Shock

Question 1

Shock def

Answer 1

Must have evidence of end organ dysfunction

NOT always associated with low BP

Question 2

Types of shock and where failure occurs

Answer 2

Hypovolemic - not enough preload

Cardiogenic and obstructive - pump failure or blockade

Distributive shcok - vessels divert to wrong place

Question 3

Obstructive vs. cardiogenic shock

Answer 3

Evidence of low CO
Inc JVP (no ev of hypovolemia)
No fever
Myocardial function is PRESERVED (normal EF)

Question 4

Massive PE and pericardial tamponda

Answer 4

PE - emboli obstruct pulm arteries leading to low stroke volume (preload) and failure or RV due to high afterload

Temponade - high pericardial pressure prevents RH filing and reduces RV stroke volume…LV stroke volume also reduced

Question 5

Hypovolemic
Cardiogenic
Obstructive
Distributive

CVP
PWP
CO

Answer 5

CVP - down, normal/up, up, normal/down

PWP - down, up, normal (or down if PE, up if tamponade), normal/down

CO - down, down, down, up in early and down in late

Question 6

CVP

Answer 6

Correlates with RVEDP

Flat neck veins - low RV pre-load…know it is mostlikely volume depletion

Elevated - volume overload, RV hypertrophy, tamponade, pneumothorax, SVC occlusion, or tricuspid stenosis

Question 7

PWP

Answer 7

Left atrial and LV pressure

If low - then dec preload

If high - could be mitral stensosis of pulmonary vein obstruction…couod also be from high pericardial or pulmonary pressures or a non-compliant LV myocardium

Question 8

PWP chest x-ray

Answer 8

13-18 - cephalization of flow…may have cardiomegaly and may get inc pedicle width

18-25 - kerley B lines, hazy borders and central vessels

over 25 - alveolar cardiogenic edema with fluffy opacities

Question 9

CO assessment

Answer 9

Pulse 
Cap refill
Extremities 
Skin for diaphoresis
Sensorium

PLUS - urinary catheter for renal perfusoion and bedside echo

Question 10

Cardiogenic shock

Answer 10

Most due to LV failure

Most get the LV failure within 1st 24 hours…5-7 hours normally

Clinically - shock with peripheral vasoconstriction and high PWP..except with predominant RV infarction where lungs may be clear and the CVP high (look for Kussmaul’s sign)

Question 11

Cardiogenic shock preogression

Answer 11

LV dysfunction…leads to low SV and CO>…compensatory tachycardia causes dec coronary artery filling tim e and inc demand as well as inc LV end systolic and diastolic volumes and pressures leads to inc myocrdsial oxygen demand….dec coronary artery perfusion gradient causes worsening myocardial iscehmia gradient…progressive dysfunction and shock

Question 12

Comps after acute MI

Answer 12

Intiial 24 hours and 3-5 days later

VSD - 90% with murmur, O2 step up in RV

Free ventricular wall rupture - 1/4 with murumur, clear X-ray, tamponade physiology

Pap muscle rupture - 50% with murmur, alveolar dedma, prominent V wave in PWP tracing

Question 13

Pericardial effusion exam and imaging

Answer 13

Heart tones diminished

Pericardial rub present (sometimes0

Lungs clear

Tamponade - inc JVP, low BP, weak pulse

IMaging - Water bottle cardiac silhoutte, clear lungs

Diff from HF by thoracic blood volumes, vascular markings, and presence of edema

Question 14

Massive PE

Answer 14

Blocks conduit from L-R heart

Right chambers will dilate and LV will reduce in size

Echo to differentiate from tamponade

Question 15

Septic shock progression

Answer 15

Symphony of cytokines - recruit immune cells, release toxic radicals, active clotting system, microvessels open to allow immune cell entry, induce NO production, kill bacteria

Out of control - plasma leakage with dec BV, microvessel injury impaires O2 delivery to tissues, maldistribution of blood flow, dec CO and dec BP…organ filure and death

Question 16

Septic shock phases

Answer 16

Early shock - dominanted by vasodilation, inc CO, and catecholamine release…can be HTN but only if good heart

Late shock - poor perfusion, dec CO, refractory hypotension and peripheral vasoconstriction

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