Resuscitation Flashcards
factors contributing to likelihood of sudden cardiac death
CV pathology: CAD, severe LV dysfunction, cardiomyopathy (hypertrophic, arrhytmogenic RV), congenital heart disease, valvular heart disease, cardiac pacemaker and conducting system disease
hereditary channelopathies: Brugada, early repolarization syndrome (ERS), long QT, short QT, catecholaminergic polymorphic VT
risk factors and triggers:
- long term risk factor mgmt: htn, hyperlipidemia, smoking, diabetes, SES
- unstable atherosclerotic plaque: psychological stress, physical activity
who is more likely to survive cardiac arrest (at home or in public)
in public
what is survival of EMS treated cardiac arrest
11.4%
what is surivival of all comers -cardiac arrest (includes DOA)
6.8%
what time of day is AMI and SCD more common
in first few hours upon wakening due to increased sympathetic stimulation
what medication helps prevent SCD
beta blockers especially in patents with CAD with previous MI and low EF
initial rhythm of ventricular fibrillation in cardiac arrest consistent with what etioology
acute coronary syndrome
when to consider ICD in patients with low EF
below 35% EF to prevent SCD
who to consider for ICD
individuals with previous documented cardiac arrest, ventricular fibrillation, hemodynamically significant or nonsustained VT, patients with first degree relative with SCD, one or more recent unexplained syncope, a max LV thickness of 30mm, abnormal BP response to exercise in presence of other SCD risk factors, or high risk children with unexplained syncope, massive LV hypertrophy or family hx of SCD
what is arrhythmogenic right ventricular cardiomyopathy
hereditary form of cardiac muscle disease that is characterized by right-sided heart failure, ventricular arrhythmias of right ventricular origin (i.e., ventricular tachycardia with a left bundle- branch block morphology), syncope, and sudden cardiac death
what ECG changes are seen in arhymogenic RV cardiomyopathy
T wave inversion in right precordial leads (V1-V3)
which congenital heart defects are often associated with sudden cardiac death
aortic stenosis coarctation of aorta Ebsteins anomaly Tetralogy of Fallot transposition of great arteries coronary artery anomalies (anomalous left coronary artery from pulmonary artery) single ventricle
what is the pathophysiology of anomalous left coronary artery from pulmonary artery
the left coronary artery traversing between the aorta and main pulmonary artery
Ischemic symptoms, ventricular arrhythmias, and sudden death can be triggered during exercise as a result of increasing venous return, which dilates the main pulmonary artery and compresses the anomalous coronary artery in the space between the aorta and main pulmonary artery
harsh, late-peaking systolic murmur at the upper-right sternal border with radiation to the neck is found with what lesion
hemodynamically significant aortic stenosis
what sequelae can occur with significant aortic stenosis
effort-induced dyspnea, myocardial ischemia, and ventricular arrhythmias, which can trigger syncope and sudden cardiac death
what is the most common cause of aortic stenosis
bicuspid aortic valve that typically calcifies and narrows its orifice in mid-adulthood or sclerosis/calcification of a tricuspid aortic valve, which can occur in individuals who are older than 70 or 80 years of age
what causes sick sinus syndrome
diffuse degenerative disease of the heart’s electrical generation and conduction system
Sick sinus syndrome affects the heart’s primary pacemaker and can cause intermittent lightheadedness, syncope, or sudden cardiac death
what is sudden arrhythmic death syndrome
udden arrhythmic death syndrome is characterized by sudden cardiac death occurring out of hospital in relatively young adults (mostly men), often during sleep or at rest, usually without any premonitory symptoms (including syncope) and with no anatomic abnormality identified at autopsy.
what is the etiology of Brugada syndrome
autosomal dominant inheritance that results in total loss of function of the sodium channel or in acceleration of recovery from sodium channel activation
what ethnicity most commonly has Brugada
SE asian, and males
ECG changes in early repolarization syndrome
notch-like J wave on the QRS down-slope, followed by upsloping ST-segment elevation, most prominently in the mid to lateral precordium but can also occur just laterally or inferiorly. There is commonly reciprocal ST-segment depression in aVR.
