Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Critical Care > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Pulmonary Edema

A

abnormal accumulation of fluid in the alveoli and intersititial spaces of the lungs. Life threatening emergency
Most common cause is Left sided heart failure
Ischemic Non-ischemic cardiomyopathy Valvular Heart disease
end inspiratory crackles (early), frothy sputum (late)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pulmonary Emboli (PE)

A

Blockage of the pulmonary artery by a thrombus, fat or air embolus, bacterial vegitation, or tumor tissue.
Embolus lodges at a narrow part of the circulatory system and in this case it is in the pulmonary vasculature
More than 90% arise from DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Venous Thromboembolism (VTE)

A

is the term to describe the process of DVT to PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pulmonary Emboli clinical manifestations

A

Dyspnea
Mild to moderate hypoxemia
Tachypnea, cough, chest pain, hemoptysis, crackles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pulmonary Emboli complications

A

Pulmonary infarction
Death
Pulmonary Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

D-Dimer

A

diagnostic test for PE measures the cross-linked fibrin fragments found as a result of clot degradation and are rarely found in healthy individuals. increase= clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Spiral CT

A

diagnostic test for PE Contrast media is injected into person and scanner illuminates pulmonary vasculature. Contraindicated in patients with Dye allergy or renal dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ventilation/ Perfusion Scan (V/Q)

A

Used if CT is contraindicated.

If ventilation is normal and Perfusion is abnormal there is a high probability of a PE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

DVT Prophylaxis

A

LMWH
Compression devices
Early Ambulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

For Patient’s identified as having PE

A

Anticoagulants
Fibrinolytic Therapy
Surgical Therapy – pulmonary embolectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cardiomyopathy (CMP)

A

Group of diseases that affect the structural or functional ability of the myocardium.
Primary (idiopathic)
Secondary (ischemic, ETOH, cardio toxicity)
CMP can lead to heart failure and cardiomegaly- leading cause of heart transplantation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Types of CMP

A 
dilated, hypertrophic and restrictive
Takotsubo Cardiomyopathy (Broken heart syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Dilated Cardiomyopathy

A

most common type
Etiology – infection, autoimmune, ETOH
Fibrosis of myocardium and endocardium
Ventricular dilation , impaired systolic function, atrial enlargement, stasis of blood (mural wall thrombi prevalent) .
Leading cause of death for DCM – sudden cardiac death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dilated Cardiomyopathy Clinical Manifestations

A

DOE, Fatigue, dyspnea at rest, PND, orthopnea, cough, increased abdominal girth, anorexia, nausea vomiting, S3 and or S4, JVD, pulmonary crackles, hepatomegaly (HJR), displaced PMI, dysrhythmias, heart block, emboli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diagnostic studies for Cardiomyopathy

A

ECHO, Chest x-ray, b-type naturetic peptide, cardiac cath, multiple gated acquisition (MUGA) nuclear scan, endometrial biopsy.
Determine EF <20% has a mortality rate of 50% within the next year.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment for Cardiomyopathy

A 
Heart Failure cocktail – ACEI or ARB, BB, nitrates, diuretics, KCL, aldosterone antagonist, antidysrhythmics if necessary and possibly anticoagulation.
Remove cause if secondary 
Recurrent and multiple episodes common
Inotropic therapy – milronone, dobutrex
Statin therapy – decreases inflammation
Ventricular assist devices
Heart Transplant
Hospice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Hypertrophic Cardiomyopathy pathophysiology

A

Nonobstructed-
Hypertrophy of the walls
Hypertrophied septum and relatively small chamber size
Obstructed-
Hypertrophy of the walls
Hypertrophied septum and relatively small chamber size
The hypertrophied septum creates an outflow track obstruction
Mital valve incompetence
Young athletes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Hypertrophic Cardiomyopathy 4 main characteristics

A

massive ventricular hypertrophy
rapid, forceful, contraction of the left ventricle
impaired relaxation(diastole)
obstruction to aortic outflow (not in all patients)
–Thickened intraventricular septum
diastolic dysfunction with RV stiffness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Hypertrophic Cardiomyopathy Clinical Manifestations

A

fatigue,DOE,angina, syncope, palpitations, dysrrthymias (SVT) AF, VT, VF), SCD, Heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hypertrophic Cardiomyopathy Diagnostic Studies

A

Assessment – exaggerated apical impulse and laterally displaced, S4, systolic murmur, ECG changes, ECHO, Nuclear testing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Hypertrophic Cardiomyopathy treatment

A

BB, CCB, Dig(only for AF), antidysrhythmics, ICD, PPM, surgery, PTSMA (percutaneous transluminal septal myocardial ablation with Alcohol)
Digoxin, nitrates and other vasodilators contraindicated with the obstructed form.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Restrictive Cardiomyopathy Pathophysiology

A

Fibrosed walls cannot expand or contract. Chambers narrowed: emboli common
Disease of myocardium that impairs diastolic filling and stretch.
Systolic function normal
Myocardial fibrosis, amyolidosis, scarcoidosis, secondary to radiation therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Restrictive Cardiomyopathy Diagnostic studies

A

Diagnostic studies the same as others

may need endometrial biopsy for diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pericarditis

A

a condition caused by inflammation of the pericardial sac (the pericardium).
The pericardial space is the cavity between these two layers. Normally it contains 10 to 15 mL of serous fluid.
Causes- Infectious or Non-Infectious, Hypersensitive or Autoimmune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pericarditis associated with MI

