Unit 3 Pathophysiology - Chapter 33 Alterations of Cardiovascular Function Flashcards
Varicosities and cause of them?
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
Chronic venous insufficiency
inadequate venous return causes change in vasculature, skin, and supporting tissues
Superior vena cava syndrome
results from compression of SVC by tumors
DVT caused by
- venous stasis (immobility, age, left heart failure)
- spinal cord injury
- venous wall damage (trauma, IV meds)
- hypercoagulabe states (pregnancy, oral contraceptives, malignancy, genetic coagulopathies)
DVT symptoms
Often asymptomatic
may l/t
* fatal pulmonary emboli
Hypertension can be ___?
Primary w/ no known cause or secondary d/t disease or drugs
Risk factors for HTN?
- positive family hx
- male gender
- advanged age
- black race
- elevated Na+ intake
- low K+, Ca++, and Mg + intake
- DM
- ciagrette smoking
- Etoh use
Cause of primary HTN?
- genetic and environmental interaction
- such as diet, smoking, age, and others
Theories for pathogenesis of primary HTN
- overactive SNS
- overactive of renin-angiotensin-aldosterone system
- altered neurohumoral mediators of blood volume + vasomotor tone (ANP, BNP, adrenomedullin)
- inflammation consisting of insulin resistance + endothelial fx
- obesity-related hormonal changes
Clinical manifestations of HTN
heart disease, renal disease, CNS problems, retinal changes
Orthostatic hypotension
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
Orthostatic hypotension clinical manifestations
- fainting
- possible falls or injury
Aneurysm
localized dilation of vessel to which aorta is susceptible, including brain
Thrombus
clot that remains attached to a vascular wall
Embolus
mobile aggregate of a variety of substances that occlude vasculature, which may include
* thrombi
* air
* amniotic fluid, bacteria
* fat
* foreign matter
Common sources of aterial thrombotic emboli from heart?
Mitral and aortic valvular disease
atrial fibrilllation
Include lower extremities, brain, and heart
Generation of air emboli
Requires connection between vascular compartment and source of air causing ischemia and necrosis when vessel completely blocked
Amniotic fluid as an embolus?
Yes, can be forced into bloodstream generating embolus during labor or delivery
Aggregates of bacteria as an embolus?
Yes, group of them in vasculature is large enough to form one
What happens when theire is trauma to the long bones?
Fat emboli can appear d/t defective fat metabolism after trauma or release of fat globules from bone marrow exposed by a fracture
Foreign matters occur how?
In a hospital setting in which intravenous and intraarterial lines are being used!
Vasospatic diosrders
- Thromboangiitis obliterans (Buerger disease) — small blood vessels that become inflamed and swollen. Then thrombosis happens => hands and feets (especially arteries susceptible)
- 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.
Atherosclerosis
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
Peripheral arterial disease
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
Coronary artery disease
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
Risk factors for CAD
- 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)
Reverisble myocardial ischemia presents in a few ways clinically
- Stable angina [chronic coronary obstruction results in recurrent preditable chest pain]
- Prinzmetal angina [abnormal vasopasm of coronary vessels in unpredictable chest pain]
- Silent ischemia [myocardial ischemia that does not cause detectable symptoms]
Stable angina tx
- stress ECG, thallium or SPECt
- management => lifestyle changes, vasodilators, antithrombotics, PCI, or CABG surgery
What happens when a sudden obstruction occurs b/c of thrombosis formation over a ruptured atherosclerotic plaque?
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
Unstable angina
transient episodes of thrombotic vessel occlusion and vasoconstriction at site of plaque damage => w/ return of perfusion before significant myocardial necrosis occurs
Myocardial infarction
Coronary blood flow is interrupted for an extended period => myocyte necrosis (including hibernating, stunning, and remodeling of myocardium)
Acute coronary syndromes can be assessed by?
- 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
Common complications of acute coronary syndromes
- dysrhythmias
- congestive heart failure
- sudden death
Pericarditis
inflammation of pericardium d/t infection, drug therapy, tumors
symptoms - physically troublesome however life threatening
Pericardial effusion
fluid may collect within the pericardial sac; cardiac fx impaired d/t large volume of fluid accumulating rapidly
Cardiomyopathies
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
How to determine if valve is abnormal?
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
Mitral valve prolapse (barlow syndrome)
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.
Rheumatic fever
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
Infective endocarditis
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
Heart failure
inability of heart to supply the metabolism w/ adequate circulatory volume and pressure
Left heart failure
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)
Cardiac output
heart rate and stroke volume
Stroke volume
depends on contractility, preload (ventricular filling, initial stretching), afterload (force or load against which heart has to contract to eject blood)
What is the most common cause of decreased contractility
MI, results in ventricular remodeling that causes progressive myocyte contractile dysfunction over time
Preload LVEDV (left ventricular (LV) end-diastolic pressure)
Increased when decreased contractility or excess plasma volume
Increased peripheral vascular resistance
increased afterload l/t
* decreased ventricular emptying
* more workload for left ventricle (causing hypertrophy and ventricular remodeling)
Increased preload and afterload consecutively? Including decreased contractility?
Worsening
Neurohumoral mechanisms of CHF?
Abnormalities w/
1. SNS
2. RAAS
3. arginine vasopressin (ADH)
4. natriuretic epptides
5. inflammatory cytokines
6. myocyte metabolism (thickening)
Management of left heart failure? (2)
- Increase contractility
- reduce preload + afterload
Clinical manifestation of left heart failure?
- pulmonary vascular congestion
- inadequate systemic perfusion
Heart failure with preserved ejection fraction can occur
- Individually
- Or with systolic heart failure
Major causes of diastolic dysfunction include
- HTN-induced myocardial hypertophy
- Ischemia w/ resultant vetricular remodeling
Right heart failure causes?
- Result from left heart failure
- And/or diffuse hypoxic pulmonary disease (COPD , cystic fibrosis, ARDs)
High output failure?
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)
