Nurs 453 test 2 Flashcards
(223 cards)
1
Q
Regulators of our blood
A
valves
2
Q
Valvular heart disease is defined by
A
Affected valve AND problem
3
Q
Stenosis:
A
narrowing valve opening
4
Q
Regurgitation:
A
backward flow of blood into the heart or between heart chambers
5
Q
Prolapse :
A
“fall out of place”, or valve leaflets move to an area where they are not intended to be
6
Q
best way to evaluate valve function or dysfunction
A
Transthoracic echocardiogram
7
Q
mitral valve
A
between the left atrium and the left ventricle
8
Q
left atrium receives
A
oxygenated blood from the pulmonary veins on the way to systemic circulation
9
Q
Gold standard for evaluating the severity of MV stenosis
A
Trans-mitral gradient (measured by echocardiogram)
10
Q
1 cause of MV stenosis
A
congenital heart disease
11
Q
MV stenosis leads to
A
Obstruction of blood flow
Pressure difference between the LA & LV
↑ of blood volume & pressure in LA causes ↑ risk of atrial fib
Hypertrophy of the pulmonary vessels= ↑ pulmonary HTN
12
Q
MV Stenosis-Clinical Manifestations
A
Exertional Dyspnea can be accompanied w/ hemoptysis - Caused by reduced lung compliance & lack of ability to move oxygenated blood out of the LV
Palpitations: Atrial fibrillation associated to enlarged RA/RV from fluid overload
fatigue, angina
13
Q
most cases of MV Regurgitation are caused by
A
MI Chronic rheumatic heart disease MV prolapse Ischemic papillary muscle dysfunction Infective Endocarditis (IE) MI with LV failure ↑ risk for acute MR
14
Q
acute MV regurgitation clinical manifestations
A
new systolic heart murmur
↑ in pressure transmits to pulmonary bed
pulmonary edema and cardiogenic shock
Thready peripheral pulses, cool, clammy extremities, low cardiac output
15
Q
chronic MV regurgitation clinical manifestations
A
may be asymptomatic for years
16
Q
MV Prolapse
A
Structural abnormality allowing MV leaflet to prolapse into LA during systole
Usually benign, but serious complications can occur, including death
17
Q
MV Prolapse Clinical Manifestations
A
Most pts are asymptomatic for life
but they can have Atypical chest pain, dysrhythmias, Palpitations, SOB, Murmur & clicks
18
Q
common dysrhythmias with MV prolapse
A
Ventricular tachycardia (V Tach) Paroxysmal supraventricular tachycardia (PSVT)
19
Q
If atypical pain occurs then during MV prolapse
A
Does not respond to Anti-Anginal treatment
Episodes occur in clusters, especially during stress
20
Q
MV Treatments Stenosis, Regurgitation, Prolapse
A
avoid caffeine and stimulants, Cath lab, mitral valve replacement
21
Q
aortic valve
A
AV is between the LV and the aorta…key to getting CO!!!
22
Q
AV stenosis
A
Obstruction of flow from LV to aorta during systole
↑ pressure on LV and ↑ myocardial O2 consumption
↓ CO which leads to Pulmonary HTN and HF (HFpEF and HFrEF)
Can be discovered in childhood, adolescence or young adulthood
23
Q
cause of AV stenosis
A
Calcification (#1)
Bicuspid AV that calcifies (seen at age 40 to 50)
24
Q
AV Stenosis Clinical Manifestations
A
Angina
Syncope
Exertional dyspnea
25
prognosis for AV stenosis
Poor prognosis if symptoms and obstruction are not relieved
26
treatment for AV stenosis
Beware of Nitroglyerine: ↓ preload necessary to help open the stiff valve
Anticoagulation: Warfarin (goal 2.0 to 3.5, higher if they have valve replacement)
Aortic Valve Replacement (AVR)
27
AV regurgitation
Blood flows from ascending aorta backs to LV
| Happens during diastole and ↑ preload
28
acute AV regurgitation is a
life threatening emergency
29
cause of acute AV regurgitation
```
Infective endocarditis (IE)
Rheumatic heart disease
Trauma
Aortic Dissection
Marfans, Lupus
```
30
AV Regurgitation Clinical Manifestations
```
CARDIOVASCULAR COLLAPSE
Abrupt onset of PROFOUND DYSPNEA
Angina…more subtle than in AV stenosis
Diastolic murmur
Hypotension
```
31
tricuspid valve
Tricuspid valve is between the RA and the RV.