A

Acute Pericarditis after MI
-48-72 hrs after MI
Late Pericarditis (Dressler syndrome)
-4-6 weeks after MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Pericarditis: Clinical Manifestations

A 
Severe sharp pleuritic chest pain
Worse with deep inspiration, cough
Unrelieved with NTG and many times Morphine
Different dyspnea
worse when lying down
improves with sitting up and leaning forward
Diffuse ECG changes (ST elevation)
Pericardial Friction Rub 
Heard with diaphragm (LLSB)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Pericarditis: Complications

A

Pericardial Effusion
Tamponade – compression of heart (emergency)
-decreased LA filling
-decreased cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Manifestations of tampanode

A
  • tachypnea and tachycardia
  • muffled heart sounds and narrow pulse pressure
  • increased pulsus paradoxus
  • dyspnea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Pericarditis Diagnostic studies

A

ECG, ECHO, Labs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Pericarditis Collaborative Care

A

Identify are treatment of underlying problem
Bacterial – antibiotics
Acute Inflammation – NSAIDS (in some cases corticosteroids)
Colchicine (Colsalide) for recurrent pericarditis
Pericardiocentesis
Pericardial Biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Pericarditis Nursing Management

A 
Assessment
Pain management
elevate HOB
NSAIDS with food or milk to decrease GI distress
Anxiety management
Monitor for signs of tamponade
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Chronic Pericarditis

A

Etiology – scaring and loss of elasticity of pericardial sac.
Manifestations vague
-dysnea, peripheral edema, fatigue, anorexia weight loss
Diagnostic studies
-Chest x-ray, ECHO, MRI, CT scan
Collaborative Management
-Pericardiectomy (Pericardial Window)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Pericardial Tampanode

A

Increased fluid accumulation in pericardial space
Signs and symptoms-
Becks triad (rarely occur all together), JVD, Distant Heart Sounds, Hypotension, Pulses Paradoxus of >10mmHg (Abnormal fall in BP with inspiration)
Patients present with dyspnea and tachypnea
Treatment Pericardiocentesis
CXR that shows a widened mediastinum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Myocarditis

A

Acute or chronic inflammation of the myocardium as a result of pericarditis, systemic infection or allergic response
causes include viruses, bacteria, fungi, radiation therapy, and pharmacologic and chemical factors.
Coxsackie A and B viruses are the most common etiologic agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Myocarditis Pathophysiology

A

The causative agent invades the myocytes and causes cellular damage and necrosis
Activation of the immune response
Autoimmune response is activated with destruction of myocytes
Results in- cardiac dysfunction, linked to DCM, associated with SCD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Myocarditis Clinical Manifestations

A

Variable from benign to heart failure and death.
Fever, fatigue, malaise, myalgias, pharyngitis, dyspnea, lymphadenopathy, and nausea and vomiting are early systemic manifestations of the viral illness.
cardiac signs appear 7 to 10 days after viral infection.
pleuritic chest pain with a pericardial friction rub and effusion. (Pericarditis)
S3 heart sound, crackles, JVD, syncope, peripheral edema, and angina. (Heart Failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Myocarditis Diagnostic studies

A

ECG, Lab Studies, Endometrial biopsy, Echocardiography, Nuclear Scans, MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Myocarditis Collaborative Care

A

Medication Therapy
-Analgesics, salicylates, NSAIDS
-Cautious use of Digoxin
-ACE inhibitors,BB,Diuretics, Afterload reducers
-Positive chronotropic agents, Anticoagulation, Immunosupressants, antidysrhythmics, antibiotics
oxygen therapy, bed rest, and restricted activity. In cases of severe HF, the use of intra-aortic balloon pump therapy and ventricular assist devices may be required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Myocarditis Nursing Management

A

assessment for the signs and symptoms of HF (decompensation)
decrease cardiac workload
monitoring.
assess the level of anxiety, institute measures to decrease anxiety, and keep the patient and caregiver informed about the therapeutic plan.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Infective Endocarditis

A

Infection of the inner most layer of the heart (Endocardium) and the heart valves.
Subacute (SBE)- involves those with pre-existing valve disease and may last months.
Acute – affects those with healthy valves and manifest as rapidly progressive disease.
Etiologies include: rheumatic heart disease, bacterial (vegetation), viral and fungal infections, IV drug use, and others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Vegitations

A

a clump of fibrin, leukocytes, platelets, and microbes that stick to the valve surface or endocardium.
Vegitations can break loose and become emboli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Infective Endocarditis Clinical Manifestations:

A

Low grade fever, chills, weakness, myalgias, weightloss, clubbing of fingers
Splinter hemorrhages – nailbeds
Petechiae – conjunctivae, lips, buccal mucosa and palate
Osler’s nodes – painful tender red or purple pea sized lesions on finger tips or toes
Janeway’s Lesions – flat painless red spots on palms and soles
New or changing murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Infective Endocarditis Diagnostic Studies

A

Blood Cultures

Echocardiography (TTE and TEE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

IE: collaborative Care

A 
Prophylactic Treatment
Drug Therapy
Based on Culture and Sensitivity
Requires weeks of therapy
Valve replacement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

IE : Nursing Management

A

Assess vital signs and heart sounds (murmur)
Examine patient for clinical evidence of IE
Goal
Normal or baseline cardiac function
Performance of ADLs
Knowledge of therapy and prevention of IE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

transducer has to be at the level of the

A

right atrium, 4th intercoastal midaxillary line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Volume

A

Preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Afterload

A

SVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Cardiac Output

A

rate, contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Pump

A

cardiac output and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Hemodynamic Monitoring

