M5 Perfusion Flashcards
Shock 101
Condition in which vital tissue and organs are not receiving enough blood
Without O2 and nutrients from blood, things start to die
Shock can happen due to any mechanism of action that disrupts
Heart function
Blood volume
Blood pressure
Subjective shock S/S
Feeling sick
Weak
Cold/hot
LOC
Objective shock S/S
Hypotension BELOW 60
SOB
Cardiac output and urinary output with shock
Decreases
Respiratory output with shock
Rate Increase resulting in Resp Alkalosis
Resp Alkalosis is an impending indicator of
SHOCK
O2 sat and shock
Drops
First organs to be affected by shock are heart and brain so what are the earliest symptoms
what about respirations
LOC
BP drop
HR increase
Cardiac output drop
rapid and shallow
5 Types of shock
Hypovolemic
Neurogenic
Cardiogenic
Septic
Anaphylactic
Shock treatment ABC
Airway
Breathing
Circulation
To treat shock, threat
Underlying cause
Supportive measures for shock
IV to expand intravascular volume
Vasopressors to increase BP
Supplemental O2
Keep PT warm
Keep environment quiet
What makes treatment difficult in the later stages of shock
Positive feedback loop
Causes for fluid loss shock
Hemorrhage
Burns
Dehydration
Vomit/diarrhea
Diuretics
Diagnostics scans for Hypovolemic shock
CT
Ultrasound
EGD
detects bleeding
Echocardiography
Labs for hypovolemic shock
ABG
Electrolytes
Renal panel
CBC
Urinalysis
Diagnostic tests for cardiogenic shock
12 lead EKG
Nuclear scan
Cardiac cath
Coronary angiography
Lab tests for cardiogenic shock
All the hypovolemic labs +
CRP
Cardiac biomarkers
Thyroid hormones drugs
Diagnostics and Lab test for neuro shock
12 lead EKG
CT MRI of brain
ABG
lytes
CBC
Urinalysis
Diagnostics and labs for anaphylactic shock
12 lead EKG
sensitization test
ABG
Lytes
CBC
Urinalysis
Diagnostics and labs for septic shock
12 lead EGK
Same as hypovolemic
Diagnostics and labs for septic shock
12 lead EGK
Same as hypovolemic+
Serum lactate
Pro-calcitonin
Coagulation factors
Blood/other CULTURES
Hypovolemic shock is defined as a loss of _% of intravascular volume
15
Difference between hypovolemic and cardiogenic shock
Fluid volume and cardiac health
S/S of hypovolemic shock
cardiac
resp
integument
rapid pulse
low BP-high SVR
rapid respirations-low preload
poor skin turgor, tenting, thirst
Hypovolemic shock management
Replace volume with
BLOOD, COLLOIDS or CRYSTALLOIDS
What hormone to give to hypovolemic shock PTs
ADH
Antidiuretic Hormone
Treat acute massive blood loss with
What is the _% for acute blood less
Whole blood
Know blood admin procedures
More than 30% of total volume
Depending on what is low during hypovolemic shock, what other blood components can we give
Plasma protein fraction
Fresh-frozen plasma
Packed RBCs
Colloids 101
what kind of pressure
Expand plasma by drawing body cell molecules in to blood vessels
Oncotic
When to use colloids
When up to 1/3 of adult blood volume is lost
Colloid types
nonblood
we can administer
Dextran
Hespan
Natural colloids in blood
Albumin
Plasma protein fraction
Serum globulin
Crystalloids 101
Types
Intravenous solutions that contain lytes
replace fluids and promote urine output
Isotonic
Hypotonic
Hypertonic
Crystalloid solution examples
NS
LR
Plasmalyte
Neuro shock patho
Sympathetic v/parasympathetic ^ = v in vascular tone = v SVR = v cardiac output = v tissue perfusion = Impaired Cellular Metabolism
Neuro shock risk factors
Spinal trauma
Regional anesthesia
Autonomic nervous system drugs
Neuro shock S/S
heart
skin
v cardiac output
hypotension
bradycardia
cold
Dusky
Volume replacement for neuro shock
Crystalloid
Colloid
Meds for neuro shock
Vasopressors
Corticosteroids
Other neuro shock interventions
Cardiac pacing
GCS (Glasgow coma) scale
Ventilation/intubation
Another name for neuro shock
Vasogenic due to dilation
When the medulla does not get enough O2 or GLUCOSE we get
neurogenic shock
SVR
Systemic vascular resistance
Resistance of blood vessels
Used to create blood pressure
Cardiogenic shock 101
Decreased cardiac output
Impaired cellular metabolism
Hypoxia in presence of adequate volume