The RA gets its unoxygenated blood from the great veins (superior and inferior vena cava).
32
TV stenosis
RA output becomes obstructed; the blood volume
| RA enlargement, elevated venous pressures
33
TV stenosis cause
Almost always in patients with IV drug use (infective endocarditis)
rheumatic heart disease…patients might also have MV or AV stenosis
34
TV stenosis treatment
valve replacement
35
Pulmonic Valve (PV)
```
Pulmonic valve is between the RV and the pulmonary artery… deoxygenated blood.
Pulmonic Valve (PV) disease is very rare
```
36
Pulmonic Valve (PV) disease
Almost always congenital- may go unnoticed for years if mild
37
Pulmonic Valve (PV) disease cause
RV problems
High pressures in the RV
Hypertrophy of RV
38
Pulmonic Valve (PV) disease clinical manifestations
Fatigue
Cyanosis
JVD
Loud mid-systolic murmur
39
labs for valve disease
CBC w/ diff
May culture if suspicion of infective endocarditis
CMP to see if there is liver, kidney or other organ dysfunction
40
diagnostics for valve disease
```
Cardiac echo (thoracic or TEE)
Goals standard best to evaluate valve function or dysfunction
12-lead, cxr
```
41
Infective Endocarditis (IE)
Infection of the endocardium
Impacts the cardiac valves
Causative agent: staph or strep
42
patients at risk for infective endocarditis
Medical hx of: IV drug use, hospital acquired infections, prior IE
HX within the past 3-6 months:
IV Drug Abuse
Dental, surgical, or GYN procedures (including OB)
43
Primary lesion of IE
Fibrin, leukocytes, platelets, microbes adhere to valve or endocardium
Embolization of portions of vegetation get into circulation
Infarction can occur
44
sub-acute IE
Longer course (months), slower onset
enterococci
Hx of previous valve disease
45
acute IE
Shorter course, rapid onset
strep, staph, viruses, or fungi
Typically have healthy valves prior to infection
46
infective endocarditis clinical manifestations
```
Acute: Non specific: symptoms are flu like
Fever in >90%
New/changing systolic murmur
Sub-acute: more generalized symptoms
Ha, back pains, body ache
```
47
infective endocarditis labs
```
CBC w/ diff
Blood cultures, both aerobic & anaerobic
Electrolytes
Troponins
Coags
```
48
infective endocarditis diagnostics
12-lead ECG
CXR – look for cardiomegaly
Echocardiogram
49
Treatment for IE
Treat the causative agent may need valve replacement
50
Modified Duke Infective Endocarditis Criteria
```
Microorganisms in vegetation
pathological lesions
positive blood cultures
evidence of endocardial involvement
IV drug use
predisposing heart condition
Vascular/ immunologic phenomena
microbiological evidence
Score determines definite, possible or no, and then determines how to treat
```
51
pericarditis
inflammation of the sac
52
pericarditis causes
```
Infectious:
- bacteria, virus, TB, fungal
Non-infectious:
- cancer, MI, trauma, uremia
Autoimmune or Hypersensitivity:
- rheumatic fever, drug reactions, rheumatoid arthritis, lupus
```
53
hall mark finding of pericarditis
Pericardial friction rub
also Severe angina, sharp & pleuritic in nature
Worse w/ deep breathing
54
complications of pericarditis
Pericardial effusion: accumulation of excess fluid in the pericardium. Can be rapid or slow.
Cardiac tamponade: effusion increases in volume, compresses the heart.