A

Direct system of measuring pressures (heart, blood pressure), Pulmonary artery pressure (PA), Central venous pressure (CVP, RA), Intra-arterial pressure, Wedge pressure
Must be in critical care unit
Called invasive monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

CVP (Volume)

A

The pressure within the superior vena cava; it reflects the pressure under which the blood is returned to the superior vena cava and right atrium (preload)
The CVP is measured with a central venous catheter in the superior vena cava
Normal CVP is 3-8 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Elevated CVP indicates

A

An increase volume (sodium and water retention)
Decreased contractility
Excessive IVF
Kidney failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Decreased CVP indicates

A

Decrease in intravascular volume
Hemorrhage
Severe vasodilation
Pooling of blood in the extremities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Measuring CVP

A 
Identifying level of the right atrium
Patient  supine
Zero the transducer to the right atrium
Patient relaxed
If on ventilator reading is taken at the point of end expiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

inflate PA catheter balloon with

A

1-1.5 mL of air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

balloon inflated only

A

on insertion or to do wedge reading

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Right atrial pressure (RA)

A

Assesses right ventricular function and venous return to the right side of heart
Proximal port of the pulmonary artery catheter (in RA)
Direct method of measuring right ventricular filling pressure (preload)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Increase in RA due to

A

right ventricular failure, hypervolemia or decreased contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Decreased CVP

A

usually hypovolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Pulmonary Artery Pressure

A

Assesses LV function
Diagnosis of etiology of shock
Assesses response to interventions such as administration of volume and medications that are vasoactive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

PAS/PAD (PA Mean)

A

Normal 15-26/5-15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

PAWP or PCWP (pulmonary artery wedge pressure or pulmonary capillary wedge pressure)

A

Wedge is achieved by momentary inflation of the balloon and watching the waveform dampen, Wedge pressure is normally 4-12 mm Hg and is reflective of the LV function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Increased wedge

Decreased wedge

A

Increased wedge
LV failure, hypervolemia, mitral regurgitation
Decreased wedge
Hypovolemia, afterload reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Cardiac Outputs

A

temperature probe (thermistor) at the end of the PA catheter and in the pressure tubing. The cardiac output monitor measures the difference in the two temperatures and calculates the cardiac output
Normal 4-7 liters per minute
Cardiac index: calculated using BSA (CO/BSA)
Normal is 2.5-4 L/min/m2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

CABG - coronary artery bypass graft

A

Candidates determined by angiogram (stent or surgery)
Surgical decision depends on the extent of the disease and the location of the lesions
Purpose is to increase blood flow to the myocardium
Use saphenous (leg) vein graft(SVG), internal mammary artery (IMA), or radial artery
** keep BP low to prevent popping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

SVG

A

Recurrence of atherosclerotic disease after surgery within 5-10 years
SVG is anastomosed to the ascending aorta and to the coronary artery beyond the blockage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

IMA

A

Arterial grafts are preferred as they do not develop atherosclerotic changes as quickly as SVG
Proximal IMA is left intact and the distal end is moved from the chest wall to the coronary beyond the blockage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

PRE-OP TEACHING Cardiac Surgery

A

Visit the ICU (patient and family)
Some medications will be discontinued prior to surgery (diuretics, digoxin, aspirin, anticoagulants)
Emotional support
Discussion of monitors, lines, tubes, ET tube (patient cannot speak with ETT), ventilator
ROM, CTs, pain control
Meticulous pulmonary care (splinting chest, TCDB, IS)
Post operative activity- Shoulder ROM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Post op equipment Cardiac Surgery

A

CTs, Epicardial pacing wires, ET tube, Mechanical ventilator, NG tube, Heart monitor, Foley, Swan, Arterial line, Dressings to sternal and leg incisions, O2 monitor, TEDs or pneumatic boots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Post op care Cardiac Surgery

A

VS q 15 minutes X4, q 30 minutes X 4 and then hourly
Hemodynamic monitoring- PA catheter to measure RA, PA, PCWP, CO, CI at same frequency as vital signs
Assess for hypothermia (vessels may be constricted). Rewarm no faster than 1.8 degrees F per hour to prevent shivering.
Assess for postoperative bleeding, peripheral circulation
Assess lab values (CBC, BMP, CK, troponins, coagulation studies)
ECG and CXR
Arterial line measures BP and site for drawing ABGs
Correlate the arterial blood pressure with the cuff blood pressure at least once per shift

72
Q

incision care

A

Surgical dressing in place for 48 hours
After 48 hours, open to air
Clean daily with antiseptic (chlorohexidine, betadine)
Patient should be taught to shower daily and use antibacterial soap, pat dry and then use antiseptic

73
Q

Chest tubes to drain the mediastinum and/or the pleural space

A

Assess for amount (should be less than 100/hr for the first few hours with a gradual decrease in the amount of chest tube drainage)
Assess for color
Assess for air leak
Usually kept in place for 24 to 48 hours and are taken out when drainage meets parameters and when there is no air leak
Assess chest tube dressing

74
Q

Ventilator and respiratory care

A

ABGs, O2 Sats
Long anesthesia time (at least 4 hours)
Atelectasis r/t surgery
Usually on ventilator 4-12 hours postoperatively
Suction as needed as evidenced by breath sound assessment Q1-2 HOURS
After extubation T, C, DB, IS q2h
Pain must be controlled postoperatively so the client can breathe effectively and for the maintenance of effective respiratory care
Up in the chair ASAP

