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Adult Health > AH2 Cardio Lecture > Flashcards

AH2 Cardio Lecture Flashcards

1
Q

serum lactate indicates

A

level of serum oxygen-hypoperfusion or hypoxia causes anaerobic metabolism and increased levels of serum lactate.
Serum lactate levels increase in lactic acidosis, severe dehydration, heart failure, respiratory failure, hemorrhage, ketoacidosis, severe infections, alcohol abuse, salicylate toxicity, shock, and liver disease. Most labs define normal as 0.5 to 2.2 mmol/L for venous blood and 0.5 to 1.6 mmol/L for arterial blood.
Administering metformin with intravascular iodinated contrast media for radiologic studies or procedures can cause lactic acidosis due to decreased kidney fxn r/t contrast medium. Metformin should be discontinued in select patients (according to facility policy and procedure) at the time of the study or procedure and for 48 hours afterward. - See more at: http://www.nursingcenter.com/lnc/journalarticle?Article_ID=933028#sthash.44B96AKZ.dpuf

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2
Q

noninvasive assessments of hemodynamics

A 
cap refill
pulse rate and quality
skin temp/color
BP
mentation
urine output
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3
Q

invasive hemodynamic monitoring

A

invasive intravascular catheters (CVP, RA, PA, Swan Ganz Catheter)
Arterial Catheter

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4
Q

fluid overload
decreased HR
sympathetic venoconstriction
increased BP

A

increased preload-nitro (venous vasodilators), morphine, diurectics

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5
Q 
dehydration
blood loss
fluid loss
loss of atrial kick
increased HR
positioning-gravity
A

decreased preload-crystalloid/colloid, vasopressors

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6
Q

lung infection
chronic lung disease
pulmonary HTN

A

causes of increased PVR

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7
Q

vasoconstriction
aortic stenosis
increased blood volume increased blood viscosity

A

increased afterload-give vasodilators

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8
Q

vasodilation
allergic rxn
loss of vascular tone
sepsis

A

decreased afterload-give vasoconstrictors

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9
Q 
monitor 
flush system
transducer
high-pressure tubing (pump to 150-300)
catheter
A

constant flow of sterile solution to maintain patency and avoid clots (saline vs heparin solution: low limb perfusion, extended time line in place, frequent blood draws, heparin sensitivity)
level and zero system every time the patient, the pole or the bed is moved
transducer position directly affects accuracy

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10
Q

phlebostatic axis

A

level with Right atrium (fourth intercostal space); catheter tip and transducer must be at same level as phlebostatic axis when using hemodynamic monitoring

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11
Q

snap shut of aortic valve

A

dicrotic notch

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12
Q 
atrial depolarization (contraction)
0.06-0.12s
possible source of variation may be disturbance in conduction within atria
A

p wave

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13
Q

ventricular depolarization

A

QRS

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14
Q

repolarization

A

t wave

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15
Q

MAP formula

A

MAP=Diastolic BP x2 + SBP/3
normal is 70-100 mm Hg
must be >60 mm Hg for the perfusion of vital organs

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16
Q

R wave

A

represents the contraction of the LV and the mvmt of blood from the aortic valve out to the body

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17
Q

S wave

A

represents the contraction of the RV and the mvmt of blood from the pulmonic valve to the lobes of the lung

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18
Q

gives measure of LV pressure

A

Swanz Catheter, pulmonary artery pressure

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19
Q

CVP

A

measures pressure in right atria

normal is 2-6 mmHg

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20
Q

acute episodes of cardiac ischemia, electrolyte imbalances, and the use of cardiac meds

A

abnormal T waves

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21
Q

hypokalemia, diabetes, ventricular hypertrophy, and cardiomyopathy

A

abnormal U waves

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22
Q

The 300 method

A

300, 150, 100, 75, 60, 50

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23
Q

PR intervals

A

0.12-0.20s

disturbance in conduction usually in AV node, bundle of His, or bundle branches, but can be in atria as well

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24
Q

QRS duration

A

0.04-0.12s
time during which both ventricles contract (depolarization)
possible variations due to disturbance in bundle branches or in ventricles

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25
Q

big box and little box durations

A

0.2 s and .04 s

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26
Q

QT interval

A

.34-.43 seconds (less than 500milliseconds)

possible variations due to drugs, electrolyte imbalances, and changes in heart rate

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27
Q

dobutamine

A

beta agonist-tx for bradycardia

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28
Q

frequent PAC’s

A

catheter in right atria? too much fluid? heart irritated due to ischemia? too much caffeine? can be precursor to atrial fib

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29
Q

atrial flutter

A

sawtooth pattern observed with P wave, regular ectopic beats; precursor to atrial fibrillation-treat

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30
Q

atrial fibrillation

A

atrial chaos; irregular rhythm, F waves, ectopic beats

give anticoagulation therapy

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31
Q

How much cardiac output comes from the atrial kick?