55
labs for pericarditis
```
Pericardiocentesis…culture the fluid
CBC w/diff
CRP/ESR
Troponins
Blood cultures
Coags
```
56
diagnostics for pericarditis
```
ECG-abnormal in 90% of cases (ST elevation)
CXR- look for cardiomegaly
Cardiac Echo
CT/MRI
Pericardiocentesis
```
57
leads with pericarditis
ST elevation present in all leads
58
Pericarditis Collaborative management
Treatment/Management is based on causative factors
Directed towards identification and tx
Management of pain and anxiety
59
myocarditis
Inflammation of the myocardium leading to cellular damage and necrosis
60
myocarditis is a common cause of
dilated cardiomyopathy
61
causes of myocarditis
Virus, bacteria, fungi
| Coxsackie A and B viruses (most common)
62
myocarditis manifestations
Can have a friction rub & pericarditis along w/ myocarditis
flu-like
large range of symptoms
63
labs for myocarditis
```
CBC w/diff
Sed rate; c-reactive protein (CRP)
Troponins
Viral titers
tissue and fluid samples
```
64
diagnostics for myocarditis
12 Lead ECG
Endomyocardial biopsy (w/in first 6 wks most definitive)
Echo
MRI
65
Treatment for myocarditis
Goals: manage associated cardiac symptoms with meds such as digoxin, diuretics, ACE or BB
If severe: consider IABP or heart transplant
66
nursing diagnosis for Inflammatory Disorders
Decreased cardiac output r/t alterations in afterload and/or preload
Activity intolerance r/t generalized weakness, arthralgia, and alteration in O2 transport secondary to valvular dysfunction
67
P wave
atrial contraction
68
PR interval
av node conduction should be 0.12-0.2
69
QRS complex
ventricular contraction should be 0.04-0.1
70
T wave
ventricular relaxation
71
QT interval
depolarization should be lass than half of the preceding R-R interval
72
HFrEF vs HFpEF heart failure
left side
73
Primary risk factors for heart failure
HTN and CAD, MI
74
HF is caused by
interference with Preload, Afterload, Myocardial Contractility and Heart Rate (which all regulate CO)
75
HFrEF
Heart Failure with reduced ejection fraction
Systolic Failure…“Failure of systole”
Inability of the heart to pump effectively
76
hallmark sign of HFrEF
Hallmark sign is decreased EF, usually less than 45%
77
HFpEF
Heart Failure with preserved ejection fraction (EF 65% and greater)
Diastolic failure…“Failure of diastole” – failure to fill
Inability of the ventricles to relax and fill during diastole, most commonly r/t hypertension
78
most common HF
left sided
79
signs of left sided HF
pulmonary congestion and edema - back up of blood into the pulmonary veins
80
primary cause of Right sided HF (for pulmonale)
left sided HF
81
signs of right sided HF
Signs: Peripheral edema, JVD, hepatomegaly, splenomegaly because blood is backing up into the systemic venous circulation
82
Compensatory Mechanisms in HF
Aimed at maintaining CO and BP (helps at first!)
Neurohormonal Response – RAAS
SNS stimulation – catecholamine
Dilation – stretch of ventricles/atrium
Hypertrophy - increase of mass & thickness – diuretics, ACEs, ARBs
83
Counter-regulatory Mechanisms
```
ANP, BNP (renal, CV, and hormonal effects)
Nitric Oxide (NO)…vasodilation
```
84
Cardiac Compensation
compensatory mechanisms succeed in maintaining adequate CO to maintain central & local perfusion
85
Cardiac Decompensation
compensatory mechanisms NO longer maintain adequate CO and inadequate perfusion results
86
what happens during Acute Decompensated Heart Failure
Engorgement of the pulmonary vascular system, as this increases, alveolar lining cells disrupted – RBCs leak w/ fluid
87
s/s of Acute Decompensated Heart Failure
Tachypnea, dyspnea and orthopnea (RR>30) – increased pulmonary congestion
Worsening ABGs – ↓ PaO2, possibly ↑ PaCO2 & progressive acidosis
Anxious, pale cyanotic, clammy, cold skin
Bilateral crackles, possibly wheezes, copious frothy, pink sputum (due increased pressure and RBC crossing the membrane)
Tachycardia – compensating
↑ BP initially – but then drops
88
meds for Acute decompensated HF
Diuretics, Vasodilators, morphine, positive inotropes
89
Diuretics
Mainstay of treatment for volume overload
| Reduces preload
90
Vasodilators
Reduces preload & afterload
| Type depends on if we are treating preload or afterload
91
morphine
Reduces preload and afterload
Improves gas exchange
Reduces anxiety and can reduce dyspnea
92
positive inotropes
```
Increases myocardial contractility and CO
Includes dobutamine (preferred), milrinone, and digoxin
```
93
meds for chronic HF
diuretics, ACE, ARB, vasodilator, Beta blocker, positive inotropes, antiarrythmic, anticoagulant
94
beta blockers
Metoprolol, carvedilol (preferred)- assists with blocking ventricular remodeling
Can help with rate control
95
anticoagulant during HF
due to pooling of blood
| Warfarin, DOACs, ASA
96
diagnostics during acute decompensation
Cardiac echo (must have…prior to discharge), 12 lead
97
labs during acute decompensation
BNP, CMP, CBC, ABGs
98
managing acute decompensation
Assess, Assess, Assess!
