Ch.18 Alterations In Cardiac Function

Front 1

Names for CHD

Back 1

Ischemic heart disease (IHD)
Coronary Artery Disease (CAD)

Front 2

What is the source of most CHD ?

Back 2

Atherosclerosis

Front 3

Atherosclerosis

Back 3

progressive narrowing of the arterial lumen

Front 4

What are major risk factors Of CHD ?

Back 4

Front 5

What is atherosclerotic place mostly composed Of?

Back 5

Lipids

Front 6

Which Lipids are associated with higher risk of atherosclerosis ?

Back 6

LDL's + Triglycerides

Front 7

What are the types of Lipids?

Back 7

LDL = BAD
Triglycerides = BAD
HDL: Good

Front 8

How are HDL's good For Athero sclerosis ?

Back 8

Transport cholesterol from peripheral tissues back to liver , thus removing plaque

Front 9

Hyperlipidemia

Back 9

Genetic
- defect in LDL receptor on liver cells
- inability of liver to efficiently remove cholesterol from blood

Front 10

How is Atherosclerotic Plaque formed ?

Back 10

1. initiated by injury to coronary artery epithelium
2. After injury endothelium-may become more permeable + recruit leukocytes
3. LDL 's leak through and Macrophages Oxidize them
4. Oxidized LDL's are damaging +timuiate recruitment of macrophages
5.macrophages engulf lipids (foam cells)
6. Macrophages + foam cells attract More leukocyteS
7.Excess lipids and debri accumulate within cell wall
8.They Colace into a lipid pool or core

Front 11

Which plaques are more prone to rupture?

Back 11

ones with large lipid cores

Front 12

What does a ruptured plaque cause?

Back 12

initiates Platelet aggregation and thrombis formation

Front 13

Which plaques are less likely to rupture?

Back 13

Older plaques because they have more Collagen and fibrin

Front 14

What happens when a plaque Occupies 75% or more of arterial lumen ?

Back 14

sig. reduction in blood flow

Front 15

Where can plaque be located?

Back 15

Anywhere in the 3 major Coronary arteries or secondary branches

Front 16

Difference between small and large lesions?

Back 16

Small = fatty streaks, precursor lesions and asymptomatic
Advanced= small lesions that acquired More free lipids, cause narrowing Of lumen and are prone to rupture
* this can cause thrombis formation

Front 17

What has to happen to be diagnosed with CHD ?

Back 17

Critical narrowing of lumen then Sudden plaque rupture and Thrombs formation

Front 18

stable plaques

Back 18

asymptomatic
associated with exercise induced agina pain (stable angina pectoris)

Front 19

What is almost always associated With Plaque rupture ?

Back 19

-Acute coronary syndrome
-Unstable angina
-MI
-.sudden Cardiac arrest

Front 20

What is ischemia?

Back 20

insufficient Oxygen apply that Causes cell death

Front 21

pathophysiology of Ischemia

Back 21

the heart is unabe to slow its activity when ATP Supplies dwindle, a Steady flow of oxygen is essential

Front 22

What are the critical factors in meeting cellular demands for Oxygen ?

Back 22

1. Rate of coronary perfusion
2. Myocardial workload

Front 23

How can coronary perfusion be impaired?

Back 23

Atherosclerotic plaque
Thrombis
vasospasm
Failure of auto regulation by microcirculation
poor perfusion pressure

Front 24

Classic or stable Angina pectoris

Back 24

When onset of ischemia is predictabe with certain activities and subsides with rest

Front 25

ACS occurs when?

Back 25

Obstruction of coronary blood flow results in Acute myocardial ischemia

Front 26

What enhances risk of thrombus formation?

Back 26

High fibrinogen levels (smokers)
Enhanced platelet adhesiveness (hyperlipidemia)

Front 27

How is a clot formed?

Back 27

Begins with adherence of Platelets to the ruptured plaque
platelets that attach attract more and form a plug

Front 28

coagulation cascade

Back 28

resluts in formation of platelet-fibrin clot that May occlude the vessel or break loose and travel

Front 29

Aspirins Role?

Back 29

long term use of small doses of aspirin reduces mortality from ischemic heart disease

Front 30

What are Vulnerable plaques?

Back 30

Those with large lipid cores, thin caps, or high Sheer stress

Front 31

Myocardial ischemia may be cased by ?

Back 31

coronary vasospasm , hypoxemia, Or low perfusion pressure

Front 32

Angina Pectoris

Back 32

Chest pain
- associate w/ MI

Front 33

What causes Angina pectoris?

Back 33

conditions that increase myocardial Oxygen demand
• exercise
• Stress
• SNS activation
• increase preload, after load, heart rate or muscle mass

Front 34

Referred pain

Back 34

pain experianced in one location but felt in another

Front 35

What may Angina pain be described as?

Back 35

burning, crushing, squeezing, or choking

Front 36

Atypical symptoms of MI ?

