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Patho1 > Cardio Patho > Flashcards

Cardio Patho Flashcards

1
Q

what is coronary artery disease?

A

the coronary arteries that come off of the aorta to supply the heart with oxygenated blood becomes arteries clogged due to atherosclerosis, then the heart muscles can die from lack of oxygenation.

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2
Q

what is the most dangerous location to have atherosclerosis related to coronary arteries - why?

A

left anterior descending artery, this supplies the left ventricle with blood, and it is responsible for perfusion to the body

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3
Q

what are the non-modifiable risk factors for CAD?

A

older age
family history (+ shared environmental exposure)
males earlier in life
postmenopausal women
ethnicity (black, hispanic, native, indigenous)

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4
Q

what are the modifiable risk factors for CAD?

A

hypertension
smoking
diabetes
obesity
diet high in salt, fat, and carbs
hyperlipidemia
depression / stress

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5
Q

describe the endothelial dysfunction with CAD, what causes it?

A

even though the vessels are entirely blocked, they constrict when they are supposed to dilate (and vice versa).
caused by DM, HTN, HPL, smoking

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6
Q

what are the clinical manifestations of CAD?

A

angina (may not have, but the more narrowed = decrease blood flow = chest pain)
complete occlusion = MI
symptoms associated with chest pain: heartburn, irregular pulse, palpitations, weakness, dizziness, nausea, cold sweats, burning in the chest / shoulder / abdomen

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7
Q

how long, on average, does stable angina last?

A

2-5 minutes

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8
Q

how long, on average, does unstable angina last?

A

> 10 minutes

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9
Q

what is stable angina often mistaken for and why?

A

indigestion - this is because it can happen after eating a large meal.

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10
Q

what causes stable angina most commonly?

A

atherosclerosis

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11
Q

what is the basic description of cardiac chest pain?

A

pressure or a tightness

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12
Q

what is the basic description of non cardiac chest pain?

A

stabbing or sharp

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13
Q

what is the general location of cardiac chest pain?

A

diffuse, poorly localized

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14
Q

what is the general location of non cardiac chest pain?

A

focal and well localized

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15
Q

what usually brings on stable angina, what relieves it?

A

exertion usually brings it, usually relieved by rest

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16
Q

when can unstable angina be triggered?

A

at rest

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17
Q

cardiac or non-cardiac chest pain: which is associated with physical exertion or other stresses

A

cardiac

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18
Q

cardiac or non-cardiac chest pain: which may be positional or spontaneous at rest?

A

non-cardiac

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19
Q

cardiac or non-cardiac chest pain: which is relieved with rest and can be resolved usually within a few minutes?

A

cardiac

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20
Q

cardiac or non-cardiac chest pain: which has no predictable relation to physical exertion?

A

non-cardiac

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21
Q

how long can non-cardiac chest pain last?

A

seconds to days

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22
Q

what are common symptoms for angina for women?

A

hot / burning or tenderness around the chest (but doesn’t always have to be the chest)
indigestion
heartburn
nausea
fatigue / weakness
lightheadedness
dyspnea

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23
Q

where can the pain be in relation to a myocardial infarction?

A

neck, jaw, upper abdomen, shoulders, and arm

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24
Q

what symptoms often accompany a myocardial infarction?

A

N/V, SOA, diaphoresis

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25
Q

what do we usually do for stable angina, in general?

A

educate the patient - encouraging rest and avoiding increased demands
nitrates
prevent and treat atherosclerosis
teach s/s of a heart attack

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26
Q

what is cardiomyopathy?

A

a disease that affects the myocardium (which is the muscle), these diseases decrease the ability of the muscle to contract and can eventually lead to HF.

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27
Q

what are the potential causes of cardiomyopathy?

A

usually idiopathic - but can be from ischemia, HTN, inherited disease, infections, toxins, myocarditis, autoimmune condition

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28
Q

what are the potential causes of dilated cardiomyopathy?

A

can be from ischemia, alcohol / drugs, infection, peri / post partum, valve disease, genetics

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29
Q

what does dilated cardiomyopathy lead to?

A

HF with decreased EF

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30
Q

what is the common cause of hypertrophic cardiomyopathy?

A

HTN

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31
Q

what does hypertrophic cardiomyopathy increase the risk for?

A

deadly arrhythmias

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32
Q

what is the least common type of cardiomyopathy?

A

restrictive

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33
Q

what is heart failure?

A

a progressive condition in which the heart muscle is unable to pump enough blood to meet the demands of the body for blood and oxygen

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34
Q

how is cardiac output affected with heart failure?

A

decreased

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35
Q

what components make up stroke volume?

A

preload, myocardial contractility, afterload

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36
Q

what is preload and afterload?

A

preload - the amount of volume in the left ventricle right before it contracts
afterload - the pressure the heart has to squeeze against when it contracts

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37
Q

how does heart failure affect cardiac output, myocardial contractility, preload, and afterload?

