Circulatory 2 Flashcards

1
Q

What are the two main valves of the heart?

A
  1. Atrioventricular valves (AV valves)– control blood flow from atria to ventricles
  2. Semilunar valves – control blood flow from ventricles to the pulmonary
    or systemic circulation
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2
Q

AV valves consist of:

A

tricuspid: between right atrium & ventricle
mitral/bicuspid: between left atrium & ventricle

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3
Q

Semilunar valves consist of:

A

pulmonic: controls flow to pulmonary artery
aortic: controls flow to the aorta

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4
Q

what problems could occur in the valves?

A

stiffening or
deformity of valves
This could be due to trauma,
inflammation, ischemia, etc
-Causes changes to the flow of blood. We will see valves that can’t open properly & valves that can’t close
properly.

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5
Q

what is valvular stenosis/ stenotic valve (narrowing)

A

-Valves that can’t open properly.
-The opening is very small, so the heart can’t pump enough blood through the valve.
-Workload of the heart increases, & the CO will drop

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6
Q

what is valvular regurgitation (incompetent)

A

-Opposite of stenosis; the valve cannot close properly.
-Blood will go backward as a result because the valve cannot close to prevent it.
-Workload of the heart increases, & CO will drop

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7
Q

When doing an assessment, some valve issues may be mild, like mild stenosis or a mild regurgitation, but not very severe & signs or symptoms may not be present (asymptomatic).
How will you know the valve problem is still there?

A

by listening to the heart, you’ll hear a murmur because that is the sound that is produced from turbulent
blood flow. When blood is trying to squeeze through a tiny space, or if blood is flowing backward, it generates abnormal vibrations that are heard as murmurs.

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8
Q

what is the pericardium? (1st layer of heart wall)

A

Fibrous sac that surrounds & holds the heart in place & protects it

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9
Q

what are the two layers of the pericardium?

A
  1. Tough outer layer resists distention (Fibrous pericardium) Doesn’t stretch. Prevents overfilling of heart.
  2. Double layer membrane, serous inner layer that lines the
    heart & the outer layer of pericardium, forming cavity that
    contains small amount serous fluid (30-50mL).
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10
Q

what is pericardial effusion?

A
  • When too much fluid gets in the pericardial space (only small amount in there to prevent friction)
  • Inflammation or infection causes fluid build-up (may be pus, serous fluid, or blood).
  • Compresses chambers of the heart & can interfere with ventricle filling & causes the CO to DROP
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11
Q

What is it called when the chambers of the heart are being compressed & can interfere with ventricle filling & cause the CO to drop?

A

if that happens we call it Cardiac tamponade
- Very critical type of illness

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12
Q

what is the thicker, muscle layer of the heart wall?

A

The myocardium performs the work of the heart. MYO= MUSCLE. Differs from skeletal muscle in that contractions are involuntary
-Thicker layer, muscle layer of the heart wall
-Performs the actual work of the heart; the contracting & relaxing

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13
Q

example of a disorder that impairs the heart MUSCLE function

A

Cardiomyopathy
- A group of disorders that affect the heart muscle; some are genetic, & others may be caused by viruses or autoimmunity.
- CO will drop due to impaired pumping ability of the heart
- Signs of heart failure

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14
Q

example of another disorder that impairs the heart’s MUSCLE function

A

Myocardial Infarction
“Heart attack”
- CO will drop due to impaired pumping ability of the heart

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15
Q

Very inside/inner layer of heart wall:

A

ENdocardium
-Thin layer that serves as the inner lining of the heart.
-Smooth & slippery
- Clots don’t form on heart walls, platelets &
microbes don’t stick to it.

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16
Q

what is the function of the endocardium?

A

lines heart wall
-Protects against infection, clots, & microbes entering the heart through the blood.

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17
Q

The most common problem that affects the endocardium:

A

Infective Endocarditis
-Inflammation of the endocardium due to infection
-The surface of the endocardium is infected by a pathogenic microorganism that leads to
the development of vegetative lesions that can destroy the tissue underneath

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18
Q

Infective endocarditis is most common in people with

A

-Most common in people who have a heart defect, especially a valve. Also, a pacemaker, defibrillator, etc. can provide areas or grooves where microbes can hang on
to & start to multiply & cause infection that will cause inflammation.
-Pathogens may enter through the blood & gain access to the heart.
-Could enter through a soft tissue wound that becomes infected, an upper
respiratory infection, a cold, etc. that enter the blood & gain access to the heart.

