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CV487 > Class 1 CV > Flashcards

Class 1 CV Flashcards

1
Q

Premature VS (HR, BP, RR)

A

120-170HR
>55/35>75/45
40-70RR

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2
Q

0-3 month VS (HR, BP, RR)

A

100-160HR
>65/45>85/55
30-60RR

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3
Q

3-6 month VS (HR, BP, RR)

A

90-120HR
>70/50>90/65
30-45RR

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4
Q

6-12 month (HR, BP, RR)

A

80-120HR
>80/55>100/65
25-40 RR

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5
Q

1-3 year VS (HR, BP, RR)

A

70-110HR
>90/55>105/70
20-30RR

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6
Q

6-12 year VS (HR, BP, RR)

A

60-95HR
>100/60>120/75
14-22RR

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7
Q

12+ year VS (HR, BP, RR)

A

55-85HR
>110/65>135/85
12-18RR

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8
Q

Palpation findings

A

Thrills vibrate
Heaves rise & fall
Bruits indicate an obstruction

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9
Q

Atrioventricular valves

A

Rigth AV; tricuspid
Left AV; bicuspid (mitral)
Open during diastole

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10
Q

Semilunar valves

A

Between ventricles and pulmonary arteries
Pulmonic valve
Aortic valve
Open during systole

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11
Q

Blood flow through the heart

A
  1. Liver to right atrium (IVC)
  2. Right ventricle through pulmonic valve to pulmonary artery
  3. Lungs
  4. Left atrium, through mitral valve to LV
  5. Aorta to body
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12
Q

Atrial systole…

A

Occurs during ventricular diastole

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13
Q

For a moment all valves…

A

Are closed during isometric contraction to exceed aortic pressure

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14
Q

After isometric contraction

A

Isometric relaxation or isovolumic relaxation

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15
Q

Normal heart sounds

A

S1; AV valves close (tricuspid & mitral) to begin systole
S2; semilunar valves close (pulmonic & aortic) ending systole
Split S2; when the aortic valve closes before the pulmonic

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16
Q

Extra heart sounds

A

S3; low intense vibration (ventricles resist filling); start of diastole
“kentucky” (ventricular gallop)

S4; low frequency vibration (atrial contraction); end of diastole when ventricle is resistant to filling
“Tennessee” (atrial gallop)

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17
Q

S3 indicators

A

Left ventricular failure (ie. volume overload, HF, mitral valve regurgitation, high CO, hyperthyroidism, anemia and pregnancy)

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18
Q

S4 indicators

A

-CAD
-Cardiomyopathy with systolic overload (after load)
-LV hypertrophy
-Aortic stenosis, HTN

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19
Q

Respirations impact on LV systole

A

MoRe to the Right; inspiration increases venous return to the right side of the heart; increases stroke volume
Less to the Left; less blood is returned to the left side of the heart; decreases ventricular stroke volume

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20
Q

Murmurs & etiology

A

Turbulence
Gentle, blowing, swooshing
Conditions: Inreased velocity blood flow, decreased viscosity of blood, structural defects in valves, or unusual openings in chambers

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21
Q

Assessing murmurs (what to listen for)

A

Timing: systole or diastole
Loudness: 6 grades
Pitch

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22
Q

Conduction of the heart

A

SA node initiates (pacemaker) to AV node to bundle of His to the apex then through the ventricles

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23
Q

PQRST waves

A

P wave; depolarization of the atria
P-R interval; interval from the beginning of the P wave to the beginning of the QRS complex
QRS complex; depolarization of the ventricles
T wave; repolarization of the ventricles

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24
Q

Cardiac output definiton & variables

A

Stroke volume x HR
Variables: HR, SV, metabolic rate & O2 demand, females

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25
Q

Neural reflexes

A

Baroreceptors are pressure sensors in the aortic arch and carotid sinus that respond to BP and HR

