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Kol- 410 Med Surg II > Exam 1 Review- CV part > Flashcards

Exam 1 Review- CV part Flashcards

1
Q

this is an early rhythm complex that occurs for the next SA impulse

A

premature complexes

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2
Q

PVC/PAC that occurs every other beat / every 2 beats / every 3 beats?

A

bigeminy , trigeminy, quadrigeminy

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3
Q

sxs of prematures complexes

A

Palpitations or symptoms of low cardiac output –> check BP

*note: may be asxs as well

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4
Q

premature complexes can be generated by other parts of the heart, what do we see when the PAC starts in the atrium?

A

see P wave that is abnormal, narrow QRS complex

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5
Q

premature complexes can be generated by other parts of the heart, what do we see when the PAC starts in the ventricles?

A

no P wave, wider QRS complex

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6
Q

brady dysrthymia = HR < ____

A

60!

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7
Q

concerns with brady-dysrhythmia - what does it to diastole? what are 3 things we are checking in patient to assess their perfusion?

A

• Prolonged diastole → improved perfusion to heart

OR

• Decreased perfusion to heart if Cardiac Output decreases (low BP)
◦ check BP! to determine if CO is poor perfusion
◦ check LOC
◦ check urine output

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8
Q

tachy dysrhythmia = HR >_____

A

100!

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9
Q

what does tachy-dysthymia do to diastole? what do we need to assess?

A

• Shortens diastole –> heart itself doesn’t get as much O2
• Increased work of heart (heart needs more O2)
◦ uses too much energy
• get BP - low from decrease stroke volume

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10
Q

sinus brady s/s

A

• Low BP, Confusion, SHOB, chest pain, dizzy, syncope

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11
Q

who might naturally have a low HR?

A

arthletes

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12
Q

is sinus brady always bad?

A

has therapeutic benefit of reducing myocardial O2 demand and allws for increased perfusion time

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13
Q

when do we use pacing- HR too slow or HR too fast?

A

hr too slow! –> patient not perfusing

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14
Q

pacemakers can pace different parts of the heart -

◦ Atrial (Sick Sinus) - initiates p wave
◦ Ventricular
◦ Biventricular (Heart failure)

the take home from this is you need to know….

A

what your patient is pacing

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15
Q

wtf are pacer spikes?

A

= initiates something to happen in the heart

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16
Q

3 types of atrial dysrthymias

A

• Premature Atrial Complexes (see above)
• Supraventricular Tachycardia
• Atrial Fibrillation

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17
Q

this type of dysrhythmia =
• Rapid stimulation of atrial tissue
• 100 bpm to 280 bpm
- No visible P wave

A

Supraventricular Tachycardia (SVT)

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18
Q

what is • Paroxysmal Supraventricular Tachycardia

A

short run of SVT and got back to normal

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19
Q

interventions for SVT

A
  • take BP
    -identify cause
    -Vagal maneuver
    -Adenosine (6mg, 12mg, 12mg)
    -Fluids
  • BB, CCB
    -Cardioversion (= synchronous shock)
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20
Q

adenosine protocol for SVT?

A

◦ causes period of asystole.
◦ feels like you are getting kicked in the chest
◦ Give 6 then 20 cc fluid, 12 then 12 if needed

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21
Q

Atrial fibrilation- what are the main causes?

A

Related to atrial fibrosis and muscle mass
◦ Hypertension
◦ Heart Failure
◦ CAD
-mitralregurgitation

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22
Q

this dysrhythmia = irritable atria, multiple rapid impulses depolarizing the atria causing decreased cardiacoutput and NO P WAVE

A

atrial fibrillation

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23
Q

do you see a P wave with A fib?

