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N361: Pathophysiology II > Module 9: Disorders of Cardiac Function > Flashcards

Module 9: Disorders of Cardiac Function Flashcards

1
Q

Where is the heart located

A

in the left side of the mediastinum

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2
Q

Epicardium

A

covers the outer surface of the heart

has 2 layers: parietal and visceral

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3
Q

Myocardium

A

the middle layer of the heart and is the actual contracting muscle of the heart

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4
Q

Endocardium

A

is the innermost layer of the heart and lines the inner chambers and the heart valves

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5
Q

The epicardium is continuous with…

A

the pleura of the lungs

this means any leakages there can compress the heart as well

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6
Q

the endocardium is continuous…

A

with the endothelium of all vessels in the body - it ends up being a closed system to allow laminar flow

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7
Q

The atrioventricular valves lie between…

A

the atria and ventricles (the bicuspid/mitral and tricuspid valves)

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8
Q

The atrioventricular valves close when?

A

at the start of ventricular contraction (to prevent blood from flowing back into the atria from the ventricles

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9
Q

When do the atrioventricular valves open up?

A

the valves open when the ventricles relax

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10
Q

The bicuspid/mitral valve is located…

A

on the left side of the heart

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11
Q

The tricuspid valve is located…

A

on the right side of the heart

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12
Q

What holds leaflets of valves closed?

A

Papillary Muscles and Chordae Tendinea

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13
Q

Which AV valve has higher pressure on it?

A

Mitral (by a lot)

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14
Q

The pulmonic semilunar valve lies …

A

between the right ventricle and the pulmonary artery

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15
Q

The aortic semilunar valve lies between…

A

the left ventricle and aorta

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16
Q

When do the semilunar valves open?

A

they open during ventricular contraction

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17
Q

When do the semilunar valves closed

A

when the ventricles begin to relax

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18
Q

What is the purpose of the semilunar valves

A

to prevent blood from flowing back into the ventricles during relaxation

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19
Q

What feeds the myocardium?

A

NOT BLOOD IN THE VENTRICLES

it is the coronary circulation that feeds it

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20
Q

Where do the coronary arteries start?

A

they root off of the aorta

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21
Q

Coronary Veins

A

return deoxygenated blood from the heart back to the circulation so the blood can mix with systemic blood

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22
Q

What causes anginal pain?

A

In something like heart failure, the perfusion of coronary circulation is bad causing pain from tissues not being fed

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23
Q

Where do the vessels of coronary circulation go?

A

Around the heart and deep into the tissues as well

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24
Q

The coronary circulation has what two major branches?

A

Left Coronary Artery
Right Coronary Artery

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25
Q

What areas of the heart does the left coronary artery feed

A

it is the foremost facing artery due to position of the heart in the chest, so it feeds the anterior part of the septum and the anterior left ventricle

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26
Q

What will happen if there is a block in the left coronary artery

A

there will be an inability to get conduction down to the bundle of HIS

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27
Q

What are the parts of the Left Coronary Artery

A

Left Anterior Descending

Left Circumflex

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28
Q

what does the left anterior descending feed

A

the anterior septum

the anterior left ventricle

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29
Q

What does the left circumflex feed

A

the lateral wall and left ventricle

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30
Q

What area of the heart does the right coronary artery feed

A

posterior septum

posterior heart

SA and AV nodes

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31
Q

What can a blockage of the right coronary artery cause

A

it can lead to inadequate perfusion, impair the SA, AV nodes and Perkinje fibers, and stop conduction occurring in those regions

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32
Q

So, blockage of coronary circulation …

A

impacts both the myocardium tissue AND the cells responsible for electrical potential for contraction and electrical activity - a dual deficit

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33
Q

___ is the pacemaker of the heart

A

SA-Node

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34
Q

Where is the SA node

A

it starts in the right atrium

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35
Q

What is the pathway of heart conduction?

A

SA node –> left and right atria/AV Node –> bundle of HIS –> right and left bundle branches –> perkinje fibers

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36
Q

What happens once conduction gets to the AV node

A

atrial contraction

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37
Q

What happens once conduction gets to the perkinje fibers

A

ventricular contraction

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38
Q

What allows fast electrical conduction through the heart

A

intercalated discs between cardiac muscle cells

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39
Q

Why is it important that the signals move through the ventricles and aorta differently?

A

Aorta are thinner and smaller while ventricles are thicker and bigger - so signals take longer to get through them

If we did not have this then the ventricles could not contract simultaneously (since the right side of the heart is a lot thinner than the left) and we would ack ventricular contraction coordination

It also allows the SA and AV nodes to get signals at the same time and allow contractions simultaneously

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40
Q

P-Wave

A

Repolarization of the Atria in response to SA node triggering

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41
Q

QRS Complex

A

Represents Ventricular Depolarization - triggers the main pumping contractions

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42
Q

T Wave

A

represents ventricular repolarization

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43
Q

PR Interval

A

delay of the AV ode to allow filling of the ventricles

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44
Q

What cannot be seen in an EKG

A

the atrial repolarization since it is lost behind the QRS complex

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45
Q

If there is a malfunction of conduction from a blockage or damage to the Bundles what can occur on an EKG?

A

there can be a delay in getting signals to the ventricles leading to a prolonged PR interval

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46
Q

SA Node

A

pacemaker of the heart that initiates each heartbeat

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47
Q

Where is the SA node located

A

at the junction of the superior vena cava and right atrium

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48
Q

How fast does the SA node generate electrical impulses?

A

60-100 times per minute

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49
Q

what controls the SA node

A

the SNS (spinal nerve) and PNS (vagus nerve)

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50
Q

AV Node location

A

in the lower aspect of the atrial septum

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51
Q

AV Node

A

a node that gets signals from the SA node that moved through the atria in order to keep the conduction going (also sets up a slower electrical impulse if SA node is damaged)

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52
Q

The Bundle of HIS (AV Bundle)

A

Another pacemaker site from the fusion of the AV node

It branches into the right and left bundle branches which will terminate into Perkinje’s fibers

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53
Q

Where do the right bundle branches extend through

A

the right side of the interventricular septum

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54
Q

Where do the left bundle branches extend through

A

extend into the left ventricle

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55
Q

If the SA node and AV node fails, the bundle of HIS can initiate and sustain a heart rate of what?

A

40-60 BPM

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56
Q

What electrical impulse speed can the AV node make

A

50 BPM

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57
Q

Can the Bundle of HIS provide electrical impulses fast enough for adequate perfusion

A

no, 40 is rather low

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58
Q

What electrical impulse speed can the Perkinje Fibers make

A

30 BPM

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59
Q

The lower the control of conduction on the heart…

A

the lower the heart rate

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60
Q

Perkinje’s Fibers

A

a diffuse network of conducting strands located beneath the ventricular endocardium

These fibers spread the wave of depolarization throughout the ventricles

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61
Q

First Heart Sound

A

“Lub”

Made when the AV shut at the start of systole due to increased ventricular pressure

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62
Q

What is the actual sound of the heart coming from?