High flow O2, consider CPAP or intubation
Cardiac monitor, IV x2, positioning (high folwers)
Daily weights, strict I&Os, Na/H2O diet/fluid restriction
99
assessment with heart failure
1st complete a history & physical exam; determine underlying cause of the HF. get BNP, troponin, cardiac echo, 12 lead, and possible Cath
100
complications of HF
pleural effusions, dysrhythmias, thrombus, hepatomegaly, renal failure
101
women and MI
SOB and fatigue are common presenting factors
Present w/ general fatigue, flu like symptoms, n/v or GI upset…
they often don’t think they are having an MI
102
cause of ACS
```
Occlusion of coronary artery…#1 cause
Endothelial damage occurs
Atherosclerotic plaque disruption “rupture”
Platelet aggregation
Thrombus formation
```
103
N-STEMI
Non-ST-segment-elevation myocardial infarction
| will have positive trops
104
Management of N-STEMI and unstable angina is
identical
105
STEMI
ST-segment-elevation myocardial infarction
Manifests w/ signs and symptoms of dyspnea, diaphoresis & change in ECG
will have positive trops
106
troponins
show cardiac ischemia!
107
chest pain work up
trop, 12 lead EKG, H&P, cardiac monitor, O2, pain relief, ASA, fibrolytics
108
STEMI management
Get the artery open ASAP, immediate cath lab
| Fibrolytics (NO cath lab available)
109
NSTEMI management
ASA, heparin, monitor and Cath lab later
110
door to needle
less than 30 minutes
111
door to balloon
less than 90 minutes
112
MD responsibility during chest pain
Interprets ECG w/in 10 min, interprets labs, gives antiplatelet therapy, β-blockers w/in 24 hr, determines STEMI vs NSTEMI, Chest Pain or
Ischemic Symptoms
113
if no Cath lab is available
Percutaneous Catheter (PCI) or fibrinolytic agent (if cath lab not immediately available) for STEMI
114
H&P with chest pain
Assess pain – PQRST or OLDCARTS
| Assess age, race, co-morbidities, risk factors, family history, recent drug use
115
does a normal ECG rule out ACS/AMI
no
116
primary identifier of STEMI
ST segment elevation in 2 or more consecutive leads
117
what differentiates old MIs from acute process
T-wave inversions and pathologic Q-waves develop after an MI
118
ST elevation
infarction
119
ST depression
Ischemia
120
Lateral leads
CIR - I, AVL, V5, V6
121
anterior leads
LAD (left anterior descending artery) - V1, V2, V3
122
Inferior leads
RCA - II, III, AVF
123
which STEMI carries the worst prognosis
anterior - Due to larger infarct size; feeds a majority of the LV
Infarct in the left coronary artery will see septal, anterior and lateral changes…left coronary artery
124
Inferior MI
Right Coronary Artery RCA
| ST elevation in leads II, III and aVF
125
nitroglycerin is a concern with
right sided MI decreases preload!!!
126
pharm management with ACS/AMI
MONA (aspirin is key), atorvastatin
127
High Sensitivity Troponin T levels
```
Negative = 6
Positive = 20
NSTEMI = 52
Critical = 100
higher trop means more myocardial damage
```
128
when to get troponin
BASELINE, then at minimum x 2 hours for three times (hour 0, hour 2, hour 14)
Chest pain centers may obtain every 4 hours, Positive is > or = 0.04
129
other cardiac markers
CK-MB
Myoglobin - Sensitive, but not specific…
Elevations occur in 1-2 hours after onset of symptoms
neither of these are specific for cardiac injury
130
Other Causes of Elevated Troponins
Sepsis
Burns
Extreme Exertion
131
Criteria for stress test:
Chest pain present
2 negative Troponins
No significant 12 lead ECG changes (pt may have abnormal but not STEMI)
Need some form of direct evaluation of the heart (prior to discharge)
132
two type fo stress test
exercise and nuclear (pharmacology)
133
exercise limitations
Women- ↑ false +
| βBlockers blunt maximum HR & maximum work so ↓ sensitivity
134
Cardiac Nuclear Stress Tests
Uses dobutamine, adenosine, or dypridamole which:
↑ myocardial work load in pts unable to exercise
Adenosine & dypridamole are contraindicated in patients w/ bronchospasm or high grade AV block
135
what can decrease the effectiveness of Cardiac Nuclear Stress Tests
Theophylline & caffeine decrease the effectiveness of the test
Also beta blockers or drugs that speed up or slow down the heart can effect the test
136
What would make us want to immediately stop a stress test?
