.S. secondary lymphedema is most requently caused by the surgical

Front 15

Understand the factors that affect blood pressure

Back 15

ncluding CO, HR, SV, SVR, Preload and Afterload.

Front 16

Heart Rate (HR):

Back 16

Number of cardiac cycles/min.

Front 17

Stroke Volume (SV):

Back 17

Volume of blood ejected with each contraction

Front 18

Cardiac Output (CO):

Back 18

Volume of blood (in liters) ejected each minute
CO = HR x SV

Front 19

Normal Cardiac Output

Back 19

4-8L/min

Front 20

Cardiac Output affects

Back 20

preload, afterload, contractility

Front 21

Preload:

Back 21

text p420, 421 and slide 19
Volume of blood in cardiac chamber prior to ejection.
Influenced by volume and cardiac compliance
Determines amount of stretch on muscle fibers
AKA- “End-diastolic volume”

Front 22

Afterload: (p21)

Back 22

text p420, 421 and slide 19
The amount of resistance the ventricles must overcome to eject blood.

Front 23

Systemic Vascular Resistance

Back 23

text p420, 421 and slide 19
is the primary determinant of afterload and the terms are sometimes used interchangeably

Front 24

Primary hypertension (p382)

Back 24

is also called essential hypertension......it does not have a clearly identifiable cause, therefore it is considered a idiopathic disorder. this differentiates primary from secondary. (Chart on the effects of hypertension on the body pg. 384)

Front 25

Secondary Hypertension (p387)

Back 25

when hypertension is found to have a specific identifiable cause, it is termed secondary hypertension
The cause may be a specific pathology or condition that results in hypertension, or the development of high blood pressure may be the result of the ingestion of certain drugs, foods, or chemicals

Front 26

Identify potential etiologies for Primary Hypertension.

Back 26

Primary hypertension does not have a clearly identifiable etiology and is therefore an idiopathic disorder.
· This unknown cause produces vasoconstriction and increased peripheral vascular resistance (PVR).
· Risk factors are increasing age, family history, obesity, tobacco use, sedentary lifestyle, etc.

Front 27

Understand the effects of Hypertension on major target organs.

Back 27

see chart at
download the chart from one of the websites provided at the following hyperlink:

http://uploadmirrors.com/download/QYSYBGUI/Effects_of_Hypertension_on_Organs.docx

Front 28

Circulatory System Flow Figure 15 - 2 p351

Back 28

1. SVC, IVC
2. RA
tricuspic valve
3. LA
4. Pulmonary artery (deoxyginated)
5. Lungs
semilunar valves
6. pulmonary veins
7. LA
mitral
8. LV
semilunar valve
9. aorta
10. body (systemic)
http://www.youtube.com/watch?v=AXKRGARMuR8

Front 29

Identify lifestyle changes that can be implemented to treat Hypertension (pg. 385, table 16-6 on pg. 387).

Back 29

Weight loss is an important intervention, with profound evidence that it reduces cardiovascular mortality.
· Dietary Approach to Stop Hypertension (DASH) diet - high in fruits & vegetables and low-fat dairy products with decreased total & saturated fat
· Decreased sodium intake – no more than 100 mmol/day.
· Moderate intake of alcohol
- Men: ≤ 2 drinks/day
- Women: ≤ 1 drink/day

Front 30

Define Orthostatic Hypotension and identify associated symptoms.

Back 30

Orthostatic hypotension is defined as decrease in systolic blood pressure greater than or equal to 20mmHg when standing (pg 389).
Symptoms include dizziness, blurred vision, confusion, and possible syncope, which may result in injuries secondary to falls.
Normally, gravity changes are compensated by reflex vasoconstriction
Normally, 10-15% of blood pools in lower extremities. When moving from supine to standing, messages are sent to have a rapid increase in blood pressure and improved perfusion to upper body, especially the brain. When this doesn’t happen you have orthostatic hypotension

p390

Front 31

Describe the pathogenesis of CAD and identify associated risk factors.

Back 31

CAD - Coronary Artery Disease
A narrowing of the coronary arteries resulting in decreased oxygen supply to the myocardium, and is associated with coronary atherosclerosis (Endothelial injury and inflammation and lipd accumulation in the intima are thought to be the primary initiators of coronary atherosclerosis)

Front 32

Risk Factors of CAD (Coronary Artery Disease)

Back 32

here are several risk factors such as: Age, male gender, family history, abnormal lipids, hyperLIPIDemia, cigarette smoking, hypertension, and obesity.

Front 33

Tests used in detecting CAD (Coronary Artery Disease)

Back 33

Abnormal Lipids:
Total Cholesterol > 200 mg/dl
LDL (Low Density lipoproteins) aka: BAD Cholesterol >130 mg/dl
Triglycerides >150 mg/dl
HDL (High Density lipoproteins) aka: GOOD Cholesterol <40mg/dl

Front 34

Describe the potential effects of CAD on cardiovascular functioning.

Back 34

The oxygen concentration is insufficient to meet the myocardial tissue demands.
Signs and Symptoms
slowed heart rate
decreased cardiac output
dysrhythmia
sudden death
ischemia
angina
Myocardial Infarction

Front 35

Differentiate between stable angina, unstable angina, and myocardial infarction.

