Exam #5 Flashcards
Shick Patho
- Too little o2 is delivered to the tissues (related to sustained decrease in MAP)
- can be due to issues with total blood volume, cardiac output, size of the vascular bed
1) compensatory phase: body begins to compensate and move blood to selected areas
- baroreceptors pick up on hypovolemia –> reabsorb sodium and water –> increase osmolarity –> fight or flight –> increased epi/norepi –> vasoconstriction –> blood shunted to brain and heart
- biggest effect is on lungs: blood is shunted to heart and brain
- blood isn’t oxygenated well due to lungs not working well
2) Progressive: if MAP continues to decrease, lactic acid levels and other harmful metabolites increase which damages tissues
- decrease in all organ function, decrease in mental status, decrease co2, decreased o2, change in LOC
- massive capillary permeability, ablumin leaks, edema, alveoli edema –> decreased o2 and respiratory issues
- ileus from decreased blood to the GI tract, necrosis of GI tissue
3) Irreversible: if this continues, MODS occurs
- all organs are damaged, necrosis of brain, DIC, massive bleed out
- MODS
categories of shock
- cardiogenic
- hypovolemic
- distributive: neurogenic, anaphylactic, septic
- obstructive
S/S of shock
- cardio: increased HR but weak pulses (compensating but weak), decreased BP (loss of fluid), low o2 sat (V/Q mismatch in compensatory stage)
- skin: cool and clammy first (blood shunted to brain and heart), warm/cool/clammy in later stage, pale, cyanotic, mottled
- respiratory: RR increases but depth is shallow (anarobic metabolism, V/Q mismatch, pulmonary edema, acidotic –> increased RR), decreased pao2 (80-100), decreased sao2
- renal/urinary: urine output decreased, specific gravity increased (very concentrated urine, fluid retained in body)
- CNS: in early shock thirst/anxiety/restlessness (decreased o2 to the brain), in later shock confusion/lethargy/coma (organs shut down)
- musculoskeletal: muscle weakness and pain (arobic to anarobic shift), decreased or absent Deep tendon reflexes
shock lab results
- increased lactic acid: muscle breakdown from anarobic metabolism (if it goes down then it means it’ shifting back to arobic)
- increased potassium: retention, acidiosis
- increased BUN/creatinine
- increased glucose: in early phase, compensatory, fight or flight mode/cortisol
- increased PaCO2: build up of waste, v/q shunt, decreased RR = co2
- decreased pao2: shunted to heart and brain
- decreased PH: acidosis
- hct/hgb: decreased if hemorrhagic, increased if dehydrated or fluid shift
- compensitory stage: metabolic acidosis with resp compensation
- progressive stage: acidosis w/o respiratory compensation
shock DX studies
- no single finding confirms or rules out shock, but changes can support the diagnosis of shock
- history and physical: car accident, fall, allergies, surgery, illness
- 12 lead ECG: decreased o2 to heart and brain, dysrhythmias
- chest xray: pulmonary infiltrates. bleeds
- pulse ox: hemoglobin may make it look false
- hemodynamic monitoring: BP, MAP, PAWP (left preload), CVP (right preload)
general shock treatment
- maintain patent airway
- oxygen to keep 02 > 90%
- fluids: for septic, hypovolemic and anaphylactic - crystalloids (LR, NS), colloids (blood, blood products, plasmanate, hetastarch, plasma expanders)
- drugs: prefered via central venous catheter, use drugs if fluids don’t help – vasopressors (dopamine, norepinephrine, make sure pt has enough fluid on board first by monitoring PAWP and CVP), inotropes (dobutamine, primacro) increase cardiac contractility and cardiac output, vasodilators (Tridil, nipride) increase cardiac perfusion
shock nursing care
- prevent: catch pt in compensatory phase, use aseptic technique, promote hydration
- assess every 15 minutes until shick is controlled then hourly
- monitor MAP
cardiogenic shock
- direct pump failure, fluid volume is not affected
- causes: systollic, diastolic or structural problems, dysrhythmias, MI, cardiac arrest
- assessment: can look like heart failure (left sided = pulmonary edema, right sided = JVD/edema), increased BNP, increased ANP
- TX: thrmobolytics (break down clots), angioplasty with stenting, CABG, valve replacement, IABP, cardiac transplant. vasodilators, diuretics, beta blockers, inotropes (increase force of contraction)
hypovolemic shock
- total body fluid decreased
- causes: absolute (actual fluid loss, hemorrhage, comiting, diarrhea, diabetes), relative (fluid shift from vascular space to extravascular space, 3rd spacing - bowl obstruction, burns, ascites, ruptured spleen, pancreatitis, sepsis)
- assessment: hct/hgb decreased with hemorrhage, hct/hgb increased with dehydration/fluid shift
- TX: 1st stop loss of fluid and restore circulating volume, 2nd give vaso drugs
Distributive shock
- fluid is shifted from central vascular space, total body fluid volume is normal or increased, loss of vascular tone
- causes: neural-induced (vasomotor center - spinal cord injury above t6, spinal anesthesia, vasomotor center depression), chemical-induced (anaphylactic - massive vasodilation after being exposed to allergy, septic - infection = massive vasodilation due to inflamm response)
Neurogenic Shock
- injury above T6, loss of vasomotor center
