Block 2 Flashcards
BP = what two parameters?
CO x SVR
SVR is determined by what?
Radius of resistance vessels
Cardiac = what two parameters?
SV x HR
CO
SVR
SV
HR
Which one is directly influenced by preload, contractility, and afterload?
SV
SVR is proportional to Afterload
Increase of (preload/contractility/afterload) increases SV
All except afterload
Increased afterload decreases SV
Increased afterload will INCREASE SVR though
Cardiac output adjusted for body weight is known as..?
Cardiac Index
= CO/BSA
What is preload? Afterload?
Preload = pressure/volume in ventricles as they fill up
Afterload = the pressure the left ventricles have to overcome for blood to flow, resistance to blood flow
How do fluids and vasopressors affect preload/afterload?
Fluids will increase preload (diuretics will decrease it)
Anything that causes vasoconstriction (like vasopressors) will increase afterload (so vasodilation will decrease it)
Increased preload = Increased end diastolic volume = Increased contractility except in what patients?
Heart Failure, stroke volume hardly changes
What are the 4 types of shock?
Hypovolemic
Cardiogenic
Obstructive
Distributive
Distributive
Hypovolemic
Cardiogenic
Obstructive
Which one has vasodilation?
Distributive
Distributive
Hypovolemic
Cardiogenic
Obstructive
Which one has vasoconstriction?
Hypovolemic (arterial side usually)
Distributive
Hypovolemic
Cardiogenic
Obstructive
Which one has a formation of a pericardial tamponade?
Obstruction
Distributive
Hypovolemic
Cardiogenic
Obstructive
Which one is seen in patients with possible edema?
Cardiogenic
Distributive
Hypovolemic
Cardiogenic
Obstructive
Which one is caused by ventricular failure?
Cardiogenic
CVP
PCWP
CO
SVR
How does hypovolemic shock affect these values?
Low fluid, therefore CVP and PCWP decreased
CO is down as a result, but SVR will compensate (vasoconstriction) and increase
CVP
PCWP
CO
SVR
How does cardiogenic shock affect these values?
Fluid status is usually increased, so CVP and PCWP are increased.
CO is still down as a result and SVR will compensate by increasing
CVP
PCWP
CO
SVR
How does obstructive (pericardium tamponade) shock affect these values?
Same as cardiogenic but different from PE obstructive shock
CVP
PCWP
CO
SVR
How does obstructive (systolic contraction/PE) shock affect these values?
Pretty much the same as obstructive and cardiogenic, but PCWP may decrease or be normal
CVP
PCWP
CO
SVR
How does distributive shock affect these values?
No treatment = everything decreased
With treatment = everything increased except SVR
Immediate goals of:
MAP
CI
MAP > 65
CI >2.2
Immediate goals of:
Hgb
O2 sat
Lactate
Hgb > 7
O2 sat >92%
Lactate < 2
Osmolarity equation?
2xNa + (BUN/2.8) + (Glucose/18)
Compared to NS, what does LR have?
Less sodium
Potassium
Calcium
Less chloride
Lactate
Compared to NS, what does plasmalyte-A or Normosol-R have?
Less sodium (but more than LR)
Potassium (higher than LR)
Less chloride (even less than LR)
Magnesium
Acetate
Gluconate
How does administering albumin help with fluids?
Draws fluids from extravascular/intracellular space to intravascular space
What did the SAFE trial say?
ICU patients, fluid resuscitation with albumin vs NS
No difference in 28-day mortality
Subgroup analysis with traumatic brain injury had a higher mortality with albumin (but wasn’t the focus of the trial)
Use crystalloids (NS) for initial resuscitation vs colloids)
Another study (CRISTAL) showed the same results except they did it with more crystalloids and colloids
What have studies shown about using more balanced crystalloids (LR, plasma-lyte) vs NS?
No mortality differences, but less AKI in LR, plasma-lyte groups
Activation of alpha 1 and 2 in the vascular smooth muscle/CNS cause vaso(constriction/dilation)
Alpha 1 = constriction
Alpha 2 = dilation in CNS, constriction in vascular space
Activation of beta 1 and 2 in the vascular smooth muscle cause vaso(constriction/dilation)
Beta 1 = increased chronotropy (cardiac muscle)
Beta 2 = dilation
Activation of dopamine and phosphodiesterase in the vascular smooth muscle cause vaso(constriction/dilation)
Dopamine = constriction
Phosphodiesterase = dilation
Activation of vasopressin 1 and 2 in the vascular smooth muscle cause vaso(constriction/dilation)
1 = constriction
2 = increases blood volume (water retention in kidneys)
Activation of alpha receptors have more of an affect on (CVP/SVR)
SVR; constriction of vascular smooth muscles typically occur on the arterial side
Venous side (CVP) doesnt change shape much
Vasopressin
V1 vs V2 receptors
Which one increases SVR? What does the other one do?
V1
V2 - increased blood volume
Both ultimately increases arterial pressure
Norepi Epi Phenylephrine Vasopressin Dopamine Dobutamine Isoproterenol Milrinone
Which drug can cause reflex bradycardia?
Phenylephrine
It targets only alpha and body will compensate by lowering HR
Norepi Epi Phenylephrine Vasopressin Dopamine Dobutamine Isoproterenol Milrinone
Which drug has differing receptor effects depending on dose?
