Unit 3 Pathophysiology - Chapter 33 Alterations of Cardiovascular Function

Question 1

Varicosities and cause of them?

Answer 1

Area of veins in which blood has pooled (saphenous veins mainly, drain blood out of leg to heart)
* damaged as a result of trauma to valves
* or by chronic venous distention d/t gravity
+ venous constriction

Question 2

Chronic venous insufficiency

Answer 2

inadequate venous return causes change in vasculature, skin, and supporting tissues

Question 3

Superior vena cava syndrome

Answer 3

results from compression of SVC by tumors

Question 4

DVT caused by

Answer 4

• venous stasis (immobility, age, left heart failure)
• spinal cord injury
• venous wall damage (trauma, IV meds)
• hypercoagulabe states (pregnancy, oral contraceptives, malignancy, genetic coagulopathies)

Question 5

DVT symptoms

Answer 5

Often asymptomatic

may l/t
* fatal pulmonary emboli

Question 6

Hypertension can be ___?

Answer 6

Primary w/ no known cause or secondary d/t disease or drugs

Question 7

Risk factors for HTN?

Answer 7

• positive family hx
• male gender
• advanged age
• black race
• elevated Na+ intake
• low K+, Ca++, and Mg + intake
• DM
• ciagrette smoking
• Etoh use

Question 8

Cause of primary HTN?

Answer 8

• genetic and environmental interaction
• such as diet, smoking, age, and others

Question 9

Theories for pathogenesis of primary HTN

Answer 9

1. overactive SNS
2. overactive of renin-angiotensin-aldosterone system
3. altered neurohumoral mediators of blood volume + vasomotor tone (ANP, BNP, adrenomedullin)
4. inflammation consisting of insulin resistance + endothelial fx
5. obesity-related hormonal changes

Question 10

Clinical manifestations of HTN

Answer 10

heart disease, renal disease, CNS problems, retinal changes

Question 11

Orthostatic hypotension

Answer 11

drop in blood pressure that occurs on standing; compensatory vasoconstriction reponse d/t standing is altered by marked vasodilation and blood pooling in muscle vasculature

Primary form d/t neurologic changes that affect autonomic reflexes that control blood pressure upon standing

Question 12

Orthostatic hypotension clinical manifestations

Answer 12

• fainting
• possible falls or injury

Question 13

Aneurysm

Answer 13

localized dilation of vessel to which aorta is susceptible, including brain

Question 14

Thrombus

Answer 14

clot that remains attached to a vascular wall

Question 15

Embolus

Answer 15

mobile aggregate of a variety of substances that occlude vasculature, which may include
* thrombi
* air
* amniotic fluid, bacteria
* fat
* foreign matter

Question 16

Common sources of aterial thrombotic emboli from heart?

Answer 16

Mitral and aortic valvular disease

atrial fibrilllation

Include lower extremities, brain, and heart

Question 17

Generation of air emboli

Answer 17

Requires connection between vascular compartment and source of air causing ischemia and necrosis when vessel completely blocked

Question 18

Amniotic fluid as an embolus?

Answer 18

Yes, can be forced into bloodstream generating embolus during labor or delivery

Question 19

Aggregates of bacteria as an embolus?

Answer 19

Yes, group of them in vasculature is large enough to form one

Question 20

What happens when theire is trauma to the long bones?

Answer 20

Fat emboli can appear d/t defective fat metabolism after trauma or release of fat globules from bone marrow exposed by a fracture

Question 21

Foreign matters occur how?

Answer 21

In a hospital setting in which intravenous and intraarterial lines are being used!

Question 22

Vasospatic diosrders

Answer 22

1. Thromboangiitis obliterans (Buerger disease) — small blood vessels that become inflamed and swollen. Then thrombosis happens => hands and feets (especially arteries susceptible)
2. Raynaud disease — fingers + toes + ears + tip of nose => feel numb and cold in response to cold temperatures or stress (constrict excessively limiting blood supply = vasospasm)

narrowing of the arteries caused by a persistent contraction of the blood vessels, which is known as vasoconstriction. This narrowing can reduce blood flow.