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26
Q

PNS

A

Decreases HR
Vagal fibers release Ach

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27
Q

Neurotransmitters from the SNS

A

Increase HR
NE, E, distended radial artery

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28
Q

Cardiac output respiratory and metabolism

A

O2 demands increase in hypermetabolic states

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29
Q

Frank starling law

A

The greater the stretch (preload), the stronger the contraction and larger ejection fraction

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30
Q

Atrial kick does what

A

Augments venous return to the heart increasing ventricular volume & pressure

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31
Q

Compliance

A

More compliant ventricles mean lower filling pressure

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32
Q

Preload

A

= Volume
Inside problem

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33
Q

Afterload

A

= Constriction
Opposing pressure generated by the ventricle to open the aortic valve
Outside problem

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34
Q

Left ventricular outflow resistance

A

Aortic diastolic pressure
SVR
Aortic valve resistance

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35
Q

Right ventricular outflow resistance

A

Pulmonary artery diastolic pressure, PVR, pulmonic valve resistance

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36
Q

Systemic vascular resistance

A

Resistance of blood flow throughout systemic circulation

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37
Q

Peripheral vascular resistance

A

Resistance of blood flow throughout pulmonary circulation

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38
Q

Increased afterload causes & etiology

A

Decreases stroke volume
Caused by: HTN, aortic or pulmonic stenosis, heart O2 demand, vasoconstriction, high BMI

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39
Q

Decreased afterload

A

Increases stroke volume
Decreases ventricular work
Decreases heart O2 demand
Vasodilation

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40
Q

Contractility definition

A

Hearts abiliy to increase the extent and force of muscle fiber shortening independent of preload/afterload

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41
Q

Factors determing contraction/contractility

A

1.Altered stretching of the ventricular myocardium caused by changes in ventricular end-diastolic volume (preload)

2.Alterations in the inotropic stimulation of the ventricles
-Positive inotropic strengthens heart contraction
-Negative inotropic weakens heart contraction

3.Oxygen supply

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42
Q

Ejection fraction definition

A

Amount of blood ejected from the ventricle compared with end-diastolic volume

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43
Q

Ejection fraction measurments

A

50-70%; normal
41-49%; mild HF
<=40%; moderate HF
<=35%; severe HF

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44
Q

Carotid artery & jugular veins

A

Reflect efficiency of cardiac function

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45
Q

Jugular veins tell us

A

About right sided activity and reflect filling pressure and volume changes

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46
Q

Hemodynamic changes with aging

A

-Systolic BP increases d/t arteriosclerosis
-Left ventricular wall thickens to accommodate vascular stiffening
-Diastolic BP decreases, increasing the pulse pressure
-HR and CO do not change with aging

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47
Q

SVT and ventricular arrhythmias (age)

A

-Increase with age
-Ectopic beats are more common in older adults which can compromise CO&BP when disease is present

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48
Q

Tachydysrhythmias in older adults

A

-Not tolerated well by older adults because the myocardium is thicker and early diastolic filling is impaired at rest
-Tachycardia not tolerated well because of shortened diastole
-Compromises organs affected by aging or disease

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49
Q

ECG in older adults

A

-P-R and Q-T intervals are prolonged; QRS complex is unchanged
-Left axis deviation related to LV hypertrophy and fibrosis in the left bundle branch; increased incidence of bundle branch blockage

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50
Q

Common cardiac findings in infants and children

A

-Sinus arrhythmia; speeding and slowing of heart
-Venous hum

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51
Q

Deep veins

A

Run along deep arteries providing most of the venous return from the lower extremeties

52
Q

Superficial veins

A

The great and small saphenous veins
Blood flows from the superficial to the deep leg veins

53
Q

Perforators

A

connecting veins that join deep and superficial veins

54
Q

Veins

A

Low pressure systems
Blood moves through them via: Contraction of skeletal muscle, the pressure gradient caused by breathing, and the intraluminal valves which prevent backflow
-Capacitance vessels because of their ability to stretch

