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NP > ACUTE EXAM 2 > Flashcards

ACUTE EXAM 2 Flashcards

1
Q

normal limits of svr

A

800-1200 dynes

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2
Q

calculation of svr

A

map-cvp/co x 80

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3
Q

cardiac index

A

measure of co adjusted to BSA; body habitus and size is individual

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4
Q

pvr is active or passive

A

passive, low normal <250 dynes

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5
Q

intrapleural pressure **

A

intrathoracic pressure

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6
Q

increased svr, cardiac output? high or low

A

low

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7
Q

high cardiac out doesn’t always mean…

A

perfusion

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8
Q

negative inotropes

A

decrease contracility

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8
Q

positive inotropes should

A

increase stroke volume and cardiac output ; start low and then go up, you can make the patient tachy and pro arrhythmic and use more myocardial oxygen

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9
Q

how does increasing contractility affect SV

A
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10
Q

inc 2g3pg

A

shift to the right

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11
Q

decrease hgb

A

shift to the right

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12
Q

shift to the left

A

alkalotic, low temo, low 23gpd; this is worse; fingers fall off and end organs fail we arent feeding the tissues; the hemoglobin and holding on tight

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13
Q

determinants of d02

A

pao2, hgb, sao2;co/ci

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14
Q

> 80 % svo2 means

A

may represent a threat to tissue oxygenation

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15
Q

<60 svo2 means

A

shift to the right a value decreases the threat to tissue oxygenation increases

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16
Q

know the components of svo2

A

hbg
vo2
co
sao2

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17
Q

if you didnt have a swan

A

coox

if you have a central line you could use it to identify changes in the patients tissue oxygen extraction

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18
Q

anaerobic metabolism what gets produced

A

lactate acid gets built up a marker of anaerobi cmetabolism; a rise is detectingin global tissue oxygenation disturbance

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19
Q

procalcitonin

A

proetin releases as an acute phase reactant in response to inflammatory stimulti, especiallybacterial********, could track and trend the course of antibitoics

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20
Q

DIACROTIC NOTCH

A

aortic valve closed

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21
Q

prefusion pressure

A

mean arterial pressure

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22
Q

mean arterial pressure

A

1/3 systolic, 2/3 diastolic

s+ (dx2)/3

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23
Q

> 13 %

A

HIGH IS DRY

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24
Q

no pa cathter for

A

right sided; you want right sided just put a cvp

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25
Q

advantages of the PAC

A

Measurement of left ventricular filling pressures (estimate)
Sampling of mixed venous blood.
Measurement of cardiac output.

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26
Q

Three factors contribute to the regulation of CVP:

A

Capacitance of the venous system
Total blood volume
Pumping ability of right side of the heart

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27
Q

right sided heart failure cvp is

A

high

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28
Q

debakey 1 &2

A

stanford a

Ascending and descending

Ascending open approach involving the aortic arch cannot do in any other fashion

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29
Q

symptoms of AA

A

chets pain pressure radiating to the back ripping tearing back pain dull ache with either rupture or dissection

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30
Q

patient has hoarseness

A

ascending or at the arch, compression on largeneal nerve;

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31
Q

abdminal and pulstile mass

A

abdmonial aneurysm

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32
Q

triple a things we find on assessment

A

Pulsitile mass. Bruit. Abdominal pain.

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33
Q

ruputred aneursym

A

hemdyabmically unstable 40 % die before treatment

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34
Q

diagnostics for aoritc aneursym

A

chests ct- gold tsandrad and doesnt even need to be with contrast now, x-ray you will see wided mediastinum, ultrasound-abdominal**, ACC, coags and cmp

Abdominal aneurysms can be seen with an ultrasound

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35
Q

differentials with an aortic aneurysm

A

renal obstruction, uti, pepic ulcer disease like a peptic ulcer perforation/gerd, or ruptured disc wit the pain in the back

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36
Q

treatmnent of AA

A

contact ct surgery or vascular; graft for a suspected rutpure or dissection

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37
Q

> 5.5cm or symptomatic

A

treat**** >6cm for open repair; 5.5> endovascular repair

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37
Q

<5cm in low risk patients

A

follow every 6-12 months; ultrasound and MRI

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37
Q

once a patient dissects

A

surgery immediate repair even if it is not that big

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38
Q

many aortic dissections are associated with

A

connective tissue disorder like marfans and HTN

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39
Q

tee or TTecho

A

sometimes you can see it the aortic

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40
Q

To assess the different levels of the vessel what test would you use

A

Aortic angiography to get more information

used to be the standard and no more

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41
Q

With aortic aneurysms our vital signmanagement with medications ranges we want what?