Question 23

Atherosclerosis

Answer 23

leading cause of coronary artery and cerebrovascular disease

an inflammatory disease that begins with endothelial injury and progresses thourhg several stages to become a fibrotic plaque

This plaque can rupture => result in thrombosis and vasoconstriction l/t obstruction of lumen and inadequate perfusion of distal tissues

Question 24

Peripheral arterial disease

Answer 24

atherosclerosis of arteries that perfuse limbs (particularly lower extremities)

often asymptomatic but can present with intermittent claudication (pain in leg on walking)

reduction and antiplatelet therapy

Question 25

Coronary artery disease

Answer 25

results imbalance between coronary supply of blood and myocardial demand for o2 + nutrients reverisble myocardial ischemia or irreversible infarction may result ================= occlusion of coronary arteries and often result of atherosclerotic lesions (buildup of plaque) that limit flow of blood to heart

Question 26

Risk factors for CAD

Answer 26

* advanced age * gender HTN * dyslipidemia * diabetes mellitus * smoking * obesity * sedentary * elevatd hs-CRP (increased risk of heart attack) * chronic kidney disease * environmental exposures (air pollution, ionizing radiation)

Question 27

Reverisble myocardial ischemia presents in a few ways clinically

Answer 27

1. Stable angina [chronic coronary obstruction results in recurrent preditable chest pain] 2. Prinzmetal angina [abnormal vasopasm of coronary vessels in unpredictable chest pain] 3. Silent ischemia [myocardial ischemia that does not cause detectable symptoms]

Question 28

Stable angina tx

Answer 28

* stress ECG, thallium or SPECt * management => lifestyle changes, vasodilators, antithrombotics, PCI, or CABG surgery

Question 29

What happens when a sudden obstruction occurs b/c of thrombosis formation over a ruptured atherosclerotic plaque?

Answer 29

Acute coronary syndrome results THEN unstable angina causes reversible myocardial ischemia and l/t possibility of impending infarction MI results d/t prolonged ischemia causing irreversible damage to the heart muscle. Sudden cardiac death can occur in any of the aute coronary syndromes

Question 30

Unstable angina

Answer 30

transient episodes of thrombotic vessel occlusion and vasoconstriction at site of plaque damage => w/ return of perfusion before significant myocardial necrosis occurs

Question 31

Myocardial infarction

Answer 31

Coronary blood flow is interrupted for an extended period => myocyte necrosis (including hibernating, stunning, and remodeling of myocardium)

Question 32

Acute coronary syndromes can be assessed by?

Answer 32

* Measuring serum enzymes - troponin * characteristic changes in ECG * Such as ST elevations (for STEMI, which requires immediate intervention) * Smaller endocardial infarctions (not ST segment elevation, non STEMI) but suggest additonal myocardium at risk for recurrent ischemia and infarction) management => thrombolytic drugs, antithrombotic drugs, vasodilators, PCI, or immediate surgery

Question 33

Common complications of acute coronary syndromes

Answer 33

* dysrhythmias * congestive heart failure * sudden death

Question 34

Pericarditis

Answer 34

inflammation of pericardium d/t infection, drug therapy, tumors symptoms - physically troublesome however life threatening

Question 35

Pericardial effusion

Answer 35

fluid may collect within the pericardial sac; cardiac fx impaired d/t large volume of fluid accumulating rapidly

Question 36

Cardiomyopathies

Answer 36

categorized as * dilated (congesitive) - weakened and enlarged * restrictive (rigid and noncompliant) - chambers stiff over time; able to squeeze well but not able to relax between beats normally - harder for heart ofill up with blood + blood backs up into the circulatory system * hypertrophic (asymmetrical) - left ventricle (main pumping) walls become thick and stiff; eventually can't take in or pump out enough blood during each heartbeat to supply the body's needs

Question 37

How to determine if valve is abnormal?