55
Q

Varicose veins

A

Have incompetent valves that cannot approximate which increases venous pressure and further dilates the vein

56
Q

Lymphatic system functions

A

-Conserve fluid and plasma proteins that leak out of the capillaries
-Form a major part of the immune system that defends the body
-To absorb lipids from the intestinal tract

57
Q

Spleen functions

A

-To destroy old red blood cells
-Produces antibodies
-Store red blood cells
-To filter microorganisms from the blood

58
Q

Types of HTN

A

-Primary: Elevated BP with no specific cause
-Secondary: Elevated BP with an underlying disorder
-Complicated: Chronic HTN occuring overtime (eg. arteriosclerosis)

59
Q

Hypertensive crisis

A

-Severe & abrupt
-Pressure impedes blood flow to cerebral capillary beds
-Hydrostatic pressure in capillaries moves vascular fluid to interstitial spaces
-Leads to cerebral edema & dysfunction

60
Q

Hypertensive emergency

A

Develops over hours to days and has caused organ damage

61
Q

Hypertensive urgency

A

-Develops over days to weeks and has not caused organ damage

62
Q

Physical exam overview in a hypertensive crisis

A

Neurological dysfunction, retinal damage, pulmonary edema, HF and renal failure

63
Q

Physical exam in a hypertensive crisis (CV)

A

-Bruits
-JVD to rule out increase volume
-Weak & thready lower extremity pulses indicating increased afterload,
-Hemodynamic instability and edema

64
Q

Physical exam in a hypertensive crisis (respiratory)

A

-Auscultate for crackles
-Pulmonary edema
-Assess for poor oxygen exchange and signs of cyanosis

65
Q

Physical exam in hypertensive crisis (renal)

A

-Monitor urine output, colour, frequency, and for signs of dehydration

66
Q

Clinical manifestations in hypertensive crisis (neurological)

A

Headache, N/V, seizures, confusion, stupor, coma, encephalopathy, blurred vision and transient blindness

67
Q

Hypertensive crisis (CV) can lead to…

A

Cardiac instability such as unstable angina to MI, pulmonary edema, and aortic dissection

68
Q

Clinical manifestations in hypertensive crisis (renal)

A

Renal insufficiency such as decreased urine output to complete renal shutdown

69
Q

Hypotension

A

<100/60
Inadequate tissue perfusion because of lowered CO
Shifts in intravascular volume

70
Q

Hypotension manifestations

A

aLOC
-Chest pain (heart is pumping rapidly without being supplied with O2 and nutrients)
-Tachypnic
-Oliguria, anuria
-Lethargic

71
Q

Hypotensive shock types

A

-Cardiogenic (heart cannot pump effectively)
-Hypovolemic
-Distributive (vasculature is not compensating for hemodynamic changes)
-Septic
-Anaphylactic
-Neurogenic

72
Q

Labs to monitor for patients with HTN

A

-CBC
-Coagulation
-Electrolytes
-Kidney function
-Lipids
-Speciality labs: Troponin, creatinine kinase, and C-reactive protein

73
Q

Labs to monitor for people with hypotension

A

-CBC
-Coagulation
-Electrolytes
-Kidney function
-Lipids
-Liver function
-Speciality labs (troponin, brain-natriuretic peptide, creatinine kinase, creatinine kinase of heart, C-reactive protein)

74
Q

Bradycardia in pediatric population that can be lethal

A

-Newborns-3 years; <100bpm
-3-9 years; <60bpm
-9-16 years; <50bpm

75
Q

Heart block

A

Impulse from SA to AV node is slowed and fails to initiate conduction

76
Q

Atrial flutter

A

-Continuous stimuli to the AV node cannot conduct all the impulses but a few get through to the ventricle
-Only involves the atria, the venticular bundle of His is functioning normally

