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Pathophysiology > Vascular System > Flashcards

Vascular System Flashcards

1
Q

What is a cardiac arrhythmia and symptoms associated with the condition?

A

LESS CARDIAC OUTPUT

  • abnormalities in the myocardial conduction (dysrhythmias), can be sustain or sporadic
  • could be asymptomatic but patient could experience: palpitations, dizziness, lightheadedness, fatigued, out of breath
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2
Q

Acute Coronary Syndromes (ACS)

A

sudden reduction in coronary blood flow leads to unstable angina and myocardial infarction (MI)- more than 90% of ACS result from disruption of an atherosclerotic plaque and formation of an intracoronary thrombus

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3
Q

Ischemic Syndromes

A
  • normal: patent lumen, normal endothelial function, platelet aggregation inhibited
  • stable angina: lumen narrowed by plaque, inappropriate vasoconstriction
  • unstable angina: plaque rupture, platelet aggregation, thrombus formation, unopposed vasoconstriction
  • variant angina: no overt plaques, intense vasospasm
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4
Q

Embolus

A

a detached clot or fragment of a clot carried into the pulmonary or systemic circulation; clogs vessel or vessels downstream that are a smaller diameter than the clot, blocks blood flow and may cause tissue necrosis

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5
Q

Arteries

A

more smooth muscle

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6
Q

Veins

A

one way valves, larger lumen

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7
Q

Thrombus

A

an intravascular clot; can occur in any vessel or within the heart

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8
Q

Vascular Occlusion

A

blockage of a vessel

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9
Q

Ischemia

A

critical reduction in blood flow- associated with arteries

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10
Q

Infarct

A

tissue necrosis from interruption of blood flow- associated with arteries

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11
Q

Thrombus formation

A

stasis: immobility, blood pool- anurisms, caused by endothelial injury: injury or surgery, hypercoagulation: conditions- pregnancy, cancer, obesity

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12
Q

Thrombus Formation

A

stasis: immobility, blood pool (aneurism), endothelial injury (injury-surgery), hypercoagulation (conditions: pregnancy, cancer and obesity)

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13
Q

Arterial Thrombi

A

platelet rich!

  • usually begin sites of turbulence or endothelial injury
  • thrombi that adhere to the walls of the heart chamber or aortic lumen
  • consists of a friable meshwork of platelets, fibrin, red cells, and degenerating leukocytes
  • arterial thrombi are frequently occulusive
  • most common sites are coronary, cerebral, femoral
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14
Q

Venous Thromosis

A
  • usually at sites of stasis or unusually slow flow

- contain more enmeshed red cells and relatively few platelets

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15
Q

Fate of Thrombus

A
  • propagation (bigger): accumulate additional platelets and fibrin
  • embolization: thrombi (usually fragment of a thrombus) dislodge and travel to other sites
  • dissolution: result of fibrinolysis, extensive fibrin deposition of cross linking and older thrombi makes them more resistant to lysis
  • organization and recanalization
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16
Q

Arterial and Cardiac Thrombi

A
  • atherosclerosis is a major cause
  • myocardial infarction may lead to cardiac mural thrombi
  • rheumatic heart disease may lead to arterial mural thrombi
  • both cardiac and aortic mural thrombi are prone to embolization
  • embolism to the brain is the most common!
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17
Q

Superficial Venous Thrombi

A
  • usually in the saphenous veins
  • local congestion, swelling, pain, tenderness
  • rarely embolize!!!
  • predispose the overlying skin to infection and ulcer (varicose ulcers)!
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18
Q

Deep Vein Thrombosis (DVT)

A
  • involves one of the deep veins in calf or those at above the knee:poplitel, femoral, and iliac
  • may embolize to the lungs: pulmonary embolism, pulmonary infarction
  • may cause pain and edema but asymptomatic in 50% of patients
  • often associated with hypercoagulable states
  • predisposing factors: bed rest, orthopedic surgery, cancer, congestive heart failure, obesity, and advancing age
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19
Q

Embolism

A
  • embolus: detached intravascular solid, liquid or gas that is carried by the blood from its original point of origin distant site- causes tissue disfunction or infarction
  • example: thromboembolism (most common dislodge thrombi), cholesterol plaque, fat droplet, amniotic fluid, tumor fragments, air bubble
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20
Q