A

30% CO results from atrial (LUB) kick

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32
Q

SA node rate

A

60-100bpm

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33
Q

AV node rate

A

40-60bpm

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34
Q

Purkinje fibers rate

A

20-40 beats/minute

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35
Q

loudest at apex of heart

AV valves close

A

S1 LUB

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36
Q

semilunar valves close

loudest at base of heart

A

S2 DUB

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37
Q

present if ventricular wall compliance is decreased and structures in the ventricular wall vibrate; this can occur in conditions such as heart failure, valvular regurgitation, fluid overload, or HTN. heard in early diastole

A

S3; may actually be normal in those younger than 30 years

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38
Q

may be heard on atrial systole if resistance to ventricular filling is present; this is an abnormal finding, and the causes include cardiac hypertrophy, CAD, aortic stenosis, HTN, or injury to the ventricular wall; heard in late diastole

A

S4

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39
Q

isoelectric

A

flat-ST segment
0.12 s
possible variations due to disturbances usually caused by ischemia, injury, or infarction

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40
Q

ventricular repolarization

A

T waves 0.16 s

possible variations due to electrolyte imbalances, ischemia, or infarction

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41
Q

Dysrhythmias Emergency Management

A

Initial: Ensure ABC’s, Administer O2, obtain vitals, obtain 12lead EKG and continuous monitoring, ID underlying rate and rhythm, ID dysrhythmia, Establish IV access

Ongoing: Vitals, LOC, O2 saturation, cardiac rhythm; anticipate need for antidysrhythmic meds and analgesics, anticipate need for intubation, prepare to initiate advanced cardiac life support (CPR, defibrillation, or transcutaneous pacing)

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42
Q

Nursing considerations for Adenoside

A

give for PSVT (paroxysmal supraventricular tachycardia)
administer IV dose rapidly over 1-2 seconds followed by a rapid NS flush
Brief period of asystole is common
observe pt for flushing, dizziness, chest pain, or palpitations

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43
Q

What is the impact of Ach on the heart?

A

PNS; slows rate and decrease contractility; PNS is stimulated when BP increase is detected

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44
Q

Where are the baroreceptors?

A

in the walls f the aortic arch and carotid sinuses

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45
Q

an elevation indicates myocardial damage and peaks at 18 hours following an acute ischemic attack.
Normal value is

A

CK-MB

normal value is 0-5% of total; total CK is 26-174 units/L

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46
Q

this cardiac enzyme rises within 3 hours or ischemic attack and persists for up to 7-10 days

A

Trop-1
0.6ng/mL
(Trop T: 0.1ng/mL)

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47
Q

this is an oxygen-binding protein found in cardiac and skeltal muscle that rises within 2 hours after cell death, with a rapid decline in the level after 7 hours

A

myoglobin

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48
Q

How is the RBC affected by the cardiovascular system?

A

RBC decreases in rheumatic heart disease and infective endocarditis and increases in conditions characterized by inadequate tissue oxygenation

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49
Q

How does the cardiovascular system affect WBC?

A

WBC increases in infectious and inflammatory diseases of the heart and after myocardial infarction bc large numbers of WBCs are needed to dispose of the necrotic tissue resulting from the infarction
WBC increase to 20,000 day after MI and remain elevated up to a week

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50
Q

What makes the Hct increase?

A

vascular volume depletion

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51
Q

What does a decreases H&H indicate?

A

anemia

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52
Q

What does a serum lipids test measure?

A 
serum cholesterol (<130, HDL=30-70) levels
**used to assess the risk of developing CAD
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53
Q

a small amount of protein in the urine (microalbuminuria)

A

has been a marker for endothelial dysfunction in cardiovascular disease

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54
Q

What increases risk for digoxin toxicity?

