What lung problems can cause a increase in alveolar-capillary membrane thickness

Match the term to the definition

Resperation, Ventalation, Compliense 

A. the air movement into and out of the pulmonary airway

B.The exchange of gas across the capillary membrane

C.The ease of lung inflation

A. Ventalation

B. Resperation

C. Compliense 

Weak inspiratory muscles- MIF < -20

Airway obstruction- CSF pnumonia 

Decreased respiratory drive- TBI, COPD

Increased membrane thickness

Decreased alveolar surface area

Decreased hemoglobin- enemia

Vasoconstriction- ↓ blood flow

Pulmonary shunt

        SaO2 (97%)  +  PaO2 (3%)

(attached to HBG + dissolved in blood)

Vasodilation or vasoconstriction based on tissue needs

How does the autonomic nervous system help controle oxygenation

Stimulation or inhibition of alpha, beta, and dopaminergic receptors in  heart, lungs, vessels

Constricts - arteries, veins, bladder neck and prostatic capsule 

dilation- pupils

(also causes ejaculation)

 ↑ the force of conctaction of the heart

heart- ↑ conduction, rate 

kidney- release of renin (stops vasoconstriction, stops Na reabsorption)

Dilation - arteriols, bronchi

Relaxation- uterus

contraction - skeletal muscle

glycogenolysis- skeletal muscle, liver

dilation- peripheral blood vessels 

Kidneys- ↑GFR, ↑ diuresis

dilation- peripheral blood vessels 

Kidneys- ↓GFR, ↓ diuresis, ↓ blood flow

↓ aldosterone (stops Na retention)

Your pt was ammited after a MVA with multipul fx and numothorax. the pt is on sadation  because of machanical ventalation.Resps are set at 10 bpm.  Today the pt has deleoped a temp of 101.

What factors are increasing this pts O2 consumption

what factors are decreasing?

increasing

hyperthermia, Trauma, Sepsis, anxity/pain  (if no meds given)

decreasing

sedation, inactivity, hypoventalation

How would you determine the adequacy of tissue oxygenation

no presences of lactic acid

SaO2 > 90

PaO2 75-100

PvO2- 40-60

hgb > 12

How is  Pulmonary Status assessed

Arterial blood gases

Respiratory muscle efficiency

Auscultation for aeration

Calculation of pulmonary shunt

What factors affect the  Arterial O2 Status

Cardiac output - Direct or indirect measurement

 Hgb - Availability of O2 binding

 Perfusion- V/Q Mismatch

When that compensatory threshold has been met VO2 drops at the same rate as DO2. At this point, patients have no reserve and are tissue oxygen consumption becomes compeltely dependent on oxygen delivery.

if Hgb is wnl, PaO2 >60, SaO2 > 90

then DO2 is wnl

CaO2 - is the amount of O2 caried to the tissues

CVO2- is the amount of oxygen left over from the tissues that is didn't use

CaO2- VaO2 = AvO2 differences

20mg- 15 mg =5mg

AvO2 differences ÷  CaO2= consumption

                  5mg÷  20mg = 25%

What happens to the Serum lactate levels when the SvO2 is  <40%

levels increase with SvO2 <40%

No

There is significant change of patient’s O2 consumption if SvO2 changes >10% and persists > 10 minutes

Pa02/Fi02 ratio: normal is more than 286, with a value of less than 200 suggesting a large shunt (i.e. 80/.40 = 200)

↓ Co, cellular anaerobic metabolism

possible asymptomatic 

sympathetic stimulated 

(↑ HR, vasoconstrict)

unresponsive to therapy

early: normal

Late: < 90mmHg systolic

early: increased

late: increased rate/weak

early: normal

late: pale

early: cool moist

late: cold

early anxious

late calm 

early: increased and deep

late: increased shallow

Hypovolemic, Transport, Obstructive,  Cardiogenic,

Hypovolemic- Volume Loss, Volume Maldistribution

 Volume Maldistribution- (Neurogenic, Anaphylactic Shock, Septic Shock)

What are the key features of Volume Loss shock?

Vasoconstriction (Increased SVR, PVR)- squeez of vessles

Decreased output (CO, BP, PAP)-

Decreased filling pressures (CVP, PCWP) - low vol.

↑HR and resp.

How is  Volume Loss shock treated?

stop fluid loss

2-3L crystalloid till blood replacement available

position pt wtih legs and head elevated with trunk of body flat. 

What are the key features of Neurogenic shock?

Vasodilation (warm, decreased SVR)

Decreased output (CO, BP)

Decreased sympathetic response (HR)

hypothermia dispight felling warm

How is Neurogenic shock treated?

Treat bradycardia- eppi, atropine, levophed, isoproterenol

vasopressors- eppi, levophed, vasopressen

Fluid resuscitation 

warming measures,

What are the key features of Anaphylactic Shock?

Respiratory distress initially

Vasodilation (warm, decreased SVR)

Decreased output (edema, CO, BP, )

↑ HR

How is Anaphylactic Shock treated?