Causes for cardiogenic shock
HF
Dysrhythmias
Valve dysfunction
Myocardial infection
Massive emboli
Cardiac temponade
Cardiac temponade
Space around heart fills with fluid
Cardiogenic shock risk factors
Age
MI/HF history
DM
CAD
Cardiogenic shock S/S
neuro
resp
integ
cardiac
GI
LOC
Tachypnea, dyspnea due to pulmonary edema
dusky skin
hypotension BELOW 60
Oliguria
Managing cardiogenic shock
Meds
Vasodilator - nitro
Vasopressor - dopamine
Beta-agonist - increase contraction force
Morphine - improve coronary perfusion
Volume replacement with cardiogenic shock
Crystalloid/colloid
Managing airway and cardiogenic shock
Intubation
Surgeries and procedures for cardiogenic shock
Intra aortic balloon
VAD
Revascularization (bypass surgery)
Septic shock 101
Gram positive TLR2 receptor or gram negative TLR 4 receptor activation = Macrophage engagement = SIRS=w/c shock=MODS
SIRS
Systemic inflammation response syndrome
S/S
Fever
Tachycardia
Tachypnea
Leukocytosis
MODS
Multiple organ disfunction
w/c shock s/s
1st warm shock
2nd cold shock
vasodilation
hypotension
hypoperfusion
inflammation
Myocardial depression
Worsening tissue hypoperfusion
Most common sites of entry for septic shock
Lung
Urinary
GI
Wound
Vascular cath
Risk factors for septic shock
age
nutrition
Hx (trauma surgery caths, HF, DM)
Immunosuppression - AIDS, steroids, chemo, post-organ transplant
Early septic shock S/S
heart
GU
Skin
Neuro
Tachycardia
^ Cardiac output
Hypo OR hyperthermia
Deranged renal system
Jaundice
Deterioration of mental status
Labs for septic shock
Culture
C-reactive proteins
Serum lactate
Pro-calcitonin
Coagulation factors
Fluids for Septic shock
Crystalloids
Colloids
Meds for septic shock
Antibiotics (central line cath)
Vasopressors
Steroids
Beta-agonists
Antipyretics
Insulin
Septic shock airway management
Intubation
Anaphylactic shock 101
Hypersensitivity reaction
vasodilation and hypovolemia=decreased perfusion and impaired metabolism
Most common allergens causing anaphylactic shock
Insect bites
Shellfish
Peanuts
Latex
Meds (pcn)
What else is a big allergen that can happen in hospitals
blood transfusion
Anaphylactic shock S/S
neuro
resp
integument
GI/GU
loc
Stridor/Wheezing
Pruritus
Hives
Swollen lips/tongue
Abdominal cramps, oliguria
Cardio S/S of anaphylactic shock
BP drop
SVR drop
Increased Cardiac Output
Meds for anaphylactic shock
Antihistamines
Bronchodilators
Corticosteroids
Vasopressors
Airway management and anaphylactic shock
intubation/ventilation
Fluid replacement to give in anaphlectic shock
Crystalloids/colloids
1st things to remove in anaphylectic shock
ANTIGEN
Vasoconstrictor/sympathomimetic for shock 101
Act on alpha-adrenergic receptors
raise blood pressure
positive inotropic effect
Vasoconstrictor/sympathomimetic meds
Norepinephrine
(Levophe, Levaterenol)
Vasoconstrictor/sympathomimetic adverse effects
tachycardia
hypertension
Vasoconstrictor/vasopressors 101
Good for early stages
Activates sympathetic system
raises BP and increases contractions
Purpose of vasopressor meds
Maintain blood flow to vital organs heart brain
decrease flow to other organs
kidneys liver
Monitoring for vasopressors
discontinue as soon as
continuous
pt is stable
How to discontinue vasopressors
GRADUALY
prevents rebound hypotension
Vasoconstrictor/vasopressors drugs
Norepinephrine (levophed) - alpha/beta agonist
Phenylephrine - alpha agonist
DDAVP- antidiuretic agent
Only use Sympathomimetic vasocontrictors or vasopressors when
Fluid and Lyte replacement has FAILED
What to monitor when pt on vasopressors
BP
HR
ECGs
Urine Output
GLAUCOMA
Extravasation of vasopressors and dopamine causes
Tissue necrosis
Titrate dose based on BP
What must be injected at Extravasation site immediately
Phentolamine (regitine)
Teach pt to monitor extravaccation via reporting
Pain and burning at IV site
Blanching and blueness of fingers
Chest pain or palpitations
Inotropic drugs 101
Strengthen contractions
Increase cardiac output
Inotropic drug names
Digoxin
Dobutamine
Dopamine
Prototype inotropic agent
treats what shock types
Dopamine
HYPERvolemic
Cardiogenic