A

hypokalemia

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55
Q

flatten and inverted T wave, appearance of U ave, and St depression

A

hypokalemia

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56
Q

tall, peaked T waves, widened QRS complexes, prolonged PR intervals, or flat P waves

A

hyperkalemia

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57
Q

What happens to sodium during Heart Failure?

A

serum sodium will decrease to indicate water excess

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58
Q

tall T waves and depressed ST segments

A

hypomagnesemia

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59
Q

muscle weakness, hypotension, and bradycardia

A

hypermagnesemia

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60
Q

Which heart disorders increase BUN?

A

heart failure or cardiogenic shock

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61
Q

What is BNP a marker for?

A

BNP is released in response to atrial and ventricular stretch and serves as a marker for heart failure
levels should be lower than 100pg/mL-higher levels indicate more severe HF

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62
Q

Holter monitor

A

id’s dysrhythmias if they occur and evaluates the effectiveness of antidysrhythmics or pacemaker therapy.

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63
Q

What are some drug considerations to be aware of prior to a stress test?

A

theophylline is usually withheld 12 hours prior
CCBs and Beta Blockers are usually withheld on the day of the test to allow the HR to increase during the stress portion of the test

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64
Q

What special drug-related consideration must be made if a procedure uses iodine dye?

A

withhold metformin (Glucophage) for 24 hours prior due to risk of lactic acidosis

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65
Q

What are nursing responsibilities for cardiac catheterization?

A

check for iodine sensitivity
withhold food and fluids for 6-18 hours before procedure
inform pt of use of local anesethsia, insertion of catheter, feeling of warmth when dye injected and possible fluttering sensation in heart when catheter is passed. Pt may be directed to cough or deep breathe when dye is injected and pt is monitored by ECG throughout procedure.
After procedure, assess circulation to extremity-check peripheral pulses q15mins for first hour, and then with decreasing frequency. Observe puncture site for hematoma and bleeding. Do not elevate HOB >15 degrees

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66
Q

an invasive, nonsurgical technique in which one or more arteries is dialted with a balloon catheter to open the vessel lumen and improve arterial blood flow

A

PTCA percutaneous transluminal coronary angioplasty

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67
Q

What do we need from the patient prior to performing a PTCA?

A

a firm commitment to stop smoking, adhere to diet restrictions, lose weight, alter his or her exercise pattern, and stop any other behaviors that lead to progression of artery occlusion

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68
Q

Which two veins are commonly used for CABG?

A

saphenous vein or internal mammary vein

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69
Q

When do you Dc diuretics prior to CABG?

A

2-3 days before surgery

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70
Q

when do you DC digoxin prior to CABG?

A

12 hours before surgery

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71
Q

when do you DC ASA and other Anticoags prior to CABG?

A

1 week before surgery

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72
Q

How long is a patient mechanically ventilated following a CABG?

A

6-24 hours post op

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73
Q

What drainage amount from chest tubes is reported?

A

drainage exceeding 100-150mL/hour

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74
Q

pulsus paradoxus, JVD with clear lung sounds

A

signs of cardiac tamponade

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75
Q

Hone care instructions for patients who have had cardiac surgery

A

avoid push/pull for 6 weeks
avoid crossing legs, restrictive clothing
elevate limb used for graft
resume sex only when client can walk one block or climb two flights of stairs without symptoms

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76
Q

When med do you give if sinus bradycardia?

A

atropine sulfate to increase HR, oxygen via nasal cannulla
apply a transcutaneous pacemaker if pt is unresponsive to atropine sulfate
monitor for hypotension

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77
Q

atrial and ventricular rates are 100-180 beats/minute

A

sinus tachycardia

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78
Q

multiple rapid impulses from many foci depolarize in the atria in a totally disorganized manner at a rate of 350-600 times/minute

A

atrial fibrillation (atrial quiver)–>leads to thrombus formation–>anticoag therapy!!

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79
Q

bigeminy

A

PVC every other heartbeat

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80
Q

Trigeminy

A

PVC every third heartbeat

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81
Q

Quadrigeminy

A

PVC every fourth heartbeat

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82
Q

Couplet or pair

A

two sequential PVCs

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83
Q

Unifocal

A

uniform upward or downward deflection, arising from the same ectopic focus

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84
Q

multifocal

A

different shapes, with the impulse generation from different sites

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85
Q

R-onT phenomenon

A

PVC falls on the T wave of the preceding beat-may proceed vfib

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86
Q

What may be a cause of PVC?