75
Q

Control of fluid balance

A

Determine if too much or too little with Swan and labs
Maintain renal output at least 30 mL/hour
Assess electrolytes. Potassium should be replaced to keep level WNL.
May need volume replacement with colloids if H and H is normal, with PRBC if H and H is low
May need platelets or fresh frozen plasma if the client is bleeding too much

76
Q

complication of cardiac surgery heart failure

A

Decreased BP, oliguria, poor peripheral vascular checks, decreased level of consciousness, crackles, chest pain
All are signs of decreased cardiac output
Client may be fluid overloaded but CO is diminished because the pump has failed

77
Q

Valvular Disorders

A

Valves direct the flow of blood
When damaged, blood backs up and pressures in the system increase
Chordae tendineae anchor the valve leaflets to the papillary muscles and the ventricular wall
Semilunar valves between the ventricles and the arteries (pulmonic and aortic)

78
Q

Anatomic Location of Tricuspid Valve

A

Fifth intercostal space to left of sternum

79
Q

Anatomic Location of Pulmonic valve

A

Second intercostal space to the left of the sternum

80
Q

Anatomic Location of Mitral Valve

A

Left midclavicular line at 5th intercostal space

Mitral area also apex and PMI (point of maximal impulse

81
Q

Anatomic Location of Aortic Valve

A

Second intercostal space to the right of the sternum

82
Q

S1 is heard when the

A

AV valves close and is heard loudest at the apex of the heart

83
Q

S2 is heard when the

A

semilunar valves close and is heard best at the base of the heart

84
Q

Mitral Valve Prolapse

A

Usually no symptoms
More likely with women
Portion of mitral valve prolapses back into atrium during systole
Blood regurgitates into LA from LV
If symptoms, may be fatigue, SOB, dizziness, syncope, palpitations, CP, anxiety
Eliminate caffeine, smoking and alcohol

85
Q

Mitral Regurgitation

A

May be problem with valve leaflets, chordae tendineae, or papillary muscle
Blood flows LV to LA and leads to hypertrophy and dilation
Decreased CO
Systolic murmur
May be asymptomatic to severe HF symptoms depending on rapidity of development
Dyspnea, fatigue, weakness, palpitations, DOE, cough from pulmonary congestion, dizziness

86
Q

Mitral Stenosis

A

Restricts blood flow LA to LV
Can be caused by rheumatic endocarditis
Hypertrophy and dilation
Backflow of blood into the pulmonary circulation
DOE, fatigue due to decreased CO, hemoptysis, cough, wheezing, palpitations, orthopnea, PND, and respiratory infections
Atrial fibrillation is common due to the strain on the atrium and therefore pulse is weak and irregular
Diastolic murmur
Atrial dysrhythmias

87
Q

Aortic Regurgitation

A

Backflow of blood from the aorta to the LV during diastole
Leaflets do not close (Endocarditis, Congenital problem, Dissecting aorta)
LV dilates and hypertrophies
SBP increases due to increased force of myocardial contraction
DBP decreases due to arteries reflexively relaxing
Widened pulse pressure
Diastolic murmur

88
Q

Aortic Regurgitation S&S

A

Symptoms of LV failure (orthopnea, paroxysmal nocturnal dyspnea)
Client may be able to feel the stronger pulse from the increased contractility
May be able to see pulsations in the carotids and temporal arteries
Fatigue, DOE
Prophylactic antibiotics are needed for invasive or dental procedures
Avoid strenuous activities (due to LV dysfunction)
Treat with valvuloplasty or AVR
Must preserve the LV

89
Q

Aortic Stenosis

A

Narrowing of the valve between the LV and the aorta
Can be congenital
Can be due to rheumatic endocarditis or calcification
LV increases the force of contraction to compensate
LV hypertrophy
DOE, dizziness, syncope (decreased CO to the brain)
Orthopnea, PND, pulmonary edema
CP (increased myocardial oxygen demand)
Systolic murmur

90
Q

Valve Replacement

A

Usually a mediastinal approach
Abrupt correction of long standing blood flow issues
Sudden changes in intra-cardiac pressures
Postoperative risk of thrombo-embolism, infection, bleeding, HF, HPTN, dysrhythmias

91
Q

Mechanical (St. Jude) Valve Replacement

A

Last longer

Need to be on coumadin for life due to the risk of thromboembolism

92
Q

Tissue or biologic valves (Pig valve, porcine, Synthetic)

A

Do not last as long
Do not need to be on coumadin
7-10 year viability

93
Q

Post-operative care of the Valvular Surgery Client

A 
ICU for 24-72 hours
Hemodynamic monitoring
VS frequent
Medications for BP, HR, CP
In hospital up to 7 days
94
Q

Rheumatic Endocarditis

A

Beta hemolytic strep is the usual culprit of rheumatic fever
Can cause endocarditis (usually of the mitral valve)
Would hear a murmur
Prevent with prompt treatment of strep throat

95
Q

Two criteria must be met before shock can be diagnosed:

A

There must be a reduction in mean systemic B/P
Clinical evidence of hypoperfusion of vital organs
This results in:
Decreased tissue perfusion and
Impaired cellular metabolism

96
Q

Shock Initial Stage (Early Stage)-

A

Occurs at a cellular level and is usually not clinically apparent.
Increased sympathetic stimulation occurs (compensation)- mild vasoconstriction & increase in heart rate
Metabolism begins to change from aerobic to anaerobic.
Lactic acid begins to build.

