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Patho Exam 3 > Cardiac Diseases > Flashcards

Cardiac Diseases Flashcards

1
Q

What are the 3 layers of the heart from outer to inner

A

epicardium
myocardium
endocardium

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2
Q

Where are the coronary arteries located

A

outside of the heart

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3
Q

What is the most important coronary artery

A

Left Coronary Artery which branches into the Left Anterior Descending - feeds most of the left ventricle (widow makers region)

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4
Q

Cardiac Conduction System

A

SA node –> AV nodie–> Bundle of His –> R and L Bundle Branches –> Purkinje fibers

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5
Q

SA node

A

pacemaker of the heart
located at top of R atrium
generate 60-100 pulses per min and is controlled by PNS and SNS

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6
Q

AV node

A

located in the lower aspect of the atrial septum - receives electrical impulses from SA node

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7
Q

Bundle of His

A

fuses with the AV node to form another pacemaker site; branches into R and L and terminates into Purkinje’s fibers
can sustain a heart rate of 40-60 beats per minute (if SA node fails)

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8
Q

Purkinje’s Fibers

A

a diffuse network of conducting strands located beneath the ventricular endocardium - they spread the wave of depolarization through the ventricles

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9
Q

1st heart sound

A

lub (S1)

AV valves close at beginning of systole d/t increased pressure in the ventricles (R - tricuspid L = Mitral)

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10
Q

2nd heart sound

A

dub (S2)

Semilunar valves shut at the end of systole due to the falling pressure in the ventricles (R = pulmonic L=aortic)

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11
Q

Physiologic split

A

Aortic vale precedes pulmonic valve closure by 0.02-0.04 seconds during expiration and 0.04-0.06 secs during inspiration

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12
Q

Atherosclerosis

A

hardening of paste
characterized by fibrofatty lesions in the intimal lining of the aorta, large and medium sized arteries, coronary arteries, and other larger vessels that supply the brain

**CORONARY ARTERIES ARE THE MOST COMMONLY EFFECTED

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13
Q

If atherosclerosis in veins

A

hard to feel pulses

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14
Q

If atherosclerosis in arteries

A

hard to feel pulses and leg pain

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15
Q

What is the most common cause of CAD

A

inflammation r/t atherosclerosis

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16
Q

Inflammation in Atherosclerosis

A

chronic inflammation condition = accumulation of fibrous plaques and lipids progressively narrows the lumen of the vessel and impedes blood flow

Progression causes vascular changes that impair diseased vessels ability to dilate (stiffens). Can result in calcification or rupture

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17
Q

What can trigger atherosclerotic CAD

A

smoking, HTN, hyperglycemia all cause release of chemicals involved in inflammatory response

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18
Q

What organisms have been identified to POSSIBLY contribute to atherosclerosis (they are bystanders)

A

Chlamydia pneumoniae
Herpes Simplex Virus
Cytomegalovirus

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19
Q

Is atherosclerosis problematic to the brain? Why?

A

yes bc its responsible for majority of cases of MI and cerebral infarction; lesions occur in the innermost layer of medium and large muscular arteries; you you have it it one part, your bound to have it in others, and since the heart pumps blood to the brain CAD can cause MI, stroke, gangrene of extremities, sudden cardiac Death

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20
Q

Fatty Streak Lesions

A

contains foam cells (macrophages filled with lipids and T cells)
migrate from smooth muscle in tunica media to tunica intema and take on the appearance of foam cells

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21
Q

Fibrous Plaque Lesions

A

connective tissue, smooth muscle cells full of lipids, macrophages, and lymphocytes; progressively thickens and may occlude the lumen
(often with necrosis and calcification)

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22
Q

What is Complicated Lesion?

A

fibrous plaque can undergo extensive degeneration and rupture. The ulcerations/cracks that occur during rupture, trigger the aggregation of platelets –> this could result in a thrombus/sudden occlusion

**takes years/decades to occur

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23
Q

What are some common sites of atherosclerosis

A

at the bifurcations
in legs (smokers and DM)
epicardial portions of coronaries
New lesions at perianastomoatic sites of CABG (bypass grafting)