A

hypoxemia-evaluate oxygen saturation

electrolytes-hypokalemia may cause PVCs

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87
Q

ventricular tachycardia

A

140-250 beats/minute or more

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88
Q

a chaotic rapid rhythm in which the ventricles quiver and there is no cardiac output

A

vfib-fatal if not terminated within 3-5 mins

client lacks pulse, BP, respirations, and heart sounds

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89
Q

Interventions for Vfib

A

CPR
defibrillate with 120-200 joules (biphasic defibrillator) or 360 joules (monophasic defibrillator)
CPr for two mins and then reassess cardiac rhythm for further defibrillation needs
administer oxygen and antidysrhythmic therapy

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90
Q

What are Vagal maneuvers for?

A

to terminate supraventricular tachydysrhythmias

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91
Q

What are some techniques besides meds to manage dysrhythmias?

A

vagal maneuvers
carotid massage
valsalva maneuver
cardioversion

92
Q

When do we used cardioversion?

A

for stable tachydysrhythmias resistant to medical therapies or an emergent procedure for hemodynamically unstable ventricular or supraventricular tacydysrhythmias
*defibrillator is synchronized to pt’s R wave to avoid discharging the shock during the vulnerable period (Twave)-if this precaution is not observed, a shock during T wave could incite vfib

93
Q

What are some considerations for elective cardioversion for atrial fibrillation?

A

pt on anticoag for 4-6 weeks preprocedure and a transesophageal echocardiogram should be performed to rule out clots in the atria prior to the procedure

94
Q

What about oxygen and cardioversion/defibrillation?

A

DC oxygen prior to shock to avoid fire!

95
Q

Implantable cardioverter defibrillator patient education

A

ICD senses VT or VF and delivers 25-30J up to four times

96
Q

what on an ECG indicates ischemia?

A

ST depression and T wave inversion

97
Q

what indicates infarction on an ECG?

A

ST elevation followed by T wave inversion and an abnormal Q wave

98
Q

occurs with activities that involve exertion or emotional stress, relieved with rest of nitroglycerin

A

stable angina (exertional angina)

99
Q

occurs with an unpredicatble degree of exertion or emotion and increases in occurrence, duration, and severity over time; lasts longer than 15 mins; characterized by chest pain that occurs days to weeks before MI; pain may not be relieved by nitroglycerin

A

unstable angina (preinfarction angina)

100
Q

angina resultant from coronary artery spasm and may occur at rest; ST segment elevation may be present of ECG

A

Variant angina (Prinzmetals or vasospastic angina)

101
Q

a chronic, incapacitation angina unresponsive to interventions

A

intractable angina

102
Q

occurs when myocardial tissue is abruptly and severely deprived of oxygen

A

myocardial infarction; obvious physical changes do not occur in the heart until 6 hours after the infarction, when the infarcted area appears blue and swollen

103
Q

What are signs of MI in a female?

A

atypical discomfort, SOB, fatigue, NSTEMI or T wave inversion

104
Q

What are signs of MI in elderly?

A

SOB, pulmonary edema, dizziness, altered mental status, or a dysrhythmia

105
Q

crushing substernal pain that may radiate to jaw. back, and left arm. Pain may occur without cause, primarily early in the morning and is unrelieved by rest or nitroglycerin but IS relieved by opioids. Pain lasts 30 mins +
n/v, diaphoresis, dyspnea, dysrhythmias, feelings of fear and anxiety, pallor, cyanosis, coolness of extremities

A

signs of MI

106
Q

dresslers syndrome

A

a combination of pericarditis, pericardial effusion and pleural effusion which can occur several weeks to month following a myocardial infarction

107
Q

signs of heart failure

A

presence of crackles or wheezes and dependent edema

108
Q

When do you lower the HOB and notify a HCP?

