shock

preload

-stretch in walls of ventricles during diastole

ex. hypovolemia = less preload

afterload

-resistance ventricles have to push against to get blood out of heart (lungs or systemic)

*if blood vessels are dilated, decrease in after load, less resistance for blood to push against

contractility

-pumping action, force of contraction

-use dig for contractility

-also calcium levels (use CCBs) -norepinephrine, and thyroid hormones impact

cardiac output formula *

CO= HR x SV

cardiac output

-volume of blood ejected in 1 min

-normal 4-8 L

stroke volume

-volume of blood ejected during each systole

(affected by preload, after load, and contractility)

shock

-decreased blood flow to organs and tissues causing inadequate oxygenation

-cellular metabolism: inconsistent oxygen & metabolic waste builds up

pulmonary artery catheter waveforms

-use to obtain pressures in heart

-look at preload, afterload, and contractility

-go in through vein to pulm art.

-can also get RV, RA pressures

to get into left ventricle

-go through artery

what does preload relate to

-pressure in right atrium

-measure pre load through venous return and compliance of ventricles

CVP (central venous pressure)

-2 to 6 mmHg

-how we measure preload (pressure in RA)

if CVP low

-less then two

-need more volume in circulatory system --> give fluids or blood

*will look dry mucous membranes, decreased urine output, low BP, pale, tachycardia

**fluids/ blood products

if CVP high

-more than 6

-fluid overloaded

-will see SOB, edema, crackles in lungs

**diuresis

with CVP each complex must have

waveform

*TELLS US BODY IS BEING PERFUSED

to measure contractility

-cardiac cath: direct measurement of flow of blood & pressures in heart

right= venous

left= arterial (EF from left ventricle)

-echo: structures and functions

pulmonary artery wedge pressure

-evaluate left ventricle and overall cardiac function

measuring afterload

-RV= PVR (pulmonary)

-LV= SVR (systemic)

**MAP

MAP

70-100

(average pressure in arterial circulation throughout cardiac cycle)

calculating MAP

(SBP + 2DBP)/3

arterial pressure monitoring

Invasive technique to monitor arterial blood pressure

**transducer must be at 4th intercostal space, zeroed, fluids in bad

*if this is low take manual BP (assess are they confused/ drowsy?)

if transducer too high or too low

too high= falsely low BP

too low= falsely high BP

*must be at 4th intercostal space

lifespan considerations neonates/ infants

-immature heart sensitive to volume and pressure

-high metabolic demands/ little cardiac reserve capacity

-HR slows throughout childhood

***hypotension in neonates = sign of late shock

pregnancy lifespan considerations

-SVR (after load)= elevated HR

-blood volume = increased HR

-CO peaks at 30-50% above preg levels

-lay on left side! (can do CPR on left side)

lifespan considerations with aging

-CO with stress = longer lasting tachycardia

-increase SVR, increase BP, decrease CO

clinical signs of shock

-sustained drop in MAP

-inadequate oxygen tissue perfusion

-anerobic metabolism

-metabolic acidosis

-cell death eating to tissue and organ death

Class I early shock

-less than 10mmHg from their normal MAP

-circulating volume decreased

s/s of early shock

-elevated HR

-increased CO (strong contractility)

-Increase arterial BP

-increase SVR due to elevated BP

compensatory shock

-MAP drops 10-15 mmHg below normal

-circulating volume drops 15-30% >1000mL

comp. mechanisms= maintain BP and tissue perfusion, prevent cell damage

*this can only last for short pd of time

compensatory mechanisms (stage II of shock)

1. stimulation of SNS: release epi and norepinephrine

**vasoconstriction of blood vessels/ skin that decreases perfusion

**vasodilation of heart, respiratory and skeletal muscle (increase HR, force of contraction of heart, RR)

2. renin- angiotensin response

*decrease blood flow to kidneys, renin release and converts to angiotensin II, kidneys reabsorb water and sodium, lose potassium, increase vasoconstriction and increase SVR, **raises BP