97
Q

Compensatory Shock-

A

Compensatory Mechanisms including neural, hormonal and biochemical are activated to maintain perfusion of Vital organs
Classic sign of shock (decreased blood pressure) is minimized by compensatory mechanisms, oxygen supply and demand mismatch

98
Q

Compensatory Shock clinical manifestations

A

Neurologic System – barrorecptors activated – stimulate SNS. SNS releases epi and nore. Vasoconstriction results. Blood flow to heart and brain maintained but shunted away from non vital organs
Cardiovascular System – heart rate increases and coronary arteries dilate
Respiratory System – decreased blood flow to lungs increases physiologic dead space (VQ mismatch). O2 levels decrease and patient will compensate with increased depth and rate of respirations
Gastrointestinal System – shunting of blood decreases gastric motility, increased risk for paralytic ileus.
Renal System – activation of RAAS, and ADA released in response to increased osmolality

99
Q

Decompensated or Progressive Shock-

A

Compensatory mechanisms Fail
Vital organs become underperfused
Overall metabolism is anaerobic- the small amount of energy created by anaerobic metabolism is not enough to keep the cell functional and irreversible damage begins to occur.

100
Q

progressive stage clinical manifestations

A

Neuro – decreased mental status
Cardiovascular – CO falls resulting in decreased perfusion. Altered capillary permeability allows protein to leak out of vascular space resulting in decreased circulating volume and intersitial edema. (Anasarca may develop).
Pulmonary – increased VQ mismatch due to constricted arterioles. Pulmonary edema.
GI – protective mucosa becomes ishemic and sets the stage for PUD, and GI Bleeding.
Renal – tubular necrosis – renal failure - elevated BUN, Creatinine.
Liver – elevated liver enzymes
Hematologic system – DIC – results in bleeding from multiple sites.

101
Q

Disseminated Intravascular Coagulation (DIC)

A

Serious bleeding and thrombotic disorder
Shock can predispose patient to DIC.
Blood pooling can lead to clotting.
This uses up clotting factors and results in bleeding

102
Q

Irreversible or Refractory Shock-

A 
anerobic metabolism
accumulation of lactic acid causes increased capillary permeability – edema
Decreased coronary blood flow
Cerebral ischemia
Severe tissue hypoxia with ischemia and necrosis
Profound hypotension and hypoxemia
Multiple organ dysfunction (MOD)
Death
103
Q

MAP=

A

(dx2)+s/3

104
Q

Hypovolemic Shock

A 
Occurs as a result of a loss of intravascular blood volume
Volume is inadequate to fill the vascular space
The volume loss may be either an absolute (d/v bleeding) or relative (internal fluid shift) volume loss 
class 1-4 of blood loss
105
Q

Class I blood loss

A

a fluid volume loss up to 15 % or an actual volume loss up to 750 ml.
May be asymptomatic,restlessness or anxiety

106
Q

Class II blood loss

A

patient has an intravascular volume deficit of 15 to 30% (actual blood loss of 750-1500ml)
decreased preload CO and BP, pallor apprehension, prolonged cap refill, increase HR and RR

107
Q

Class III blood loss

A

occurs when blood volume loss reaches 30 to 40%(actual volume loss of 1500 to 2000 ml)
(All compensatory mechanisms are in full action and beginning to fail)
decrease BP cap refill UO, anxious, confused, increase HR RR

108
Q

Class IV blood loss

A

blood volume deficit is greater than 40% (actual volume loss of more than 2000 ml)
(Compensatory mechanisms are exhausted)
impaired organ function, organ failure, irreversable shock

109
Q

Collaborative Management(Hypovolemic Shock)

A

Give isotonic fluids while waiting for blood (packed red blood cells) ,IV crystalloids

110
Q

Cardiogenic Shock

A

The result of failure of the heart to pump blood forward effectively
Etiology- systolic dysfunction (decrease contraction), diastolic (decreased filling), dysrhythmias (tachy or brady), structural factors (valve disease)
Can be defined as a low CO and hypotension with clinical signs of inadequate blood flow to tissues
Low urine output
Changes in mental status
Decreased peripheral pulses- Cool & clammy skin

111
Q

most common event leading to cardiogenic shock

A

Acute myocardial infarction (AMI)
The risk of cardiogenic shock increases as the area of myocardial necrosis increases
When more than 40% of the left ventricle is destroyed in the AMI process, cardiogenic shock is likely within 48 hours of the acute event

112
Q

Clinical Manifestations of Cardiogenic Shock

A

tachycardia, hypotension, narrowed pulse pressure, increased SVR, decreased cardiac output (less than 4L/min), Cardiac Index (less than 2.5L/min), Pulmonary crackles on auscultation, Cyanosis, pallor, mottling, Edema, decreased U/o, Anxiety, restlessness, confusion

113
Q

Cardiogenic Shock Assessment

A

Left ventricular ejection fraction is usually less than 30%
Other S&S- hypotension, reduced CO, increase in respiratory rate, development of crackles (secondary to pulmonary congestion), urine output decreased, restlessness, agitation, confusion

114
Q

Cardiogenic Shock Collaborative Management

A

restore the balance between oxygen supply and demand.
Definitive measures to restore blood flow include: thrombolytics, angioplasty, or coronary revascularization
IV fluids may be administered (if needed) to obtain maximal stretch of the myocardial fibers and optimal contraction
Positive inotropic agents-dobutamine (Dobutrex) increase MAP, dopamine (Intropin)
Vasoactive drugs-sodium nitroprusside (Nipride) decrease MAP, nitroglycerin (Tridil)
Intra-aortic balloon counterpulsation (IABC) is a treatment used to stabilize the patient with cardiogenic shock