A

when systolic BP is <100mm Hg or 25 mm Hg lower than previous measurement

109
Q

the inability of the heart to maintain adequate cardica output to meet the metabolic needs of the body bc of impaired pumping ability

A

heart failure

110
Q

an inadequate output of the affected ventricle cuases decreased perfusion to vital organs

A

forward failure

111
Q

blood backs up behind the affected ventricle, causing increased pressure in the atrium behind the affected ventricle

A

backward failure

112
Q

leads to problems with contraction and ejection of blood

A

systolic failure

113
Q

leads to problems with the heart relaxing and filling with blood

A

diastolic failure

114
Q

dependent edema, JVD, abdominal discomfort, hepatomegaly, splenomegaly, anorexia and nausea, weight gain, nocturnal diuresis, swelling of fingers and hands

A

right-sided failure

115
Q

signs of pulmonary congestion, dyspnea, tachypnea, crackles, dry, hacking cough, paroxysmal nocturnal dyspnea

A

left sided heart failure

116
Q

severe dyspnea and orthopnea, pallor, tachycardia, expectoration of large amounts of blood tinged frothy sputum, wheezing and crackles, gurgling respirations, acute anxiety, apprehension, restlessness, profuse sweating, cold, clammy skin, cyanosis, nasal flaring, use of accessory breathing muscles, tachypnea, hypocapnia (evidenced by muscle cramps, weakness, dizziness, and paresthesias)

A

signs of acute pulmonary edema

117
Q

Nursing Actions for pulmonary edema

A 
high fowler's
oxygen
vitals, lung sounds
IV access
diuretic+morphine (morphine reduces preload, decreases anxiety, and reduces work of breathing)
foley
intubation or ventilator?
doc event, actions taken, and client response
118
Q

Which activities might a heart patient want to avoid as they increase pressure in the heart?

A

isometric activities

119
Q

hypotension

urine output

A

signs of cardiogenic shock

120
Q

What will a Swan-Ganz catheter record if pt has cardiogenic shock?

A

increased pulmonary capillary wedge pressure (PCWP) and a decreased CO

121
Q

what is central venous pressure?

A

pressure within the superior vena cava on its way to right atrium; normal is 3-8 mm Hg

122
Q

What may cause CVP to increase?

A

increased blood volume, sodium/water retention, excessive IV fluids, alterations in fluid balance, kidney failure

123
Q

What may cause a decrease in CVP?

A

decrease in circulating volume due to fluid imbalance, hemorrhage, severe vasodilation with pooling of blood in the extremities that limits venous return

124
Q

where is the right atrium?

A

midaxillary line at the fourth intercostal space

125
Q

what position must you place the client for hemodynamic monitoring?

A

HOB 45 degrees, transducer at level of right atrium; to maintain patency of the line, a small amount of fluid is delivered under pressure

126
Q

what is the pulmonary artery wedge pressure an indicator of?

A

left ventricular end diastolic pressure
normal is 4-12 mm Hg
elevations indicate LV failure, hypervolemia, mitral regurgitation, or intracardiac shunt
decreases may indicate hypovolemia or afterload reduction

127
Q

What is normal PAP (pulmonary artery pressure)?

A

15-26mmHg systolic/5-15mmHg diastolic

128
Q

What is the target MAP for optimal organ tissue perfusion?

A

60-70 mm Hg

129
Q

pain is grating and aggravated by breathing (particularly inspiration), coughing, and swallowing; pain is worse in supine position and may be relieved by leaning forward; pericardial friction rub is heard upon auscultation, fevers, chills, fatigue, malaise, elevated WBC, ST elevation, afib, signs of right HF

A

pericarditis-may lead to HF or cardiac tamponade

130
Q

acute or chronic inflammation of the myocardium as a result of pericarditis, systemic infection, or allergic resposne

A

myocarditis

131
Q

fever, pericardial friction rub, gallop rhythm, murmur, pulsus alternans, signs of HF, fatigue, dyspnea, tachycardia, chest pain

A

signs of myocarditis-assist client to high fowlers or leaning forward

132
Q

inflammation of inner lining of heart and valves and occurs primarily in pts who are IV drugs abusers, have had valve replacements or repair of valves with prosthetic materials, or other structural cardiac defects

A

endocarditis

133
Q

fever, anorexia, weight loss, fatigue, cardiac murmurs, HF, embolic complications from vegetation fragments travelling through the circulation, petechiae, splinter hemorrhages in nail beds, Osler’s nodes (reddish, tender lesions) on the pads of fingers, hands, toes, Janeway lesions (nontender hemorrhage lesions) on the fingers, toses, nose, or earlobes, splenomegaly, clubbing of the fingers

