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Foundations EXAM 1 > Cardiovascular (EXAM2) > Flashcards

Cardiovascular (EXAM2) Flashcards

1
Q

Blood is oxygenated through ___, ___, and ___ of respiratory gases

A

Ventilation
Perfusion
Transport

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2
Q

__ and ___ regulators control rate and depth fo respiration in response to changing tissue oxygen demands

A

Neural and chemical regulators

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3
Q

Pumps blood through the pulmonary system to oxygenate the blood

A

R Ventricle

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4
Q

Pumps oxygenated blood through the systemic circulation

A

L ventricle

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5
Q

Brings blood back to heart from the bottom part of the body to the heart

A

Inferior vena cava

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6
Q

4 chambers, 2 atria, 2 ventricles are called the:

A

Myocardial pump

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7
Q

Diseases that decreased ejection fraction (% squeeze the heart can pump).

A
  • Coronary artery disease (CAD)
  • Cardiomyopathy
  • Cardiomegaly (enlarged heart)
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8
Q

Heart’s ability to stretch for filling of the heart (more chambers fill, the stronger the chambers will push blood out)

A

Starling’s Law

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9
Q

S1

A

Mitral and tricuspid valve closing

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10
Q

S2

A

Pulmonary and aortic valves closing

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11
Q

Heart muscles is called ___

A

Myocardium

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12
Q

Coronary artery circulation supply blood to:

A

Myocardium of heart. Provide nutrients and remove waste

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13
Q

Systemic circulation supplies blood to:

A

Arteries and veins

To body

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14
Q

Coronary arteries (3)

A
  1. Right coronary artery
  2. Left Coronary artery (most abundant blood supply)
  3. Circumflex artery
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15
Q

Coronary artery circulation

-general-

A

-branch off of aorta

(LCA)- brings flow to myocardium of ventricles of heart.

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16
Q

The coronary arteries wrap around the ___ of the heart

A

Outside

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17
Q

Left Main Coronary Artery (LMCA)

A

Supplies blood to left side of the heart muscle

Divides into 2 different arteries: left anterior descending artery , circumflex artery

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18
Q

Left anterior descending artery

A

Branches off of the left coronary artery and supplies blood to the front of the left side of the heart

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19
Q

Circumflex artery

A

Branches off the left coronary artery and encircles the heart muscle. Supplies blood to the outer side and back of the heart.

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20
Q

Right Coronary Artery

A

Supplies blood to the right ventricle, the right atrium, and the SA and AV nodes.

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21
Q

The right coronary artery divides into smaller branches: (2)

A
  1. Right posterior descending artery

2. Acute marginal artery (R atrium and R ventricle and bottom portion of both ventricles)

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22
Q

The Main portion of the right coronary artery provides blood to the __ ____ of the heart, which pumps blood to the ___

A

Right side

Lungs

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23
Q

Left Loves the Heart

A

Supplies the main blood supply for the heart.

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24
Q

The amount of blood ejected from the left ventricle each minute

A

Cardiac output

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25
Q

Normal amt for cardiac output

A

4-6L/min

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26
Q

Amount of blood pumped from the LV with each contraction

A

Stroke Volume

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27
Q

Body needs to change circulation based on your metabolic demand. Ex of metabolic demand:

A

-exercise
-pregnancy
-fever
^ CO and O2 demand

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28
Q

The blood that is in left ventricle at the end of diastole

A

Preload

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29
Q

The more the ___ on the ventricular muscle the greater the ____

A

Stretch

Contraction * Starling’s law

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30
Q

The resistance to the left ventricular ejection

A

Afterload

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31
Q

In ___ the afterload increases which makes cardiac workload increase

A

HTN

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32
Q

Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume

A

Frank-Sterling Law of the Heart

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33
Q

___ Preload lead to ___ EDV leads to ___ stretch of myocardium : ______

A

^, ^, ^ : ^ stroke volume

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34
Q

Influences their ate of impulse generation and speed of conduction pathways

A

Autonomic NS

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35
Q

Originates with the SA nod or pacemaker, transmitted to the AV node, bundle of HIS and Purkinje fibers

A

Conduction system

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36
Q

Increases the rate of impulse generation and impulse transmission and innervates all parts of atria and ventricle

A

Sympathetic NS (SOS)

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37
Q

Decreases the rate and innvervates atria, ventricles, sinoatrial and atria-ventricular nodes

A

Parasympathetic NS

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38
Q

“Pacemaker of the heart”

A

SA node

60-100 beats per minute (BPM)

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39
Q

SA Node rate of impulses:
AV Node rate of impulses:
Bundle of His and Purkinje Fiber impulse rate:

A

60-100 bpm
40-60 bpm
20-40 bpm

40
Q

If the heart rate is at 43 BPM, what can you infer from this?