Airway management

Epinephrine and antihistamines

Fluid resuscitation 

position pt with legs elevated, facilitate ventilation, enhancing volume

What are the key features of Septic Shock

early and Late

EARLY (hyperdynamic phase), Febrile / warm to hot skin

Increased output (HR, BP, CO) ↑ resp

LATE (hypodynamic phase)- Classic shock -  cold, ↓ resp. ↓ CO

Antibiotic therapy - First dose within 1-3 hours depending on circumstances of admission

Fluid resuscitation-  8-12 L first 24 hours

Xygris- stops clotting cascade

Tight BGM control- Insulin gtt for BGM 80-150 (Mortality increased significantly in the presence of hyperglycemia alone.)

Steroids- alows adrenal glands to rest and ↓ inflimation.

What are the causes of Transport shock?

Decreased hemoglobin volume- Anemia, Hemorrhage, Hemodilution (Crystalloid)

Inappropriate hemoglobin binding- Carbon monoxide poisoning, Heavy metal poisoning

What are the key features of Transport Shock

Decreased hct / hgb

Increased carboxyhemoglobin

How is Transport Shock treated?

cristoliods first then blood replacement

Hyperbaric therapy

What are the causes of Obstructive shock

Cardiac tamponade

Pulmonary embolus

Tension pneumothorax

What are the key features of Obstructive Shock

Tamponade - Pulsus paradoxus, Beck’s triad (JVD, muffled heart sounds, hypotention)

Pulmonary embolus - SOB, hypoxia, hypotension

Pneumothorax - Absent breath sounds

↑SV02,PAP,HR 

How is Obstructive Shock treated?

Tamponade - Remove pericardial fluid

Pulmonary embolus - Thrombolytics

Pneumothorax - Chest tube placement

What are the causes of Cardiogenic shock?

Myocardial ischemia

Cardiac structural defect / damage

Cardiac dysrhythmias

Vasoconstriction (cool, increased SVR)

Decreased output (HR, CO, BP, PAP)

Increased filling pressures (CVP, PCWP)

How is Cardiogenic Shock treated?

Support myocardium (IABP, VAD)

Revascularization (thrombolitics)

+ inotropic drugs

Antidysrythmics

vasodilators for reducing preload and afterload

A pt is brought to the ED unconscious and is unclear as to the cause and is in asystole.

What drugs should you prepare to give?

o   Lidocaine

o   Epinephrine (for contractility and anyphylaxis)

o   Atropine (for symptomatic bradycardia)

o   Narcan (antidote for narcotics)

How can you help your pt to Minimize O2 consumption

o   Decrease pain and anxiety

o   Normal temperature

o   Minimize activity

BP +/-  20 mmHg pre-shock state

Temp: WNL

HR: 60 – 100 beats per minute

Alert & Oriented: Glasgow to pre-shock (is one of the best indicators of cardiac output)

How will your pts Urine output

  apper if they are out of shock?

Urine output > 30cc/hr (is one of the best indicators of cardiac output)

septic shock

Which of the following are clinical manifestations of cardiogenic shock:

decreased PAP

decreased right arterial pressure

decrease cardiac index

decrease SVR

decrease cardiac index

(it will have increased PAP, increased right arterial pressure and increased SVR)

which of these is a major consequence of hematological shock:

microvascular thrombus

DIC

ALI

your patient is in shock and is hypotensive. Which of the following medications is most appropriate:

nitroprusside

Phenylephrine

dobutamine

labetalol

Phenylephrine- is a vasoconstrictor

(alpha adrenergic agonist)

(nitroprusside is a vasodilator, dobutamine is a + inotropic drug but has no effect on vasoconstiction, labetalol is a beta blocker)

which of these steps are included in severe Sepsis and septic shock management:

low-dose dopamine for renal protection

keeping blood sugar levels less than 150 mg/dl

. Tripoli for anemia

anti-thrombolytic therapy

which of the following shock states include hypotension despite adequate fluid resuscitation along with perfusion abnormalities such as lactic acidosis and oliguria:

bacteremia

systemic inflammatory response syndrome

multiple organ dysfunction syndrome

septic shock

Your pt valuse are:

(Volume maldistribution)

Your pt valuse are: 

↑SV02,PAP,HR 

Your pt valuse are: 

Your pt valuse are: 

↑HR ,CO/CI,RR, temp, SV02,WBC

(Volume maldistribution)

Your pt valuse are: 

(Volume maldistribution)

Your pt valuse are: 

(Volume Loss)

Your pt has the fallowing S/S:

Pale cool clammy skin, vertigo, confusion, decreased

and dark urine bounding pulse. 

What type of shock are they in

(Volume Loss)

Your pt has the fallowing S/S:

What type of shock are they in

(Volume maldistribution)

Your pt has the fallowing S/S:

Increased carboxyhemoglobin

What type of shock are they in

Your pt has the fallowing S/S:

Massive peripheral dilation

Hypotension, bradycardia, hypothermia and warm dry skin. warmth is lost  due to no vasoconstriction

What type of shock are they in

(Volume maldistribution)

Your pt has the fallowing S/S:

What type of shock are they in

Your pt has the fallowing S/S:

What type of shock are they in

Your pt has the fallowing S/S:

Vasodilation  

(Volume maldistribution)