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24
Q

Atherosclerotic Risk Factors

A 
Men >45 Women >55 (or early menopause)
Family history of CHD
dyslipidemia
Smoking
HTN
High LDL or Low HDL
DM
Obesity
Low Birth weight in newborns
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25
Dyslipidemia
Cholesterol >200 mg/dl and increased LDL d/t genetics, dietary, or overproduction/deficient removal Increases risk of CAD could also be d/t DM, renal disease, alcoholism, hypothyroidism
26
Smoking
accelerates atherosclerosis and 3-5X greater chance of CAD Each year you don't smoke you risk goes down
27
DM
4x greater risk for an MI Gangrene of Lower Extremities Women more prone than men and often goes with hyperlipidemia Want to control Blood sure and Blood Pressure
28
HTN
5x great risk when 160/95 than normotensive Tx decreases CAD, CHF or cerebrovascular disease **MOST TREATABLE ASPECT OF ATHEROSLCEROSIS
29
Obesity and Inactivity
Obesisty associated with hypertryglceridemia, hypercholesterolemia, glucose intolerance, and HTN Inactivity can lead to decreased HDLs
30
What are some causes of atherosclerosis
``` High blood serum cholesterol and triglycerides High BP Infection High blood iron levels High blood homocysteine (correlation) ```
31
Atherosclerosis raises the systolic pressure by
Decreasing arterial distensibility, and vessel lumen diameter
32
Coronary Artery Disease Facts
Leading cause of death and disability in US 1:3 men 1:10 women <60 Mortality/death is declining d/t CPR, HTN management, and lower cholesterol diets
33
Manifestations of CAD:
Sudden Cardiac Death - can occur within 1 hour and occur more frequently in AM (6am-12pm) D/T hyper coagulable state One death every 90 seconds Peaks btwn ages of 0-6months (SIDS) and 45-75 years
34
Causes of Sudden Cardiac Death
75% d/t CAD 25% d/t myocardial abnormalities (hypertrophy, valvular disease) Narrowing of the coronary arteries >75% Old AMI ACUTE THROMBOSIS AT SITE OF FISSURED PLAQUE Lethal Dysrhythmias (rhythm problem) (Ventricular fibrillation, aystole, bradycardia)
35
Sudden Cardiac Death Lifesaving Tx
BLS (basic life support) ALS (advanced life support Pacemaker
36
What is the primary cause of death in sudden cardiac death
lethal dysrhymias
37
Coronary Artery Disease
narrowing or obstruction of the coronary arteries d/t atherosclerosis which causes a decreased perfusion of myocardial tissue and myocardial O2. Leads to HTN, angina, dysrhythmias, MI, CHF, and death
38
Why is occlusion of the coronary arteries in a young individual more lethal than in an older individual
The development of collateral circulation takes time; people who are older have arteries that have anastomitized which can help supply blood to occluded areas
39
What is the goal of tx in CAD
lather the atherosclerotic progression
40
CAD Manifestations: Angina
discomfort within or adjacent to the chest; typically provoked by exertion or anxiety Lasts for several minutes, alleviated by rest and does not result in myocardial necrosis Potential sequelae: AMI & Death
41
What can decrease myocardial oxygen demand
Decreased ventricular volume
42
Angina
chest pain resulting from myocardial ischemia caused by inadequate myocardial blood and oxygen supply **Imbalance btwn O2 supply and demand
43
Causes of Angina
obstruction of the Coronary Blood Flow d/t atherosclerosis, Coronary artery spasm, and conditions increasing myocardial oxygen consumption
44
Goal of Tx of Angina
provide relief of an acute attack, correct the imbalance between myocardial O2 supply and demand, and prevent the progression of the disease and further attacks to reduce the risk of MI
45
What is the most important concept relating to Angina
Most people have increased O2 demand and diminished O2 supply; they hear always extracts max O2 from blood even under minimal demand; Coronary blood flow can increase up to 7x to try and meet the O2 demands. CAD prevents body from meeting it's O2 demands
46
Types of Angina
Stable - person can predict that this is going to happen Unstable - occurs at lower levels of exertion or begins to intensify at rest (can result in MI 20%) Variant/ Prinzmetals - rest pain and V-arrhymias caused by CA spasm (no plaque; just spasms) (**could be r/t cocaine)
47
What are some descriptions/manifestations of Angina
Exertional chest discomfort Lasting several minutes in duration (>20 min suspect MI) Relieved by rest Any area between lower jaw and epigastrium - can radiate to neck arms "tightness" "heaviness" or "choking sensation" Provoked by walking up hill, stairs, vigorous arm work, intercourse, following a meal etc.
48
Physical findings of Angina
Increased HR and BP S4 d/t atrial contraction in a ventricle stiffened by ischemia S3 in Left ventricular failure Systolic mumur d/t mitral regurgitation as a result of ischemia