A

That the SA node is not firing and the AV node is doing all the work. AV node rate for bpm (40-60bpm)

41
Q

Contraction of the atria (EKG) wave

A

P wave

42
Q

The electrical signal passes through the bundle of his to the R and L bundle branches in the septum (EKG) wave:

A

Q wave

43
Q

(EKG) The contraction of the Left Ventricle. Which wave?

A

R wave

Electrical signals passes across the ventricles through the Purkinje fibers making the ventral contract

44
Q

(EKG) the contraction of the Right ventricle

A

S wave
Electrical signals forces the ventricles to push blood through the pulmonary valve and aortic valve, into the lungs and into the systemic circulation

45
Q

(EKG) the relaxation of the ventricles

A

T wave

46
Q

No flow of current. Cardiac cells are resting

A

Polarization

Diastole

47
Q

The flow of electrical current (or electrical connection/action potential) which results in a contraction of tissue

A

Depolarization

Systole

48
Q

The process of returning to a state of polarization

A

Repolarization

49
Q

Cardiac monitoring purpose:

A
  • identify the patient’s baseline
  • recognize significant changes
  • recognize lethal dysrhythmias that require immediate intervention
50
Q

Tachycardia

A

> 100

51
Q

Bradycardia

A

Less than 60

52
Q

Ectopic

A

Extra beats in rhythm

53
Q

Supraventricular

A

Above the ventricles

54
Q

Juncitonal

A

Within the AV node

55
Q

Ventricular

A

In the ventricles

56
Q

Irregular and often rapid heart rate that can increase your risk of stroke, HF, and other heart-related complications

A

Atrial fibrillation

57
Q

Atrial Fibrillation symptoms:

A
  • heart palpitations
  • shortness of breath
  • weakness
58
Q

Abnormal ventricle contractions in a very rapid and UNCOORDINATED manner

A

Ventricular fibrillation

59
Q

Symptoms of ventricular fib

A
  • dizziness
  • lightheadedness
  • Palpitations
  • Loss of consciousness
60
Q

May be brief, lasting for only a few seconds, or last long. Can cause your heart to stop (sudden cardiac arrest)

A

Ventricular tachycardia

61
Q

Ventricular tachycardia symptoms

A

-dizziness, lightheadedness, palpitations, or even loss of consciousness

62
Q

Characteristic rhythm of the healthy human heart. Present in adults if hr is between 60-100 bpm

A

Normal sinus rhythm (NSR)

63
Q

When the hr is >100

A

Sinus tachycardia

64
Q

Sinus tachycardia symptoms:

A 
SOB
Lightheadedness
Rapid pulse rate
Heart palpitations
Chest pain 
Syncope
 (Heart is beating too fast so heart cant fill completely to perfuse blood)
65
Q

Normal physiological response to exercise and conditions in which catecholamine release is physiologically enhanced or less commonly, when PNS system is withdrawn.

  • also caused by other bad things
A

Sinus tachycardia

66
Q

Underlying causes of Sinus Tachycardia

A

Fever
Infection
Neuro injury

67
Q

Lifestyle modifications to tx sinus tachycardia

A

DASH DIET

Exercise

68
Q

Medications for Tachycardia

A

Beta blockers
Ca++ blockers
Na++ sodium blockers- slows rate of repolarization of heart
K+ blockers- delay replorization in SA & AV node
Fluids

  • pacemaker
69
Q

A slow, regular, HR resulting from a low rate of pacing by SA node. (Regular rhythm) slow pace.

A

Sinus bradycardia

70
Q

What type of pt’s is sinus bradycardia normal for?

A
  • high physical fitness

- hypothyroidism (metabolic rate reduced)

71
Q

Medications that create Sinus Bradycardia:

A
  • acetylcholine, acetylcholinesterase inhibitors
  • sympatholytic drugs (beta blockers, methyldopa, clonidine)
  • opioids and sedative
  • digitalis
  • Ca++ blockers (diltiazem, verapamil)
  • Amiodarone (antiarrhythmic drugs)
  • hepatitis C: sofosbuvir, daclatasvir
72
Q

Etiology of sinus bradycardia:

A
  1. ) acute myocardial infarction
  2. ) sleep apnea
  3. ) exaggerated vagal activity
  4. ) ^ IC pressure
  5. ) infectious causes- typhoid, dengue, viral fevers, sepsis**
  6. ) other- hypothyroidism, hypothermia, anorexia, prolonged hypoxia
73
Q