A

Not the valves closing but the disruption of laminar flow of blood they cause - turbulence

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63
Q

Second Heart Sound

A

Occurs when the semilunar valves shut at the end of systole from falling ventricular pressure - the pressure in the ventricles drops below that in the great vessels so these close to prevent backflow

“Dub”

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64
Q

Physiologic Split

A

The aortic valve closes slightly sooner than the pulmonic valve in order to allow the same amount of blood to go through from both areas

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65
Q

Atherosclerosis

A

Athero = Gruel/Paste ; Sclerosis = Hardening

It is the characterized by fibrofatty lesions in the intimal lining of the aorta, large and medium arteries (more than small), coronary arteries, and carotid arteries and other larger vessels that supply the brain

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66
Q

The most commonly affected vessel with atherosclerosis is…

A

the coronary arteries

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67
Q

The number 1 cause of death in the US is

A

heart disease

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68
Q

The third most common cause of death is

A

stroke

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69
Q

A major risk factor for atherosclerosis is…

A

hypercholesterolemia

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70
Q

The most common cause of CAD is…

A

inflammation r/t atherosclerosis

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71
Q

How does atherosclerosis cause blocks?

A

accumulation of fatty fibrous plaques and lipids progressively narrows the lumen of the vessel and impedes blood flow to the myocardium

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72
Q

Progression of atherosclerosis causes…

A

vascular changes that impair the diseased vessels ability to dilate

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73
Q

In advanced atherosclerosis what can occur?

A

rupture or calcification

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74
Q

What is another disease that is related to heart disease?

A

Gum disease - a portal of entry for bacteria to get through is the gums and along with non laminar flow from deposits and calcification bacteria can grow and start inflammatory processes

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75
Q

Atherosclerosis = ___ + ___

A

fat plaque build up + inflammation

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76
Q

Atherosclerosis was once thought of as a ___ problem, but we now know…

A

plumbing; now we know its inflammation thats also related

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77
Q

What may be high d/t the inflammation in atherosclerosis

A

C reactive protein levels

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78
Q

Evidence from research increasingly suggests that ___ is a significant part of atherosclerosis

A

inflammation! (with the fibrofatty plaques)

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79
Q

Common risk factors for the inflammation r/t to atherosclerosis?

A

All these release pro inflammatory cytokines

Smoking
Hypertension
Lipoproteins
Hyperglycemia

(All common heart disease risks)

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80
Q

What may also have a role, that we are not too sure of, in atherosclerosis?

A

Infection (chlamydia, herpes, CMV)

But we do not know whether they cause it or entered the disease vessel opportunistically

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81
Q

The majority of cases of myocardial and cerebral infarction are due to?

A

Atherosclerosis

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82
Q

The principal cause of death among men and women in the US and western Europe is

A

Atherosclerosis

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83
Q

In what layer of the blood vessels does atherosclerosis lesions tend to occur?

A

in the innermost layer - the intima of the medium and large muscular arteries

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84
Q

What are some potential sequelae of atherosclerosis?

A

MI (block C artery)

Stroke (block Ce Artery)

Gangrene (Block leg/arm)

Sudden Cardiac Death (instant death)

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85
Q

Surprisingly one of the first manifestations of atherosclerosis can be ___

A

death

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86
Q

Atherosclerosis occurs in what age groups?

A

ANY AGE

occurs in all ages, present at birth in some infants, and is common in young children too

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87
Q

As the atherosclerosis lesion develops what stages will it undergo?

A

Fatty streak –> fibrous plaques –> complicated lesions

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88
Q

Fatty Streaks

A

A reversible time for lesion development of atherosclerosis

It contains foam cells

During this smooth muscle from the tunica media migrate into the tunica intima and take on the appearance of foam cells

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89
Q

Foam Cells

A

macrophages filled with lipids and T cells

present in fatty streaks

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90
Q

Fibrous Plaques

A

Progressive thickening that can occlude the lumen with necrosis and calcification

it is made of connective tissue, smooth muscle cells full of lipids, macrophages, and lymphocytes

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91
Q

As the fibrous plaque expands, what does the artery do?

A

It inflames to form a fibrous cap that separates the plaque from the lumen which ends up causing decreased blood flow and increased blood pressure

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92
Q

Complicated Lesion

A

a fibrous plaque that has undergone extensive degeneration and may rupture

The softer lesions are more likely to rupture and the bleeding can cause occlusion leading to MI

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93
Q

How does a complicated lesion lead to occlusion for something like MI

A

The lesion has ulcerations, cracks from the plaque rupture serving as sites for platelet aggregation

this can allow the platelets to form a thrombus and have sudden occlusion of the vessel

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94
Q

___ lesions are more likely to rupture

A

softer

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95
Q

Most MI are due to what …

A

rupture of a vessel, bleeding, and clot formation that causes acute occlusion

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96
Q

Common sites for atherosclerosis vessel occlusion

A

Aorta

Femoral Artery

Popliteal Artery

Tibial Artery

Coronary Arteries

Carotid Arteries

Cerebral Arteries

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97
Q

Occlusions and Atherosclerosis most commonly occurs are ___

A

bifurcations (since it is more turbulent leading to debris collection or damage)

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98
Q

Atherosclerosis of the legs is more common in ___ and ___

A

smokers and DM

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99
Q

What is the most common region of plaque build up for the coronary arteries

A

the epicardial region

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100
Q

Can lesions occur in sites from CABG

A

yes. if you have bypass surgery you can get a lesion at the new stitched together vessels (perianastomotic sites)

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101
Q

Risk factors for Atherosclerosis

A

Male over 45

Women over 55 or early menopause

Family hx of premature CHD, AMI, or sudden death

Smoking

HTN (greater than 140/90)

High LDL cholesterol (greater than 160)

High triglycerides (greater than 250)

Low HDL cholesterol (lower than 35)

DM

Obesity and inactivity

Low birth weight

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102
Q

How does hyperlipidemia relate to atherosclerosis as a risk factor?

A

CAD and Chronic Hypercholesterolemia are clearly associated - with high cholesterol and LDL (and low HDL) increasing risk x5!!!

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103
Q

What are some causes for hypercholesterolemia?

A

Dietary

Genetic

Overproduction

Deficient Removal

(Familial Hypercholesterolemia gets 500-1000 mg/dL due to faulty receptors)

DM

Renal disease

alcoholism

hypothyroidism

corticosteroids

estrogens

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104
Q

Why do we need cholesterol?