77
Q

Atrial fibrillation

A

-Worse than atrial flutter
-The atria of the heart quivers

78
Q

Premature ventricular contractions

A

-Extra contraction that originates in the ventricle
-Occasional PVC is normal, three in a row indicates that the patient has increased cardiac irritability and >10 in a minute may precipitate an MI or Vtach
-Vtach is worse than atrial flutter and atrial fibrillation

79
Q

Ventricular tachycardia & K+

A

-Irritable focus of an impulse within the ventricle
-Life threatening and can lead to ventricular fibrillation
-Too much K+ causes cardiac irritability (decreased CO)

80
Q

Ventricular fibrillation

A

-Quivering of the ventricle
-Impedes pumping function of the heart
-No O2 to the brain

81
Q

Pertinent labs to monitor in dysrhythmia

A

Na+
K+; impaired kidney function (not excreting K+)
Ca+; hypocalcemia influences dysrhythmias more than hypercalcemia, increased risk for vtach
Mg+

82
Q

Angina and MI primary cause

A

-Can be caused my atherosclerosis

83
Q

Angina definition

A

-Diminished blood flow and lack of oxygen in the arteries in the heart leading to myocardial ischemia

84
Q

Angina manifestations, precipitating factor, eventuality and types

A

-Chest pain
-Often occurs during activity
-Precursor to MI
-May be stable, unstable, or variant

85
Q

Stable angina

A

-effort induced chest pain
-lasts few seconds to 15 minutes
-relieved by rest, removal of provoking factors, or NTG

86
Q

Unstable angina

A
  • lasts longer and occurs more frequently
  • may be exertional or occurs at rest
  • often referred to as crescendo angina, preinfarction angina, nocturnal angina
87
Q

Variant (prinzmetal) angina

A
  • chest pain that occurs at rest in early hours of the morning
  • is often associated with ST segment elevations
    -often cyclical
88
Q

Acute MI

A

-Interruption of blood supply to the cardiac muscle
-Result of sustained ischemia leading to myocardial cell death
-Location of the infarction correlates with the involved coronary circulation

89
Q

Causes of acute MI

A

-Anything impeding blood flow
-Plaque rupture
-Thrombus formation
-Coronary artery embolism
-Coronary spasm (cocaine)
-Hypotension
-Decrease in O2 delivery to tissues (anemia, shock, hypoxemia)
-Post procedure
-Spontaneous Coronary Artery Dissection

90
Q

Type I MI

A

-Thrombosis of the coronary artery or a plaque rupture.
-Spontaneous symptoms
-Men>women

91
Q

Type II MI

A

-Disrupted O2 supply or demand in the absence of a blockage
-Women>men
-Less chest pain and dyspnea
-May not present with ischemic events on the ECG

92
Q

Angina vs acute MI discomfort

A

Angina; chest pain, pressure, squeezing, tightness

Acute MI; Same as angina + abdominal pain and SOB

93
Q

Angina vs acute MI location and radiation

A

Angina; midsternal, neck, jaw, arms, and back

AMI; same as angina + increased pain and radiation

94
Q

Angina vs acute MI intensity

A

Angina; mild-moderate

AMI; more intense, silent, and severe

95
Q

Angina vs acute MI duration

A

Angina; 3-15 minutes

AMI; >20-30 minutes

96
Q

Angina vs acute MI precipitating factors

A

Angina; exercise, weather, large meal, sex and stress

AMI; same as angina but may occur at rest

97
Q

Angina vs acute MI associated S&S

A

Angina; none

AMI; Diaphoresis, SOB, abdominal pain, indigestion, fatigue, pale, tachycardia, and palpitations

98
Q

Angina vs acute MI lab values

A

Angina; none

AMI; high sensitivity troponin, CKMB

99
Q

Overview of acute MI manifestations + LV dysfunction/RV dysfunction

A

-Pain, ashy, clammy, cool to touch
-If LV dysfunction; crackles may be heard in the lungs
-If RV dysfunction; JVD, hepatic engorgment and peripheral edema
-Extra heart sounds
-N/V, fever