S/S of sinus bradycardia

A
  • chest pain
  • fatigue
  • SOB
  • weakness
  • dizziness
  • syncope
  • confusion/memory issues
  • diaphoresis
  • tiring during physical activity
74
Q

TX of sinus bradycardia

A
  • atropine, Epi, NE, Dopamine
  • saline bolus
  • treat underlying cause
  • pacemaker
  • Na
  • O2
  • monitor vitals, K+, ABGs, Na, Ca++
75
Q

Nursing care for bradycardia

A
  • know baseline vitals
  • monitor for hypotension, syncope, diaphoresis, dyspnea, altered mental state
  • monitor vitals, pulse ox, telemetry
  • PT in TRENDELENBURG (head facing down to ground)
  • or lay down flat
76
Q

Atrial Firbrillation

A
  • no discernible p-waves
  • multiple foci rapidly discharging
  • no organized electrical activity in atria
  • rhythm is irregular

A Fib CONTROLLED= rate < 100 bpm
A Fib UNCONTROLLED= rate >100 bpm

77
Q

If its V-Fib you …..

A

De Fib!

* clear*

78
Q

Elective procedure where client is awake but sedated. Synchronized with QRS and is 50-200 Joules

A

Cardioversion

79
Q

Caused by electrical impulses that didn’t originate from the SA node (disrhythmias)

A

Disturbance in conduction

80
Q

Insufficient volume is ejected into the systemic and pulmonary circulation

A

Altered cardiac output

81
Q

Acquired or congenital disorder of a cardiac valve by stenosis or regurgitation

A

Impaired valvular function

82
Q

Coronary artery flow to the myocardium insufficient to meet myocardial oxygen demands

A

Myocardial ischemia

83
Q

Release of catecholamines from sympathetic nervous system: ^ HR, contractility, vasoconstriction, and ^ tendency of blood to clot

  • suppress immune and inflammatory system
  • release cortisol from adrenal cortex
A

Stress

84
Q

R sided heart failure -

A
  • Impaired functioning of the right ventricle
  • Elevated PVR (pulmonary vascular resistance)
  • Blood begins to “back up”
85
Q

S/S of right sided heart failure

A

weight gain,
distended neck veins, hepatomegaly,
splenomegaly,
dependent peripheral edema

86
Q

Left sided heart failure

A
  • Decreased functioning of the left ventricle

- Decreased cardiac output

87
Q

S/S left sided heart failure

A

-fatigue,
-shortness of breath,
-dizziness and confusion from tissue hypoxia
-crackles in lungs
- dyspnea on exertion (DEO)
- paroxysmal nocturnal dyspnea
*** pulmonary congestion
Monitor lung sounds closely

88
Q

Transient imbalance between myocardial oxygen and demand

A

Angina

-relieve with rest/coronary vasodilators

89
Q

MI

A
  • Pain occurs at rest or exertion
  • CELLULAR DEATH occurs after 20 minutes.
  • Rest, position change and nitroglycerin do not relieve pain
  • Men and women may have different symptoms
  • men- crushing, squeezing, elephant sitting on my chest
  • women- short of breath, fatigue, indigestion, mid back hurts, jaw pain.
90
Q

Heart enlargement

A

Cardiomyopathy

91
Q

Plaque build up inside coronary arteries

A

Coronary artery disease

92
Q

Mitral valve, aortic valve abnormalities

A

Heart valve abnormalities

- lots of regurg

93
Q

Peripheral Vascular disease

A

Functional PVDs don’t involve defects in blood vessels’ structure. (The blood vessels aren’t physically damaged.) These diseases often have symptoms related to “spasm” that may come and go.

• Organic PVDs are caused by structural changes in the blood vessels. Examples could include inflammation and tissue damage.
Peripheral artery disease (PAD) is a type of organic PVD. It’s caused by fatty buildups (atherosclerosis) in the inner walls of arteries. These deposits block the normal blood flow.

94
Q

Oxygen transport abnormalities (2)

A
  • anemia

- carbon monoxide

95
Q

Carbon monoxide poisoning ( cardiovascular abnormalities)

A

** cherry red appearance**
CO binds to cardiac myoglobin with an even greater affinity than to hemoglobin; the resulting myocardial depression and hypotension exacerbates the tissue hypoxia.
Carbon monoxide binding with hemoglobin results in carboxyhemaglobin. This has a cherry red color visually. This is why the hypoxic patient doesn’t appear blue or ashen. Their skin is pink.

Foundations EXAM 1 (9 decks)

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