A

it is an ingredient in bile and the lipoprotein bilayer of every cell

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105
Q

How does smoking impact heart disease and atherosclerosis?

A

It accelerates atherosclerosis

has a 3-5x greater risk for CAD

has a 70% death rate

(It increases BP, impacts vascular tone, decreases myocardial O2, increases LDL oxygenation, contributes to inflammation, damages the endothelial lining, etc)

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106
Q

Good news regarding smoking as a risk for heart disease?

A

Smoking cessation reduces risk to that of non smokers within 1 year (risk of heart disease; lung cancer not so much)

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107
Q

How is Diabetes mellitus a risk factor for atherosclerosis and CAD?

A

Gives a 4x greater risk of MI

Can lead to gangrene of lower extremities

Women get more prone to it than men

changes metabolism of fats leading to differing HDL and LDL issues

Often coincides with hyperlipidemia

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108
Q

What is the goal with DM patients

A

control blood sugar and blood pressure (to lower CAD risk)

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109
Q

Bad News about Hypertension and heart disease

A

risk is 5x greater when you have a BP of 160/95 than normotensive

can be idiopathic and be a silent killer

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110
Q

Good news regarding HTN and heart disease

A

treatment can decrease cardiovascular disease, CAD, and CHF significantly and there are many great treatments

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111
Q

The most treatable risk factor for heart issues is ___

A

hypertension

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112
Q

Reducing the risk of MI also reduces risk of ___

A

stroke

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113
Q

What is obesity associated with that contributes to heart disease risk

A

hypertriglyceridemia

hypercholesterolemia

glucose intolerance and DM

HTN

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114
Q

What is inactivity associated with that contributes to heart disease risk?

A

it can cause HDL levels to drop

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115
Q

What are some of the theories on what causes atherosclerosis to occur?

A

High serum cholesterol and triglycerides

High BP

Infection (and inflammation)

High Blood Iron Levels

High Blood Homocysteine Levels

(Different initiating events are involved to different degrees in different people)

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116
Q

What is the theory on why atherosclerosis may be higher in men than pre menopausal women?

A

Women lose 30 mg of iron a month and get 30 a day, so they go even but men do not leaving them potentially more predisposed to atherosclerosis if it partly from blood iron levels since it can deposit in vessels

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117
Q

Why is it believed high homocysteine levels contributes to atherosclerosis?

A

It is an AA that increases rates of heart disease and stroke and has an unclear relationship with alzheimers and osteoporosis

Also too much can irritate blood vessel linings leading to scarring, hardening, and narrowing increasing workload and coronary events and contributing to clotting

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118
Q

The leading cause of death and disability in the US is

A

CAD

(1 in 3 men, 1 in 10 women over 60; 800000 new AMIS each year, 450000 recurrences each year)

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119
Q

Why is the mortality rate of CAD declining some in recent years?

A

CPR

management of HTN

lower cholesterol diets

use of antibiotics

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120
Q

Risk of atherosclerosis and CAD is equal to that of men for women after…

A

menopause

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121
Q

Sometimes the first and only manifestation of CAD is

A

sudden cardiac death (25% of cases)

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122
Q

CAD r/t sudden cardiac death only takes how long to cause death?

A

1 hour

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123
Q

When is peak risk for sudden cardiac death related to CAd

A

between 0-6 months and 45-75 years

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124
Q

Why is sudden death, stroke, and MI more frequent in the morning between 6a and 12p for CAD?

A

that is a time of hypercoagulability and the greatest platelet aggregation can occur then

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125
Q

What are the major factor causes of sudden cardiac death

A

75% of cases are from CAD

25% are from myocardial abnormalities such as hypertrophy, dilated cardiomyopathy and valvular disease

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126
Q

What are some other causes of sudden cardiac death

A

narrowing of the coronary arteries

an old AMI

acute thrombosis at the site of fissured plaque

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127
Q

Sudden cardiac death can occur when ___% of the coronary artery vessel is narrowed

A

75%

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128
Q

In 90% of sudden cardiac deaht cases actual death is a result of…

A

LETHAL DYSRHYTHMIAS

(Ex: ventricular tachycardia, ventricular fibrillation, bradycardia, or asystole)

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129
Q

If Sudden Cardiac Death events are left untreated…

A

there is irreversible brain damage in 3-5 minutes followed by death

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130
Q

Possible lifesaving treatments for sudden cardiac death?

A

BLS (CPR)

ALS: Defibrillation, pacing for bradyarrhythmia’s, and drugs

Electrophysiologic testing to ID appropriate drug therapy

Implanted cardioverted/defibrillator

Resection of diseased myocardium

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131
Q

What percentage of sudden cardiac death patients are revived with defibrillation and how many discharge alive?

A

40-50% revive, and of those 50% leave alive

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132
Q

Describe CAD

A

a narrowing or obstruction of the coronary arteries d/t atherosclerosis, an accumulation in the arteries of fatty plaques made of lipids

This causes a decreased perfusion to the myocardium and inadequate myocardial O2 supply

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133
Q

What manifestations can the decreased perfusion of myocardial tissue and inadequate myocardial O2 supply lead to?

A

Hypertension

Angina

Dysrhythmias

MI

Congestive Heart Failure

Death

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134
Q

Angiogenesis

A

the formation of new blood vessels

especially important in coronary arteries

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135
Q

How does collateral circulation related back to CAD

A

If there is more than one artery supplying, if one is blocked then the blood can take another path

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136
Q

Collateral Circulation formation process

A

it takes time and happens when chronic ischemia occurs to meet metabolic demands

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137
Q

Who is more likely to die of an MI: A young person or older person

A

young person (does not have the collateral vessels)

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138
Q

When do CAD symptoms occur

A

when the coronary artery is occluded to the point of inadequate blood supply to the muscle, causing ischemia

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139
Q

When is coronary artery narrowing significant?

A

If the left lumen diameter is reduced 50% or any other major branch is reduced 75%

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140
Q

The goal of CAD treatment is to…

A

alter the atherosclerotic progression

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141
Q

The Widow Maker

A

This is referring to the left main artery of the coronary circulation

It feeds the anterior septum, bundle of HIS, and anterior left ventricle, and since 50% occlusion is only needed here to cause an MI, there is a much higher rate of death

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142
Q

Anything above ___% occlusion requires a stent

A

70%

143
Q

Angina

A

discomfort within or adjacent to the chest

lasts for several minutes, is alleviated by rest, and does NOT result in myocardial necrosis

144
Q

Potential Sequelae of Angina

A

AMI and Death

145
Q

What typically provokes angina?