Dopamine
Low - Dopamine and small beta 1
Medium - Dopamine, Beta 1 and small beta 2
High - Dopamine, Beta 1,2, and alpha
What receptors do norepi and epi target?
Norepi - alpha + beta 1
Epi - alpha, beta 1 + 2
Norepi Epi Phenylephrine Vasopressin Dopamine Dobutamine Isoproterenol Milrinone
Which drug is a PDE3 inhibitor?
Milrinone
What targets do dobutamine and isoproterenol target?
Both target beta 1 and 2
Dobutamine however targets alpha which can sort of prevent hypotension
Norepi Epi Phenylephrine Vasopressin Dopamine Dobutamine Isoproterenol Milrinone
Which drugs could cause hypotension?
Dobutamine
Isoproterenol
Milrinone
How is cardiogenic shock treated?
Treat the underlying cause
Small amounts (250-500ml) of crystalloids in absence of pulmonary edema
Diuretics (caution)
Norepi is first line
You may do norepi + another vasopressor + inotropes (watch for hypotension)
Mechanical devices if nothing else works
Cardiogenic shock goal?
MAP >60-65mmHg
What did the SOAP II trial show?
Higher mortality rate with dopamine use in cardiogenic shock. That’s why dopamine is not recommended in treatment
Also causes more arrhythmias
How is distributive shock treated?
Crystalloids and then norepi as first line BUT you may add vasopressin or epi on top
Target MAP is at 65mmHg
Steroids can be used but is controversial
Antimicrobials within 1 hr for 7-10 days
What condition is common in distributive shock?
Sepsis
What is the SIRS criteria?
Must be ≥2 to be qualified for sepsis
Temp >38 or <36
HR>90
RR>20
WBC>12 or <4
What does the SOFA score look into?
Organ failure assessment (used in the newest sepsis scoring assessment)
Whats in the qSOFA scoring?
RR≤22bpm
Altered mentation
SBP≤100mmHg
≥2 suggest poor outcome
How much crystalloid should you give in distributive shock and for what reason?
30ml/kg
For hypotension or lactate ≥4
What is the ACTH stimulation test?
Uses cosyntropin to stress adrenal glands to measure increased cortisol levels
≤9 is insufficient
What did the CORTICUS study show?
When given 50mg q6hrs x 5 days it reversed shock quicker but also increased hyperglycemia
What did the HYPRESS trial show?
Corticosteroids for refractory shock only
If patient needs steroids, what is the dose?
50mg q6 hrs
or
100mg q8 hrs
Pros and cons of angiotensin 2 drugs?
Improve MAP within 3 hours but tapers off
AE of thrombotic and peripheral ischemia
Obstructive shock treatment?
Modest fluids (diuresis for pulmonary HTN, fluids for PE)
Vasopressors (NE)
Thrombolytics for MASSIVE PE; Alteplase 100mg (90 for stoke) over 2 hrs
Hypovolemic shock treatment?
<1.5 L of isotonic crystalloids
Adjunct vasopressors if life-threatening hypotension
Hemostatic resuscitation eat at least 2 erythrocyte like 1 plasma:1 PLT
Distributive
Hypovolemic
Cardiogenic
Obstructive
Which one contains sepsis, neurogenic, and immune mediated shock?
Distributive
What are the indications for mechanical ventilation?
Hypoxia
Hypoventilation
Respiratory fatigue (anxiety, dyspnea, status asthmaticus)
Seizures
GCS<8
What is FiO2?
Fraction of inspired oxygen
Ranges from 21% (environmental air) to 100%
What does the TLC ventilator mean?
Trigger - when breath starts
Limit - how fast breath enters
Cycle - when breath changes from inhalation to exhalation
What does the continuous mandatory ventilation do?
Ventilator does all the work
Patient cannot trigger own breath
Which ventilator option is mode of choice for ARDS?
Assist-control ventilation
What does a assist-control ventilation do?
Assist pt to a full breath. Triggers when pt tries to inhale, if there is no breath, then it’ll act as a continuous mandatory ventilator
Causes hyperventilation and respiratory alkalosis
What is a synchronized intermittent mandatory ventilator?
No assistance when patient triggered breath occurs
Allows them to contribute to their own respiratory effort
What is a pressure support ventilator?
Full spontaneous respiratory effort by patient
What is continuous positive airway pressure?
No inspiratory assistance
Can be given to intubated or non-intubated pt via mask
What are the noninvasive ventilators?
BiPAP (usually for acute care)
CPAP
ARDS is caused by a triad of symptoms which are:
Dyspnea
Tachypnea
Hypoxemia
What is the Berlin Definition of ARDS?
Within 1 week
BILATERAL opacities
Not explained by HF or fluid overload
PaO2:FiO2 <300
Mild 201-300
Severe ≤100
Moderate inbetween
Risk Factors of ARDS?
- Pneumonia
- Sepsis
- Trauma
Mechanical ventilation and ARDS?
TV
PaCO2
PEEP
Tidal volume = 4-6ml/kg IBW
Permissive hypercapnia using A/C mode (PaCO2 50-55mmHg
PEEP of 5cm H20
What are the pharmacological treatments used in ARDS?
Nimbex
EARLY use of low/moderate dose of methylprednisolone or decadron