3. andrenal glands release aldosterone

4. ADH relases

5. fluid shift

decompensated/ progressive shock

-sustained decrease in MAP >20 mmHg below normal

-30-40 % blood volume loss

-comp. mechanisms unable to maintain MAP

***VASOCONSTRICTION everywhere impeding blood flow and causing poor oxygenation

***LACTIC ACID production

(anaerobic metabolism)

what we will see with decompensated shock

-tachycardia, vasoconstriction, poor perfusion to skin, skeletal muscles, kidneys, GI (starts in periphery and moves up trunk)

-heart and brain start to become hypoxia, sends organs into ischemia and anoxia

*rapid treatment to live

refractory shock

-irreversible

-tissue anoxia and cell death throughout body

-no effective treatments

-death of cells, tissues, organs then body

neurologic effects of shock in each stage

-decrease cognition, LOC

early--> restless, agitated

decompensated --> lethargy

refractory --> coma

cardiovascular effects of shock in each stage

-tachy, thready pulse, MAP changes, steady decrease in CO

early--> no profound changes

decompensated --> slight increase in BP and HR, thready pulse

refractory stage --> MAP

resp effects of shock

-tachypnea

-resp acidosis

can have ARDS

GI effects of shock

-hypoactive BS

-paralytic ileus

-ulcerations of GI mucosa

-bowel necrosis

GU effects of shock

-decrease in urine output

-decrease in GFR

-kidney failure

-oliguria

hepatic effects of shock

early --> increased glucose production

decompensated --> decrease in glucose production, decrease lactic acid conversion (acidosis)

increase risk of infection

more effects of shock

**hypothermia, thirst

-pallor, cool moist skin

edema in late stages

diagnostics for shock

-CBC w/ diff

-blood cultures

-ABG

-BMP

-urine specific gravity

-serum cardiac enzymes

-liver enzymes

-lactic acid trending

-CXR, CT, MRI

-central venous cath

hypovolemic shock

-decrease in intravascular volume

-decrease preload*

-decrease CO*

-increase SVR* (less volume in heart)

*most common

what does neurogenic shock cause

Bradycardia

cariogenic shock

-impaired pumping

-decrease preload

-decrease CO

-increase SVR

•Impaired pumping ability of heart

•Sustained drop in MAP

•Inadequate oxygen to tissues

•Anaerobic metabolism, acidosis

•Cell death leads to tissue & organ death

cariogenic shock causes

-massive MI (most common cause)

-tampenode

-pericarditis

-cardiac arrect

-frequent vfib/ vtach

-pump failure

-open heart surgery

-cardiomyopathy

-potassium/ electrolyte imbalances

-alcohol abuse disorders

risk factors of hypovolemic shock

-surgery

-trauma

-GI bleed

-coagulation disorders

-esophageal varices (alcoholics)

-burns

-malnutrition

-vomiting/ diarrhea

-NG suction

-diuretics

-diabetes insipidus

-post partum bleeding

early stage hypovolemic shock manifestations

•Slight decrease BP

•Slight increase HR

•Respirations normal

•Skin cool, pale, moist

•Alert & oriented

•Slight decrease in output

•Thirsty

•Slow capillary refil

compensatory/ decompensated hypovolemic shock manifestations

•Hypotension

•Rapid thready pulse

•Increase respiration

•Skin cool, pale, poor turgor, edema with fluid shift

•Restless, anxious, confused

•Oliguria (

refractory stage of hypovolemic shock manifestations

•Severe hypotension MAP

treatment of hypovolemic shock

- fluids

-stop bleeding

-surgical reapair

(give protamine sulfate if on heparin)

*can't give meds until we replace volume

may give amioderone, calcium, morhpine, dig

supporting vital function until perfusion is restored in hypovolemic shock

neuro: rest, orient, monitor LOC

CV: fluid volume, sodium bicarb, vasopressors

resp: O2, mech ventilation paO2 >80

GI: NPO

GU: monitor urine output, may require dialysis

*can't give meds until we replace volume

why is morhpine given in shock

dilate veins & anxiety

neuro effects of cariogenic shock

-restless, anxious, lethargic, comatose

CV effects of cardiogenic shock

-rapid thready pulse

-JVD

-hand veins distending

-hypotension

-dependent edema

-elevated CVP

-elevated PCWP

(HEART PRESSURES)