A

Exertion or Anxiety

146
Q

What makes Angina different from Infarction

A

Angina does not cause myocardial death/necrosis (however it can turn into an MI if you keep pushing it)

147
Q

What do we measure in the blood to determine if heart cells are dying?

A

Troponin protein levels since the cells will release that upon death

148
Q

Symptoms of myocardial ischemia occur when …

A

O2 demand is above O2 supply

149
Q

Most common causes of angina/myocardial ischemia

A

ASHD (Atherosclerotic Heart Disease)

Hypertrophic Cardiomyopathy

Aortic Stenosis

150
Q

ASHD

A

Atherosclerotic Heart Disease

it is classic heart failure when the ventricular wall is thin and flabby and cannot pump well

151
Q

Diastolic Heart Failure

A

Hypertrophic cardiomyopathy

The cells hypertrophy but on an X ray it looks like a normal heart size with a small interior left ventricle chamber

152
Q

Why is hypertrophy a problem for the heart?

A

the cell increases in size and needs more O2, but the vessels will still be providing the same amount

153
Q

Determinants of O2 demand in the heart include…

A

HR

Contractility

Ventricular Wall Tension (no stretch = creating greater demand)

154
Q

Physiologic states that increase O2 demand

A

Exercise

Emotional stress

States of SNS activity

155
Q

How does Anxiety decrease perfusion to the heart

A

it increases BP which decrease perfusion

But also SNS activity is determined by beta 1 receptors in the heart leading to a higher HR, contractility, and conduction which all contributes to decreased delivery from increased myocardial demand

156
Q

Angina is chest pain resulting from…

A

myocardial ischemia caused by inadequate myocardial blood and O2 supply

157
Q

Angina is caused by an imbalance between…

A

O2 demand and supply

158
Q

Angina causes include…

A

obstruction of coronary blood flow due to atherosclerosis

Coronary artery spasm (like with drugs_

conditions increasing myocardial oxygen consumption

159
Q

The goal of angina treatment is to do what?

A

provide relief of an acute attack

correct the imbalance between myocardial O2 supply and demand

prevent the progression of the disease and further attacks to reduce the risk of MI

160
Q

4 Key concepts of Angina

A
  1. Heart always extracts near maximal O2 from blood even under minimal demand- this can only increase with more RBC
  2. Coronary blood flow can increase 7x as O2 demands
  3. In CAD, blood flow cannot get through, coronary spams occur, or plaque disruption occurs
  4. Most people have myocardial O2 demand AND diminished supply
161
Q

Types of Angina

A

Stable

Unstable

Variant or Prinzmetal’s Angina

162
Q

Stable Angina

A

Relatively constant pattern of pain with regard to severity and precipitating factors

163
Q

Unstable Angina

A

recent onset (within the last 2 months), occurs at lower levels of exertion or at rest, has begun to intensify over time

Represents a continuum of symptoms between stable angina and MI

Also if the pattern of stable angina changes it is once again considered unstable Angina

164
Q

20% of Unstable Angina progresses to…

A

MI within 3 months

165
Q

Variant/Prinzmetal’s Angina

A

RESTING pain and ventricular arrhythmias caused by CA spasms

Can happen at anytime like rest, sleep, or activity

It is from coronary artery spasms

166
Q

Classic angina includes..

A

stable and unstable angina

167
Q

One drug commonly given for angina is ___

A

nitroglycerin

168
Q

What can help control CA spasms and Prinzmetal’s Angina

A

Calcium Channel Blocked decreases them

169
Q

The most powerful tool for diagnosing angina is…

A

the history and physical

170
Q

When taking the H&P of a patient with potential Angina what things should be asked?

A

Character

location

radiation

duration

precipitating/alleviating factors

accompanying symptoms

any changes in pattern over weeks or days

171
Q

Typical manifestations of Angina

A

exertional chest discomfort

several minutes duration

relieved by rest

in the region of the sternum (or anywhere between the lower jaw and epigastrium) - but its different in women

may radiate to neck or lower jar, arms (especially left), but not commonly in the back or epigastrium

described as a “tightness” “heaviness” or “choking sensation” rather than definite pain

172
Q

Angina is provoked by…

A

walking uphill

stairs

vigorous arm work

intercourse

exercise in cold weather

emotions (fear, anxiety, anger)

following a meal (since more blood goes to GI tract)

173
Q

Physical findings of Angina we can assess

A

HR and BP

S4 from atrial contraction in a ventricle stiffened by ischemia (like a baseball hitting a board than a glove_

S3 in L ventricular failure

Systolic murmur due to mitral regurgitation as a result of ischemia to the papillary muscles

174
Q

The issue with Angina is many things can have similar physical findings, so what needs to be ruled out?

A

GERD

PUD

Cholecystitis

Asthmatic Bronchitis

PE

MI

175
Q

Lab measurements for Angina

A

ECG (during attack)

176
Q

What is seen different on an EKG during Angina

A

ST Segment depression or elevation

Mostly if the muscle is ischemic ST depresses, an ST elevation indicated MI

177
Q

If angina occurs for more than 20 minutes…

A

we must suspect an impending MI or unrelated to myocardial ischemia issue and investigate

178
Q

Diagnostic Studies for Angina

A

ECG

Stress Test

179
Q

To diagnose angina, an ECG will show what during rest compared to times of activity?

A

Rest: ST depression or elevation and/or T wave inversion during times of pain

180
Q

What will a stress test show that is indicative of angina?

A

Chest pain or changes in the ECG or vital signs during testing which may indicate ischemia

181
Q

On an ECG if you see a tombstone shape…

A

that means death is imminent - very bad

182
Q

Who always needs to be present for a stress test

A

a cardiologist in case the patient has an MI

183
Q

What are the cardiac enzyme findings like in Angina

A

normal since none of the cells have died so no troponin has been released

184
Q

What is the only way to get a definitive diagnosis of Angina by finding the cardiac enzyme levels and information about the patency of the coronary arteries?

A

Cardiac Catheterization

185
Q

Exercise ECG AKA “Stress Test”

A

Exercise on a treadmill until ischemia ECG changes, angina, or dyspnea occur

May have radionuclide studies added during exercise if there’s no uptake in ischemia or prior infarctions

186
Q

Persantine

A

an alternative to the exercise ECG stress test for patients unable to exercise

it provides dilation of the coronary arteries while lying in bed to get similar results

187
Q

What are contraindications for the Stress test

A

significant aortic stenosis

untreated HTN

CHF

unstable Angina

188
Q

The Gold standard for diagnostic testing and visualization of the heart is…

A

Cardiac catheterization

189
Q

The most precise means to document presence of CAD is…

A

via a cardiac catheterization

190
Q

Cardiac catheterization can give visualization of the coronary arteries and also…

A

measurements of left ventricular function (LVEDpressure; LVED volume; ejection fraction)

191
Q

When is a cardiac catheter indicated

A

patients with sever angina

recurrent chest pain of uncertain etiology

survivors of cardiac arrest

192
Q

If there is coronary artery stenosis of greater than 70% –> ?