Tissue Infarctions

A
  • areas of ischemic necrosis due to thrombus or embolus
  • most commonly caused by arterial occlusion
  • whether an occluded vessel will lead to tissue damage (cell death) depends on: availability of alternate blood supply, rate of occlusion, tissue tolerability to hypoxia
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21
Q

Pulmonary Embolism

A
  • most originate from a leg DVT
  • fragments of the DVT are carried from site of origin back to the right side of heart and then into the pulmonary arterial vasculated where they lodge
  • depending on size, they: occlude the main pulmonary artery, straddle the pulmonary artery bifurcation (saddle embolus), pass into and occlude smaller branching pulmonary artery
  • frequently a shower of multiple emboli
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22
Q

Systemic Thromboembolism

A
  • most arise from intracardiac mural thrombi
  • also arise from: aortic aneurism, atherosclerotic plaques, valvular vegetation (bacterial growth), venous thromboembolism (paradoxical embolism), cancer (trosseau syndrome)
  • the end location of arterial emboli depends on the location of the source (lower extremities: brain)
  • IN GENERAL= tissue infarction
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23
Q

Examples of Infarctions

A
  • myocardial infarction: due to coronary artery occlusion!!
  • stroke: ischemic- due to cerebral artery occlusion (emboli from cardiac mural thrombi or carotid artery), hemorrhagic!!
  • pulmonary infarct
  • renal infarct
  • digital infarct
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24
Q

Shock

A
  • low cardiac output, reduced blood volume, or decrease systemic vascular resistance !!reduced tissue perfusion!! which leads to cellular hypoxia (skin, kidney, brain)
  • initially reversible cellular injury which prolong shock- irreversible cell damage or death
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25
Q

Types of Shock

A
  • hypovolemic (low volume)
  • distributive (smooth muscle has unequal distribution of fluid)
  • obstructive (obstruction that leads to: cardiogenic- inadequate pumping)
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26
Q

Cardiogenic

A

inadequate pumping by heart- myocardial damage, extrinsic compression, obstruction to outflow

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27
Q

Hypovolemic

A

fluid loss caused by massive hemorrhage or severe burns

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28
Q

Distributive

A
  • septic: overwhelming bacterial or fungal infection- toxin production, release of inflammatory mediators, coagulation activation, multiple organ dysfunction
  • anaphylactic (severe allergic rxn)
  • neurogenic: spinal cord injury, loss of sympathetic tone to peripheral blood vessels, extreme vasodialation
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29
Q

Blood Pressure

A
  • low blood pressure= hypotension, <90/60mmHg, inadequate organ perfusion- may lead to dysfunction/shock
  • high blood pressure= hypertension, END ORGAN DAMAGE- stroke, cardiac hypertrophy, or heart failure
  • BP= cardiac output (CO) X peripheral resistance (PR)
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30
Q

Hypertension (HTN)

A

If left untreated- END ORGAN DAMAGE: ischemic heart disease or congestive heart failure, stroke, or kidney injury- can be treated with blood pressure lowering therapy which decreases morbidity and mortality

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31
Q

Causes of Hypertension

A
  • essential hypertension (primary HTN): 90-95% of cases, idiopathic: reason unknown
  • secondary hypertension: due to identifiable cause
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32
Q

Mechanisms of Essential HTN

A
  • genetic factors
  • reduced renal sodium excretion
  • vasoconstrictive influences
  • environmental factors (stress, lack of exercise, high salt consumption, obesity)
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33
Q

Atherosclerosis

A

formation of atheromatous plaque (atheroma) in the intima of blood vessels: raised lesion with a soft core of lipids and covered by a fibrous cap- typically involves lower abdominal aorta, coronary arteries, popliteal arteries, internal carotid arteries, vessel of circle of willis

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34
Q

Consequences of Atherosclerosis

A

myocardial infarction, stroke-cerebral infarction, aortic aneurysm, peripheral artery disease(PAD) aka peripheral vascular disease(PVD)-symptoms include caudication (pain with exercising) and gangrene of the toes

35
Q

Risk Factors of Atherosclerosis

A

genetics, age, gender, modifiable risk factors(hyperlipidemia- increased LDL/decreased HDL, hypertension, smoking, diabetes mellitus), inflammation (C-reactive protein), metabolic syndrome, lipoprotein a(Lp[a]), lack of exercise, stress