- assessment: bradycardia with low BP, flaccid paralysis below level of lesion, loss of reflex activity, cool or warm skin (poikilothermia), dry skin
- TX: depends on the cause, vasopressors (constricts vessels), atropine, give fluids cautiously (not a fluid issues, brain issue), no colloids (not a fluid volume issue just vasomotor issue)
Anaphylactic shock
- allergy to med, food, bug bite, etc
- assessment: dyspnea, wheezing, stridor, flushing, pruritis, uticaria, swelling of lips, tongue
- TX: prevention is key, epinephrine (constricts and increases BP), antihistamines (benadryl, stops inflamm), bronchodilators (open airway), aggressive fluid resuscitation with colloids (hetastarch, albumin, dextran), IV corticosteroids (only if low BP persists)
1st give Epi, then antihistamine, then fluid replacement
Septic Shock
- systemic infection
- assessment:
1s phase - hyperdynamic - initially everything speeds up, aggressive, agitation
- vasodilation (skin pink, warm, flushed), increased cellular metabolism, increased fever greater than 104
- increased HR and BP, bounding pulses
- WBC with left shift (increased bands)
2nd phase - hypodynamic - sudden onset, rapid decline, poor prognosis
- skin cool and mottled
- temp below normal
- low BP, low CO
- DIC
- decreased heart and brain function
- treatment
- large amount of fluid replacement (isotonic and colloids)
- IV abx with cultures
- vasopressors (norepi, dopamine, vasopressin) when increased PAWP & CVP
- may need inotropes (dobutamine), increase contractions
- IV corticosteroids used occasionally
- xigris (treats systemic infections)
- in 1st phase, heparin to prevent DIC
- in 2nd phase, clotting factors (FFP, Cryo) to treat DIC
obstructive shock
- problems that impair the ability of the normal heart muscle to pump effectively , total body fluid volume is not affected
- causes: tamponade, pneumothorax, superior vena cava syndrome, abdominal compartment syndrome, PE, pulmonary HTN, thoracic tumor, pericarditis – all affect normal blood flow to heart
- assessment: JVD, pulsus peradoxus (pulse changes with breathing), bradypnea is a late sign
- TX: early recognition and tx to relieve obstruction - mechanical decompression, radiation/debulking, thrombolytics
SIRS
- systemic inflammatory response syndrome, generalized inflammation in organs remote from the initial insult
- clinical response to a nonspecific insult of either infectious or noninfectious origin
- 2 or more of the following variables: Fever of more than 38°C (100.4°F) or less than 36°C (96.8°F), Heart rate of more than 90 beats per minute, Respiratory rate of more than 20 breaths per minute or arterial carbon dioxide tension (PaCO 2) of less than 32 mm Hg, Abnormal white blood cell count (>12,000/µL or 10% immature [band] forms)
- systemic inflammation (doent have to be caused by infection)
- can be caused by ischemic or necrotic tissue (MI, pancreatitis), endotoxin release, bacteria, trauma, burns
- S/S: increased temp ( > 100.4), increased HR ( > 90), increased RR ( >20), WBC high or low
MODS
- multiple organ dysfunction syndrome
- failure of 2 or more organ systems such that homeostasis cannot be maintained without intervention
- results from SIRS
- both SIRS and MODS = respiratory is the first system to show symptoms (ARDS), mental status changes, acute kidney injury, hypermetabolic and catabolic state, liver dysfunction (decreased albumin = edema), DIC, electrolyte imbalances
- S/S of MODS and SIRS = development of ARDS, Myocardial depression, change in neuro status, hyperglycemia, renal hypoperfusion, ATN, mucosal ischemia, GI bleeds, jaundice, hepatic encephalopathy, increased bleeding times, decreased platelet count,
nursing care for MODS and SIRS
- detect early signs of deterioration
- prevent hospital aquired infections
- prevent hypoxemia: lungs are first to be affected
- prevent malnutrition: excess calories needed to promote healing/immunity
- control blood sugars
- support failing organs
adrenergic drug indications
- beta 1: heart, increases HR, increases renin release which increases BP
- beta 2: lungs, bronchodilation, increases glycogenolysis
- alpha 1: vasoconstriction
1) respiratory: beta 2 adrenergic, bronchodilation - asthma, bronchitis
- exp: albuterol, ephedrine, formoterol, levabuterol, salmeterol
2) topical nasal decongestants: alpha 1 adrenergic - constrict dilated arterioles, reduction of nasal blood flow
- exp: ephedrine, naphazoline, oxymetazoline
3) cardiovascular: used to support CV during cardiac failure or shock, vasoconstrictive
- exp: dobutamine, dopamine, ephedrine, norepinephrine
adrenergic adverse effects
- alpha adrenergic: causes vasoconstriction – headache, restlessness, excitement, insomnia, euphoria, chest pain, hypertension, tachy, palpitations, dysrhythmias
- beta adrenergic: increases HR and BP – mild tremors, headache, nervousness, dizziness, nausea, vomiting, increased HR, palpitations, fluctuations in BP
Adrenergic Toxicity, management of overdose
- manage symptoms and support the patient
- majority of adrenergic drugs have a very short hald life and need to be given IV drip
- two life threatening effects = CNS and CV - seizures (diazepam) and intracranial/systemic hemorrhage (esmolol)