Back 36

Back pain
fatigue
weakness

Front 37

3 patterns of angina pectoris?

Back 37

1. stable Angina
2. Prinzmetal variant angina
3. Unstable or Crescendo Angina

Front 38

Stable Angina

Back 38

* Most Common form
* Classical or typical
* reduction of coronary blood flow
* predictable
* relieved by rest and nitroglycerin

Front 39

What is nitroglycerin used For and what does it do?

Back 39

Relieves stable Angina
ceases peripheral and Coronary Vasodilaton, reduces preload, and reduces myocardial workload

Front 40

Prinzmetal variant angina

Back 40

* unpredictable attacks of anginal pain
* most have sig. coronary atherosclerosis
* atherosclerosis is NOT what causes ischemic symptoms
* Vasospasm is the Culprit
* Treatment = Calcium channel blocking agents

Front 41

What are patients with Angina at risk for developing?

Back 41

Acute Coronary Syndrome (ACS)

Front 42

Acute Coronary syndrome

Back 42

* A mix of unstable angina and MI
* Cause Chest pain that may be more severe and lasts longer than typical angina
* may occur in those who were previously asymptomatic
* Plaque rupture With thrombus formation Occurs

Front 43

Difference between unstable Angina and MI?

Back 43

Unstable = Occlusion is partial or Clot will dissolve before the death of myocardial tissue
MI = occlusion is complete and thrombus persists long enough for development of irreversible damage to myocardial cells (necrosis)

Front 44

What has to be present to determine MI?

Back 44

Bio-Markers
* CK-MB, Troponis I+T

Front 45

What is Reperfusion Therapy?

Back 45

Treatment that restores blood back through blocked arteries
* only effective early in course of infarction

Front 46

Who is a candidate for reperfusion therapy?

Back 46

patients with Chest pain and STEMI

Front 47

what is a STEMI ?

Back 47

ST-segment elevation

Front 48

When does MI occur?

Back 48

When prolonged or total disruption of blood flow to myocardium Causes cellular death by necrosis or apoptosis

Front 49

What is the initiating event that causes MI?

Back 49

thrombus on plaque
* sudden Change in plaque structure

Front 50

What is the role of platelets in Acute MI?

Back 50

Platelets adhere to cracked plaque and forma plug, activate clotting cascade
* Thrombus grows until it occludes the vessel and triggers MI

Front 51

Where are most infarcts located?

Back 51

Left ventricular walls

Front 52

When can morphologic changes from MI be detected ?

Back 52

6-12 hours after infarct

Front 53

When does the infarct become Obvious to detect and why?

Back 53

18-24 hours after infect
* area becomes yellowish + soft with a rim of red vascular connective tissue

Front 54

When is the necrotic tissue progressively degraded and Cleared from the site?

Back 54

1 to 2 week after infarct
* myocardium is weak and susceptible to rupture at this time

Front 55

When has the necrotic tissue been replaced by scar tissue?

Back 55

6 weeks after infarct

Front 56

What is the diagnosis of a MI made from?

Back 56

1. S+S
2. ECG changes
3. Elevaticn in Specific marker proteins

Front 57

MI pain can be described as?

Back 57

Severe crushing, excruciating Chest pain.... may radiate to arm , Shoulder, neck, back

Front 58

Are MI's relieved by nitroglycerin ?

Back 58

NO

Front 59

How long do MI's normally last longer than?

Back 59

15 minutes

Front 60

How is necrotic tissue shown on an ECG?

Back 60

* Abnormally deep Q waves
* Inverted T waves
* Elevation of ST

Front 61

List the serum markers

Back 61

CK-MB
Troponin I
Troponin T

Front 62

How long does the CK-MB Stay elevated for?

Back 62

48-72 hours after MI

Front 63

What are the markers of Choice for detecting MI?

Back 63

Troponin I + T
* because they remain elevated for longer periods of time
* Not good for new infarction (reinfaction)

Front 64

What causes the Q Wave findings?

Back 64

totally ischemic cells, which die and become electrically silent
* release serum marker proteins

Front 65

What is responsible for ST elevation ?

Back 65

Abnormal iron flux

Front 66

Treatment for MI is directed at?

Back 66

*decreasing 02 demand
* increasing Myocardial 02 supply

Front 67

What is sudden cardiac Arrest?

Back 67

unexpected death from cardiac arrest within 1 hour of the onset of symptoms
* CAD usually cause
* high risk of having another if you survive the first

Front 68

Chronic Ischemic Cardiomyopathy

Back 68

Heart failure develops insidiously as a Consequence of progressive ischemic Myocardial damage
* had a history of angina or mi
* common in the old

Front 69

Stenosis

Back 69

Failure of a Valve to Open Completely

Front 70

Regurgitation (insufficiency)

Back 70

inability of a valve to close completely

Front 71

What are the primary causes of stenosis?