A

there is limited flow to the myocardium and a greater risk for a coronary event

this is a significant finding

193
Q

What is some general management rules for Angina

A

counseling and education regarding the potentially serious and unpredictable nature of the issue

drugs and other treatments to prolong survival and alleviate symptoms

hospitalization and intensive drug therapy and catheterization if angina is unstable

risk factor modification

search for correctable contributing factors

194
Q

What are some risk factors for angina that can be modified?

A

low fat, low cholesterol diet

smoking cessation

BP control

195
Q

What are some correctable contributing factors to angina

A

Aortic stenosis

hyperthyroidism (hyper metabolic need state)

severe anemia

tachyarrhythmias

196
Q

CAD + Anemia = ??

A

highly lethal

197
Q

Why do we need to treat tachyarrhythmias in angina patients

A

we should give meds to slow the heart rate and make pumping more effective since the increased heart rate will increase metabolic demand

198
Q

How to implement immediate management of angina?

A

Assess pain

provide bed rest

administer O2 at 2-4 L nasal cannula as prescribed (this goes first!!!)

Administer nitroglycerin as prescribed

obtain a 12 lead ECG

provide cont cardiac monitoring

199
Q

What does nitroglycerin do for an angina patient

A

dilates coronary arteries

reduces O2 requirements of myocardium

relieves chest pain

200
Q

What 3 things contribute to the workload of the heart

A

Preload (blood volume)

the heart itself (rate and contractility)

Afterload (resistance against which it must pump)\

we wanna decrease these!!

201
Q

Why is venous dilation so important for angina treatment

A

it will decrease preload and arterial dilation will decrease afterload and decreasing any of the 3 factors will help the heart

202
Q

How do beta blockers help?

A

they block beta 1 receptors in the heart and cause contractility, heart rate, and conductivity to decrease

203
Q

How do calcium channel blockers help?

A

they help prinzmetal angina in particular by stopping vasospasms

204
Q

Goal of Angina pharmacologic management

A

restore balance between myocardial O2 demand and supply by decreased O2 demand and/or coronary blood flow

205
Q

Major Drug Classifications for Angina Pharma Management

A

Nitrates (nitroglycerin)

Beta blockers

calcium channel blockers

206
Q

How should antiplatelet therapy be done for unstable angina?

A

Daily aspirin to prevent new clots

hospitalization for IV heparin and aspirin if needed

Plavix if there is a stent

207
Q

Invasive Angina Surgical Procedures

A

PTCA

Laser Angioplasty

Atherectomy

Vascular Stent

CABG

208
Q

Percutaneous Transluminal Coronary Angioplasty

A

PTCA

One of more arteries are dilated with a balloon cath to open the lumen and improve arterial blood flow by pressing back plaque too

has a shorter hospitalization than a CABG

209
Q

What can occur after a PTCA for a patient?

A

They can re-experience occlusion and may need the process repeated

210
Q

Complications of PTCA

A

arterial dissection or rupture

immobilization of plaque fragments

spasm

acute MI

injury to epithelium

211
Q

What is the indications for a PTCA

A

same as CABG with different contraindications

212
Q

When is a PTCA cardiac cath contraindicated?

A

left main coronary artery stenosis

severe diffuse multi vessel disease

213
Q

A PTCA is done via a…

A

cardiac catheter

214
Q

PTCA can diagnose need for…

A

open heart surgery

215
Q

Stent

A

something that can be placed in the Coronary artery to keep it open after PTCA

it will need to either be heparinized or take a med like Plavix to prevent clots of it

After a while the intimal layer will cover over it and the body will not longer attack it as foreign

216
Q

Laser Assisted Angioplasty

A

a laser probe is advanced through a cannula similar to PTCA and it can vaporize the plaque rather than compress it

The heat from the laser vaporizes the plaque and opens the occluded artery

217
Q

When is a Laser Assisted Angioplasty done

A

clients with small occlusions in the distal superficial femoral, proximal, popliteal, and common iliac arteries

Used more for small occlusions around the body

218
Q

Atherectomy

A

removes plaque from an artery by the use of a cutting chamber on the inserted catheter or a rotating blade which pulverizes plaque

Risk of causing travelling debris though

219
Q

When is Atherectomy used

A

to improve blood flow in those with ischemic limbs in those with Peripheral arterial disease

220
Q

Intermittent Claudication

A

may be in those with PAD

increased O2 demand when walking leaving the legs in pain, but if the legs are in a dependent position (sitting) perfusion is aided and pain subsides

221
Q

Venous Stasis

A

opposite to intermittent claudication

this is veins not arteries like PAD

Dependent position hurts here so the legs must be up to return blood flow to the heart

222
Q

Coronary Artery Bypass Graft (CABG)

A

Attachment of the saphenous vein between the ascending aorta and stenotic coronary artery

coronary cath is done to detect need for this type of open heart surgery though

the blockage comes from cholesterol build up, so the surgeon makes it so the new vein goes from the aorta directly past the blocked location to provide blood

may need more than just one though, may need 2,3, 4 or more grafts

223
Q

The chance of a perioperative (during surgery) AMI during CABG is

A

2-10%

224
Q

What is common after 1 year or 6 years for CABG grafts

A

by one year 10% reocclude and by 6 years 2% reocclude

225
Q

Angina can reoccur after CABG if…

A

grafts re occlude or CAD progresses

226
Q

Saphenous Vein

A

vein taken from the leg and grafted upside down (to stop valves from blocking flow) in a CABG to provide blood flow in the heart

227
Q

Mortality during a CABG is 1-3% higher when…

A

the patient :

has disease of left main coronary artery (LMCA)

significant left ventricular dysfunction

is over 65

228
Q

Coronary Revascularization

A

200,000 + done a year

They are surgical methods (PTCA and CABG) to allow for reperfusion of the coronary/myocardium regions

229
Q

Indications for Coronary Revascularization surgeries?