A

CO = decrease
MC = decrease
preload + afterload = increase

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38
Q

what are the 4 hallmarks of heart failure?

A

volume overload (can’t pump it out)
impaired ventricular filling
weakened ventricular muscle
decreased ventricular contractile function

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39
Q

what are the potential causes of HF?

A

repeated ischemic episodes (stable angina, cardiomyopathy)
MI
chronic HTN
COPD - causes right sided
dysrhythmias (d/t decreased output)
valve disorders, mitral insufficiency, aortic stenosis
PE

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40
Q

what are the risk factors of developing HF?

A

hypertension (biggest one)
within 6 months of a MI
men and postmenopausal women
black / african american
family hx
age
DM
ischemic heart disease
smoking
sedentary
COPD
anemia
congenital heart defects
viruses
alcohol / drug abuse
CKD

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41
Q

what type of HF would cause increased left ventricles?

A

left sided heart failure

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42
Q

what is left sided heart failure?

A

congestion backed up into the left ventricles causing backflow into the pulmonary veins

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43
Q

what are common findings for left sided heart failure?

A

cough, crackles, wheezes
frothy, pink tinged sputum
paroxysmal nocturnal dyspnea
orthopnea

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44
Q

what is right sided heart failure?

A

heart failure commonly caused by COPD causing congestion in the right chambers of the heart snd backflow into the vena cava. This decreases blood flow to the lungs.

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45
Q

what are common findings with right sided heart failure?

A

JVD
dependent edema
weight gain
hepatosplenomegaly

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46
Q

other names for heart failure with reduced ejection fraction?

A

HFrEF or systolic HF

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47
Q

what is the EF for someone who has HFrEF?

A

< 40

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48
Q

what causes HFrEF?

A

impaired contractile function, increased afterload, cardiomyopathy, and mechanical problems

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49
Q

what is heart failure with reduced ejection fraction?

A

left ventricle loses the ability to generate pressure to eject blood, the weakened muscle can’t generate a strong enough stroke volume to get the blood out. Eventually the LV fails and fluid backs up and causes accumulation.

50
Q

what are other names for heart failure with preserved ejection fraction?

A

HFpEF, diastolic HF

51
Q

what is HFpEF?

A

inability of the ventricles to relax and fill during diastole, this leads to a high filling pressure and a decreased SV and CO, causing fluid congestion

52
Q

what is the EF for a patient with diastolic HF?

A

normal or moderately decreased (40-49%)

53
Q

what is ventricular remodeling, what disease process does it come with?

A

HF
this happens when the body recognizes that the heart isn’t working right. The body releases substances (angiotensin II, ADH, endothelin, TNF-alpha, catecholamines, insulin-like growth factors, and growth hormones) that actually end up hurting the body over time (causes genetic changes, apoptosis, hypertrophy of cardiac myocytes, collagen deposits, and fibrosis). All of this leads to changes that cause enlargement and increased dilation in the LV, worsening the HF.

54
Q

when does S3 happen, what does it indicate?

A

S3 happens during the filling of the ventricles (after S2). This means that there is still fluid left in the left ventricle which is commonly indicative of HF.

55
Q

define automaticity

A

ability to generate an electrical impulse

56
Q

define excitability

A

ability to respond to an outside impulse

57
Q

define conductivity

A

ability to receive an electrical impulse and conduct it on

58
Q

define contractility

A

ability to myocardial cells to shorten in response to an impulse

59
Q

what 2 electrolytes are responsible for the action potentials in the heart?

A

Na+ and K+

60
Q

is atrial / ventricular depolarization systole or diastole?

A

systole

61
Q

is atrial / ventricular repolarization systole or diastole?

A

distole

62
Q

atrial depolarization is indicated by what wave on an EKG?

A

P wave

63
Q

ventricular depolarization is indicated by what complex on an EKG?

A

QRS complex

64
Q

ventricular repolarization is indicated by what wave on an EKG?

A

T wave

65
Q

what 2 structures are specifically responsible for telling the ventricle to contract?

A

bundle of Hiis and purkinje fibers

66
Q

where in an EKG reading would you see atrial repolarization?

A

QRS complex

67
Q

what is the normal PR interval?

A

0.12 - 0.20 seconds

68
Q

what is the normal QRS interval?

A

< 0.12 seconds

69
Q

for sinus rhythms where does the electrical conduction originate?

A

SA node

70
Q

what is the time represented by the individual boxes on an EKG strip?

A

0.04 seconds

71
Q

what is sinus arrhythmia?

A

a degree of variability in the heart rate, is considered normal still. will not change CO. still normal bpm, PR interval, and QRS complex. this is most common in younger people. heart rate will change with respirations or autonomic nervous system.

72
Q

what is a dysrhythmia?

A

an abnormal cardiac rhythm that will affect cardiac output

73
Q

what 3 things can potentially cause dysrhythmias?