what is characterized by prolongation of the corrected QT interval (QTc), syncope, and sudden
death caused by torsade de pointes and ventricular fibrillation
long QT syndrome
0.35 to 0.44 second is normal
how to calculate QTc
QTm / square root of (R-R)
QTm is the measured QT interval in seconds, and R-R is the interval
between any two consecutive R waves on the electrocardiogram in seconds. Because the QT interval is heart-rate dependent, the formula “corrects” the measured QT interval to a heart rate of 60 beats/min (at which the R-R interval is 1 second)
management of patients of long QT syndrome
avoidance of QT prolonging drugs, high-intensity sports, and refer to cardiology/EP
hereditary long QT syndromes associated with nerve deafness
autosomal recessive - Jervell and Lange-Neilsen syndrome
short QT time
less than 0.34s
causes of long QT
hypokalemia, hypomagnesemia, hypocalcemia, anorexia, ischemia, central nervous system pathology,
terfenadine-ketoconazole combinations, or certain antipsychotic or antiarrhythmic drugs
causes of short QT
hypercalcemia, hyperkalemia, acidosis, systemic inflammatory syndrome, myocardial ischemia, or increased vagal tone or can be inherited in an autosomal
dominant genetic pattern
presentation of catecholaminergic polymorphic VT
Affected individuals have exercise- and stress-related ventricular tachycardia, syncope, and sudden cardiac death, usually in childhood or early adulthood. Although there are no characteristic abnormalities in the electrocardiogram pattern, a significant number of affected individuals have sinus bradycardia that is not otherwise explainable. Almost half of these individuals carry a diagnosis of epilepsy as the cause of their recurrent syncope before the true cause (i.e., catecholaminergic polymorphic ventricular tachycardia) is identified.
premonitory symptoms in SCD
most common premonitory symptoms reported by sudden cardiac death survivors or family members of victims are chest discomfort, dyspnea, and “not feeling well
what did the Cardiac Arrhythmia Suppression Trial show
potent class I sodium channel–blocking antiarrhythmic drugs (encainide, flecainide, and moricizine) are proarrhythmic and paradoxically increase the odds of developing sudden cardiac death, as compared with placebo, in patients at relatively low risk for death
prevention of SCD techniques
The benefits of β-blockade, sotalol, and amiodarone in decreasing mortality from sudden cardiac death pale in comparison with the protective effects of the implantable cardioverter-defibrillator in high-risk patients,36 including those who have been resuscitated from ventricular fibrillation or cardioverted out of sustained ventricular tachycardia.37 Although these devices are expensive to insert, their effectiveness over conventional therapy results in a cost of less than $30,000 per year of life saved, which makes them relatively cost-effective for implantation in high-risk individuals.
what did Public Access Defibrillation randomized clinical trial show
laypersons trained and equipped to use automated external defibrillators in public places can double survival to hospital discharge compared with that which can be achieved by layperson rescuers who can only perform CPR while awaiting EMS arrival
survival of cardiac arrest if initial rhythm not VF/pulseless VT
<5%
define bradyasystole
ventricular rate <60 beats/min or periods of absent heart rhythm (asystole)
what is primary vs. secondary bradyasystole
Primary bradyasystole occurs when the heart’s electrical system fails to generate and/or propagate an adequate number of ventricular depolarizations per minute to sustain consciousness and other vital functions. Secondary bradyasystole is present when factors external to the heart’s electrical system cause it to fail (e.g., hypoxia).
causes of bradyasystolic arrest
myocardial ischemia or infarct sick sinus syndrome hypoxia hypercarbia stroke opiates, B-blockers, CCBs, adenosine, or parasympathetics
what is the underlying pathophysi of PEA
a marked reduction in cardiac output due to either profound myocardial depression or mechanical factors that reduce venous return or impede the flow of blood through the cardiovascular system
conditions that cause PEA
hypovolemia tension pneumothorax pericardial tamponade pulmonary embolism massive myocardial dysfunction due to ischemia or infarction, myocarditis, cardiotoxins, etc. drug toxicity (BBs, CCBs, TCAs) profound shock hypoxia acidosis severe hypercarbia auto PEEP hypothermia hyperkalemia pseudo-PEA
4 main mechanisms of shock
hypovolemic
obstructive
distributive
cardiogenic
cardiac output determined by
CO= HR x SV
MAP is determined by
MAP = CO X SVR
oxygen delivery is determined by
oxygen delivery = cardiac output x arterial oxygen content
Do2 = CO × [(1.39 × Hb × Sao2) + (Pao2 × 0.0031)]
Do2 is the amount of O2 delivered to the tissues per minute. A normal value is 1000 mL O2 per minute
how to calculate arterial oxygen content
Arterial Oxygen Content = Amount of Oxygen in the Blood
Cao2 = (1.39 × Hb × Sao2 ) + (Pao2 × 0.0031)
how to calculate oxygen consumption
Oxygen Consumption = Cardiac Output × (Arterial O2 Content – Venous O2 Content) V̇o2 = CO × (Cao2 – Cvo2)
how to calculate shock index
SI = HR/ SBP
A normal value is 0.5–0.7. A persistent elevation of the shock index (>1.0) indicates an impaired left ventricular function (as a result of blood loss or cardiac depression) and carries a high mortality rate.
hemodynamic changes seen in hypovolemic shock
decreased preload
increased SVR
decreased CO
etiologies of hypovolemic shock
hemorrhage
capillary leak
GI losses
burns
hemodynamic changes seen in cardiogenic shock
increased preload
increased afterload
increased SVR
decreased CO
aetiologies of cardiogenic shock
MI, dysrhythmia, heart failure, valvular heart disease
hemodynamic changes in obstructive shock
decreased preload
increased SVR
decreased CO
aetiologies of obstructive shock
tension pneumothorax, PE, pericardial tamponade
hemodynamic changes in distributive shock
decreased preload
decreased SVR
mixed CO
aetiologies of distributive shock
sepsis, anaphylaxis, neurogenic
physical examination findings in shock
temp: hyper or hypothermia may be present
HR: usually elevated, can be bradycardic due to hypogylemic, BB use or pre-existing cardiac dz.