A

no P wave on afib

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24
Q

A Fib interventions

A
  • O2
    -decrease anxiety
    -Meds (dilt (drip) + amiodoarone (drip) + anticoag)
    -Cardioversion (synchronized)
    -Ablation
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25
Q

type of dysrhytmia with HR of 140-180 fired from ventricles

A

V tach

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26
Q

risk factors for V tach

A

◦ Myocardial Ischemia
◦ Cardiomyopathy
◦ Low K+
◦ Drugs
◦ Shock

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27
Q

type of dysrhythmia with electrical chaos is ventricles meaning the ventricles can’t contract =

A

v fib

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28
Q

V fib risk factors

A

• CAD
• MI
• Low K+
• Low Mg
• Surgery, Procedure
• Trauma

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29
Q

interventions fr V fib =

A

defibrilate
CPR
• Antidysrhythmic

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30
Q

you have a person in V fib and you shock their ass. Are they gonna be cool now?

A

must fix underlying cause— can go back into v fib after you defibrillate

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31
Q

type of dysrthymia with no impulses being conducted in the ventricle leading to no cardiac output =

A

ventricular asystole

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32
Q

interventions for ventricular asystole

A

CPR, ventilate, epinephrine

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33
Q

3 types of defibrillators

A

-AED
-Implantable
-Wearable

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34
Q

dysrhythmias are typically the result of another…..

A

pathology or disease state so we have to treat that!

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35
Q

list the mumur for each valve thing

mitral valve stenosis
Mitral Regurgitation
Mitral Valve Prolapse
Aortic Stenosis
Aortic regurgitation

A

mitral valve stenosis = diastolic murmur
Mitral Regurgitation = High pitched systolic murmur, S3
Mitral Valve Prolapse= late systolic murmur
Aortic Stenosis = systolic murumur
Aortic regurgitation = Diastolic murmur

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36
Q

stenosis vs regurgitation

A

stenosis = stiffening, narrowing, smaller
regurgitation = back flow

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37
Q

stenosis effects the heart velve when it is open or closed?

A

OPEN –>can’t open enough and blood is having a hard time getting through the valve

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38
Q

regurgitation effects the heart valve when it open or closed?

A

CLOSED –> valve is not closed well enough and blood flows backwards

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39
Q

how is mitral valve stenosis different then mitral valve prolapse?

A

stenosis = • Valve leaflets fuse, become stiff and chordae tendineae shorten • Narrow valve opening

prolapse = • Enlarged valvular leaflets that prolapse into left atrium during systole (should turn in towards the ventricle but don’t!)

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40
Q

what will mitral valve stenosis lead to?

A

• Prevents normal blood flow from left atrium to left ventricle
◦ Increased atrial pressure
◦ Dilated left atrium
◦ Increased pulmonary pressure
◦ Right ventricle hypertrophy
◦ Pulmonary congestion
◦ Right sided HF –>Left sided HF (Reduced Preload)

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41
Q

assessment findings for mitral valve stenosis?

A

• May be asymptomatic
• Difficulty breathingPulmonary edema
• Coughing
• JVD
• Edema in extremities
• Development of A-fib?
• Diastolic murmur

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42
Q

what does mitral valve regurgitation lead to ?

A

• Backflow of blood into left atrium during left ventricle contraction
◦ Hypertrophy of left ventricle and atrium

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43
Q

causes of mitral valve regurgitation?

A

• Fibrotic and calcific changes that prevent the mitral valve from closing during systole
• Caused by aging process, endocarditis, congenital abnormalities, RHD

44
Q

assessment findings for mitral valve regurgitation

A

• Asymptomatic for many years
• Symptoms occur when the left ventricle can no longer overcome the blood volume
• Decreased Cardiac output
• Fatigue
• Weakness
• Anxiety
• Difficulty breathing
• Palpitations
• Chest pain
• **Afib – highest risk of all the valvular disorders
• Right sided failure…
• **High pitched systolic murmur, S3

45
Q

mitral valve prolapse causes?

A

• Often congenital (downs syndrome, marfans syndrome)

46
Q

mitral valve prolapse assessment findings

A

• Asymptomatic or Symptomatic
◦ Chest pain
◦ Dizziness
◦ Palpitations
◦ Midsystolic click, late systolic murmur

47
Q

what will aortic stenosis lead to?