49
Diagnostic Tests for Angina
EKG during the pain Stress Test - chest pain or changes in ECG/VS during testing may indicate ischemia Cardiac Enzymes - normal enzymes/no random enzymes leaking = so it's probably just angina Cardiac Catheterization- GOLD STANDARD definitive way of looking into vessel
50
Cardiac Stress Test
Exercise on treadmill until ischemia EKG changes, angina, or dyspnea occur SHOULD NOT BE PERFORMED - SIGNIFICANT AORTIC STENOSIS, UNTREATED HTN, CHF, UNSTABLE ANGINA
51
PERSANTINE (dypridamole thallium IV)
for pts unable to exercise this drug will dilate the coronary arteries just the like exercise does
52
Coronary Arteriography/Cardiac Catheterization
GOLD STANDARD - and most precise means of documenting CAD. Takes pictures of artery where the occlusion is. Also gives measures of Left Ventricular Function **good for people with recurrent angina or lots of angina
53
Management of Angina
Counseling to tell them how serious it is Drugs can alleviate sx/ prolong survival Modify Risk Factors - Low fat and Low cholesterol diet, stop smoking, and control BP Search for correctable contributing factos (ex aortic stenosis, hyperthyroidism, sever anemia) Unstable - hospitalize and catheterization
54
Angina Implementation
Assess Pain AdMINISTER O2 AND 2-4 LITERS NITROGLYCERIN -TO DILATE the coronary arteries + reduce O2 requirements (only for healthy people without/ not related to atherosclerosis)
55
Surgical Procedures of Angina
Percutaneous Transluminal Coronary Angioplasty (PTCA) Laser Assisted-Angioplasty Vascular Stent Coronary Artery Bypass Graft (CABG)
56
Percutaneous Transluminal Coronary Angioplasty (PCTA)
dilate the artery/vessel with a ballon catheter to open the lumen and improved arterial blood flow
57
Complications of PCTA
arterial dissection/rupture immobilization of plaque fragments spasm Acute MI
58
Contraindications to PCTA
LEFT MAIN ARTERY STENOSIS SEVERE MULTI-VESSEL DISEASE **if vessel completely occluded you probably can't do this
59
Stent
metal cage inserted into blood vessels so it prevents the occlusion from reoccurring after the ballon is removed (maintains latency)
60
Laser Assisted Angioplasty
A laser probe is advanced through the artery; heat from the laser vaporizes the plaque to open the occlude artery * *used for clients with small occlusions in (distal superficial femoral, proximal popliteal, and iliac arteries) * If laser in wrong place it can blast the vessels
61
Atherectomy
USED IN THE 90s catheter with cutting chamber that aches the plaque (packman); works best in straight lesions NOT curvy vessels **Breaking clot is good, but the broken pieces can travel to the brain!
62
Coronary Artery Bypass Graft (CABG)
Attach a saphenous vein between ascending aorta and stenoic coronary artery - give the blood another way to go, except usually get occlusions there too after about a year (10%)
63
Coronary Revascularization has 2 forms...what are they?
CABG PCTA **ways of restoring blood flow to the area
64
Acute Myocardial Infarction Causes **Acute MI same as MI
almost all are d/t thrombotic occlusion r/t CAD infective endocardidtis emboli (infection of the heart muscle/valves) atrial thrombi vasospasm from cocaine, amphetamine use small vessel disease in DM trauma
65
Myocardial Infarction (process and tissues)
occurs when Myocardial tissue is abruptly/severely deprived of Oxygen; ischemia leads to necrosis if blood flow isn't restored Infarction does not occur instantly but evolves over several hours **Obvious physical changes will not occur until 6 hours after the infarction has occurred (swollen and blue tissue) After 48 hours the infarct turns grey with yellow streaks as neutrophils invade the tissue 8-10 days after the infarction granulation tissue forms Over 2-3 months the necrotic area develops into a scar which permanently changes the size and shape of the left ventricle
66
MI Key factors
Angina (especially if pain has changed/increased when at rest) Absence of exacerbating factors (ex anemia, htn, chf, hypothyroidism) - this could reflect changes in plaque resulting in intermittent thrombosis Q wave infarcts = indicate the entire portion/thickness of LV is involved Only take 20-40 minutes for muscle death to start occurring
67
What does the Size of the Infarct spent on
extent, severity, and duration of ischemia amount of collateral circulation metabolic needs of myocardium at time of the event
68
What does a Q wave infarct indicate?
``` AKA TRANSMURAL (ACROSS THE WALL) damage in the heart muscle has gone through all 3 layers of the heart muscle **damage typically begins from the inside (endocardium) ```
69
Common Locations for MI
Coronary Arteries (LAD 40-50%)
70
What is the result of MI on the affected portion?