A

signs of endocarditis

134
Q

Client education r/t endocarditis

A

tell patient to inform all HCPs of hx of endocarditis and ask about the use of prophylactic antibiotics prior to invasive respiratory procedures and dentistry

135
Q

flank pain radiating to the groin, hemturia, and pyuria

A

renal emboli-potential complication r/t endocarditis

136
Q

sudden abdominal pain radiating to left shoulder and the presence of rebound abdominal tenderness on palpation

A

splenic embolic-potential complication of endocarditis

137
Q

confusion, aphasia, dysphasia

A

potential central nervous system emboli-potential complication of endocarditis

138
Q

pleuritic chest pain, dyspnea, cough

A

pulmonary emboli-potential complication of endocarditis

139
Q 
pulsus paradoxus
increased CVP
JVD with clear lungs
distant, muffled heart sounds
decreased CO
narrowing pulse pressure
A

cardiac tamponade

140
Q

cardiac tamponade interventions

A

place client in critical care for hemodynamic monitoring
admin fluids to manage decreased CO
prepare client for pericardiocentesis

141
Q

heart valves cannot fully open

A

stenosis (diastolic murmurs)

142
Q

heart valves cannot close completely

A

regurgitation or insufficiency (systolic murmurs)

143
Q

What is the window for tPA therapy with DVT?

A

within 5 days after onset of symptoms

144
Q

what do you monitor during Coumadin therapy?

A

PT/INR

145
Q

what do you monitor during heparin therapy?

A

aPTT

146
Q

stasis dermatitis or brown discoloration along the ankles extending up to the calf, edema, ulcer formation (edges uneven, ulcer bed is pink and granulation is present)

A

venous insufficiency

147
Q

sclerotherapy

A

a solution is injected into a varicose vein, followed by the application of a pressure dressing
incision and drainage of the trapped blood in the sclerosed vein is performed 14-21 days after the injection, followed by the application of a pressure dressing for 12-18 hours

148
Q

chronic disorder in which partial or total arterial occlusion deprives the lower extremities of oxygen and nutrients-most commonly caused by atherosclerosis

A

PAD

149
Q

intermittent claudication, REST PAIN relieved by placing extremity in dependent positon, lower back or buttock discomfort, loss or hair and dry scaly skin on the LE, thickened toenails, cold and gray-blue color of skin in LE, elevational pallor and dependent rubor in LE, decresased or absent peripheral pulses, signs of arterial ulcer formation occurring on or between toes or on the upper aspect of the foot that are painful

A

PAD signs

150
Q

what is rest pain?

A

associated with PAD; characterized by numbness, burning, or aching in the distal portion of the LE which awakens the client at night and is relieved by placing the extremity in depended position

151
Q

Do you advise a patient with PAD to elevate affected extremity?

A

bc swelling of the extremities prevents arterials blood flow, the client with PAD is instructed to elevate the feet at rest, but not above heart level bc extreme elevation slows blood flow to feet. In severe cases of PAD, clients with edema may sleep with the affected limb hanging from the bed or they may sit upright (without leg elvation) in a chair for comfort

152
Q

fusiform

A

type of aortic aneurysm with diffuse dilation that involves the entire circumference of the arterial segment

153
Q

saccular

A

type of aortic aneurysm with distinct localized outpouching of the artery wall

154
Q

dissecting

A

type of aortic aneurysm created when blood separates the layers of the artery wall, forming a cavity between them

155
Q

false or pseudoaneurysm

A

occurs when the clot and connective tissue are outside the arterial wall as a result of vessels injury or trauma to all three layers of the arterial wall

156
Q

pain extending to neck, shoulders, lower back, or abdomen, syncope, dyspnea, increased pulse, cyanosis, weakness, hoarseness, diff swallowing

A

thoracic aneurysm

157
Q

prominent, pulsating mass in abdomen at or above the umbilicus, systolic bruit over the aorta, tenderness on deep palpation, abdominal or lower back pain

A

abdominal aneurysm

158
Q

severe abdominal or back pain, lumbar pain radiating to the flank and groin, hypotension, increased pulse rate, signs of shock, hematoma at flank area

A

rupturing aneurysm

159
Q

insertion of an intracaval filter (umbrella) that partially occludes the inferior vena cava and traps emboli to prevent pulmonary emboli

A

vena caval filter

160
Q

suturing or placing clips on the inferior vena cava to prevent pulmonary embolic; done via abdominal laparotomy

A

ligation

161
Q

prehypertension

A

120-139/80-89

162
Q

Stage 1 hypertension

A

140-159/90-99

163
Q

Stage 2 hypertension

A

160/100 or higher

164
Q

HA, visual disturbances, dizziness, chest pain, tinnitus, flushed face, epistaxis

A

htn s/sx

165
Q

Whats the big deal about a hypertensive crisis?