A

• Ventricular hypertrophy
◦ Over time, left ventricle cannot meet the needs of body on exertion
**Left sided HF –> Right sided failure

–> may need surgery

48
Q

assessment findings for aortic stenosis

A

• Fixed cardiac output (can’t accommodate increased demand)
◦ poor perfusion abilities (decreased pulses, kidney function)
• Angina
• Difficulty breathing
• Syncope
• Fatigue
• Debilitation
• Peripheral cyanosis
• Systolic murmur –> aortic valve is open during systole

49
Q

what happens in aortic regurgitation?

A

• Aortic valve leaflets don’t close well during diastole
• Blood flows back from aorta to left ventricle
◦ Dilated ventricle/ Hypertrophy

50
Q

causes of aortic regurgiation?

A

• Infective Carditis
• Congenital anatomic abnormalities

51
Q

what will aortic stenosis lead to?

A

left sided heart failure

52
Q

assessment finding for aortic stenosis

A

• Left failure symptoms
• Difficulty breathing
• Nocturnal dyspnea/ angina
• Diaphoresis
• Bounding pulse –> development of R side HF –> later finding
• Widened pulse pressure
• Diastolic murmur

53
Q

drugs we give to help with heart valve stuff?

A

◦ Diuretics- preload
◦ Beta Blockers - slow heart rate to reduce heart demand
◦ Digoxin- contractility
◦ Oxygen
◦ CCB’s - afterload
◦ Anticoagulants -afib and risk for clot

54
Q

prosthetic vs biologic valves- duration? anticoags?

A

‣ prosthetic valve lasts longer –> increased risk of clotting –> anticoagulation for life

‣ biologic –> don’t last as long –> don’t require anticoagulation (old person)

55
Q

after surgery for valve stuff patient is at great risk for

A

ENDOCARDITIS! ABX is have dental procedure
Clots –> anticoags

56
Q

most common culprits of infective endocarditis?

A

◦ Streptococcus viridans
◦ Staphylococcus aureus

57
Q

risk factors for infective endocardiits?

A

• IV Drug Use
• History of valve replacement
• Systemic Infection
• Structural cardiac defect

58
Q

infective endocarditis populations are risk examples

A

• Post operative patient with insufficient venous access (and subsequent PICC line insertion)
• A mother of four with strep throat
• A patient with sepsis related to a UTI
• A patient who had his molars removed

59
Q

when does sxs onset of infective endocarditis occur?

A

2 weeks after exposure

60
Q

sxs of infective endocarditis

A

◦ Fever (might not show up in elderly)
◦ Murmurs
◦ S3 and S4
◦ Heart failure
• Organ dysfunction
• PE/ Pulmonary infarct
• Stroke
• Petechiae
• Splinter hemorrhages

61
Q

_____ occurs in about 50% of infective endocaridits cases

A

emoblization

62
Q

right vs left endocarditis- what is it associated with?

A

◦ right side with IV drug –> first place it hits when introduced to body
◦ left side used to be more common

63
Q

1 diagnostic for infective endocarditis?

A

blood cultures

64
Q

interventions for infective endocardiits?

A

• Antibiotics–>administered IV/ 4-6 weeks
• Rest/ Activity
• Support Heart Failure
• Surgery (if neccessary)
◦ Remove infected valve
◦ Repair injured valve
◦ Drain abscesses

65
Q

most common type of cardiomyopathy that involves both ventricles being dilated

A

dilated cardiomyopthy

66
Q

dilated cardiomyopthhy results in impaired ______ function

A

systolic

67
Q

causes of dilated cardiomyopthy

A

Alcohol, Chemotherapy, Infection, Inflammation, Poor Nutrition

68
Q

type of cardiomyopathy common in athletes?