A

When meds have failed

If there is improved chance for survival in those with 50% stenosis of L main CA, 3 vessel disease, EF between 30-50%, and those with angina following an AMI

Basically when all else fails and you can improve survival by preserving myocardial function

230
Q

Acute Myocardial Infarction

A

Leading cause of death in the US (30% of cardiac deaths; kills over half a million yearly and hospitalized 3/4 of a million)

many survive but often live with heart failure chronically

231
Q

What is the most common cause of AMI

A

AMI d/t thrombotic occlusion superimposed on CAD

instability of atherosclerotic plaques with hemorrhage, fissuring, rupture – > acute thrombotic occlusion

232
Q

Causes other than CAD for AMI

A

infective endocarditis emboli

thrombi from prosthetic valves

atrial thrombi

vasospasm from cocaine or amphetamine use

trauma

small vessel disease in DM or collagen vascular disease

anything that stops laminar flow

233
Q

When does MI occur

A

when myocardial tissue is abruptly and severely deprived of O2

This ischemia can cause necrosis of myocardial tissue if the blood flow is not restored

234
Q

How does MI progress/when does it occur?

A

it does not occur instantly, but rather evolves over several hours

235
Q

When do obvious physical changes occur in the heart following MI?

A

6 HOURS LATER AFTER INFARCTION

the infarcted area appears blue and swollen at this time \

cells will release enzymes during this time that cause more damage

236
Q

After 48 hours what happens to the infarct area?

A

the infarct turns gray with yellow streaks as neutrophils invade the itssue

237
Q

8-10 Days after infarction what occurs?

A

granulation tissue forms (this can become necrotic)

238
Q

What happens 2-3 months post infarct

A

necrotic area develops into a scar

the scar tissue permanently changes size and shape of the entire left ventricle causing potential bad contractions

239
Q

__ is critical to a heart attack

A

time (the sooner you restore blood flow - like maybe in the Cath lab- the less likely morbidity is)

240
Q

Manifestations of AMi

A

sudden death

new onset angina

unstable angina

occurrence of angina with less effort or at rest

protracted angina with pain like that of an infarct

acceleration of angina despite intense medical treatment

241
Q

If the anginal pain is changed –>

A

pay attention and worry about an infarct

242
Q

If there is an absence of anginal exacerbating factors like anemia, HTN, CHF, hypothyroidism, and obesity …

A

this reflects changes in plaques and resulting intermittent thrombosis that causes AMI

243
Q

Transmural Infarct / Q Wave Infarct

A

if the clot is not broken down and thrombi persist –> ta very dangerous infarct involving the entire thickness of the left ventricle occurs

244
Q

Onset of muscle death after an infarct is…

A

20-40 minutes (20!!!)

245
Q

Size of an infarct depends on…

A

extent, severity, and duration of ischemic episode

amount of collateral circulation

metabolic needs of myocardium at time of event (younger die easier too; what you were doing during infarct can change impact too -shoveling v sitting)

246
Q

40-50% of AMI occur…

A

in the LAD

this impacts the heart apex, anterior left ventricle, and interventricular septum (and papillary muscles and Bundle of HIS)

247
Q

30-40Z% of AMI occur…

A

in the RCA

this impacts the inferior/posterior wall of the L ventricle and R ventricle (also impacts conduction like in LAD since it impacts septum and this impacts SA and AV nodes)

248
Q

15-20% of AMI occur…

A

in the L circumflex

this impacts the lateral L ventricle

249
Q

Most common MI site

A

LAD - the widow maker since it feeds so much

250
Q

What is the result of an AMI on the affected portion

A

decreased contractility with abnormal wall motion

altered compliance (Stretch)

decreased stroke volume leading to decreased ejection fraction

more LVEDP

251
Q

EDV

A

end diastolic volume

amount of blood in ventricle at end of diastole (rest period)

about 100 mL

252
Q

SV

A

stroke volume

amount ejected from ventricles

70-75 mL normally but can be less with damage

253
Q

ESV

A

end systolic volume

difference between EDV and SV and it is what remains in the ventricle

25-30 mL

254
Q

Ejection Fraction

A

the % amount of ejected blood (in MI you may get a lower stroke volume causing a lower EF)

255
Q

The lower the EF…

A

the lower the cardiac output and the lower the ability to perfuse

256
Q

LVEDP

A

left ventricular end diastolic pressure

pressure in the ventricle at the end of diastole

the more blood left the greater the pressure

these pressures are supposed to get lower than atrial pressure when passively filling, but if the pump is affected you get higher pressures and it interferes with heart functioning

257
Q

What does the area of infarct look like after an AMI?

A

central area of necrosis

surrounded by minimally surviving injured cell area that can come back and function if blood flow is restored

it is an area surrounded by ischemia

the myocardium will NOT regenerate and the necrosis tissues will be replaced with scar tissue

258
Q

Q Wave infarcts are preceded by…

A

fatigue

chest discomfort

malaise in days preceding

259
Q

A Q Wave infarct involves __ __ of the myocardium

A

full thickness (MI)

260
Q

When does infarction usually occur during the day?

A

in the early AM since platelet aggregation and clotting is higher

261
Q

What does it mean if an MI is clinically silent?

A

May not feel the heart attack due to impairment of the nervous system (neuropathy in DM) or having a high pain threshold (women)

However, it is usually found later on an ECG

262
Q

MI that obstructs the LAD results in…

A

anterior or septal MI or both

263
Q

MI that obstructs the circumflex artery results in ..

A

posterior wall MI or lateral wall MI

264
Q

MI that obstructs the right coronary artery results in…

A

inferior wall MI

265
Q

What obstruction locations impact electrical conductivity most?

A

LAD or RCA

266
Q

Risk Factors for MI

A

Atherosclerosis

CAD

elevated cholesterol levels

smoking

HTN

obesity

physical inactivity

impaired glucose tolerance

glucose

many are modifiable

267
Q

S/S of AMI

A

Pain

Diaphoresis

cool clammy gray skin

weakness

sense of impending doom

profound restlessness

confusion

fever in 24-48 hours usually above 101 r/t inflammation

respiratory issues like increased RR, cough, wheezing, frothy sputum, crackles, SOB

extremity issues like peripheral cyanosis, edema, and pallor

pre renal failure

JVD

268
Q

What is the pain like in an AMI

A

intense, severe, crushing - like an elephant on your chest

Unremitting pain for 30-60 minutes (but only takes 20 minutes for tissue death)

retrosternal pain location

often pain radiates down the ulnar side of the arm, neck, teeth, and jaw

269
Q

AMI impaired L ventricular filling —>?

A

pulmonary vascular congestion (pulmonary edema) –> SOB, tachypnea, orthopnea, moist crackles usually in lung bases

270
Q

AMI tachycardia d/t SNS activity –> ?

A

dysrhythmias (EP and NEP)

271
Q

BP may initially be normal in AMI, but with R ventricular or severe L infarction…

A

it may be hypotensive

272
Q

S3 v S4 indicates

A

S3 is pathonomic for heart failure

S4 is more of a wall compliance issue

273
Q

What sort of changes occur for the heart after an AMI

A

displacement of PMI

soft S1 S3 and S4

mitral regurgitation murmur

friction rub (pericardial inflammation)

dysrhythmias (PVCs and V tach)

palpitations occur

274
Q

PVC - Premature Ventricular Contraction

A

a ventricular contraction not preceded by atrial contraction (no P wave!!)