Substernal chest pain, ST elevation on ECG or lethal rhythm
137
coronary angiography also called
Cath lab - gives direct visualization of coronary arteries
138
who gets immediate Cath lab
STEMI pt
139
shock state primary problem
perfusion
140
What do we need to maintain perfusion? what if these things are altered
Adequate cardiac pump
Adequate vasculature or circulatory system
Sufficient blood volume
When these are severely altered…shock states occur!!!
141
shock is characterized by
ineffective tissue perfusion
decrease tissue perfusion
acute circulatory failure
impaired cellular metabolism – cellular level move in to anaerobic metabolism
142
shock leads to
imbalance between the supply and demand for oxygen/nutrients
143
4 stages of shock
initial, compensatory, progressive and refractory
144
Initial stage of shock
Begins at cellular level, not clinically apparent
Oxygen to cells impacted by perfusion
decrease cardiac output
Metabolism changing from aerobic to anaerobic
145
Anaerobic Metabolism =
lactic acid buildup
146
Compensatory Stage of Shock
Activation of compensatory mechanisms
Goal: maintain homeostasis
Neural: ↑ HR, contractility, arterial/venous congestion, shunting of blood to vital organs
Hormonal: activation of RAAS-causes vasocontraction, ADH and ACTH
Drop in BP
Immediate response of baroreceptors activating SNS
increase HR & vasoconstriction (most common)
147
Compensatory stageClinical manifestations
```
Oriented x 3 (restless, apprehensive)
Shunting of blood to heart and brain
↑ contractility and HR
↓ BP
↑ renin, aldosterone and ADH
↓ blood flow to lungs
↓ GI blood supply
↓ renal blood flow
```
148
Progressive Stage
Compensatory mechanisms fail
Trying to prevent multiple organ dysfunction syndrome
Continued ↓ in cellular perfusion
↓ cerebral perfusion = ↓ responsiveness
↑ cap permeability
Critical dysfunction first seen in lungs (ARDS)
First signs of MODS
149
Progressive StageClinical Manifestations
Cardiovascular collapse – ↓ perfusion
Worsening of metabolic acidosis
Renal: ARF,AKI – increased BUN = decreased perfusion to the kidney
GI: Dysfunction – (bleeding, impaired absorption) – obstruction (ileus) , decreased bowel sounds
Liver: ↑ LFTs, altered drug/waste metabolism – decreased perfusion to liver
DIC (Disseminated intravascular coagulation)
Seen more in sepsis
Clotting and bleeding at the same time – seen in shock states
150
Systemic Inflammatory Response Syndrome (SIRS)
Generalized inflammation in organs remote from the initial insult
151
Multisystem organ dysfunction syndrome
Failure of 2 or more separate organ systems
Acute illness
Homeostasis cannot be maintained without interventions
152
clinical manifestations of Multisystem organ dysfunction syndrome
Clinical manifestations…Depends on the organ
153
DIC
Bleeding and Clotting disorder
ALWAYS a complication of another disorder
Massive trauma (hemorrhagic shock)
Sepsis
154
what happens in DIC
Pro-inflammatory cytokines activates clotting cascade causing microclots forming in capillaries = widespread microvascular coagulation
Systemic Clotting factors are being used up at microvascular level
No clotting factors left = bleeding everywhere!