36
Q

Vasculitis

A

vessel wall inflammation, clinical features depend on the vascular bed affected, main mechanism of pathology: immune-mediated inflammation, invasion of vascular walls by infectious pathogen, physical and chemical injury

37
Q

Raynaud’s Phenomenon

A

inappropriate vasoconstriction of arteries and arterioles in the extremities (usually affected fingers and toes), intermittent intense cold and color change- triggered by cold or emotion

38
Q

Varicosities

A

abnormally dilated and tortuous veins

  • varicose veins of the legs: commonly involve greater saphenous vein, incompetent venous valves
  • hemorrhoids: varicose veins of the venous plexus at the anorectal junction- due to pregnancy or constipation
  • esophageal varices: due to increased pressure in the portal vein, varicose veins at the gastroesophageal junction
39
Q

Heart Failure

A

characterized by a progressive decrease in cardiac output and tissue perfusion (forward failure), as well as pooling of blood in the venous capacitance system (backward failure)- congestive heart failure= heart failure with fluid overload
CO= heart rate(HR) X stroke volume(SV)

40
Q

Heart Failure Etiologies

A
  • impaired ventricular contractility
  • increased afterload
  • impaired ventricular relaxation and filling
  • HF most commonly results from conditions of impaired left ventricular function
41
Q

Compensatory Mechanisms in Heart Failure

A
  • frank-starling mechanism: increased filling volumes dilate the heart, increased myocardial cross bridges and contractility
  • ventricular hypertrophy and other remodeling: with or without chamber dilation
  • neurohormonal alterations: norepinephrine increases cardiac contractility and vascular resistance, renin-angiotensin-aldosterone system increases filling volumes, atrial natriuretic peptide (ANP) increases filling volumes
42
Q

Ejection Fraction(EF)

A

EF= stroke volume(SV) X end-diastolic volume(EDV)

  • normal ejection fraction= 50-70% is pumped out
  • borderline ejection fraction= 41-44% is pumped out
  • reduced ejection fraction= <40% is pumped out
43
Q

Heart Failure Causes

A
  • systolic dysfunction (HFrEF): progressive deterioration of myocardial contractile function- MOST FREQUENT CAUSE! caused by ischemic injury or pressure/volume overload- cause dilation
  • diastolic dysfunction (HFpEF): inability of the heart chamber to expand and fill sufficiently during diastole- following left ventricle hypertrophy- myocardial fibrosis
44
Q

Heart Failure categorized by Left Ventricular Ejection Fraction

A
  • HF with reduced EF (HFrEF): primarily systolic dysfunction, <40% EF, major cause is coronary artery disease (CAD) with previous myocardial infarction (MI)
  • HF with preserved EF (HFpEF): primarly diastolic dysfunction, >50% EF, major cause is hypertension
45
Q

Systolic Dysfunction (HFrEF)

A

heart failure that results from an abnormally of ventricular emptying due to: impaired contractility, greatly excessive afterload- results in insufficient ejection fraction

46
Q

Diastolic Dysfunction (HFpEF)

A

heart failure caused by abnormalities of diastolic relaxation or ventricular filling which is caused by heart tissue remodeling- left ventricle becomes abnormally stiff and cannot relax during diastole, cannot meet increased metabolic demands of peripheral tissues- backs up into pulmonary and systemic circulations

47
Q

Mechanisms Involved in Myocardial Hypertrophy

A

angiotension II, aldesterone, endothelin-1, insulin-like growth factor, beta-adrenergic signaling and desensitization, expression of fetal genes

48
Q

Two Patterns of Hypertrophy

A
  • pressure overload hypertrophy: due to hypertension or aortic stenosis (narrowing of the aortic valve), new sarcomeres are predominantly assembled in parallel to old cells which expands the cross-sectional area of myocytes in ventricles
  • volume overload hypertrophy: new sarcomeres being assembled in series within existing sarcomeres, causing myocytes to elongate leading primary to ventricular dilation
49
Q

Symptoms of Pulmonary COngestion due to Left Heart Failure

A

dyspnea (shortness of breath), orthopnea (sensation of labored breathing while lying flat), and paroxysmal nocturnal dyspnea (breathlessness that wakes patient from sleep and is relieved by sitting up)