A

inappropriate automaticity - a cell initiating an action potentials when it isn’t supposed to (usually in the atria)
triggered activity - extra impulse during or after a repolarization
re-entry - this is where a part of the heart continues to depolarize after the main impulse is done

74
Q

where does sinus bradycardia originate?

A

SA node

75
Q

what is the rate of sinus bradycardia?

A

< 60 bpm

76
Q

how are the PR interval and the QRS complex different in sinus bradycardia?

A

they aren’t different, just farther in general

77
Q

what are the causes of sinus bradycardia?

A

hyperkalemia
vagal responses
digoxin toxicity
late hypoxia
CCB, BB, amiodarone
MI

78
Q

what are the clinical manifestations of sinus bradycardia?

A

lightheadedness, dizziness, fatigued, syncope, dyspnea, chest pain, confusion

79
Q

where does sinus tachycardia originate?

A

SA node

80
Q

what is the rate for sinus tachycardia?

A

100-150 bpm

81
Q

how are the PR interval and the QRS complex different in sinus tachycardia?

A

PR intervals and QRS complex is normal

82
Q

how are P waves different in sinus tachycardia?

A

they may be hard to see because it is faster, but they should be the same

83
Q

what are common causes of sinus tachycardia?

A

exercise
pain
strong emotions
fever
FVD *
medications - epi, albuterol, beta-agonist
caffeine, nicotine, cocaine
early hypoxia

84
Q

what is PSVT?

A

paroxysmal supraventricular tachycardia

85
Q

what is the rate of PSVT?

A

150-250 bpm

86
Q

where does the impulse for PSVT happen?

A

above the ventricles, maybe the AV node

87
Q

how are the P waves different in PSVT?

A

usually no P wave, if there is they look weird

88
Q

what is the QRS complex interval in PSVT?

A

normal

89
Q

what usually causes PSVT?

A

re-entry phenomenon

90
Q

what do patients typically say they feel when having PSVT?

A

a sudden heart racing

91
Q

what are common causes of PVST?

A

overexertion
emotional stress
stimulants
dig tox
rheumatic heart diesase
CAD
wolff-parkinson-white
right sided HF

92
Q

what are clinical manifestations of PVST?

A

palpitations
chest pain
fatigue
dizziness
dyspnea

93
Q

what is PAC?

A

premature atrial contraction

94
Q

how do the P waves change with PAC?

A

early P waves that may look a little weird

95
Q

how does the PR interval and QRS change with PAC?

A

they are the same, QRS does follow a run of PAC

96
Q

what dysrhythmia does having PAC’s put the patient at risk for?

A

afib

97
Q

what two things should the nurse monitor if a patient has PAC’s?

A

electrolyte levels and O2

98
Q

where does the impulse generate for atrial flutter?

A

AV node

99
Q

what physiological process causes atrial flutter?

A

re-entry

100
Q

what is the atrial rate of atrial flutter?

A

can be > 250

101
Q

how are P waves and QRS different in atrial flutter?

A

there is not a QRS complex after every P wave
P wave have a sawtooth appearance
QRS timing is normal when it happens

102
Q

where does the impulse generate for atrial fibrillation?

A

random irritable spots in the atria

103
Q

what is the rate for atrial fib?

A

100-175 bpm

104
Q

how do P waves change with atrial fib?

A

there is no identifiable P wave

105
Q

what are the common causes of a-fib?

A

electrolytes
hypoxia
cardiovascular diseases

106
Q

what are the complications of a-fib?

A

decreased cardiac output
heart failure
embolism
stroke

107
Q

patients with a-fib have an increased risk of having what?

A

a stroke

108
Q

what is PVC?

A

premature ventricular contraction

109
Q

where does the impulse for PVC come from?

A

an ectopic focus in the ventricles

110
Q

how are P waves and QRS complexes different in PVC?

A

QRS complex comes earlier than it should and doesn’t come after a P wave
QRS is WIDE and DISTORTED ( > 0.12 s)

111
Q

what are common causes of PVC?

A

stimulants
electrolytes
hypoxia
fever
exercise
emotional stress
CVD

112
Q

when you begin to see PVC regularly what is the concern and what should you check?

A

check electrolytes
worries about the patient decompensating and going into a more dangerous rhythm

113
Q

what is VTACH?

A

ventricular tachycardia - made up of 3 PVCs back to back

114
Q

where does the impulse for VTACH originate from?

A

ectopic focus in the ventricle

115
Q

do atrial contractions happen with VTACH?

A

no

116
Q

how does cardiac output get affected by VTACH?

A

severely decreased

117
Q

what is the rate for VTACH?

A

150-200 bpm

118
Q

how are P waves and the PR interval different in VTACH?

A

no P wave
PR interval is not measurable because there is no P wave

119
Q

what 2 rhythms are considered deadly?

A

VTACH and Vfib

120
Q

what is vfib?

A

ventricular fibrillation

121
Q

how is cardiac output affected with vfib?

A

no effective contractions - no cardiac output

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