155
LABS that will be decrease for DIC
```
Decreased:
Hgb/Hct - bleeding
Platelets (key…rapid decline)
Fibrinogen
aPTT (early DIC)
```
156
LABS that will be increased for DIC
PT/INR
aPTT (late DIC)
D-dimer
Fibrin degradation products
157
Nursing Interventions for DIC
```
ABCs, ongoing assessment, I/Os
Administer:
Crystalloids
Blood products as needed:
PRBCs
FFP, cryoprecipitate, platelets
Heparin (may be given)
```
158
Refractory Stage
↓ perfusion from peripheral vasoconstriction & ↓ CO exacerbate anaerobic metabolism Low BP
Lactic acid leads to cap permeability and loss of vascular fluid Edema
As decrease perfusion and hypoxic state continues, organs fail
MODS
Profound hypotension & hypoxemia
Ischemic gut, Anuria, progression of DIC
Hypothermia
159
cold shock is
dead shock
160
Goals of Care for Shock patients
Improvement and preservation of tissue perfusion
161
Labs for shock
```
depends on the type fo shock but should have stuff like
RBCs/H/H
WBCs
Troponin
CPK
DIC screen
electrolytes
BUN/Creat
Liver enzymes
Lactate
```
162
Cardiogenic Shock
Impaired ability of ventricle to pump blood forward
163
Cardiogenic Shock manifestations
Early presentation similar to decompensated HF
Increased: HR, SVR, pulmonary pressures
Decreased: B/P, cardiac output/index, urine output
Chest pain, tachypnea, crackles, cyanosis, anxiety
164
mortality rate of Cardiogenic Shock
60% despite aggressive RX
165
cause of cardiogenic shock
Acute MI – most common cause of systolic dysfunction
Cardiopulmonary arrest, acute decompensated HF
Trauma, Septic or hemorrhagic shock
166
care for cardiogenic shock
Restore blood flow to the heart through Cardiac Cath w/ angioplasty or stent or Thrombolytic Therapy (tPA, streptokinase) if cath unavailable
Pulmonary Artery Catheter, IABP or VAD
167
meds for cardiogenic shock
inotropes, vasopressor, diuretics, vasodilators, antidysrhythmic agents
168
what is the issue with cardiogenic shock
Hypovolemia is generally NOT an issue
Think the patient is in extreme PUMP FAILURE…
Afterload and Preload issues
169
dobutamine
inotrope - commonly used for acute HF or cardiogenic shock
it stimulates beta receptors in the heart
beta 1 - increases contractility, HR, and CO
beta 2 - decreases SVR and after load (vasodilation)
170
Intra aortic balloon pump (IABP)
balloon that sits in the aorta to decrease after load
171
Left Ventricular Assist Device (LVAD)
Used to stabilize patients awaiting heart transplantation
| Pulls blood from the LV and sends out to the aorta
172
Hypovolemic Shock
Loss of intravascular fluid volume
173
Hypovolemic Shock manifestations
Decreased: B/P, CVP, preload, SV, UO, cap refill; Hgb/Hct
Increased: HR, SVR, RR
Pallor, anxiety, confusion, agitation
Depends on severity of volume depletion - how much and how fast is volume lost
174
Interventions with Hypovolemic Shock
ABCs
2 large bore IVs
fluid resuscitation
175
diagnostics with Hypovolemic Shock
imaging
| labs: type and cross, CBC w/ diff, CMP
176
treatment with Hypovolemic Shock
stop hemorrhage or prevent fluid loss
Surgery
IR
177
How will we know when our interventions are successful?
↑ in BP…don’t forget to look at MAP
| ↓ in HR
178
Obstructive Shock
Physical obstruction impeding the filling/outflow of blood flow occurs resulting in ↓ CO
179
causes of Obstructive Shock
Cardiac tamponade, tension pneumothorax, abdominal compartment syndrome, massive pulmonary embolism
180
Anaphylactic Shock
Acute life-threatening hypersensitivity reaction to a sensitizing substance
181
manifestations of Anaphylactic Shock
↓B/P, ↑ HR, massively decreased SVR
| swelling of the lips and tongue (angioedema), laryngospasm, wheezing, stridor, rhinitis, urticaria
182
types of distributive shock
sepsis and anaphylactic
183
medications for Anaphylactic Shock
Epinephrine, Benadryl, Bronchodilators, fluids, Corticosteroids, H2 Blockers
184
epinephrine
good in crisis - typically used for severe sepsis or anaphylaxis. triggers beta 1 in the heart to increase inotropy, HR, and CO. triggers beta 2 to bronchodilate and alpha 1 to increase SVR and BP
185
Leading cause of inpatient death in non-coronary adult ICUs in the US
septic shock
186
most common cause of shock
sepsis
187
sepsis
systemic inflammatory and coagulopathic response to infection- Life-threatening organ dysfunction caused by dysregulated host response to infection
188
septic shock
Persisting BP requiring vasopressors to maintain MAP ≥65 and LA >2 despite adequate volume resuscitation. (Surviving Sepsis Campaign)
189
3 major pathophysiologic effects of septic shock
Vasodilation
Maldistribution of blood flow
Myocardial depression
190
infection leads to
an immune response that releases immune mediators from WBC and vascular endothelium. This leads to increase in inflammation, endothelial damage and coagulation/ decrease in fibrinolysis.