Dopamine activates what receptrs
Both Alpha and Beta
Inotropic drug digoxin
increases contractility
gets essential oxygen to critical tissue quickly
Inotropic drug dobutamine
Beta 1 agent
increases contractility
best for HF
Half life - 2MIN
IV ONLY
What to monitor for Inotropic drugs
BP
Telemetry
IV site
RENAL function
Because inotropic drugs work on heart pt will have continues _ monitoring
Cardiac
What to teach pt to report on Inotropics
Chest pain/palpitations
SOB
burning/pain at IV site
numbness or tingling in extremities
Sympathomimetic for anaphylaxis 101
Epinephrine (Adrenalin)
Nonselective adrenergic agonist
Supports system by preventing hyperresponse
Assessment for epinephrine use in anaphylactic shock
Vitals
Lungs
Renal (BUN, creatinine)
LOC
Goals for patient with anaphylactic shock
Client will report itching SOB
Maintain urine output at 50ml/hr
Maintain Systolic BP at 90mmHg
Client will remain A&O
Preload
Venous blood return to the heart
Substances to increase blood volume
PRBCs
Albumin
Normal saline
Substances to decrease blood volume
Diuretics
Ace inhibitors
Substances to increase venous dilation
Nitroglycerine
Ca+ channel blockers
Clonidine
Morphine
Substances to decrease venous dilation
Dobutamine
Contractility
Forcefulness of contractions
Substances that increase contractility
Digoxin
Dobutamine-dopamine
Milrinone
Afterload
Work required to open aortic valve and eject blood
RESISTANCE to flow in arteries
Substances that increase afterload
HIGH dose of dopamine
Substances that lower afterload
Ace inhibitors
Nitro
Ca+ channel blockers
Beta blockers
Normal heart rate
60-100 bpm
Substances that lower HR
Beta blockers
Ca+ channel blockers
Substances that increase HR
Atropine
Dopamine
5 steps of the electrical pathway of the heart
SA node
AV node
Bundle of His
Left/right bundle branches
Purkinje fibers
Atrial depolarization initiated by the SA node causes the _ wave
P
After depolarization the impulse in delayed at the AV node
this is the _ segment
actually ends at _
PR segment
PQ
Ventricular depolarization begins at the apex, causing the _ complex.
This is also where… occures
QRS
Atrial repolarization
the _ segment marks ventricular depolarization
ST segment
Then ventricular repolarization begins at apex casing the _ wave
T
MI
CRUSHING s/s
Chest pain
Radiating to left arm jaw back
Unrelieved by nitro
Sweating
Hard to breath
Increase in HR and BP
N/S
Getting anxious
MI s/s women excpetion
No chest pain
paint is lower, just above abdomen
MI and diabetic neuropathy
Silent MI due to damaged nerves not feeling pain
Labs 1hr with MI
Myoglobin in blood
Labs 2-4hr with MI
Troponin is released at 0-0.4ng/ml
Labs 4-6hr with MI
CKMB is released at 0-0.4ng/ml
24-36h post MI
Inflammation and neutrophils
Could lead to
Pericarditis (Friction rub)
Pump failure
Cardiogenic shock
Arrhythmias
STEMI
ST elevated myocardial infarction
on EKG
ST segment elevated
NSTEMI
Non-ST elevated myocardial infarction
on EKG
ST will depress or invert
If ST slopes down or stays horizontal before coming up for the T, this indicates
Ischemia
MI first meds
AONM
Aspirin
O2
Nitro
Morphine
With MI time is
Muscle
What to assess in MIs
Chest pain
Cardiovascular system
Bedside monitoring
Blood ressure
Resp sounds
What to assess for in cardiovascular system with MI
12 lead EKG
ST elevation/depression
T waves
What is continuous bedside monitoring for MIs
Telemetry
What lung sounds will you hear in MIs
crackles
fluid overload due to heart dying
blood is backing up
basic interventions for MI
O2 2-4L
Working IV
Bedrest
MI labs
Troponin
CKMB
What to do in first 10 min of MI pt arrival
Vitals
O2 sta
IV access
12 lead ECG
Blood sample
Fibrinolytic therapy is used for what MIs
when to be given
STEMI
within 12h of symptom onset
Fibrinolytic MOA
Breaking down of clots
Fibrinolytic med contradictions
Post OP
Hemorrhage
Ulcers
Pregnancy
Acute Angina means
Artery Blockage
Cardiac Complication
Most common anticoagulants
Heparin
Lovenox
What to monitor with Antigcoagulants
PTT
Normal 25-35
Therapeutic 60-80
Antiplatelet meds 101
Decrease platelet aggregation