decreased contractility with abnormal wall motion altered compliance/stretch decreased Stroke Volume --> decreased EF Non contraction Non Stretching Non Filling
71
What does the area of infarct look like?
``` Central area of necrosis Surrounded by injured area Surrounded by ischemia Myocardium does NOT regenerate Replaced by scar tissue ```
72
Manifestations of MI
Onset of MI usually occurs in the early AM d/t increased platelet aggregation Q wave infarct preceded by fatigue , chest discomfort, malaise in days preceding May be clinically "silent" (found later on ECG) Ex. DM damages nerves in Blood vessels, so you could not notice the symptoms
73
Risk Factors for MI
``` Athereoslcerosis CAD Elevated cholesterol levels Smoking HTN Obesity Physical Inactivity Impaired Glucose Tolerance Stress ```
74
Signs/Sx of AMI
Intense severe, crushing pain unremitting for 30-60 min Diaphoresis Cool, Clammy, Grey Skin Weakness
75
What does impaired L ventricular filling result in
pulmonary edema/congestion (blood backs up to the lungs) = SOB, tachypnea, orthopnea and moist crackles
76
Will BP be increased or decreased with AMI?
BP increased initially, but with R Ventricular/L infarction may be hypotensive/drop in BP
77
What are some things that may happen with the heart later after an MI?
displacement of PMI soft S1 S3 and S4 mitral regurgitation friction rub
78
Diagnostic Tests for MI
Creatine Kinase Troponin AST (aspartate aminotransferase) LDH (Lactic dehydrogenase)
79
Creatine Kinase Test
CK or CPK - enzyme found in the heart, brain, and skeletal muscles. Serum CK levels are elevated when muscle or nerve cells are injured If you have increased muscle mass you will have more CK. There are 3 isoenzymes CK-MM = found in skeletal muslce CK-MB = found in cardiac muscle CK-BB = found in brain and lung Elevated CK-MB can help you determine timing, quantity, and resolution of MI
80
Troponin T test (specific)
regulatory protein found in skeletal and cardiac muscles; specific antibody can detect cardiac troponin-T and is specific for myocardial injury
81
Troponin I test
GOLD STANDARD this protein is found in cardiac muscle complex -specifically the myocardium and will return to nL sooner (8-16 hrs after onset) than Troponin T.
82
During an MI when do enzymes peak
fastest enzymes (Troponin-I and CK) rise within 4-6 hours after onset of MI - helps determine when person had MI
83
When does CK-MB peak
18 hours after onset
84
When does Troponin - I peak
11 hours after onset
85
When do CK-MB and Troponin -I return to normal?
CK-MB = 2 days Troponin-I = 4 days
86
Hemodynamic Monitoring
ICU related tests and catheters that can go into the heart to measure it's pressures which can help monitor MI
87
On EKG what may indicated an MY
elevated ST inverted T wave Deep Q wave will be on there for the rest of the persons life after a MI
88
What is a non-Q waves infarct?
partial heart attack
89
Echocardiogram
ultrasound of heart - takes from 30-90 min depending on the pts condition; it evaluates: how well the heart is moving how well the valves are working the size of the heart and it's pumping chambers/ventricles
90
What is the most serious complication after an MI
DYSRHYTHMIAS (A-fib) d/t tissue ischemia, hypoxia, SNS and lactic acidosis causes decreased CO and increased cardiac irritability which will further decrease myocardial perfusion
91
What is the most common cause of death after an MI outside of the hospital
V fib
92
What are other complications after an MI
CHF Cardiogenic shock = L ventricular failure Thromboembolism = too much bed rest - can travel to brain kidneys and spleen Ischemic pericarditis= inflammation of the pericardium (chest hurts) Myocardial Rupture = immediate death Ventrical Aneurysm - thin and bulging with pressure- eventually pops and blood comes pouring out
93
AMI prehospital tx
ems now trained in defibrillation AEDs are now publicly available analgesia with morphine = venus dilation and decreased preload aspirin therapy = anti platelet effect/reduces chances of clots
94
AMI hospital tx
CCUs (coronary care units) reduce mortality by 50% - Defibrillate, continuous ECG Telemetry monitoring for arrhythmias - can go with pt and hospital can watch whats going on in the heart Stool softeners to prevent straining Bed rest no more than 1 day O2 therapy to avoid hypoxemia
95
What do we do after an MI?
prevent recurrence with calcium channel blockers or beta blockers and aspirin anticoagulation for 6 months discuss risk facts cardiac rehab - mild monitored exercise to increase tolerance
96
The main difference between myocardial infarction and angina is
with MI the pt is more likely to experience radiation pain to the neck and arm; with angina the pain is more localized

Patho Exam 3 (4 decks)

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