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19
Q

heart murmur = at risk for

A

infective endocarditis ex: going to the dentist
Medication
-Prophylactic/Prophylaxis

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20
Q

infective endocarditis leads to

A

vegetative lesions (microorganisms & cellular debris all tangled up in strands of fibrin)

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21
Q

3 Problems to worry about

A
  1. they have pathogens in the vegetative lesions, as blood passes through vegetative lesions, it can pick up pathogens and spread them to other places in the body.
  2. they damage/destroy the underlying tissue
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22
Q

Predisposing factors of infective endocarditis:

A

environment conducive to
bacterial growth (ex:
preexisting heart defects,
valvular disease,
prosthetic heart valves,
damage to endocardial
surface, etc.)
* portal of entry for bacteria
(ex: oral lesion, dental
procedure, URI, skin
lesion, etc.

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23
Q

Congestive heart failure

A

“heart failure” = failure of the heart as a pump.

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24
Q

when the heart stops beating that is called

A

cardiac arrest

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25
Q

Congestive Heart Failure (CHF):

A

accumulation of fluid somewhere in the body.

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26
Q

what are the forward effects of heart failure?

A

Forwards effects: problems that are caused because blood is not pumping forward where it is supposed to.

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27
Q

what are the backward effects of heart failure?

A

-Backward effects: problems due to blood back-up where it’s not supposed to be.

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28
Q

PF to heart failue

A
  1. impaired cardiac function (anything that decreases CO, or impairs the pumping ability of the heart) ex: cardiomyopathy, myocardial infarction, heart valve diseases, etc..
  2. Excessive work demands: overworked = fails ex: chronic high htn(has to work harder to pump blood) ex: fluid overloaded (higher blood volume, has to pump extra fluid vol.)
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29
Q

Primary problem in heart failure?

A

poor cardiac output (2 groups: diastolic HF & systolic HF)

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30
Q

what is systolic HF?

A

When CO drops because there is a problem with systole (contraction) & there is an issue with
getting a strong contraction, so CO drops. A heart attack & cardiomyopathy fall into this category

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31
Q

What is diastolic HF?

A

Diastolic Heart Failure: When the heart relaxes, it is supposed to fill with blood. Diastolic HF is when CO drops because the ventricles aren’t filling adequately. If they don’t fill, they can’t pump out enough blood to meet the body’s needs.
Anything that impairs the filling of the ventricles can lead to a diastolic HF, such as cardiac tamponade; the ventricles can’t fill due to compression of the heart by fluid in the pericardium.

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32
Q

Examples of diastolic HF?

A

chronic HTN: makes ventricular walls hypertrophy(thickened)
cardiac tamponade: compression of ventricles so they can’t fill = CO drops

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33
Q

what happens to the size of the ventricle chamber when the left ventricle walls have hypertrophied/ thickened?

A

it gets smaller (cant fill with as much blood=CO will DROP)

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34
Q

Ejection Fraction

A

the percentage of blood that gets ejected from the ventricle when it contracts.

35
Q

Normal ejection fraction range?

A

not 100% of blood but normal is 50- 75%
always a little of blood left end there
usually measured by ultrasound.

36
Q

Reduced Ejection Fraction Failure

A

if the heart is having a hard time contracting

37
Q

Preserved Ejection Fraction failure

A

ventricle can still contract just fine, it just doesn’t fill properly.

38
Q

Compensatory mechanism #1:

A

When the CO drops, SNS kicks in & triggers fight or flight & HR increases & force of contraction also
increases & increases CO. But in the long run, the workload increases & contributes to overworking of the
heart & makes HF worse.

39
Q

Compensatory Mechanism #2

A

When CO drops, bp drops
when bp drops, that activates the RAAS: Renin Angiotensin Aldosterone System & the kidney produces renin & causes vasoconstriction & makes you retain water. Tries to fix the problems that started the whole thing (high BP); it will increase the BP & blood volume & therefore CO. Works in the short term, but in the long term, will lead to overworking of the heart & the heart gets overwhelmed.

40
Q

activating RAAS will cause

A

vasoconstriction and increased BP= increased workload against all the pressure

41
Q

Compensatory Mechanism #3

A

when the CO drops, the body releases several hormones that cause hypertrophy and thickening of the left ventricle wall = goal of generating more force of contraction and improving CO but overtime, the chamber will get smaller & CO
will decrease because there’s no space for blood. Now needs more blood, and nutrients, due to increased size & may predispose to heart attack.