275
Q

V Tach

A

PVCs stack up one after another leading to ventricular tachycardia

276
Q

Non Specific Diagnostic tests for AMI

A

CBC

ESR

Myoglobuin

277
Q

CBC (AMI)

A

checks WBC and seeing if leukocytes are combatting infection and inflammation

278
Q

ESR (AMI)

A

non specific measurement of infection or inflammation

rate rises with elevated levels of fibrinogen or globulins are present

RBC settle faster with inflammation

279
Q

Myoglobin Test (AMI)

A

O2 binding protein found in striated muscle

Releases O2 at very low tensions

Any injury to skeletal muscle will cause its release into blood

non specific with limited usefulness in diagnosing AMI

280
Q

Creatinine Kinase Diagnostic Test

A

CK or CPK - enzyme found in the heart, brain, and skeletal muscles

a non specific test for AMI

an isoenzyme with 3 types

mostly use CK-MB for MI diagnosis

281
Q

What person might have higher Creatine Kinase levels

A

those with larger muscle masses

282
Q

CK-MM

A

Creatine kinase in skeletal muscle

283
Q

CK-MB

A

creatinine kinase mostly in cardiac muscle

this one is viewed for non specific MI diagnosing

284
Q

CK-BB

A

creatine kinase in brain and lungs

285
Q

What is one of the most commonly used markers for detecting MI?

A

Troponin

286
Q

Troponin types

A

Troponin T
Troponin I

287
Q

Troponin Test

A

A diagnostic test for AMI

288
Q

Troponin T

A

a regulatory protein found in skeletal and cardiac muscle fibers

skeletal and cardiac muscle shave different forms of this protein

specific antibodies can detect cardiac troponin T and is specific for myocardial injury

289
Q

Troponin I

A

a protein in the troponin cardiac muscle complex

specific to the myocardium

usually returns to nL sooner than troponin T

290
Q

Which troponin is the gold standard

A

Troponin I (since T can indicate an MI from weeks ago)

291
Q

AST Test

A

Aspartate aminotransferase

enzyme found in the heart, kidneys, brain, RBCs, liver, lungs, pancreas, & skeletal muscle

many conditions can produce elevation

not a great test for diagnosing MI but can be looked at with others

292
Q

LDH test

A

Lactic Dehydrogenase

is present in almost all metabolizing cells, but is especially high in the heart, kidneys, brain, RBCs liver, & skeletal muscles

requires electrophoresis to separate out its 5 isoenzymes

an older and not great marker either for AMI

293
Q

What replaced LDH testing

A

CK-MB testing

294
Q

LDH is still useful, what are LHD1 and LHD2 useful for

A

assessing extent of myocardial damage

295
Q

What is important to keep in mind about Troponin I and T rising?

A

They both rise at around the same time, but T lasts longer than I elevated and can indicate something old

296
Q

which is more important:

CK or CK-MB?

LDH or LDH1?

A

CKMB

LDH1

297
Q

When do the following things begin to rise, peak and return to normal: CK, CK-MB, Troponin I, Troponin T, AST, LDH, LDH 1

A

CK - begins rise 4-6 hours - peak 24 hour- normal 3-4 days

CK-MB- 4 hour - 18 hour peak - 2 days to normal

Troponin I - 4-6 hr - 11 hr - 4 days

Troponin T - 4-6hr - 11 hr - 10 days

AST - 8 hour - 24-48 hour - 4 days

LDH - 24 hour - 3 days - 8-9 days

LDH 1 - 24 hours - 3 days - 12 days

298
Q

Hemodynamic Monitoring: CVP

A

central venous pressure

reflects amount of blood returning to the heart

hemodynamically monitor via a catheter in the right atrium

299
Q

Hemodynamic Monitoring: CO

A

cardiac output

function of heart rate and stroke volume

hemodynamically monitor via a pulmonary artery catheter equipped with a special thermistor probe

300
Q

Hemodynamic Monitoring: PCWP

A

Pulmonary capillary wedge pressure

pressure measured in the pulmonary artery; provides an indication of L ventricular function

measured via a Swan Ganz cath through the peripheral vein –> R heart –> pulmonary artery

301
Q

P Wave indicates

A

contraction of the atrial muscles (depolarization of the atria)

302
Q

QRS complex indicates

A

contraction of the ventricles (depolarization of the ventricles)

303
Q

T Wave indicates

A

electrical changes during the relaxation phase of the ventricles (repolarization of ventricles)

304
Q

What is lost in an ECG?

A

Repolarization of the atria

305
Q

What EKG results may appear in damaged heart muscle

A

inverted T wave

Raised ST segment

Deep Q Wave

306
Q

Ischemia leads to what ECG result

A

ST depression and T wave inversion

307
Q

Infarction with death of tissue leads to what ECG result

A

ST elevation (tombstone) and possible T wave inversion

308
Q

If you have a Q wave infarct, what happens in ECG results

A

whole thickness of wall is affected so the Q wave depresses - very serious

309
Q

Echocardiogram

A

noninvasive procedure that uses sound waves

gel is applied, transducer wand moved over chest to get internal structure pic of heart

takes 30-90 minutes depending on condition and echo type

Wonderful test for how the heart works in real time - see valve opening and closing, wall movement, ventricular filling and contraction, atrial filling, can outline ventricle at end of systole and diastole and measure end diastolic volume, stroke volume, EF, and end systolic volume - can see regurgitation with leaflet movement too

310
Q

Echocardiogram tests evaluate…

A

how well the heart is moving

how well the valves are working

the size of the heart and its pumping chambers (ventricles)

311
Q

Complications d/t MI (afterward)

A

Dysrhythmias

CHF

Cardiogenic Shock

Thromboembolism

Ischemic pericarditis

Myocardial rupture

ventricular aneurysm

312
Q

Why do dysrhythmias occur post MI

A

d/t tissue ischemia, hypoxia, SNS, lactic acidosis

it will cause decreased CO, cardiac irritability and further decreases in perfusion

and conduction issues from this may require a pacemaker

313
Q

The most common cause of death outside of the hospital related to a complication of MI is…

A

ventricular fibrillation

314
Q

What does CHF cause after an MI

A

decreased contractility and abnormal wall motions

decreased stroke volume

315
Q

What does Cardiogenic shock cause after an MI

A

profound L ventricular failure from massive AMI (10-15 % of post MI patients with an 80% mortality rate)

316
Q

What does Thromboembolism cause after an MI

A

may travel to the brain, kidneys, or spleen

these clots form from lack of laminar flow

bed rest and heart failure predisposes people to venous thrombus and PE (not as common with early ambulation and anticoag tho)