A

100-120 sip

heart rate at 60

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42
Q

aortic rupture can be caused by

A

trauma and or aortic aneurysm;

ruputrue severe s0b, chest pain, difficulty swallow, shck like state, bleeding into the chest, deviation, wided mediastiunum, what would you do? 50% mortality triple a rupture

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43
Q

pulmonary htn normal

A

> 20/25, 25 is the old classification on right heart cathetrization

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44
Q

what leads you to doing a cardiac cath to diagnosis PHtn

A

an echo

estimates the pressures in the heart and quantifies right-sided pressures, thus leading to a right heart cath

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45
Q

confirm diagnosis of PHth

A

right heart cath

45
Q

prostacyclin agonist

A

augment the pathways for more camp, more vasodilation, open the blood flow to the pulmonary vessels

flown, iv infusion- veltri continuous or inhaled
epoprostenol

at all timessss half life very short, need to change the bag right away

46
Q

PH on an ECG

A

right axis deviation but that can also be heart failure

47
Q

endothelia receptor antagonist bostentan

A

first oral specific for PH

block receptor on vascular smooth muscle that cause constriction

48
Q

pde5 inhibitors

A

sildenafil and tadalafil, viagra

higher doses erectile dysfunction

49
Q

1st we need to rule out right sided heart failure with what diagnostics

A

chest xray ekg and echo 1st

50
Q

what are symptoms & signs of right sided heart failure

A

jvd edema stop eating feeling full; tricupsid murmur, enlarged liver

51
Q

2nd we need to rule out lung disease what diagnostics?

A

pft,ct and osa

52
Q

3rd if we what to rule out a pe what diagnostics?

A

ct angio

53
Q

A hole in the septum that divides the atria
Left to right shunt

A

atrial septal defect

25 % of children, its a tissue defect***

54
Q

atrial septal defect present like?

A

right sided heart failure, pulmonary htn, afib and tricuspid regurg

55
Q

signs of ASD

A

Dyspnea
Fatigue
Exercise intolerance
PNA
Palpitations

sob on exertion exercise intolerant, palpitation, less common pulmonary infections **

56
Q

how do we determine ASD #1 choice

A

echo

echo with doppler, visulaize the flow acorss the heart

To determine if closure is feasible
Quantify the degree of left to right shunting
Assess RA and RV dilation
Assess RV dysfunction
Assess degree of pulmonary hypertension

57
Q

using contrast to determine ASD versus PFO

A

Syringe of saline, agitated to get bubbles to infuse air into the syringe, shoot into the central line, trace the bubbles

Will see the shunting left to right.

to diagnosis, bubble/contrast to visualize the shunt

58
Q

symptomatic ASD management?

A

surgical closure, usually with a patch, mini-thoracotomy and could also use a transcatheter versus open

59
Q

what is a PFO

A

In utero the atrial septa are separate allowing right to left blood flow as part of the fetal circulation.

After birth, the septum seals, producing an intact atrial septum. 25% of the time it remains patent is a PFO.

venous blood going into the left atrium

60
Q

Risks of a PFO

A

paradoxical embolism associated with right to left shunting when the RA pressure exceeds the LA pressure.

61
Q

clinical manifestation of PFO

A

Venous clots can go into the systemic circulation

Most patients are asymptomatic.
The usual presentation is a TIA or stroke or migraine-like headache

Only a 2mm thrombus can cause a stroke

62
Q

how do you diagnosis a PFO

A

echo with contrast

transcranial doppler

63
Q

management of PFO

A

No indication for prophylactic management

TIA or stroke
Medical therapy with ASA or warfarin
Percutaneous closure

64
Q

VSD is what?

A

Hole in the wall that separates the right and left ventricles of the heart.

could happen:
Post infarction & Congenital

65
Q

clinical manifestation of VSD

A

cardiogenic shock, acute pulmonary edema and loud holosystolic murmur

66
Q

how do you diagnosis a VSD

A

cath and 2d echo

higher oxygenation levels in the right side and we dont have that since the right side hold deoxygenated blood

67
Q

acute management of a VSD

A

Inotropes to increase cardiac output
IABP
Cardiac Cath
Coronary angiogaphy

**When acute, need to wait for pt to scar down before can do surgery

68
Q

Abnormal dilation of the arterial wall, resulting in bulging of the intima

A

aortic aneurysm

69
Q

types of AA

A

Thoracic
Abdominal
Thoracoabdominal

70
Q

aortic dissection clinical manifestations

A

Severe chest pain
Sharp, stabbing, tearing, or ripping
Felt below the chest bone, then move under the shoulder blades or to the back
Radiates to arms and legs as aortic dissection worsens

71
Q

AA causes

A

Hypertension
Athero-sclerosis
Infections
Genetic congenital

72
Q

aortic rupture clinical manifestations

A

Dyspnea
Chest
pain
Abdominal pain
Difficulty swallowing
Shock

73
Q

Beurgers disease

A

Smoking men greater than women and ages 20-40. Smoking triggers an immune inflammatory response. 50% of men end up with amputations

74
Q

Smoking and diabetes puts you at a greater rest for what disease

A

Peripheral vascular disease

75
Q

The “p’s” of peripheral artery disease

A

Pain pallor poliko paralysis loss of pulse less

76
Q

Time constrain for a patient with critical limb ischemia

A

4-6 hours considered a medical emergency

77
Q

Definition of critical limb ischemia

A

Symptoms have been significant for less than 2 weeks by vascular definition

The ischemia has happened in less than two weeks in duration

Category 1-3. Two b more loss. By cat 3 loss of motor function and the damage is done.