Back 71

Rheumatic heart disease and Valvular Calcification with aging

Front 72

What are Valvular disorder often associated with?

Back 72

Abnormal turbulence of blood that produces Murmurs

Front 73

Mitral Stenosis

Back 73

Flow of blood from the left atrium into the left ventricle is impaired
* not enough blood coming out
* decrease cardiac output
* increased left atrium Pressure from back Flow

Front 74

S+S of Mitral Stenosis

Back 74

left atrium hypertrophy
Afib
clots , embolism , Stroke
Pulmonary Congestion
* orthopenea
* cough
* dyspnea(exertional)=Most common complaint
* poor 02 sat

Front 75

Mitral Regurgitation

Back 75

Backflow of blood from left Ventricle to left atrium during ventricular systole
* giant V wave
*high after load increases regurgiant flow
*hypertrophy + dilation
*eventually lead to left sided HF

Front 76

S+S of Mitral Regurgitation

Back 76

Pulmonary congestion
poor cardiac Output
Chronic weakness + fatigue

Front 77

Mitral valve Prolapse

Back 77

Mitral ValVes that balloon into the left atrium during systole

Front 78

Aortic Stenosis

Back 78

Obstruction to aortic outflow from the left ventricle into the aorta during systole
*Could lead to left heart failure
* cause is age related calcification
*FORMATION OF CALCIUM DEPOSITS ON CUSPS!!
*70-90 years old
*high pressure in left ventricle

Front 79

S+S of Aortic stenosis

Back 79

Diminished Cardiac output
* syncope
* fatigue
* low systolic BP
* faint pulses
Pulmonary complications later on

Front 80

aortic Regurgitation

Back 80

blood leaks Back from aorta into left ventricle during diastole
* left ventricle becomes overloaded
* left Ventricle hypertrophy + dilation
* large stroke volume , high systolic bp

Front 81

S+S of Aortic Regurgitation

Back 81

bounding peripheral pulsation
* head may bob with each systole
* complain of palpitations and a throbing or pounding heart
* left sided heart failure

Front 82

Rheumatic Heart Disease

Back 82

From rheumatic Fever = acute Inflammatory disease from strep
* damage from immune attack on the individuals own tissues

Front 83

Infective Endocarditis

Back 83

inflammation of Endocordium
*vegetation on valves
* biggest cause = strep
* blood born
•IV users
• recent value replacement
• major surgery
-antibiotics b4 procedures

Front 84

Myocarditis

Back 84

inflammation, leukocyte infiltration and necrosis of cardiac muscle cells

Front 85

Acute myocarditis

Back 85

left ventricular dysfunction or dilation of all four chambers
* myocardium of Ventricle is flabby With patchy or diffuse nerotic lesions

Front 86

Cardiomyopathy

Back 86

Weakening of heart muscle
* heart becomes thick, rigid, or enlarged

Front 87

Dilated Cardiomyopathy

Back 87

Ardiac failure associated With dilation of one or both ventricular Chambers

Front 88

Causes of DCM

Back 88

Alcohol toxicity
genetic abnormalty
pregnancy
Post viral myoccrditis

Front 89

Hypertrophic Cardiomyopatty

Back 89

characterized by thickend, hyperkinetic Ventricular muscle mass
* left and\ or right ventricular hypertrophy
* asymetric
* usually involves septum
* genetic

Front 90

restrictive Cardiomyopathy

Back 90

Rarest form
* Stiff, fibrotic Ventricle with impaired diastolic filling
* reduced diastolic size of either or both ventricles
* idiopathic

Front 91

Pericardial Effusion

Back 91

Accumulation of fluid in the pericardial sac
* normally has 30 -50mL of clear thin fluid

Front 92

Types of effusions

Back 92

Serous= transudate secondary to heart failure or hypoproteineMia

Serosanguineous= serous fluid and blood

Chylous = collection of lymph from Obstruction of lymphatic drainage

Blood = hemopericardium usually resulting from penetrating trauma to the heart

Front 93

Cardiac Tamponade

Back 93

large fluid accumulation that causes Compression of the heart Chambers Which causes impaired filling

Front 94

S+S of Cardiac Tamponade

Back 94

3 classical findings
•hypotension
•distended neck veins
•muffled heart sounds
reduce stroke volume
increase heart rate
systemic venous congestion
*distended neck veins
waxing and waning of BP

Front 95

Acute Pericarditis

Back 95

*80% are idiopathic -viral
* resolves spontaneously within 2 weeks
* NSAID's only therapy
* presents with chest pain
* rubing of pericardial layers may be heard as a friction rub
- squeaky or like scratch sandpaper

Front 96

Chronic Pericarditis

Back 96

Healing of an acute form of pericardial inflammation
• destruction of pericardial sac
• adhesion of heart to surrounding mediastinai structures
• impaired cardiac contraction

Front 97

Constrictive pericarditis

Back 97

results in a fibrous, Scarred pericardium that restricts cardiac filling