A

Hypertrophic Cardiomyopathy

69
Q

type of cardiomyopathy with asymmetric ventricular hypertrophy –>Stiff Left Ventricle causes Obstruction in left ventricular outflow?

A

Hypertrophic Cardiomyopathy

70
Q

sxs of Hypertrophic Cardiomyopathy

A

-Asymptomatic until death (Athletes)
• DOE
• Palpitations
• Dizziness

71
Q

-Rarest Cardiomyopathy, poorest prognosis of the cardiomyopathy
-Stiff ventricles that restrict filling =

A

Restrictive Cardiomyopathy

72
Q

s/s of Restrictive Cardiomyopathy

A

• Symptoms of R/L HF

73
Q

causes of Restrictive Cardiomyopathy

A

Sometimes related to Sarcoidosis or Amyloidosis

74
Q

type of cardiomyopthy where Myocardial tissue replaced with fibrous and fatty tissue

A

Arrhythmogenic Right Ventricular Cardiomyopathy

(family association)
(usually R ventricle)

75
Q

HCM has a high rate of….

A

ventricular dysrhythmias

76
Q

interventions for dilated and restrictive cardiomyopthy

A

Treat for Heart Failure
• Diuretics
• Vasodilators
• Digoxin

77
Q

HCM intervetnions

A

• ICD (implanted cardiac defib)

• Beta Adrenergic Blockers
• Calcium Channel Blockers
–>Reduce outflow obstruction
–>Decrease HR/ Symptom relief

78
Q

HCM interventions- what cant we give them? what can’t they do?

A

No vasodilators, diuretics or digoxin
No Extreme Exercise

79
Q

type of cardiomyopthy that usually ends with heart transplant?

A

DCM/ Restrictive

80
Q

shock is our bodies response to a lack of ______ in the tissue

A

oxygen

81
Q

shock is classified by what the cause is- what are the types of shock?

A

-hypovolemic
-cardiogenic
-distributive (sepsis, neurogenic, anaphylactic)
-obstructive

82
Q

what is mean arterial pressure? how do we calculate the mean arterial pressure?

we want the map to be > _____

what is the MAP for 120/80 and 90/50?

A

Average arterial pressure in one cardiac cycle
◦ (Systolic Pressure + Diastolic + Diastolic) / 3

◦ want it >65 (means organs are being perfused)

• 120/80 (MAP = 93)
• 90/50 = (MAP = 63)

83
Q

causes of hypovolemic shock

A

• Blunt trauma
• GI bleeds/ ulcers
• Post surgery bleeding
• Dehydration
• Bleeding

84
Q

assessment findings for hypovolemic shock

A

•History
•Tachycardia
•Tachypnea –> trying to blow off CO2
•Restlessness, anxiety
•Low Urinary output
•Decreased MAP
•Weak pulses
•Cool, moist skin
•Mottling
•Increased Capillary refill time
•Thirst
•Confusion/ unconscious

85
Q

re hypovolemic shock - what ABG do we expect ? what will H&H be?

A

ABG –> lactic acid causes metabolic acidosis

H &H –> depends on if they are bleeding (low) or dehydrated (high)

86
Q

interventions for hypovolemic shock:

A

•Identify and manage the cause
•Restore blood volume
•Prevent complications
•Oxygen
•IV fluids
•Blood products

87
Q

2 drug classes in particular we give for hypovolemic shock - give examples of each

A

Inotropes and Vasopressors

vasopressors:
•Dopamine
•Norepinephrine (Levophed)
◦ use in sepsis -first line
•Phenlephrine (Neosynephrine)
•Epinephrine
Induce vasoconstriction → Raise MAP

inotropes:
•Dobutamine
•Milrinone
•Activate Beta Adrenergic receptors → Improve Contractility

88
Q

what kind of line do we give vasopressors through?

A

central line

> > risk of necrosis and limb loss in peripheral line

89
Q

cardiogenic shock is most commonly cause by what? What happens?