191
who's at risk for sepsis
over 65, neonates, immunocompromised, invasive procedures, specific types of infections, prior antibiotics, critically ill, genetic predisposition
192
1 hour bundle
for sepsis
- measure lactate level
- rapidly administer 30 mL/kg cystalloid for hypotension or lactate greater than or equal to 4 mmol/L
- apply vasopressors after fluids - Norepinephrine (Levophed) is first, then others
193
levophed (norepinephrine)
common first line pressor for sepsis, cardiogenic shock, or nuerogenic shock. stimulates beta 1 heart receptor which increases HR and CO. and stimulates alpha 1 - increases SVR and BP (vasoconstriction) and beta 2 - protects blood flow to organs
194
phenylephrine (neosynephrine)
peripheral pusher - alpha 1- increase SVR and BP but can cause reflex bradycardia
195
vasopressin (ADH)
commonly used as an adjunct to norepinephrine - vasoconstriction and increases volume by increasing H20 reabsorption
196
signs of sepsis
increase temp, tachypnea, warm and flushed skin, respiratory alkalosis
197
septic shock signs
cool and mottles (cold shock is dead shock), respiratory failure, GI bleed or paralytic ileus, myocardial dysfunction
198
septic shock care
assess! ABCs, fluids, vasopressors, lactate levels, antibiotics, hemodynamic monitoring
199
nursing diagnosis for cardiogenic shock
Decreased CO r/t alterations in contractility, HR
200
nursing diagnosis for anaphylactic shock
Deficient fluid volume r/t relative loss
| Decreased CO r/t alterations in preload
201
nursing diagnosis for hypovolemic shock
Deficient fluid volume r/t active blood loss
202
Thrombolytic/Fibrinolytic Therapy
When no access to cardiac cath lab or patient to unstable to transfer.
Advantages:
Widely Available
Rapidly administered
203
indications for Thrombolytic/Fibrinolytic Therapy
Chest pain typical of MI ≤ 6 hours
+ ECG
PCI not available or to far away.
204
contraindications for Thrombolytic/Fibrinolytic Therapy
Active Internal Bleeding; Hx Cerebral aneurysm, stroke and more
205
labs needed for Thrombolytic/Fibrinolytic Therapy
```
Need rainbow of labs:
Troponin
H/H
Pt/Ptt
CBC
Type and cross
```
206
what else do you need besides labs for Thrombolytic/Fibrinolytic Therapy
2-3 IV lines and neuro assessment (assess for brain bleed)
207
The Gold Standard of Treatment for someone having a MI
Percutaneous Cardiac Intervention (PCI )
208
Cardiac Catheterization aka PCI
Venous and arterial access to the right and left side of the heart.
209
what do you need to do before Cardiac Catheterization
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Medication Hx & Allergies
assess pulses!
Check Labs (Which Ones & Why?)
Pt/Ptt/INR – need to know clotting
kidney function labs
IV assess
pt understands procedure and consent
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210
Takotsubo
broken heart syndrome - Chest pain, ST elevation, mildly elevate troponins - caused by stress
211
post Cardiac Catheterization
position leg straight, monitor for reclusion- s/s ischemia, thrombosis, bleeding and Trops will go up first then down. monitor pulses
212
concerns post cardiac cath
Decreased LOC
Hypotension & Tachycardia
bleeding
213
Cardiac Mapping/Ablation
Provides information about SA and AV nodes
| Determine the origins of a dysrhythmia
214
CORONARY ARTERY BYPASS GRAFT (CABG)
A procedure in which the patient’s diseased coronary arteries are bypassed with the patient’s own venous (saphenous vein) or arterial (internal mammary artery [most common]) vessels.
215
who is a CABG for
Failed Medical Mgt
| Have Left Main or 3 diseased vessels with significant blockage.
216
who is not a candidate for CABG
Failed PCI
Newly added criteria
Diabetes Mellitus
Expected longer term benefits/outcomes
217
Alpha 1
vasoconstriction
218
alpha 2
blocks sympathetic activity
219
beta 1
increase contractility HR and renin
220
beta 2
dilation of bronchioles
221
vasoconstrictors/vasopressors
epinephrine, norepinephrine, phenylephrine, vasopressin
222
inotropes
DOBUTAMINE, DOPAMINE
223
dopamine
(hulk)- squeeze! - vasoconstriction