50
Q

Symptoms of Right Heart Failure

A

peripheral edema (swollen ankles and feet, GI tract, and ascites- free fluid in abdominal cavity), weight gain (accumulation of interstitial fluid), heptic congestion, jugular vein distention(JVD), and hepatojugular reflux(HJR)

51
Q

Causes of Right Heart Failure

A

most frequently a consequence of left ventricular failure
-con pulmonale= right ventricular hypertrophy and dilation due to pulmonary hypertension
acute- sudden, massive pulmonary embolism
chronic- due to COPD, pulmonary fibrosis

52
Q

Common Heart Attack Warning Signs

A
  • pain or discomfort in chest
  • lightheadedness, nausea, or vomiting
  • jaw, neck, or back pain
  • discomfort or pain in arm or shoulder
  • shortness of breath
53
Q

Subendocardial Infarct

A

involves the inner most layers of the myocardium

54
Q

Transmural Infarct

A

spans the entire thickness of the myocardium

55
Q

Reperfusion

A

restoration of blood flow to ischemic myocardium threatened by infarction

56
Q

Factors that Affect the Amount of Tissue Affected by an Infarct

A
  • mass of myocardium perfused by the blocked vessel
  • the magnitude and duration of impaired coronary blood flow
  • the oxygen demand of the affected region
  • the adequacy of collateral vessels that provide blood flow from neighboring nonoccluded coronary arteries
  • degree of tissue response that modifies the ischemic process
57
Q

Complications of Myocardial Infarctions (MI)

A
  • abnormal cardiac rhythm
  • left ventricular failure
  • extension of the infarct
  • rupture of myocardial free wall
  • aneurysms
  • mural thrombosis and embolism
  • pericarditis
58
Q

Congenital Heart Defects

A
  • acyanotic (left-to-right shunt), typically less severe!: atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA)
  • cyanotic (right-to-left shunt), less oxygen in circulation: transportation of the great arteries- circulations in parallel not in series
  • obstructive lesions: coarctation of the aorta
59
Q

Atrial Septal Defect (ASD)

A

a hole in the interatrial septum that allows direct communication between the left and right atria- RIGHT SIDE MUST OVERCOMPENSATE WHICH CAUSES RIGHT SIDE FAILURE- most common site is midseptal around the foramen ovale (ostium secundum ASD), which accounts for 90% of all ASD- asymptomation before the age of 30, then symptoms include: heart failure, paradoxical embolism, pulmonary arterial hypertension- ASD closed via surgery or catheter (patch)

60
Q

What is a cardiac arrhythmia and symptoms associated with the condition?

A

LESS CARDIAC OUTPUT

  • abnormalities in the myocardial conduction (dysrhythmias), can be sustain or sporadic
  • could be asymptomatic but patient could experience: palpitations, dizziness, lightheadedness, fatigued, out of breath
61
Q

Asystole

A

no electrical activity

62
Q

Sinus Bradycardia

A

slow heart rate- slowing of the normal heart rhythm due to a decreasing firing of the sinoatrial (SA) node to a rate of <60bpm

63
Q

AV Conduction System includes:

A

AV node, bundle of his, left and right bundle branches

64
Q

First, Second, and Third-Degree AV Block

A

-first-degree AV block: prolongation delay between atrial and ventricular depolarization, such that PR lengthened
-second-degree AV block: intermittent failure of AV conduction, resulting in some P waves not followed by a QRS complex, could be:
type 1 block: impaired conduction of the AV node- usually benign
type 2 block: sudden intermittent loss of AV conduction- usually a block beyond the AV node
-third-degree AV block: complete heart block- complete failure of conduction between atria and ventricles, no relationship between P waves and QRS

65
Q

Tachycardia

A

increased heart rate

66
Q

Tachyarrhythmias

A
  • when HR is >100bpm for 3 or more beats
  • result from: enhanced automatically, triggered activity, reentry
  • categorized by: those that arise above the ventricles (originating from the atrium), those that arise within the ventricle (ventricular)
67
Q

Reentry Circuit

A

an electric impulse circulates repeatedly around a reentry pathway, repeated depolarizing a region of cardiac tissue