SBP: may increase slightly initially when cardiac contractility increases,then decreases as shock progresses
DBP: may rise early in shock and then fall when cardiovascular compensation fails
pulse pressure: increases in early shock, then decreases before SBP begins to drop
MAP: often low <65
CNS: acute delirium, restlessness, disorientation, confusion, and coma secondary to decreased CPP
skin: pale, dusky, cyanosis, swearing, altered temp, increased cap refill time of > 2-3s
CV: may have flat or distended JVP based on type of shock, tachycardia and arrhythmia, S3 in high output states, decreased coronary perfusion can lead to ischemia, decreased ventricular compliance, increased left ventricular diastolic pressure, and pulmonary edema
resp: Tachypnea, increased minute ventilation, increased dead space, bronchospasm, and hyper- or hypocapnia with progression to respiratory failure
splanchnic organs: Ileus, GI bleeding, pancreatitis, acalculous cholecystitis, and mesenteric ischemia can occur due to low flow states
renal: decreased GFR
metabolic: Hyperglycemia, hypoglycemia, and hyperkalemia; as shock progresses metabolic acidosis occurs with resp. compensation
initial investigations in shock
CBC, lytes, urea/Cr, lactate, glucose, coags, ABG, transaminases/LFTs ECG UA CXR blood cultures; other appropriate cultures pregnancy test cortisol level imaging if indicated
use of POCUS in shock
Cardiac Evaluation with Sonography in Shock protocol looks at cardiac function, inferior vena cava dynamics, pulmonary congestion, sliding and consolidation, abdominal free fluid, abdominal aortic aneurysm, and leg venous thrombosis to assist in differential diagnosis generation or narrowing
end points of resuscitation in ED
goal- directed approach of MAP >65 mm Hg, central venous pressure of 8 to 12 mm Hg, Scvo2 >70%, and urine output >0.5 mL/kg/h during ED resuscitation of septic shock
questions to ask if patient has persistent shock or hypotension despite resuscitation
is patient monitored properly?
equipment malfunction? ie. dampening of art line
is the IV tubing connected and running well
are the vasopressor infusion pumps working
are the vasopressors mixed adequately and in correct dose
does mentation/clinical appearance match degree of hypotension
is pt. adequately volume resuscitated
did the pt get a pneumo after placement of central venous access
has pt been assess for occult penetrating injury
is there hidden bleeding from a ruptured spleen, large vessel aneurysm, or ectopic pregnancy
does the pt have adrenal insufficiency ?
is the pt allergic to medication given or taken before arrival?
is there cardiac tamponade in the dialysis or cancer pt?
is there associated AMI, dissection, or PE
when to use bicarb in shock
In settings of a low pH and when evidence of decreased contractility (despite ongoing resuscitative efforts) or development of a dysrhythmia, partially correct the metabolic acidosis, either with sodium bicarbonate boluses or a drip.
Consider situations, such as end-stage renal disease and renal tubular acidosis, that cannot reclaim bicarbonate through normal renal processes and whether bicarbonate may be indicated.
adverse effects of bicarb
Bicarbonate administration shifts the oxygen-hemoglobin dissociation curve to the left, impairs tissue unloading of hemoglobin-bound oxygen, and may worsen intracellular acidosis.
etiology of trauma-induced coagulopathy
combination of factors beginning with loss of coagulation factors from hemorrhage, followed by hemodilution from crystalloid resuscitation, and then exacerbated by acidosis (evidenced by a base deficit) and hypothermia that occur during the course of ongoing hemorrhage and resuscitation.
define anaphylaxis
- Urticaria, generalized itching or flushing, or edema of lips, tongue, uvula, or skin developing over minutes to hours and associated with at least one of the following:
Respiratory distress or hypoxia
or
Hypotension or cardiovascular collapse
or
Associated symptoms of organ dysfunction (e.g., hypotonia, syncope, incontinence)
2.Two or more signs or symptoms that occur minutes to hours after allergen exposure:
Skin and/or mucosal involvement Respiratory compromise
Hypotension or associated symptoms Persistent GI cramps or vomiting
3.Consider anaphylaxis when patients are exposed to a known allergen and develop hypotension