42
Q

ventricle hypertrophy

A

Can be due to high blood pressure. Ventricles are trying to pump blood against the high pressure,
so the walls thicken to generate more force, but the size of the chamber gets smaller & ventricular filling drops. Eventually,
CO will drop

43
Q
  • 2 peptides that get released as compensatory mechanisms:
A
  1. ANP (Atrial Natriuretic Peptide) released by atria in response to increased pressure in the atria
  2. BNP (Brain Natriuretic Peptide) B type- released from ventricles
44
Q

When there is extra pressure in the atria & the ventricles, these 2 peptides get released & help…

A

counteract some of the
negative consequences of the other compensatory mechanisms above.

45
Q

effects of ANP & BNP

A

-decrease SNS activity
- decrease Na/H2O retention
decrease vasoconstriction
will help counteract negative effects of compensatory mechanisms

46
Q

can we measure BNP levels in the blood?

A

yes if someone came in the ER experiencing HF, we can see how severe the HF is
the higher the level= the more severe the HF is

47
Q

can we give BNP synthetically to pts?

A

only to pts with severe HF to try to get some of these useful effects. usually given in IV form, needs to be monitored.

48
Q

circulation through the heart

A

blood is going to return to the heart from the venous system🡆when the blood returns to the heart it comes back to the RIGHTTTTTTTTT side of the heart 🡆right side of the heart pumps blood to the lungs🡆from the lungs, the blood goes to left side of the heart🡆arterial system

49
Q

where is the right side of your heart supposed to be pumping blood to?

A

to lungs. so if the right heart FAILS, the forward effects are going to be that it does not pump blood to the lungs 🡆 it does not pick up O2 which results is someone hypoxia, SOB bc blood isn’t being pumped forward to the lungs to be oxygenated

50
Q

what about the backward effects of right heart failure?

A

if the right heart is not pumping the blood forward, that must mean the blood is backing up to the venous system🡆in the jugular veins (distention)

51
Q

circulation through the heart WRITE THIS FOR THE TEST

A

venous system 🡆 right heart 🡆
lungs 🡆
left heart 🡆 arterial system

52
Q

jugular vein distention:

A

excess blood in jugular veins

53
Q

RHF recap

A

-Right Ventricle fails & blood cannot get to the lungs & will not be oxygenated. Symptoms are: forward & backward effects

54
Q
  • Forward effects: Blood is not being pumped to lungs with leads to what s/s
A

-Oxygenation problems
-bluish lips
-tachycardia
-SOB/ fatigue/ tired
-Anxiety
- Anorexia

55
Q
  • Backward effects: Blood is not going forward to the lungs, so it’s backing up in the atria & can exit out into the venous system because there are no valves in the atria.
A

-Neck vein distention (jugular) one of the first signs of blood backing up into the venous system.
- Peripheral edema if blood continues to back up because veins can only hold so much so some fluid is pushed out into
the tissues, like in the legs, etc.
-AKA Dependent edema (lower than the heart, legs or sacral if laying down)
-If blood continues to back up, some of the abdominal organs getting engorged (Edema). Splenomegaly, hepatomegaly,
etc. RUQ Pain, GI tract may be distended so GI discomfort is common.
-Ascites-If the fluid ends up in the peritoneal space. Weight gain.
-Every pound of weight gain =500 mL of fluid

56
Q

LHF recap

A

Left Ventricle has failed & blood will not get to systemic circulation & symptoms include: forward and backward effects

57
Q

Forward effects: Tachycardia: Blood not getting to systemic circulation. BP low. Hypotensive

A

-Tired
-SNS kicks in due to low CO
-HR will increase to try to bring CO back up
-Pale, clammy skin, tachycardia, etc.
*If failure is severe & CO drops a lot:
-Person may go into shock: When CO & BP drop & person can no longer perfuse major body organs, so person
goes into multiple organ failure=Cardiogenic Shock (Indicates that shock originated from the heart)

58
Q
  • Backward effects: Not pumping blood into systemic circulation so blood backs into the lungs.
A

pulmonary edema, crackles, orthopnea

59
Q

peripheral edema is also referred to as

A

dependent edema

60
Q

what are the dependent areas of the body

A

areas below the heart (depends on what position your body is in ex: lying down or standing)

61
Q

Hepatomegaly vs splenomegaly

A

hepatomegaly: enlarged liver RUQ pain
splenomegaly: enlarged spleen

62
Q

Ascites

A

-If the fluid ends up in the peritoneal space=Weight gain.
-Every pound of weight gain =500 mL of fluid***