A

can lead to death caused by stroke, kidney failure, or cardiac disease

166
Q

HIgh BP, HA, drowsiness and confusion, blurred vision, changes in neurological status, tachycardia and tachypnea, dyspnea, cyanosis, seizures

A

hypertensive crisis

167
Q

What do you do if your client develops hypotension during antihypertensive medication therapy?

A

put client in supine position

168
Q

digoxin toxicity

A

GI are eary symptoms, aong with confusioin and fatigue. additiona manifestations incude HA, hypotension, and cardiac dysrhythmias

169
Q

Ulcer is pale and deep and surrounding tissue is cool to touch. Skin is dry and there is often a loss of hair.

A

Arterial ulcer caused by tissue ischemia a from inadequate arterial blood supply of oxygen and nutrients.

170
Q

Ulcer with a dark red base and is surrounded by brown skin with local edema

A

Venous stasis ulcer is caused by the accumulation of waste products of metabolism that are not cleared as a result of venous congestion

171
Q

Treatment for DVD

A

Bed rest, limb elevation, relief of discomfort with warm, moist heat, and analgesics as needed. Ambulatory is contraindicated because such activity can cause the thrombus to dislodge and travel to the lungs

172
Q

First degree heart block

A

Prolonged pr interval

173
Q

What does the development of a waves signify?

A

Myocardial necrosis

174
Q

What finding on an EKG indicates a bbb?

A

A widened qrs complex

175
Q

Which cardiac med is best for variant angina?

A

CCBs

176
Q

What is an early indication of decreased blood volume?

A

Early decreases in fluid volume are compensated for by an increase in pulse rate

177
Q

What is the purpose of carotid massage?

A

To decrease heart rate and bp

178
Q

What is the physiological effect of stimulating alpha 1 receptors?

A

Found in peripheral arteries and veins, alpha 1 adrenergic receptors cause a powerful vasoconstriction when stimulated

179
Q

What is the physiological effect of stimulating beta 1 receptors?

A

Found In arterial and bronchial walls, beta 1s cause vasodilation and bronchodilator when stimulated

180
Q

What is the physiological effect of stimulating beta 2 receptors?

A

Found in the heart, the beta 2 receptors increase hr av node conduction, and contractility when stimulated (that’s why we use cardio-selective beta blockers for hf and mi pts)

181
Q

WhT is the physiological effect of stimulating alpha 2 adrenergic receptors?

A

Found in several tissues, alpha 2 receptors cause smooth muscle contraction, inhibition of lipolysis, and promotion of platelet aggregation

182
Q

What is the therapeutic effect of digoxin?

A

Increases strength and contraction of the heart-hold if apical rate is less than 60

183
Q

what does the pr interval represent?

A

Travel time for impulse for. as node to purkinje fibers

184
Q

A loss of communication between the atrium and ventricles from av node dissociation

A

Third degree heart block

185
Q

Slower heart rate with exhalation and increased heart rate with inhalation

A

Sinus dysrhythmias

186
Q

A gradual lengthening of pr interval until a qrs is dropped.

A

Wenckebach heart block

187
Q

Early occurrence of a wide, distorted qrs complex

A

PVC s

188
Q

A sinus rate above 100 beats/min with normal p waves

A

Sinus tachycardia

189
Q

What is a common diagnostic test following episodes of syncope?

A

Head up tilt test

190
Q

A patient in a systole is likely to receive which drug treatment?

A

Epi or atropine

191
Q

What drugs are given for PVC ?

A

Lidocaine and amiodorone

192
Q

What drugs are given to control ventricular rate?

A

Digoxin and procainamide

193
Q

What drug is given to slow heart rate?

A

Beta blockers

194
Q

What drug is given to increase heart rate?