Answer 37

Characteristic heart sounds, cardiac murmurs (whooshing or swishing made by rapid, turbulent blood flow through heart, and systemic complaints Prosthetic heart valve may be surgiclaly implanted

Question 38

Mitral valve prolapse (barlow syndrome)

Answer 38

Common finding, especially young women * mitral valve leaflets do not position themselves properly during systole; mitral valve prolapse may be completely asymptomatic or progress to mitral regurgitation (left side, stretchy valve Mitral valve regurgitation is a condition in which the heart's mitral valve doesn't close tightly, which allows blood to flow backward in the heart.

Question 39

Rheumatic fever

Answer 39

inflammatory disease d/t delayed autoimmune response to a streptococcal infection; resolves without sequelae (previous diseases or injury) if treated injury Untreated l/t rheuamtic heart disease => potentially disabling cardiovascular d/o affectring the heart valves

Question 40

Infective endocarditis

Answer 40

infection + inflammation of endocardium, especially cardiac valves if left unchecked * severe valve abnormalities * chronic bacteremia (in blood stream) * systemic emboli (can occur as vegetations break off the valve surface and travel via blood stream) antibiotic treatment essential

Question 41

Heart failure

Answer 41

inability of heart to supply the metabolism w/ adequate circulatory volume and pressure

Question 42

Left heart failure

Answer 42

heart failure w/ reduced ejection fraction (systolic) or heart failure with preserved ejection fraction (diastolic) Heart failure w/ reduced ejection fraction defined as inability for heart to generate an adequate cardiac output to perfuse vital tissue While preserved ejection fraction => left ventricle unble to fill properly with blood during the diastole phase (less blood is being pumped out than normal)

Question 43

Cardiac output

Answer 43

heart rate and stroke volume

Question 44

Stroke volume

Answer 44

depends on contractility, preload (ventricular filling, initial stretching), afterload (force or load against which heart has to contract to eject blood)

Question 45

What is the most common cause of decreased contractility

Answer 45

MI, results in ventricular remodeling that causes progressive myocyte contractile dysfunction over time

Question 46

Preload LVEDV (left ventricular (LV) end-diastolic pressure)

Answer 46

Increased when decreased contractility or excess plasma volume

Question 47

Increased peripheral vascular resistance

Answer 47

increased afterload l/t * decreased ventricular emptying * more workload for left ventricle (causing hypertrophy and ventricular remodeling)

Question 48

Increased preload and afterload consecutively? Including decreased contractility?

Answer 48

Worsening

Question 49

Neurohumoral mechanisms of CHF?

Answer 49

Abnormalities w/ 1. SNS 2. RAAS 3. arginine vasopressin (ADH) 4. natriuretic epptides 5. inflammatory cytokines 6. myocyte metabolism (thickening)

Question 50

Management of left heart failure? (2)

Answer 50

1. Increase contractility 2. reduce preload + afterload

Question 51

Clinical manifestation of left heart failure?

Answer 51

1. pulmonary vascular congestion 2. inadequate systemic perfusion

Question 52

Heart failure with preserved ejection fraction can occur

Answer 52

1. Individually 2. Or with systolic heart failure

Question 53

Major causes of diastolic dysfunction include

Answer 53

1. HTN-induced myocardial hypertophy 2. Ischemia w/ resultant vetricular remodeling

Question 54

Right heart failure causes?

Answer 54

1. Result from left heart failure 2. And/or diffuse hypoxic pulmonary disease (COPD , cystic fibrosis, ARDs)

Question 55

High output failure?

Answer 55

High-output heart failure is a condition in which your heart is initially working normally (either with reduced or preserved ejection fraction) but can't keep up with your body's increasing need for more blood. Your heart ultimately becomes weak and can no longer pump blood effectively throughout your body. Causes * Anemia * Septicemia * Hyperthyroidism (overactive thyroid can overtax heart and cause heart failure, body also needs increased blood and o2) * Beriberi (deficient in vitamin B1)