Cat one is viable limb cold painful leg. At cat one we are revacularization

If they have a pulse

78
Q

Category three treatment of critical limb ischemia

A

Surgery to amputation

Treatment of choice

Complete loss of motor function. It is irreversible

79
Q

Risk factors for DVT

A

DVT age obese females

Increase weight on the vessels
Prolonged standing
Pregnancy
Oral contraceptives
HTN
A lot is genetics

80
Q

Rest and elevation

A

Relief for pvd

81
Q

Clinical manifestations of pvd

A

Burning swelling throbbing cramping shiny skin hyperpigmentation ulceration edema restless leg syndrome leg fatigued heaviness and aching

The brown socks tan color from rbc damage the swelling and Edema

Skin is taught and edema. Ulceration is a hallmark of

82
Q

CVI management

A

Weight loss exercise elevation and compression

All based on disease severity

83
Q

Contraindications for compression

A

ABI <0.6
Severe atherosclerosis disease

Combination of pad and cvi

Arterial bypass don’t squeeze and you’ll blow that graft

Don’t squeeze the legs you could squeeze DVT

Very low platelets

Patients with severe heart failure monitoring them closely. Ny class 3

Diabetic neuropathy and sensory loss

84
Q

Normal ABI

A

> 1

85
Q

Interventions for CVI

A

Stripping stents ablative therapy or sclerotherapy

86
Q

class one hemorrhage shock

A

no fluid therapy <15 % blood loss

87
Q

classes of hypovolemic

A

based on blood loss

88
Q

31-40% blood loss

A

class 3 need blood products, replace

88
Q

15-30% blood loss

A

class 2 colloids or/and cystralalloids

89
Q

initial bolus for fluid replacement

A

500ml to 1L

89
Q

after 2L of fluid resuscitation

A

they might need blood

89
Q

> 40% blood loss

A

class four definitely we are transfusing

90
Q

treatment for first line stabilizing the patient in hypovolemic shock

A

isotonic
ringers lactate versus normal saline

LR=liver turns to bicarb, buffer the fluid, doesn’t move in or out, doesnt work as large molecule; volume expander. —liver patients cannot get; switch to normal saline

normal saline hydrates same tonicity

91
Q

20ml/kg

A

initial bolus

92
Q

hgb 8/9

A

“normal”

93
Q

map normal minimum to perfuse

A

60

94
Q

scvo2 4 things**

A

co/hgb/vo2/fio2

95
Q

1unit of prbc will increase hct approx….

A

3ml/dl and hgb by 1

96
Q

for every 4-5 units of prbc

A

one unit of ffp should be infused

97
Q

colloids (starches,gelatins)

A

Increase in plasma volume
Plasma protein fractions like albumin and plasmanate are given when volume loss is due to plasma like in burns or third spacing, bowel obstr.

98
Q

low cardiac output wedge> 18

A

cardiogenic shock

99
Q

morphine

A

48 minute in the recording***

100
Q

dopamine and dobutamine

A

mid dose range positive inotropy dose

1-4 renal dose, 5 is a mid dose and then higher ranger in pressor support

can cause arrhtyhmias

101
Q

clinical manifestations of anaphylactic shock

A

stridor wheezing, tachycardia, cutaneous puritius angioedema, restlessness, impending sensing of doom, n/v/d

102
Q

loss of vasomotor tone

A

distributive shock

103
Q

identify a patient with a known infection

A

Hyperdynamic (warm) shock
Fever, Chills
Warm, flushed skin
AMS
BP normal or slightly increased
Increased HR and RR
Decreased PaO2 despite O2 therapy

104
Q

early stage of septic shock

A

blood pressure could be OK

105
Q

hypodynamic cold shock

A

Cold, clammy skin
Increased HR, RR
Decreased BP
Resp Failure/ARDS
Metabolic Acidosis d/t lactic acidosis
Oliguria
s/s DIC
Edema

106
Q

neurogenic clinical manifestation

A

hypotensive, hypothermia, brady, hyporefelxxia; warm dry skin

107
Q

bicarb give when ph is less than 7.15

A

then give, otherwise, give fluids and hydrate

108
Q

Chronic htn damages and causes what

A

Bulging outward AA

109
Q

Aortic aneurysms causes

A

HTN infections atherosclerosis and scary is the congenital weakness

110
Q

More specific debakey one

A

Ascending and descending the whole thing and it looks like a number 1

111
Q

More specific debakey 2

A

Ascending and invoking the aortic valve

112
Q

How does the treatment look like for debakey 3 Stanford B

A

A graft

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