A

Dopamine

195
Q

Atrial fibrillation with a rapid ventricular response

A

Supra ventricular tachydysrhythmias; perform synchronized cardio version

196
Q

St depression and t wave inversion

A

Myocardial ischemia

197
Q

St elevation

A

Myocardial injury

198
Q

St elevation with a widened and deep q wave

A

Previous mi

199
Q

torsade de pointes

A

twisty rhythm; give magnesium!! looks like a double helix; -shock after giving mag

200
Q

asystole

A

CPR, give EPI (1mg q3-5 mins) look for the cause of asystole

201
Q

Pulseless electrical activity

A

EPI, CPR, look for cause

202
Q

o2, IV, monitor

A

priorities when an arrhythmia is present

203
Q

sinus bradycardia

A

atropine

less than 60 bpm

204
Q

sinus tachycardia

A

give beta blocker

greater than 100 bpm

205
Q

PACs

A

give beta blockers

206
Q

PSVT

A

150-222bpm

vagal stimulation and adenosine!!

207
Q

Atrial flutter

A

200-350
ccb, beta blcokers
cardioversion or radiofrequency catheter ablation
COUMADIN to decrease stroke risk

208
Q

Atrial fibrillation

A

350-600
CCBs, Beta Blockers, Digoxin, Dronedarone, Amiodarone
Coumadin 3 weeks before elective cardioversion and for 2 weeks after
radiofrequency catheter ablation
Maze procedure (cryoablation)

209
Q

Second Degree Heart Block Type 1

A

give atropine and/or temp pacemaker

210
Q

Second Degree Type II and Third Degree Heart Block

A

pacemaker

211
Q

PVC

A

lidocaine or amiodarone

212
Q

Vtach

A

digoxin or procainamide

cardioversion of defirillation (defib if no pulse)

213
Q

torsades de pointe

A

give magnesium and shock

twisty vfib

214
Q

roths spots, splinter hemorrhages, oslers nodes, janeways lesions

A

Infective Endocarditis

215
Q

complications of Infective endocarditis

A

stroke, pulmonary edema, and HF

216
Q

pericardial friction rub

complications include pericardial effusion and cardiac tamponade

A

pericarditis

217
Q

compression of heart due to fluid in pericardial sac. hallmark sign is pulsus paradoxus

A

cardiac tamponade, a common complication of pericarditis. assess for pulsus paradoxus q4h if pericarditis

218
Q

colchicine

A

antiinflammatory for gout, is sometimes given to pts with pericarditis

219
Q

clinical manifestations mimic HF and cor pulmonale (hypertrophy of right heart with or without HF due to pulmonary HTN)

A

Chronic constrictive pericarditis-treat with pericardectomy

220
Q

ACEI, beta blockers, digoxin, and diuretics
vasodilators if no hypotension
anticoags
immunosuppressive therapy to redcue myocardial inflammation and to prevent myocardial damage
oxygen, bed rest, restricted activity
intraaortic balloon pump therapy or ventricular assist devices to reduce workload of heart

A

treatment for myocarditis

221
Q

Aschoff’s bodies

A

nodes present in rheumatic heart disease and that turn to fibrous scar tissue with age

222
Q

carditis (murmurs, cardiac enlargement, pericarditis)
monoarthritis or polyarthritis
sydenham’s chorea (Major CNS involvement)
Erythema marginatum lesions (worse in warm water, maplike macular lesions)
elevated ESR, WBC, CRP

A

Rheumatic heart disease

223
Q

enhance cardiac contractility and decrease preload and afterload
cardioversion, ICDs, and ventricular assist devices

A

dilated cardiomyopathy

224
Q

impaired ventricular filling as the ventricle becomes noncompliant and unable to relax

A

hypertrophic cardiomyopathy-reduce ventricular contractility and relieve ventricular outflow obstruciton with beta blockers or CCBs
ICD is option if risk for SCD

225
Q

impaired diastolic filling and stretch with unaffected systolic function.
fatigue, exercise intolerance, dyspnea
heart transplant is considered

A

restrictive cardiomyopathy

226
Q

Ventricular gallop

A

S3 I. Occurs with decreased compliance of either ventricle

227
Q

Atrial gallop

A

S4. Occurs later is diastole during atrial contraction and active filling of the ventricles. Stiff ventricles, mi, hypertension, hyper trophy, fibrosis, cardiomyopathy, Cor pulmonale, aortic stenosis, pulmonic stenosis

Adult Health (18 decks)

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