115
Q

Intra-aortic balloon counterpulsation

A

IABP decreases myocardial workload by improving myocardial supply and decreasing myocardial demand
IABP achieves this by improving coronary artery perfusion and reducing left ventricular afterload

116
Q

Distributive Shock

A

Results in inadequate perfusion of the tissues through a maldistribution of blood flow
Intravascular volume and heart function are both normal, but blood is not reaching the tissues
It develops when acute vasodilation occurs without an increase in intravascular volume
3 types- septic shock, anaphylactic shock, & neurogenic shock

117
Q

Sepsis

A

A documented infection with at least 2 of the 4 systemic inflammatory response criteria caused by infection
Sepsis is most commonly caused by Gram-negative bacteria (E. coli, Pseudomonas, Klebsiella)
Gram-positive bacteria represents the second most common causative organisms (Staphylococcus, Streptococcus)

118
Q

Systemic Inflammatory Response Syndrome

A

Manifested by 2 or more of the following:
Temp higher than 38 C (100.4 F) or lower than 36 ° C (96.8 F)
HR more than 90 beats per min
Respiratory rate greater than 20 breaths per min or Paco2 less than 32 mm Hg
WBC count more than 12,000 cells/mm3, less than 4000 cells/mm3, or more than 10% immature (bands) forms

119
Q

Findings to support sepsis indicating organ dysfunction

A 
Creatinine > 2.0
Urine output ,0.5 ml/Kg/hr for 2 hours
Bilirubin >2 mg/dl
INR >1.5 (nl 1.0)
PTT > 60 (nl 25-35 sec)
Lactate (Lactic Acid) > 2mmol/L
Platelets < 100,000
Acute respiratory failure
120
Q

Procalcitonin (PCT)

A

Help differentiate infectious from non infectious causes of systemic inflammatory response syndrome.
PCT is increased in bacterial sepsis and decreased in most patients who progressed favorably.
PCT mean levels were 3.0 ng/mL in SIRS
PCT mean levels were 16.8 ng/ml in patients with Sepsis
PCT may be used to determine antibiotic utilization

121
Q

Sepic Shock

A

Sepsis with hypotension (systolic B/P less than 90 mm Hg or a reduction of 40 mm Hg from baseline) despite adequate fluid resuscitation along with the presence of perfusion abnormalities, that may include lactic acidosis, scant urination, or an acute alteration in mental status
Tissue hypo-perfusion after crystalloid fluid resuscitation SBP < 90 MAP < 65
Or
Lactate (Lactic Acid) level > or equal to 4 mmol/L

122
Q

Three major pathophysiologic effects of septic shock

A

vasodilation – resulting and relative hypovolumia
maldistribution of blood flow
myocardial depression
give alpha to constrict

123
Q

Septic shock and respiratory failure

A

May also be accompanied by respiratory failure.
initial hyperventilation results in alkalosis then as compensatory mechanism fail acidosis occurs.
85% will develop respiratory failure
40% will develop adult respiratory distress syndrome

124
Q

Septic Shock Assessment

A 
Patient’s with septic shock can present in 2 states:
An early (hyperdynamic) state, or
A late (hypodynamic) state
125
Q

Septic Shock Hyperdynamic Phase

A 
Decreased vascular resistance, while B/P is barely maintained
Peripheral vasodilation
Normal to high CO
Hypotension or normotension
Fever
Slight alterations in sensorium
Moderate tachycardia
Tachypnea
Normal urine output
126
Q

Septic Shock Hypodynamic Phase

A 
Profoundly impaired perfusion
Decreased CO
Mental status changes (lethargy &amp; coma)
Clammy, pale skin
Tachycardia, dysrhythmias, hypotension
Pulmonary congestion
Central cyanosis
127
Q

Treatment of septic shock

A

IV fluids (normal saline, Ringer’s lactate solution)
Vasoconstrictors (Dopamine)
Eliminating the source of infection
Administering appropriate antibiotics

128
Q

Anaphylactic Shock

A

due to an antigen-antibody reaction that occurs in blood vessels throughout the body in response to contact with a substance to which the person has a severe allergy
S&S can include skin rash/flushing, pruritis, sneezing/coughing, wheezing, urticaria, dizziness, chest pain, incontinence, angioedema, and restlessness, confusion, sense of doom
Life-threatening S&S can include respiratory stridor, bronchospasm and laryngeal edema

129
Q

Anaphylactic Shock Assessment

A

The peripheral vasodilation and increased capillary permeability produce pooling of blood in the periphery and a decrease in preload
Can be severe enough to decrease CO and B/P
Will see a decrease in SVR (dilation of peripheral vessels)

130
Q

Anaphylactic Shock Collaborative Management

A

ABCs of emergency care (ensure patent airway)
Volume expansion
Vasoconstricting agents
Epinephrine- first-line agent
Antihistamines, bronchodilators and corticosteroids

131
Q

Neurogenic Shock

A

Causes: spinal cord injury, spinal anesthesia, depressant action of drugs
These conditions result in the loss of sympathetic vasoconstrictor tone
This results in massive vasodilation with severe hypotension
Bradycardia develops due to the unopposed activation of the parasympathetic nervous system.
Develop impaired thermoregulation because of the loss of vasomotor tone in the cutaneous blood vessels (that dilate and constrict to maintain body temp)
Become poikilothermic (assume the temperature of the environment)