317
Q

What does Ischemic pericarditis cause after an MI

A

inflammation of the pericardium

sever sudden constant pain

worse pain with inspiration

tachycardia

moderate fever

pericardial friction rub heard with every beat

318
Q

Myocardial ruptures lead to…

A

instant death

319
Q

What do ventricular aneurysms cause after an MI

A

late complication*

filled with clots and debris an embolus can form (like a ballooning out from the vessel)

320
Q

AMI Pre Hospital Treatment

A

EMS personnel trained in defibrillation

AEDs

Adequate analgesia with morphine

Aspirin therapy - anti platelet effect

321
Q

What is the benefit of analgesia with morphine for hospital pre treatment

A

it causes venous dilation dropping the preload on the heart

322
Q

65% of AMI deaths are in the first hour, but 40% can be saved with ___

A

AED/Defibrillation

323
Q

AMI Hospital Treatment

A

Cardiac Cath lab (CCU) to reduce mortality 50% with defib, continuous ECG, swan ganz

Diet of liquids for the first 24 hours d/t risk of aspiration with N/V and to not let blood go toward GI too much

telemetry monitoring for arrhythmias

stool softeners to prevent straining (and vagal activation)

bed rest for 1 day for uncomplicated cases

gradual monitored resumption of ambulation

oxygen therapy to avoid hypoxemia

324
Q

What needs to be done in the convalescence period after an AMI?

A

prevent recurrence with calcium channel blockers, beta blockers, and aspirin

Anticoagulation for 6 months for high risk

Risk factor modification

Cardiac rehabilitation

Prompt detection of progression of CAD (ex: Angina)

325
Q

Stenotic Valves

A

valves that are hard (narrowed) and calcified

Failure of the valve to OPEN completely

326
Q

Regurgitant Valves

A

Valves that do not close like they should (leaky)

also called “Insufficiency” or “Incompetent”

Inability of valve to CLOSE completely

L Vent will have to push hard against this which can make push backward causing leaky mitral valve

327
Q

Causes for Valve Disease

A

Myxomatous Degeneration (pathological weakening of connective tissue - mitral valve prolapse for example)

Calcific Degeneration

Congenital Defects

Ineffective Endocarditis

CAD

AMI

328
Q

The pattern goes S1, ___, S2 __, S1

A

S1 Systole S2 Diastole S1

329
Q

What are the AV valves like in Systole

A

closed

a problem at this time leads to mitral regurgitation

330
Q

What are the SL valves like in Systole

A

open

a problem at this time leads to aortic stenosis

331
Q

What are the AV valves like in diastole

A

Open

a problem at this time is mitral stenosis

332
Q

What are the SL valves like in diastole

A

Closed

a problem at this time is aortic regurgitation

333
Q

While not a definitive diagnostic, what does murmurs heard in certain areas correlate to?

A

All People Eat Turkey Meat

If heard on pulmonic area, its a pulmonic problem - if over tricuspid area, its a tricuspid problem

334
Q

If I hear a murmur between S1 and S2 that means its a murmur in ___

A

systole

335
Q

If I hear a murmur after S2 it is a murmur in __

A

diastole

336
Q

If I hear a murmur when valves are closed during systole what problems could it be?

A

If it is the mitral or tricuspid that should be closed its a regurgitation problem

If its the pulmonic or aortic its a stenosis problem

337
Q

If I hear a murmur when valves are closed during diastole what problems could it be?

A

If it is mitral or tricuspid its a stenosis problem

if its the pulmonic or aortic that should be closed its a regurgitation problem

338
Q

What is more serious a systolic problem or diastolic problem?

A

Diastolic because there is less blood to inject in circulation

Systolic problems can be overcame for a time because of the strength of the ventricle forcing blood, but diastolic problems means less blood to do so with and it cannot be overcame in this case

339
Q

Mitral Valve Stenosis

A

A diastolic murmur impeding flow from the LA –> LV

lack of passive filling is occurring

This problem occurs in diastole

340
Q

Manifestations of Mitral Valve Stenosis

A

Atrial Fibrillation: Clotting and Embolism

Pulmonary Congestion: Orthopnea, cough, poor oxygenation

Decreased SV: Fatigue, activity intolerance, weakness

341
Q

Mitral Valve Prolapse (MVP)

A

Mid systolic click or murmur

Blood from the atria goes into the pulmonary veins, but the chordae tendinea let go allowing blood to back up into the lungs leaving less blood flow in the left ventricle

Decreased EDV and less blood for ventricular contraction then occurs

342
Q

Manifestations of MVP

A

palpitations

rhythm disturbances

dizziness

dyspnea

chest pain

anxiety

angina exacerbation

syncope

343
Q

Why do dental procedures (or any invasive procedure) need prophylactic antibiotics?

A

there is a risk that organisms can get in and get to areas without laminar blood flow to grow and cause infective endocarditis

344
Q

Aortic Valve Stenosis

A

Systolic Murmur

LV hypertrophy –> LV failure

Hard aortic valve (SL valve)

345
Q

Manifestations of Aortic Valve Stenosis

A

angina

syncope

fatigue

hypotension

decreased peripheral pulses

346
Q

Aortic Regurgitation

A

“Aortic Insufficiency”

Diastolic Murmur

LV hypertrophies and dilates (but valve leaflets wont close so dramatic icnrease in EDV - starlings law makes it so it can only extend and stretch so much)

(Aortic regurg on left and pulmonic regurg on right)

347
Q

Manifestations of Aortic Regurgitation

A

Main: huge EDV

Increased SBP and decreased DBP and Widened plse pressure and bounding peripheral pulses

348
Q

Ways to diagnose valvular diseases

A

cardiac auscultations

CXR (not super helpful with diastolic HF since you cannot see it)

echocardiography (can find SV, EDF, and EF and see valve and wall movement)

electrocardiography (check electrical activity)

coronary angiography (helpful with CAD related valve issues)

MRI (expensive)

doppler ultrasound

349
Q

Medications used to reduce the workload of the heart

A

Digitalis

Diuretics

Anticoagulants

Beta Blockers

calcium channel blockers

350
Q

Valvular Disease Surgeries

A

Commissurotomy

Valvuloplasty

Valve Replacement

351
Q

Commissurotomy

A

separation of the flaps of the mitral valve to relieve mitral stenosis

352
Q

Valvuloplasty

A

surgery performed on a heart valve

353
Q

Valve Replacement

A

can be a donor, animal part, plastic, or metal valve put in place

354
Q

What is the risk associated with replacement valves

A

they are foreign material so there is a risk of clots attacking it

N361: Pathophysiology II (20 decks)

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