Back 35

Angina: Chest pain caused by myocardial ischemia

Types
Stable Angina: Chest pain associated with intermittent myocardial ischemia.
Unstable Angina: Pain occurring with increasing frequency, severity & duration
Prinzmetal Angina: Coronary artery vasospasm

Silent: Asymptomatic

Front 36

Stable Angina

Back 36

is the most common form and is therefore called CLASSIC or TPICAL Angina. Stable angina is charcacterized by stenotic atherosclerotic coronary vessels that reduce coronary blood flow to the critical level. Under conditions of increased myocardial workload, such as physical exertion or emotional strain, coroncary perfusion is inadequate and ischemia results. This type of pain is generally predictable and elicited by similar stimuli each time. It is generally relieved by rest and nitorglycerin (drug that causes coronary and peripheral vasodilation, reduces preload, and therefore reduces myocardial workload)

Front 37

Unstable Angina

Back 37

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Front 38

Myocardial Infarction

Back 38

MI results when prolonged or total disruption of blood flow to the myocardium causes cellular death by necrosis or apoptosis. Acute MI is an important form of CHD resulting in more than 150,000 death annually in the US. It is estimated that an American male has a greater than 1 in 5 chances of sustaining an MI or fatal ischemic event before that age of 65. (The initiating even in most MIs is believed to be development of a thrombus on top of an ulcerated or cracked atherosclerotic plaque).

Front 39

Define MI

Back 39

Localized area of cardiac necrosis most often associated with coronary heart disease.

Front 40

What is the pathogenesis of MI?

Back 40

This occurs when myocardial tissue is abruptly and severely deprived of O2. When blood flow is quickly is quickly reduced by 80 to 90%, ischemia develops. Ischemia can lead to injury and necrosis of myocardial tissue if blood is not restored. Most MIs are result of atherosclerosis of a coronary artery, rupture of plaque, subsequent thrombosis, and occlusion (blockage) of blood flow. Other factors may be involved such as coronary artery spasm, platelet aggregation, and emboli from mural thrombi (thrombi lining the walls of the cardiac chambers).

Front 41

Define dysrhythmia

Back 41

Dysrhythmias (arrhythmias) - refers to an abnormality of the cardiac rhythm of impulse generation or conduction. A normal heartbeat is initiated at an appropriate rate in the (SA) node, and follows a consistent pathway of depolarization through the atria, (AV) node, His-Purkinje system, and finally the ventricular myocardium.

Front 42

and identify possible etiologies of dysrhythmia

Back 42

Dysrhythmias are believed to arise from 3 mechanisms:
Inappropriate Automaticity - implies that the atrial or ventricular cell that normally doesn't spontaneoulsly depolarize acquires the ability to initiate action potentials.
Triggered Activity - occurs when an impulse is generated during, or just after repolarization because of depolarizing oscillatio of the membrane potential.
Reentrant Mechanisms - Reentry is thought to be the culprit in most tachydysrhythmias, including atrial and ventricular tachycardia, flutter, and fibrillation.
reentry p475- a complex process in which a cardiac impulse continues to depoloarize in a part of the heart after the main impulse has finished its path and the majority of the fibers have repolarized

Front 43

possible causes of dysrhythmia

Back 43

Possible Causes
ischemia of cardiac muscl
hypoxia
electrolyte imbalance
trauma
inflammation
drugs

Front 44

What are the three categories of dysrhythmias

Back 44

Categories of Dysrhythmia
abnormal rates of the sinous rhythm
abnormal sites of impulse initiation (ectopic)
disturbances in conduction pathway

Front 45

polarized

Back 45

resting (power point slide # 45)

Front 46

depolarized

Back 46

electrical stimuli

Front 47

repolarized

Back 47

returning to resting phase

Front 48

Valvular Stenosis

Back 48

Stenosis
valve narrowing blocks the flow from the left ventricle to the aorta
and produces high pressure in an attempt to overcome the resistance
blocks flow leaving the ventricle
blood is not coming backwards in stenosis (stenosis is considered an obstruction)

Front 49

Insufficiency or Regurgitation

Back 49

backflow of blood due to inability of valve leaflets to shut completely.

the incompentent valve allows blood to flow back into the left ventricle
it becomes volume overloaded
atttempts to compensate via hypertrophy and dilation

Front 50

Understand the pathophysiology associated with diseases of the Aortic valve.

Back 50

more stroke volume->rapid decline in diastolic->result in bounding peripheral pulse-> the head may bob with each systole

The Hallmark of this type of disorder is Calcium Deposits on the Aortic Cusps...
Aortic stenosis is characterized by an abnormal left ventricular (LV) to aortic pressure gradient.
Aortic regurgitation

Front 51

Identify the etiology of Acute Pericarditis.
Textbook p451 - 453

Back 51

It is inflammation of the pericarditis.


It is estimated that 80 -90% of cases of acute preicarditis are idiopathic, and most of these are presumed to be Viral. Typically resolves spontaneously and non-steroidal anti-inflammatory aganets (NSAIDS) may be the only therapy used.