100
Q

Nursing assessment of acute MI (neurological)

A

-Pain, anxiety, LOC, fear, pyschosocial and diaphoresis

101
Q

Nursing assessment of acute MI (CV) (IPAP)

A

-Dysrhythmias, extra heart sounds, murmurs, cap refill, JVD, peripheral edema, BP

102
Q

Nursing assessment of acute MI (respiratory)

A

Rate and depth, crackles (if LV involved), oxygenation

103
Q

Nursing assessment of acute MI (GI)

A

N/V, aMotility

104
Q

Nursing assessment of acute MI (renal)

A

Urine output

105
Q

Pertinent labs to monitor with acute MI

A

-Hemoglobin
-Electrolytes
-Kidney function (creatinine & BUN will be high)
-Lipids & blood glucose
-Liver function tests (drawn in ALL labs)
-Troponin
-BNP (HF)
-CK-MB (only cardiac)

106
Q

Types of acute MI

A

NSTEMI; non ST elevated MI

STEMI; ST elevated MI

107
Q

Orthostatic hypotension definition

A

A decrease of 20 mm Hg (or more) in SBP or a decrease of 10 mm Hg (or more) in DBP

108
Q

Orthostatic hypotension causes

A

-Intravascular volume loss (e.g., with diuretic therapy or dehydration)
-Inadequate vasoconstrictor mechanisms related to disease or medications

109
Q

Unstable angina and MI diagnostic studies (not labs)

A

ECG
Serum cardiac markers
Coronary angiography

110
Q

Paroxysmal supraventricular tachycardia (PSVT)

A

Dysrhythmia originating in an ectopic focus anywhere above the bifurcation of the bundle of His

111
Q

Inferior wall myocardial infarction

A

Occurs from coronary occlusion with resultant decreased perfusion

112
Q

Anterior wall myocardial infarction

A

Blockage in the left descending coronary artery leads to injury of the anterior myocardial tissue

113
Q

Lateral wall myocardial infarction

A

Caused by plaque rupture with subsequent thrombus formation in the left circumflex (LCx) coronary artery or its branches

114
Q

Posterior wall myocardial infarction

A

Thrombus in the posterior descending artery

115
Q

Septal wall myocardial infarction

A

A patch of dying or necrotic tissue on the septum caused by delayed blood flow in the septal branch of the left anterior descending coronary artery

116
Q

Etiology of pulseless electrical activity (PEA); 6 H’s & 6 T’s

A

Hyperkalemia, hypoxia, hypothermia, hydrogen ion excess (acidosis), hypovolemia, and hypoglycemia
-Tamponade, tension pneumothorax, thrombosis (pulmonary embolus), thrombosis (myocardial infarction), toxins, and trauma

117
Q

Inferior MI

A

-Blockage of the right coronary artery leads to an inferior MI
-Right sided problem

118
Q

Anterior MI (widow maker)

A

Blockage the of left anterior descending artery (LAD) leads to an anterior MI
-Left sided heart problem

119
Q

Lateral wall MI

A

Atherosclerotic plaque rupture with thrombus formation in the left circumflex
-Left sided heart problem

120
Q

Posterior MI

A

Occlusion of the circumflex
-Left sided heart problem

121
Q

S3 means…

A

Left ventricular problem

122
Q

STEMI is blank than NSTEMI

A

Worse

123
Q

50ng/L of troponin

A

Lowest number indicating an MI

124
Q

Flipped T waves

A

Indicate ischemia

125
Q

STEMI indicates more what

A

Muscle damage and ST segment is elevated

126
Q

ST depression and flipped T’s mean

A

Ischemia

127
Q

ST elevation indicates

A

Injury

CV487 (15 decks)

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