Aspirin
Plavix
Aspirin
Plavix
side effects
asa GI bleed
Plavix - Thrombocytopenia purpura
Stop antiplatelet meds like aspirin and plavix how many days before surgery
5-7
Morphine for chest pain route
IV ONLY
Nitroglycerin 101
Vasodilates coronary arteries
Increases blood flow
Nitro watch for
Headache
Flushing
Dizziness
How to monitor pt on nitro
MUST monitor
BP
EKG
Chest pain
Ace inhibitors 101
“April”
Blocks RAAS system
Vasodilator
Decreases BP and workload
ACE side effects
Nagging cough
K+ increase
Arbs ArTan 101
side effects
Specifically block angiotension II part of RAAS
Vasodilators
also increase K+
Statins 101
Lower cholesterol LDL
increases HDL
What to monitor with Statins
MUSCLE Pain
CPK level - indicate muscle breakdown
LIVER function
Ca+ channel blockers 101
Blocks calcium from entering smooth myocardial muscles = vasodilation
Ca+ channel blocker meds
Norvasc
Cardizem
Ca+ channel med side effects
Hypotension
Gum enlargement (oral hygiene)
Peak or hyper acute Ts indicate
MI
EBT
Electron Bean CT
Echocardiography
Detects Heart Disease in earliest stages 2-6
Only detects later stages only 5-6
Other forms of heart health monitoring include
Heart cath
Exercise stress test
Tetralogy of fallot
PRAV
CYANOSIS
Ventral septal defect
Aortic override
Pulmonary stenosis
Right ventricular hypertrophy
The degree of CYANOSIS with tetralogy of fallot depends on the
Size of the ventricular septal defect
Degree of ventricular outflow obstruction
Obstruction of blood flow from right ventricle to the pulmonary artery results in deoxygenated blood being shunted across the … and in to the
Ventricular septal defect
Aorta
Ventricular outflow obstruction can occur at any of the 3 levels
Pulmonary valve stenosis
Infundibular stenosis
Supra-valvular stenosis
In tetralogy of fallot the right ventricle eventually becomes
Hypertrophied
At birth with tetralogy of fallot TOF, neonates O2 sat is
Normal, then decreases
When is cyanosis initially observed in TOF
crying and exertion
Other TOF S/S
Polycythemia (^RBC)
Exercise intolerance
Tachypnea
LOC
TOF home treatment
Soothe
place in knee to chest position
TOF hospital treatment
Knee to chest
Morphine sedation
O2
Beta-blockers
Phenylephrine to increase vascular perfusion
Diagnosing TOF
Auscultation
CRX
ECG
Cardiac cath
Auscultation and TOF
Harsh systolic ejection mrmur
CXR and TOF
Boot shaped heart
(right vent hypertrophy)
ECG and TOF
Doppler study and color flow mapping
Cardiac catheterization and TOF MOST DIFINITIVE DIAGNOSTIC
before surgery to ID number of septal defects
Med management of TOF
O2 sat
Growth and development
Monitor hyper cyanotic spells
Endocarditis prophylaxis
Restrict stranuous activity
Life long TOF care
Assess R ventricular outflow
Monitor exercise tolerance
Monitor arrhythmias
TOF complications
Hypoxia
Hyper cyanotic spells
CHR
Polycythemia
Arrhythmias
Nursing and TOF
Assess vitals pulses cap refil (standing sitting lying)
Monitor cyanotic attacks
Knee-chest
Monitor during exercise
Monitor intake and output
VSD Ventricular septal defect
Hole in the wall of 2 ventricles
Pulmonary stenosis
Narrowing of pulmonary valve resulting in low blood volume reaching lungs
Right ventricular hypertrophy
Right ventricle muscle thickens up
Overriding aorta
Aorta located over VSD, as such O2 poor blood gets in to aorta
Mothers risk factors for TOF
Rubella
Viral infections
Poor nutrition
Age over 40
Diabetes
tet
blue spells due to acute cyanosis or hypoxia
TOF can result in
Emboli
Seizures
LOC
TOF psych problems
Stress
Depression
Substance abuse
School problems
Non-compliance with meds in teens
During crying or feeding TOF baby’s skin will turn “tet”
Blue
TOF treatment
Beta blockers
O2
squatting - increases afterload
fluids
TOF surgeries
VSD closure
Complete repair
Palliative shunt
Modified blalock - accesses pulmonary artery but also distorts it
Consequences of total correction surgery
less than 3% mortality
CHF
heart block
sudden death
What to monitor for in TOF correction surgery post op
S/S of rejection
Infection
side effects of immunosuppression meds