Front 52

Identify the clinical manifestations of Acute Pericarditis.
Textbook p451 - 453

Back 52

Symptoms may be: inflammation and pericardial damage, that include fever, leuckocytosis, malaise, and tachycardia. Always presents with chest pain, and may be confused with anginal pain. The rubbing of the visceral and parietal pericardial layers cause pain that may radiate to the back, and be associated with esophageal discomfort, and dysphagia (difficulty swallowing).

Front 53

Define Pericardial Effusion

Back 53

Pericardial Effusion is an accumulation of NON-inflammatory fluid in the pericardial sac.

Front 54

What are the types of fluid that may accumulate in the pericardial sac?

Back 54

serous, serosanguinous, chylous, blood

Front 55

Serous

Back 55

a transudate secondary to heart failure, or hypoproteinemia

Front 56

Serosanguineous-

Back 56

a mixture of serous fluid and blood that may follow blunt chest trauma, heart surgery, or cardiopulmonary resuscitation.

Front 57

Chylous-

Back 57

a collection of lymph from obstruction of lympathtic drainage.

Front 58

Blood-

Back 58

hemopericardium usually resulting from penetrating trauma to the heart.

Front 59

Describe the pathogenesis of Cardiac Tamponade.

Back 59

Cardiac Tamponade - Large amount of fluid in pericardial space, Prevents filling of atria and ventricles, Decrease in SV and CO, and Increase in venous pressure, congestion, right heart failure

Front 60

Define heart failure

Back 60

Heart failure is the Inability of the heart to pump enough blood to meet the needs of the body... HF is diagnosed by x-ray and echocardiograph (measures the chamber size, volume, and dynamics during diastole and systole as well as determine ejection fraction.) Also a blood test for B-type natriuretic peptiede (BNP) may also be used to help indentify patients with HF.

Serious forms of heart disease have the potential to end in heart failure...

Heart Failure develops over time, and can affect the left side, the right side, or even both sides of the heart... LEFT Ventricular failure is the MOST COMMON PRESENTATION of heart failure, that then leads to Right sided HF ( a condition that is termed biventricular failure)... Left think LUNGS!! Right think Rest of BODY (kidneys)!!

Front 61

Etiology of Heart Failure is:

Back 61

Coronary Artery Disease, Myocardial Infarction (MI), Cardiomyopathy, Hypertension, Pulmonary Hypertension, Valve Disease, Chronic Kidney Disease.

Front 62

CM of Heart Failure

Back 62

Manifested as confusion, fatigue, tachycardia, reduced urine output, and poor peripheral circulation.

Front 63

Define ejection fraction

Back 63

Ejection fraction is the stroke volume divided by end-diastolic volume; indicates pumping efficiency of the ventricle.

EF is calculated by dividing stoke volume by end-diastolic volume. A normal EF is 60%-80%. Patients with systolic failure have charcteristically low ejection fractions (<40%). Patients with EF greater than 50% do not have significant systolic dysfunction and are categorized as HF with normal EF (HFnlEF). Many patients with low EF alsl ohave impaired diastolic function.

Front 64

Left sided HF

Back 64

(most often associated with left ventricular infarction, cardiomyopathy, aortic and mitral valvular disease, and systemic hypertension) is characterized by pulmonary congestion wich may manifest with Dyspnea (difficulty breathing), Orthopnea (difficulty breathing laying down), crackles, cough, pulmonary edema, and hypoxemia

Front 65

Right sided HF

Back 65

(since the right and left ventricles function in a series, left ventricular failure eventually increases the burden on the right ventricle and may cause it to fail as well; therefore the causes of right ventricular failure must therefore includes all the causes of left ventricular failure) is charcacterized by systemic venous congestion, which mya manifiest with (JVD) jugular vein distention, hepatomegaly (abnormal enlargement of the liver that is usually a sign of disease), splenomegaly (an abnormal enlargement of the spleen, as in associated with portal hypertension, hemolytic anemia), and peripheral edema.

Front 66

Define shock and identify the general clinical manifestations associated with shock.

Back 66

"SHOCK!" - is (Circulatory Failure) - resulting in Insufficient delivery of Oxygenated Blood...

Patho - Sever Trauma, Blood Loss, Heart Failure, Sever Infection (systemic)...

Cardiogenic (MI, Cardiomyopathy, Valvular Heart disease, ventricular rupture, congenital heart defects, papillary muscle rupture)

Obstructive- (Pulmonary embolism, cardiac tamponade, tension pnueumothorax, aortic aneurysm)

Hypovolemic Shock – Burns, pancreatitis, vomiting, diarrhea, acute hemorrhage.

Distributive – anaphylaxis, neurotrauma, spinal cord trauma, sepsis, spinal anesthesia

Front 67

CM of Shock

Back 67

Clinical Manifestations of Shock: Narrow pulse pressure with or without hypotension, tachycardia greater than 100 beats/min, fast and deep respirations, decreased urinary output, increased specific gravity, cool, clammy skin, altered mentation, dilated pupils