A

= Heart muscle can’t pump blood adequately
•Decreased Cardiac Output that leads to —>Decreased MAP (Blood pressure)
•Most commonly caused by myocardial Infarctions

90
Q

what happens in distributive shock? where is the blood/fluid?

A

=There is enough blood, it just isn’t where it is supposed to be
• Blood vessel dilation (no afterload)
• Capillary leakage (less blood going back to heart)
• Blood leaks into interstitial tissue
• Pooling of blood in capillary beds

91
Q

what happens in obstructive shock? where is the blood? main cause(s)?

A

• Heart is normal, but blood cannot get to heart or get out of heart for another reason
• Most commonly caused by Cardiac Tamponade –> fluid building up and pressing on heart
◦ can also be caused by tension pneumothorax

92
Q

cardiac tamponade is associated with which type of shock?

A

obstructive shock

93
Q

type of shock:

• MAP is lost because of loss/ reduction in Sympathetic Nerve impulse
• Smooth muscles relax → vasodilation

A

neural induces distributive shock

94
Q

what happens to HR and BP in neurogenic shock

A

bradycardia and hypotension

95
Q

chemical induced shock is caused by what?

A

• Chemicals cause the blood vessel wall to change
• Chemicals may be endogenous or exogenous
• Most commonly caused by Anaphylaxis or Sepsis

96
Q

Why do you get acidosis in shock? what is a normal lactic acid?

A

• build up of lactic acid
• kidneys are not being perfused to make bicarbonate
• normal lactic acid = <2

97
Q

how does SIRS relate to sepsis

A

SIRS leads to sepsis

sirs = Widespread Inflammation: WBC’s, cytokines, vasodilation, capillary leakage
◦ Microthrombi form in organ capillaries –> hypoxia

98
Q

code sepsis criteria =

A

• 2 or more signs of SIR + suspected infection

99
Q

SIRS criteria (not sure if we need to know this?)

A

temp > 38 or <36
HR > 90
RR >20
WBC >12,000 or <4,000

need 2 o these 2 have sirs

100
Q

s/s of septic shock

A

•In the setting of infection or suspected infection
•Tachypnea
•Altered mental status
•Reduced blood pressure
•Other Signs of organ dysfunction
•Infection
◦ Fever
◦ Tachycardia
◦ Rigors
•Poor Perfusion
◦ Cool extremities
◦ Mottling
• cool vs warm sepsis
◦ warm (compensating) comes before cool

101
Q

interventionsfor septic shock (3)

A

•Pan Cultures (sputum, urine, blood)
•Antibiotics within one hour (after cultures)
•ABG with lactate and/or lactic acid

102
Q

interventions for shock - what do we need to do w/in 1 hour

A

◦ Measure lactate
◦ Obtain cultures and administer antibiotics
◦ Administer crystalloid fluids for hypotension or lactate > 4

103
Q

interventions for septic shock

A

•Treat underlying cause
•Support
◦ Oxygen
◦ fluid
◦ glucose management
•Within 1 hour
◦ Measure lactate
◦ Obtain cultures and administer antibiotics
◦ Administer crystalloid fluids for hypotension or lactate
>4
•Use vasopressors to maintain MAP > 65 During or after fluid administration

104
Q

what are the 3 stages of sepsis

A

sepsis = sirs + infection
severe sepsis = sepsis + organ failure
septic shock = severe sepsis + refractory hypotension

105
Q

go to page 767 of the 7ed Saunders and look at the EKG strips for Vfib (lil irregular squiggles) and V tach (big rapid regular spikes)

A

yay….

106
Q

when are valves open and closed?

mitral valve: diastole/systole
aortic valve: diastole/ systole

A

mitral valve: diastole OPEN /systole CLOSED

aortic valve: diastole CLOSED/ systole OPEN

it helps if you draw a picture of the heart with the valves
SSystolic / SSqueeze –> big # on top = big energy to SSSSqueeze it out of the heart
dIastolic / fILL

Kol- 410 Med Surg II (27 decks)

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