63
Q

RHF s/s

A

fatigue
increased peripheral venous pressure
ascites
enlarged liver & spleen
distended jugular veins
anorexia & complaints of GI distress
swelling in hands & fingers
WEIGHT GAIN=FLUID IS HEAVY

64
Q

Left ventricle failure
circulation through heart

A

left heart is supposed to pump blood to the arterial system 🡆 if it’s not doing that, now body tissues aren’t getting oxygenated blood = pts complain of being tired/fatigued/poor activity tolerance

65
Q

cardiogenic shock

A

: When CO & BP drop & person can no longer perfuse major body organs, so person
goes into multiple organ failure=Cardiogenic Shock (Indicates that shock originated from the heart)

66
Q

what is pulmonary edema?

A

-Fluid ends up in the lung tissue & alveoli, so there is no surface are available for gas exchange
-Only in left heart failure are the oxygenation problems due to pulmonary edema

67
Q

Listen to the Lungs & if:

A

Crackles are heard when listening to the lungs. When a person breathes in (air moving through the fluid). A person may have a wet-sounding cough & Orthopnea (Difficulty breathing when you lay down) fluid rushes to the lungs from the lower body & causes difficulty breathing
-Orthopnea AKA Paroxysmal Nocturnal Dyspnea (PND): episodes of difficulty breathing at night.

68
Q

chronic vs acute?

A

chronic issues take alot longer to develop, symptoms are not so bad to start with but they get bad overtime and once you have it, you have it forever. ex: disease
acute issues come on more quickly and suddenly, s/s more severe to start with, but can eventually go away ex: clots

69
Q

if a pt has atherosclerosis in an artery leading to their foot, will you have trouble with blood getting to feet or cant get it back to heart?

A

trouble getting blood back to feet 🡆pale, cool, weak pulses, capillary refill slow, paresthesias (numbness/tingling)
pain in legs=intermittent claudication

70
Q

why do pts complain of leg pain when their legs are elevated?

A

when legs are elevated, now arteries have to get blood to your foot against gravity.

71
Q

7 P’s acute: quickly arterial occlusion

A

pallor
polar (cold)
pulselessness
pain
paresthesias
paralysis
“pistol shot”

72
Q

blood pools in veins

A

blood collecting in veins=venous stasis

73
Q

stasis means

74
Q

acute symptoms are very often due to

75
Q

arterial vs venous ulcers

A

arteria: dry and pale
venous: wet and red

76
Q

both arterial and venous

A

venous=swelling
arterial= discoloration and toenails

77
Q

thrombosis means

78
Q

DVT

A

deep vein thrombosis: / thrombophlebitis 🡆 inflammation in a vein due to a clot

79
Q

virchow’s triad

A

venous stasis
hypercoagulability: anytime the blood is more likely to clot (dehydration or blood disorder
injury to blood vessel wall

80
Q

Right Heart Failure vs. Left Heart Failure:

A

Right Heart Failure: Think of it like a backed-up pump sending blood to the lungs. It causes swelling in the legs and abdomen because blood isn’t moving well from the body to the lungs.

Left Heart Failure: Imagine a clogged pump trying to send blood to the body. It leads to fluid buildup in the lungs, making it hard to breathe.

81
Q

Chronic vs. Acute Arterial Impairment:

A

Chronic Arterial Impairment: Picture a slow, steady blockage in the arteries, like a gradually narrowing road. It can lead to symptoms like pain during movement or rest.

Acute Arterial Impairment: This is like a sudden roadblock in the arteries, causing severe pain, paleness, and even tissue death if not treated quickly.

82
Q

Chronic vs. Acute Venous Impairment:

A

Chronic Venous Impairment: Imagine a sluggish river that’s not flowing well. It leads to symptoms like swelling, heaviness, and skin changes over time.

Acute Venous Impairment: This is like a sudden dam in the river, causing swelling, pain, and possibly blood clots that need urgent attention.

83
Q

Arterial Impairment vs. Venous Impairment:

A

Arterial Impairment: Think of it as a problem with the highways that carry blood away from the heart. Symptoms include pain, coolness, and pale or blue skin because tissues aren’t getting enough oxygen.

Venous Impairment: This is like a problem with the return journey of blood back to the heart. It causes symptoms like swelling, heaviness, and sometimes visible varicose veins.