Shock + Arrhythmias Flashcards
Hemodynamic findings in the different types of shock
(CVP, PCWP, SVR( Hypovolemic - dec, dec, inc Cardiogenic -LVF - norm, incr, incr -RVF - incr, norm, incr -Both - inc, inc, inc Distributive -Early - dec, dec, dec -Late - inc, inc, dec Obstructive - inc, inc, inc
Type of shock w/ highest mortality
Cardiogenic - 65-90%
Downstream effects of shock for types of shock
all similar - ischemia, decreased perfusion
Stages of Shock
Initial - hypoxia, lactic acidosis Compensatory - catecholamine release, cytokine release, hyperventilation Progressive - microsludging, increased blood viscosity, metabolic acidosis, MODs Refractory - irreversible organ and tissue damage, ATP to adenosine
Systemic response to shock
Increased CO Tachypnea Decreased renal, GI, UT function Blood shunting to vital organs Vasoconstriction
Organs and their damage
Kidney - tubular necrosis Lung - ARDS Liver - elevated enzymes, congestion GI - ischemia, hemorrhage, peritonitis
LV myocardial tissue and cardiogenic shock
Loss of >40% of LV tissue = correlates w/ cardiogenic shock development
Cardiogenic shock; hemodynamics
Systolic BP of >90mmHg or loss of >30 mmHg Reduced CI Increased PCWP
Cardiogenic shock; treatment
If BP <90 mmHg - use positive inotropes to stabilize -Increase filling time -Increase perfusion and coronary perfusion —-Vasopressors - NE, Epi, Vasopressin —-Positive inotropes - dobutamine, dopamine, milrinone —-IABP, assist devices *Use inoconstrictors - NE, Epi, dopamine (NeED
Cardiogenic shock; myocardial damage
Decreased CO = tachycardia = increased myocardial O2 demand Increased wall stress Lactic acidosis - damages myocardium ALL COMPENSATORY MECHANISM LEAD TO INCREASED O2 DEMAND AND FURTHER DAMAGE
Cardiogenic shock; compensation
SNS activation RAAS activation Overall increase in preload and afterload = increased O2 demand = increased damage and worsening shock
Cardiogenic shock; diagnosis
Lactic acid levels - correlate w/ mortality Echo - fast, quick diagnosis
Septic shock; stages
SIRS to Sepsis to Severe Sepsis Septic Shock to MODs
Septic shock; SIRS
Two of the following criteria -Tachypnea -WBC 12000 -Tachycardia -Hyperthermic or Hypothermic
Septic shock; Sepsis criteria
SIRS + presence of an infection
Septic shock; Septic shock criteria
Presistent hypotension; SIRS + Infection + Hypotension
What is MODs (septic shock)
Multiple organ dysfunction syndrome -Primary - directly injured by infection -Secondary - due to host response to infection; inflammation
What is special about septic shock?
All other forms of shock can lead to septic shock
Septic shock treatment
Fluid resuscitation: use crystalloids –renal damage –use albumin if high levels of crystalloids are indicated Vasopressors -NE = first choice -add vasopressin if needed Dobutamine - if myocardial dysfunction occurs W/in 3 hours - measure lactate level, empirical Ab therapy, crystalloid if hypotensive or lactate > 4mmol/L W/in 6 hours - apply vasopressors, remeasure lactate
Hypovolemic shock; hemorrhagic shock therapy
Volume therapy -crystalloids, albumin, etc. -Use blood products if O2 delivery < O2 need (class III, IV)
Anaphylactic shock treatment
Volume therapy - crystalloids Epinephrine
What are the supraventricular arrhythmias
Sinus tachycardia Atrial premature beat
SVTs- atrial flutter, atrial fibrillation, paroxysmal SVTs
Paroxysmal SVTs- AVNRT, Atrioventricular reentry tachycardia (WPW and non-WPW)
What is sinus tachycardia
Inc SNS/dec PNS = >100 bpm
Normal EKG/waves
What is atrial premature beat
- due to automaticity or reentry
- 3 or more premature beats = atrial tachycardia
- Abnormal p-wave
What is atrial flutter
-reentry - tricuspid annulus circuit
—-tricuspid caval isthmus
—-counterclockwise -Saw tooth appearance
-Tx
—-rate control
—-rhythm control
———-Flecainide = paradoxical VT; 1:1 A:V conduction ———-Electric cardioversion
What is atrial fibrillation
-multiple reentry circuits and foci - atrial and pulmonary vein
————chaotic
-Tx
—–anticoagulants - CHA2DS2VASc score
—–Rate control
—–Rhythm control - cardioversion if >48 hours
What is AVNRT
- most common paroxysmal SVT -two AV nodal pathways - fast and slow
- two directions
——-down slow + up fast = typical
——-down fast + up slow = atypical
-Tx
——Acute - adenosine, valsalva maneuver, rate control ——Class I and III rhythm control
——Abalation of slow pathway; removal of fast = AV block
What is atrioventricular reentry tachycardia
-Presence of an accessory pathway (fast)
——anterograde = WPW
——retrograde = non-WPW
What is WPW
-Sinus rhythm
——Early ventricular depolarization through accessory path = disorganized, wide QRS
——Late ventricular depolarization through AV node = delta wave
-Tx - DO NOT USE RATE CONTROL
——-Acute = cardioversion
——-IV amiodarone + procainamide
——-Catheter ablation of accessory pathway
What is PVC
- Ectopic ventricular foci
- Wide QRS, no p-wave or retrograde p-wave
- >20% PVCs = systolic dysfunction
- Tx = observation or beta-blocker
What is VT
-3 or more PVCs in series
——–sustained = >30 seconds
——–unsustained = <30 seconds
- Wide QRS + >100 bpm
- Torsades de Pointes = polymorphic VT
——–Acute = Mg, isoproterenol (shortens QT)
——–Chronic = beta-blocker, ICD
-Tx
——-Cardioversion; sedate if patient is stable
What is VFib Tx
-Tx - immediate defibrillation
———IV amiodarone
SNS/PNS effects on ANS regulation
SNS - increase phase 4 slope, decreased threshold
PNS - decreased phase 4 slope, increased threshold, decreased diastolic membrane potential
*PNS dominates at rest
