Shock + Arrhythmias Flashcards

1
Q

Hemodynamic findings in the different types of shock

A

(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

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2
Q

Type of shock w/ highest mortality

A

Cardiogenic - 65-90%

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3
Q

Downstream effects of shock for types of shock

A

all similar - ischemia, decreased perfusion

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4
Q

Stages of Shock

A

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

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5
Q

Systemic response to shock

A

Increased CO Tachypnea Decreased renal, GI, UT function Blood shunting to vital organs Vasoconstriction

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6
Q

Organs and their damage

A

Kidney - tubular necrosis Lung - ARDS Liver - elevated enzymes, congestion GI - ischemia, hemorrhage, peritonitis

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7
Q

LV myocardial tissue and cardiogenic shock

A

Loss of >40% of LV tissue = correlates w/ cardiogenic shock development

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8
Q

Cardiogenic shock; hemodynamics

A

Systolic BP of >90mmHg or loss of >30 mmHg Reduced CI Increased PCWP

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9
Q

Cardiogenic shock; treatment

A

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

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10
Q

Cardiogenic shock; myocardial damage

A

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

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11
Q

Cardiogenic shock; compensation

A

SNS activation RAAS activation Overall increase in preload and afterload = increased O2 demand = increased damage and worsening shock

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12
Q

Cardiogenic shock; diagnosis

A

Lactic acid levels - correlate w/ mortality Echo - fast, quick diagnosis

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13
Q

Septic shock; stages

A

SIRS to Sepsis to Severe Sepsis Septic Shock to MODs

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14
Q

Septic shock; SIRS

A

Two of the following criteria -Tachypnea -WBC 12000 -Tachycardia -Hyperthermic or Hypothermic

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15
Q

Septic shock; Sepsis criteria

A

SIRS + presence of an infection

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16
Q

Septic shock; Septic shock criteria

A

Presistent hypotension; SIRS + Infection + Hypotension

17
Q

What is MODs (septic shock)

A

Multiple organ dysfunction syndrome -Primary - directly injured by infection -Secondary - due to host response to infection; inflammation

18
Q

What is special about septic shock?

A

All other forms of shock can lead to septic shock

19
Q

Septic shock treatment

A

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

20
Q

Hypovolemic shock; hemorrhagic shock therapy

A

Volume therapy -crystalloids, albumin, etc. -Use blood products if O2 delivery < O2 need (class III, IV)

21
Q

Anaphylactic shock treatment

A

Volume therapy - crystalloids Epinephrine

22
Q

What are the supraventricular arrhythmias

A

Sinus tachycardia Atrial premature beat

SVTs- atrial flutter, atrial fibrillation, paroxysmal SVTs

Paroxysmal SVTs- AVNRT, Atrioventricular reentry tachycardia (WPW and non-WPW)

23
Q

What is sinus tachycardia

A

Inc SNS/dec PNS = >100 bpm

Normal EKG/waves

24
Q

What is atrial premature beat

A
  • due to automaticity or reentry
  • 3 or more premature beats = atrial tachycardia
  • Abnormal p-wave
25
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
26
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
27
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
28
What is atrioventricular reentry tachycardia
-Presence of an accessory pathway (fast) ------anterograde = WPW ------retrograde = non-WPW
29
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
30
What is PVC
- Ectopic ventricular foci - Wide QRS, no p-wave or retrograde p-wave - \>20% PVCs = systolic dysfunction - Tx = observation or beta-blocker
31
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
32
What is VFib Tx
-Tx - immediate defibrillation ---------IV amiodarone
33
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