132
Q

Neurogenic Shock Pathophysiology

A 
Disruption of sympathetic nervous system
Loss of sympathetic tone
Venous &amp; arterial vasodilation (pooling of blood in the periphery)
Decreased venous return
Decreased stroke volume
Decreased cardiac output 
Decreased cellular oxygen supply
Decreased tissue perfusion
133
Q

Neurogenic Shock Assessment

A

Presenting S&S include hypotension, HR less than 60, warm, dry skin, and hypothermia
Additional signs of hypoperfusion can include a decrease in urine output, changes in LOC, decrease in peripheral pulses, and a capillary refill of more than or equal to 3 seconds
Respiratory patterns need to be assessed (rate, rhythm, depth)

134
Q

Neurogenic Shock Collaborative Management

A

For patients with spinal cord injuries, early and proper stabilization of the spinal cord is critical to preventing or limiting neurogenic shock
Treatment goals include the ABCs, fluid resuscitation and vasoconstrictors to increase B/P
Bradycardia may be treated with atropine
Hypothermia is treated with warming measures and environmental temperature regulation

135
Q

Obstructive Shock

A

A physical obstruction to outflow of the heart such as
-Cardiac tamponade, tension pneumothorax, Pulmonary embolism.
S&S depend on obstruction. May include; JVD, pulsus paradoxus

136
Q

Treatment of Anaphylactic, Septic and Neurogenic

A

“Fill up the tank”
fluid resuscitation (crystalloids and possibly colloids)
serial measurement of blood pressure and temp.

137
Q

treatment of shock- Hypotension

A

fill up the tank first
-Vasopressor (goal to achieve and maintain MAP greater than 65 mmHg)
-norepinephrine (Levophed) dopamine (Intropin) phenylephrine (Neosynephrine) Vasopressin (Pitressin)
-Inotropic Agent
-Vasodilators – to reduce afterload, decreases myocardial workload and O2 requirements, Keep MAP greater than 65 mmHg
nitroglycerine (Tridil) Nitroprusside (Nipride)
-Diuretics may be needed in Cardiogenic shock
-Parenteral Nutrition

138
Q

Epidermis

A

outermost layer of skin
Protective barrier
Regenerates every 28 days

139
Q

Dermis

A

this is the layer where new skin is created.
Vascular connective tissue
Nerves, lymphatic tissue, hair follicles and sebaceous glands

140
Q

Subcutaneous Tissue

A

Not part of the skin but attaches to the skin
Loose connective tissue and fat cells
Insulation, regulates temperature and provides shock absorption.

141
Q

Burn size

A

Small burn – localized response
Large burns
25% or more of BSA for adult , 10% or more for child

142
Q

Thermal Injury or Burn

A 
An Injury to the tissue caused by Heat, Chemicals, Electric Current, Radiation
Associated injury= Smoke Inhalation
The result of a burn depends on
Temperature of the burning agent
Duration of Contact time.
Type of tissue exposed
143
Q

priority nursing action with burn

A

Assess for airway patency
Administer oxygen as needed
Obtain vital signs
Initiate IV access and fluid administration
Elevated extremities if no fractures are obvious
Maintain body heat
NPO

144
Q

Smoke Inhalation Injuries

A

Result from inhalation of hot air or noxious chemicals
Cause damage to respiratory tract
Airway is a priority concern
Major predictor of mortality in burn victims
Of the 12,000 fire deaths each year in the U.S., 50% - 60% are due to inhalation injuries
Need to be treated quickly

145
Q

Carbon monoxide (CO) poisoning

A

Treat with 100% humidified oxygen.
CO poisoning may occur in the absence of burn injury to the skin.
Skin color may be described as “cherry red” in appearance.

146
Q

Electrical burn

A

caused by heat generated by electrical energy as it passes through the body, Results in internal tissue damage
Voltage, type of current, contact site and duration of contact are important to identify
most damage occurs beneath the skin- Iceberg effect
Patients are at risk for dysrhythmias, severe metabolic acidosis, and myoglobinuria.
May cause muscle contraction that is strong enough to fracture bones
Release of Myoglobin and Hemoglobin can result in ATN and Renal Failure

147
Q

Chemical burn

A

Alkali, Acid, Organic compounds

148
Q

Time/Temperature Relationshipto Full-Thickness Injury

A

ADULTS
30 sec=130 15 sec=135 5 sec= 140 1.8 sec= 150
CHILD
10 sec= 130 4 sec=135 1 sec=140 0.5 sec=149

149
Q

Superficial partial-thickness burn

1st degree

A

epidermis only, mild swelling, local pain, erythema, blanches with pressure, no vesicles or bullae (sunburn)

150
Q

Deep Partial Thickness Burn

2nd degree

A 
Epidermis &amp; dermis (not entirely)
vesicles or bullae present
moist- pink  or  red
very painful
Mild to moderate edema
151
Q

Full- Thickness Burn

A

Involves entire dermis & epidermis, possibly SQ tissues
Color varies: waxy white, red, brown, black, tan, yellow
Dry & leathery
Thrombosed vessels may be visible
Pain insensitivity

152
Q

rule of nines

A

front of leg-9 back of leg nine, chest- 18, back- 18, front of arm-4.5, back of arm- 4.5, face- 4.5, back of head- 4.5

153
Q

Emergent (resuscitative) phase of burn management

A

Pre-Hospital Care and Emergency Department
Airway, oxygenfluids
Usually lasts up to 72 hours
concerns of hypovolemic shock and edema.
begins with fluid loss and edema formation and continues until fluid mobilization and diuresis begin (decreased BP increase Pulse)

154
Q

Acute (wound healing) phase of burn management

A

time in hospital- for each 1% burn is about 1 day (without complications)
Begins when hemodynamically stable.
mobilization of extracellular fluid and subsequent diuresis.
The acute phase is concluded when the burned area is completely covered by skin grafts, or when the wounds are healed.
Bowel sounds return.