68
Q

Sinus Tachycardia

A

SA node discharge rate >100bpm, normal P waves and QRS complexes

69
Q

Atrial Flutter

A
  • rapid, regular atrial activity at a rate of 180-350bpm
  • many of these fast impulses reach the AV node during its refractory period- slower ventricular rate
  • caused by reentry over a large fixed area
  • P waves have sinusoidal or “sawtooth” appearance
70
Q

Atrial Fibrillation (AF) and its Consequences

A
  • chaotic rhythm
  • super fast atrial rate (350-600 discharges/min)- distinct P waves not discernable on EKG
  • many of the atrial impulses hit refractory tissue at the AV node
  • consequences include: rapid ventricular rates may decrease cardiac output, leading to hypotension and pulmonary congestion; also lack of organized atrial contraction promotes blood stasis in the atria which increases the risk of thrombus formation
71
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

A
  • sudden onset and termination
  • arterial rates between 140-259bmp
  • narrow (normal) QRS complexes (unless aberrant conduction present)
  • most common mechanism is reentry involving AV node, atrium, or an accessory pathway between an atrium and ventricle
72
Q

Ventricular Tachycardia

A
  • ventricular premature beats (VPB) arise when an ectopic ventricular focus fires an action potential
  • a series of 3 or more VPBs
73
Q

QT Prolongation

A
  • long QT syndrome (LQTS): prolonged QT intervals
  • indicates a lengthened action potential duration
  • increased risk for torsades de pointes and fatal ventricular arrhythmias
  • cause: certain drugs and rare inherited conditions
74
Q

Torsades de Pointes

A

“twisting of the points”

prolonged QT intervals predisposes a patient, can degenerate into ventricular fibrillation

75
Q

Ventricular Fibrillation

A

LIFE THREATENING ARRHYTHMIA

  • disordered, rapid stimulation of the ventricles with no coordinated contractions
  • immediate cessation of cardiac output and death if not quickly reversed
76
Q

Patent Foramen Ovale (PFO)

A

persistence of fetal anatomy

  • typically, foramen ovale closes after birth and eventually permanently seals to become the depression of the right atrium called the fossa ovalis, but in this case it fails to fuse
  • usually asymptomatic unless right atrial pressure elevates which creates potential for paradoxical embolism
77
Q

Ventricular Septal Defect (VSD)

A
  • an opening in the interventricular septum- small VSDs may remain asymptomatic, but large VSDs results in early symptoms of CHF
  • symptoms such as: high left ventricular pressure (left to right shunt), thickening pulmonary arteries, increased pulmonary vascular resistance, right heart failure
  • surgery needed during infancy
78
Q

Patent Ductus Anteriosus (PDA)

A
  • ductus arteriosus connects pulmonary trunk and the aorta which fails to close after birth
  • small PDA usually asymptomatic, but large PDA early CHF
  • treatment includes indomethacin (a prostaglandin inhibitor that constricts the ductus) or surgery
79
Q

Tetralogy of Fallout

A

characterized by 4 anatomical changes:

  1. ventricular septal defect
  2. pulmonary stenosis
  3. overriding aorta (aorta moved to the right- receives blood from both ventricles)
  4. right ventricular hypertrophy
    - associated with other cardiac defects
    - CYANOTIC congenital heart defects
    - corrected with surgery
80
Q

Transposition of the Great Arteries (TGA)

A

The aorta originates from the right ventricle and the pulmonary artery originates from the left ventricle (a switch!), intervention required because mixing between the two circulations is lethal so, ultimately surgery required to reverse great vessels to their natural state

81
Q

Coarctation of Aorta

A
  • discrete narrowing of the aortic lumen
  • severe coarctation: shortly after birth the patient experiences heart failure
  • mild coarctation: without PDA, asymptomatic until adulthood, discrepancy in blood pressure between upper and lower extremities
  • treatment: surgery, balloon dilation during cardiac catheterization
82
Q

Aortic Stenosis

A
  • narrowing of the aortic valve opening (restricts blood flow from left ventricle to aorta- left ventricular hypertrophy)
  • frequently due to congenital bicuspid aortic valve (surgical valve replacement)
83
Q

Mitral Regurgitation

A

allows backflow of blood into left atrium

Pathophysiology (4 decks)

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