-dysrhythmias

respiratory effects of cardiogenic shock

-increased work of breathing

-crackles/ wheezes

-pulmonary edema (*blood tinged sputum)

GU effects of cardiogenic shock

-oliguria/ anuria

integumentary effects of cardiogenic shock

-pale, cyanosis

-cold/ moist

cardiogenic shock treatment

-treat underlying cause (stent? CABG?)

*fluid infusions may cause more stress to heart

**inotropes: dobutamine is first line

-may need sodium bicarb or antidysrhythmics

how do you know dobutamine (inotropes) are effective for cardiogenic shock

-MORE URINE OUTPUT

how do you know if fluids were effective in hypovolemic shock

MAP

intra-aortic balloon pump

-inflates at beginning of diastole to augment coronary perfusion & deflates prior to systole to reduce after load

(working to perfuse myocardium)

*vascular complications: check pulses, check groin, keep leg/ extremity straight

(make sure perfusion in leg is adequate)

vasoconstrictors

-increase BP

-norepinephrine (levophed)

-phenylephrine

-epinephrine

with hypovolemic shock after replacing fluids may give

norepinephrine to increase MAP

-evaluate effectiveness by looking at MAP

**first line is norepinephrine after we replace volume

inotropes

-increase force of contractility (increase HR and CO)

-dobutamine

-isoproterenol

-dopamine

dopamine vs dobutamine

**dobutamine does not have effect on HR like dopamine does

*use dobutamine to help pump in cardiogenic shock

what do you give dobutamine for

cardiogenic shock

**inotrope think PUMP

-dopamine can set person back

sympathomimetics (inotropes and vasoconstrictor) considerations

-improved tissue perfusion & oxygenation

-increased SC, HR, CO

*caution in elderly

-continuous IV

-document lung sounds/ VS hourly

-monitor HR, BP, dysrhythmias, urine output, IV site

***CANNOT STOP FOR BLOOD DRAWS

norepinephrine can

cut off circulation to digits

(lose fingers/ hands etc.)

vasodilators

-affect arteries and veins

-decrease oxygen demand on heart muscle & pulmonary congestion

*nitropresside

*nitroglycerin

*titrate to keep MAP 70-100 (these bring pressures down)

what do you give in cardiogenic shock if pressure is too high

vasodilators

-nitroprusside

-nitroglycerin

colloid sollutions

-volume expanders

-increase CO by increasing circulatory volume, increases tissue perfusion

-albumin 5% and 25%

-dextran 40, 70

-hetastarch

when are colloid solutions used

-hypovolemic shock

*protein that comes from blood donors and pulls water back into circulatory system, seen a lot with renal patients

nursing considerations for vasodilators

-mix with dextrose, monitor sugar frequently

-nitro= headaches

-watch position changes

epinephrine

-vasopressor

low dose: positive inotropic effects and bronchodilation

high dose: vasoconstriction

-subQ for anaphylaxis

-can cause tissue necrosis

-IV, continuous infusion, IM

dopamine

-vasopressor

low does: increased renal blood flow

moderate dose: positive inotropic effects

high dose: vasoconstriction

indications: renal insufficiency, septic shock, cardiogenic shock

-titrate, can have rebound hypotension

-nectrotizing tissue

s/s of cardiogenic shock

-tachy, hypotensive, crackles, decreased urine output

nitroprusside

-Vasodilation arterioles and veins

•Indications: cardiogenic shock

•Nursing considerations:

•Continuous IV infusion

•Monitor:

•Nausea

•Disorientation

•Muscle spasms

•Decreased/absent reflexes

•Short half-life

•Decreases BP rapidly

•Reflex tachycardia

•Metabolizes to cyanide (blue)

•Protect from light

•Compatible with Dextrose 5%

iv fluids

what do we transfuse HGB under

7!!