155
Q

Rehabilitative (restorative) phase of burn management

A

after grafting, 6-12 months at home
The rehabilitation phase begins when Burn wounds are healed and Patient is able to resume a level of self-care activity
Monitor Three Areas: Positioning Contractures Hypertrophic Scaring (From not wearing garments or facemask)

156
Q

Fluid Replacement

A

Large bore angiocath
Crystalloid Solutions (Lactated Ringer’s, Saline)
Colloid solutions (Albumin)
Begin as soon as possible

157
Q

Fluid replacement calculation

A

4ml X % burnX wt (Kg)

give half in first 8hrs, give 1/4 next two 8 hour

158
Q

Initial Debridement

A

Removes debris and loosens necrotic tissue
Reduces surface bacteria
Makes it easier to estimate the size and depth of injury
Begins preparation of area for grafting if indicated

159
Q

Silvadene

A

for full thickness burns

160
Q

Bacitracin

A

for partial thickness burns

161
Q

Eucerin

A

are used as the burns and grafts are healing

162
Q

Methods of debridement

A

Mechanical- Hydrotherapy, washcloths, scissors and forcepts
Enzymatic- Application of topical enzymes
Surgical- Excision of tissue in surgery
-Tangential Technique- Thin layers excised until bleeding occurs
-Fascial Technique- Wound excised to the level of the superficial facia. Only used for deep and extensive burns

163
Q

mesh grafts

A

used on not visible skin, net to cover more SA

164
Q

Sheet grafts

A

used on hands and face

165
Q

nutrition and burns

A

Hypermetabolic state
Resting metabolic expenditure may be increased by 50% to 100% above normal.
Core temperature is elevated.
Caloric needs are about 5000 kcal/day.
Early, continuous enteral feeding promotes optimal conditions for wound healing.
Supplemental vitamins and iron may be given.
Patients should be weighed regularly.

166
Q

Hemodynamic resuscitation goals

A

CVP greater than 12 mmHg (Filling the tank)

MAP greater than or equal to 65 mm Hg

167
Q

Crystalloids

A

Isotonic (0.9% NS)
Hypotonic (0.45% NS) rarely used in shock
Hypertonic (3% NS) given slowly

168
Q

Colloids

A

Large proteins:
Albumen
Hespan
Dextran

169
Q

Alpha 1 receptor agonist

A

work on smooth muscle to cause vasoconstriction and increase SVR

170
Q

Beta 1 receptor agonist

A

stimulate myocardial cells resulting in increased myocardial contractility (inotropy) and heart rate (chronotropy)

171
Q

V1 receptors

A

in the vascular smooth muscle leads to vasoconstriciton of peripheral arterial beds

172
Q

Norepinephrine (Levophed)

A 
Mechanism of action:
Vasopressor
Stimulation of alpha receptors cause vasoconstriction and subsequent increase in SVR
Dose: 
0.05-1 mcg/kg/min
Adverse Events
Tachycardia Peripheral and GI ischemia
173
Q

Epinephrine (Adrenalin)

A

Mechanism of action:
Stimulation of beta 1 receptors increase heart rate and contractility of the heart (inotropic and chronotropic effect)
Stimulation of alpha receptors cause vasoconstriction and subsequent increase in SVR
Dose:
0.05-0.5 mcg/kg/min
Adverse Events
Tachycardia Peripheral and GI ischemia

174
Q

Dopamine (Intropin)

A

Mechanism of action:
stimulation of dopaminergic receptors cause renal mesenteric, coronary and cerebral arteries to dilate and increase the flow of blood.
Stimulation of beta 1 receptors increase heart rate and contractility of the heart (inotropic and chronotropic effect)
Stimulation of alpha receptors cause vasoconstriction and subsequent increase in SVR
Dose:
2-20 mcg/kg/min
Adverse Events
Tachycardia Arrhythmias
Dopaminergic doses should not be used for treatment of shock.

175
Q

Phenylephrine (Neosynephrine)

A 
Mechanism of action:
Stimulation of alpha receptors cause vasoconstriction and subsequent increase in SVR
Dose: 
0.5-5 mcg/kg/min
Adverse Events:
Reflex Bradycardia
176
Q

Vasopressin (Pitressin)

A

Mechanism of action:
Augments the effects of the other vasopressor agents
V1 receptors in the vascular smooth muscle leads to vasoconstriction of peripheral arterial beds
Dose:
0.04 units/min
Not titrated
Used in addition to other vasopressors (norepinephrine)
Adverse Events
Higher doses is associated with cardiac ischemia

177
Q

Dobutamine (Dobutrex)

A 
Mechanism of action:
Stimulation of beta  1 and 2 receptors 
Dobutamine is a synthetic catecholamine with strong affinity for both beta1 and beta2 receptors in a 3:1 ratio. 
“Stimulation of cardiac beta1 receptors, resulting in potent inotropic activity with weaker chronotropic activity. On vascular smooth muscles, dobutamine (at lower doses) can decrease SVR as a result of reflex vasodilation and beta2 receptor activation leading to significant hypotension “ (2. Department of Surgical Education, Orlando Regional Medical Center)
Dose: 
5-20 mcg/kg/min
Adverse Events
Arrhythmias
Hypotension

Critical Care (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions