Health and Illness 3 Exam 2

10/19 - Includes review from last exam

Chronic Stable Angina vs Unstable Angina

Chronic Stable Angina:

• Decreased blood flow to heart from CAD

• Often occurs at predictable times (ie during exercise)

• Position pt upright, encourage rest

• Apply O2

• Nitroglycerin (can pre-treat)

• As plaque increases and blood flow decreases over time, unstable angina may occur

Unstable Angina:

• Partial rupture of artery - no permanent damage - a type of acute coronary syndrome

• Often new onset

• Less predictable

• Occurs at rest

• More prolonged and severe >10 min

• Cardiac markers not elevated - distinguishes from NSTEMI and STEMI

• ST segment depression, T wave inversion

STEMI vs NSTEMI

STEMI:

• Classic heart attack - extensive muscle damage

• Occur abruptly from stopped blood flow - usually from disrupted arthroscelertoic plauqe that becomes a thrombus and occludes blood flow

• Cardiac markers are elevated

• ST segment elevation. - appears as tombstones - T wave inversion

NSTEMI:

• Intermediate form of ACS - less extensive heart damage

• Cardiac markers are elevated

• ST segment depression, T wave inversion (also seen in unstable angina)

Medications for HF

1. Reduce afterload (lowers heart workload)

Via vasodilation

• ACEs/ARBs - Stop RAAS system - Monitor creatinine and BUN for kidney function

• Nitrates

• Hydralazine

• Valsartan

• CCBs (not diltiazem)

2. Reduce preload (lowers heart workload)

• Diuretics

3. Inhibit SNS

• BETA blockers

4. Improve Contractility (Makes heart beat BETTER, not faster) (+ Inotropes)

• Dobutamine (increases contraction strength and vasodilates)

• Milrinone (increases contraction strength and vasodilates)

• Digoxin (watch potassium lab!) (if on furosemide or HCTZ especially) (low K = digoxin toxicity)

• Norepinephrine and epinephrine - weaker but used to vasoconstrict during shock

Sepsis 1-Hour Bundle

1. Measure lactate levels (repeat if >2)

2. Draw blood cultures (2 sets peripherally from different sites) (drawn before antibiotics)

3. Administer antibiotics

4. Fluid resuscitation (isotonic crystalloids LR or NS) (30mL/kg)

5. Vasopressor administration if fluids fail to restore a MAP >65 (norepinephrine, epinephrine, vasopressin)

Intracranial Pressure

Normal 5-15 mmHg

• Monroe-Kellie Doctrine says that if there is an increase in one factor (CSF, intravascular blood, or brain tissue) there must be a corresponding decrease in one or both of the other factors to maintain normal intracranial pressure.

• If there is too much increase, displacement occurs which leads to herniation and brain death

Cerebral Perfusion Pressure Calculation

MAP - ICP = CPP

• Normal CPP is 60-70 mmHg

• If abnormal - interventions to either increase MAP or decrease ICP (or both) are done

Clinical Manifestations of Increased ICP

• Loss of consciousness

• Dizziness and fainting

• Change in memory

• Headache

• Projectile vomiting

Cushing Triad (late sign) - Impending Brainstem Herniation

• Profound bradycardia (<50)

• Abnormal respirations (cyanne-stokes)

• Increasing pulse pressure (distance between diastolic and systolic increases) (high systolic and low diastolic) (ie 160/70)

Glasgow Coma Scale

3 is worst, 15 is best

13-15 Mild TBI

9-12 Moderate TBI

3-8 Severe TBI / Coma

External Ventricular Device (EVD)

Placed into ventricles of brain where CSF resises

• Mesures ICP and drains excess

• Brain ICP goes above a set # (for example 20) then the EVD drains off some CSF until ICP is back below desired number

• Must stay above pts ear

Only waveform to know: Impending herniation

• Waveform giving you the middle finger (see photo)

Nursing Interventions to Reduce + Maintain Low ICP

• Head midline - avoid neck flexion

• AIRWAY!

• HOB 30 degrees (if no spinal)

• DO NOT cluster care - ICP goes up when you interact with patient - sustained increased ICP = BAD. Take breaks

• Avoid suctioning

• Keep lights off, no talking - educate families

• Paralytic medications to reduce agitation (propofol, fentanyl)

• No bearing down/straining/coughing

• Treat pain promptly (avoid opiates w/ pt’s not on the vent)

• Mannitol (osmotic diuretic) to decrease brain swelling

• Hypertonic saline (3% or higher) (not too much - bad for kidneys)

• Phenytoin for seizure prevention

Concussion

Minor TBI - no identified brain damage - may result in post concussion syndrome >3mo

Diffuse axonal injury

Diffuse axonal injury -

• widespread axonal damage (trauma changes function of axon resulting in swelling and disconnection)

• not seen right away on CT

• approx 90% of patients will remain in vegetative state

• decortication, decerebration

Contusion

Bruising of brain tissue

• Often associated with coup (primary impact) and countercoup (brain hitting back of head/secondary impact) injury

• Associated with closed head injuries

• Can re-bleed (blossoming) - monitor for seizures

Epidural Hematoma

Bleeding between dura and inner surface of skull

• Brief lucid interval followed by decreased LOC - ie pt wakes up fine immediately, then rapidly deteriorates and doesn’t recover

• Neurological emergency - needs surgical intervention/evacuation

Subdural Hematoma

Bleeding between dura and arachnoid layers

• Acute (24-48h) - immediate deterioration - craniotomy, evacuation, decompression

• Subacute (within 2-14 days) - s/p severe trauma - AMS as hematoma develops - evacuation, decompression

• Chronic (weeks-months s/p injury) - usually older adults - risk for misdiagnosis as initial injury seemed benign - evacuation, decompression

Emergency Management of a TBI

• Stabilize cervical spine until spinal injury r/o

• Airway support - intubate if GCS less than 8

• Control external bleeding

• Maintain warmth

• Caution with fluid admin

• CT scan

• PREVENT SECONDARY INJURY - prevent seizures, hypotension

Basic Brain Anatomy

Frontal lobe: cognition, language, motor

Temporal: sensory info processing, understanding language

Parietal: interpreting sensory information

Occipital: interpreting visual information

Brainstem: bodies vital functions

Cerebral Edema vs Increased ICP

Cerebral edema is swelling of the actual brain r/t increased ICP

• High ICP and rigidity of the skull interfere with BBB and prevent blood and CSF from traveling around

• Causes O2 deprivation and tissue damage

Mannitol notes

May cause hyponatremia r/t diuretic properties

• Watch for pulmonary edema (lung sounds, JVD)

• Watch for AKI

• Use filtered IV line

Seizure Phases

Prodromal - anxiety, mood changes (may be hours-days before)

Early ictal/aura - (seconds to minutes before)

Ictal - 1st manifestation until seizure ends

Postictal - until pt reaches baseline again

Types of Generalized Seizures

1. Tonic - Sudden onset of increased tone that is maintained

2. Clonic - Begins with loss of consciousness, sudden loss of muscle tone - rhythmic limb jerking

3. Myoclonic - sudden excessive jerk or twitch of body/extremities (maintains consciousness and some awareness)

4. Atonic - Involves tonic episode followed by sudden loss of muscle tone, resulting in a fall.

Tonic clonic:

• Loss of consciousness

• Body stiffens (tonic) with jerking (clonic)

• Fencing position

Subclinical Seizures

1. Typical absence seizures - staring spell, only a few seconds but can occur many times if untreated - usually only peds

2. Atypical absence seizures - staring spell with other manifestations (blinking, lip movement, >10 seconds, continues into adulthood)

Status Epilepticus

Seizure activity longer than 5 min within rapid succession w/o return to consciousness between seizures

• Neurons can become exhausted leading to permanent brain damage

• Hypoxemia, dysrhythmia, increased ICP, rhabdomyolysis, acidosis, SUDEP

• Give lorazepam first

Treatment/Interventions for Seizures

1. Maintain airway

2. Protect head - soft items under and around

3. Turn to side (not when actively seizing)

4. Loosen clothing

5. Suction after - not during

6. Time the seizure

7. Supplemental O2

Medications:

1. Lorazepam: Benzodiazepine used for acute seizure control, acting quickly to calm the nervous system via GABA enhancement. Watch for respiratory depression, hypotension, tachycardia, dysrhythmias

2. Phenytoin: Blocks repetitive activation of sodium channels - watch for gingival hyperplasia, hirsutism, and cardiac effects. Regular monitoring of serum levels is necessary.

Acute Kidney Injury

Rapid loss of kidney function - hours to days - impaired fluid, electrolytes, acid base and waste regulation (acute or chronic)

Dx Criteria:

1. Acute decrease in UOP (<0.5 for >6 hours) (may have normal UOP)

And/OR

2. Elevation in serum creatinine >0.3 mg/dl within 48 hours or >1.5x baseline within 7 days

S/S of AKI

• Hypertension

• Dysrhythmias

• Edema, crackles, JVD, S3 sounds

• Too little or too much UOP

• Muscle twitching, seizures

• Increased BUN, Creatinine, Potassium and Phosphate

• Decreased calcium and HCT

Types of AKI

1. Pre-renal

Before the kidney - not enough blood flow causing decreased GFR - r/t dehydration, hypovolemia, hemorrhage, shock, sepsis - fluid challenge

2. Intrarenal

Direct kidney tissue damage - acute tubular necrosis impairs filtration - r/t nephrotoxic, contrast, rhabdomyolysis, glomerulonephritis

3. Postrenal

Urine cannot get out and backs up - raises kidney pressure - obstruction, kidney stones, tumor, kinked/clotted foley, bladder retention - if obstruction is removed within 48 hours damage can be avoided

1st Phase of AKI

Oliguric - begins with kidney insult

• Lasts 10-14 days

• UOP <400 mL/day

• Fluid volume overload - edema, crackles, JVD, S3 gallop

• Hyperkalemia

• Hyponatremia

• Metabolic acidosis

• Azotemia (nitrogenous waste build up leading to LOC changes)

2nd Phase of AKI

Diuretic

• Lasts 1-3 weeks

• UOP 1-5 L/day - lots of UOP but not good quality waste clearing urine

• BUN/Creatinine begin to normalize

• Hypovolemia

• Hypotension (admin IVF)

• Hyponatremia

• Hypokalemia

3rd Phase of AKI

Recovery

• May take up to 12 months

• GFR increases steadily

• BUN/Creatinine plateau then fall - some may never go back to baseline

• Tubule function restores

• Watch for residual CKD - CKD occurs if recovery does not

Assessment Priorities for Patient in AKI

• Strict I/O - hourly UOP if unstable w/ foley

• Monitor electrolyte labs closely (sodium and potassium especially)

• Daily weights - best fluid trend indicator

• Avoid foods high in potassium and sodium

• High protein diet r/t rate of protein breakdown that occurs with AKI

RED FLAGS

• Potassium elevation - ECG changes

• New pulmonary edema/hypoxia

• Rapidly decreasing UOP

• Severe metabolic acidosis

• Altered LOC, seizures (r/t sodium changes)

Treatment for AKI

• Stabilize ABCs/hemodynamics (O2, IVF, Pressors)

• Stop the HIT (hold nephrotoxic meds, tx sepsis, relieve obstruction, renal dose meds)

• Manage complications (hyperkalemia, acidosis, pulmonary edema, uremia, infection risk (kidneys play role in immunity)

• Dialysis (intermittent, peritoneal, CRRT)

Hyperkalemia management:

• Give calcium gluconate to buy time during hyperkalemia to protect the heart from potassium effects

• Insulin + dextrose to force potassium to move into cells (also buying time)

• Loop diuretics/K-exulate to make potassium leave in urine and feces

Intermittent Hemodialysis

Done for stable patients, CKD

Over a few hours 3x/week

Fastest type of dialysis - via fistula, graft, CVC

• Anticoagulants to prevent filter clotting

Watch for:

• Hypotension (slow rate if occurs)

• Disequilibrium syndrome (r/t solutes moving out of body too quickly) (HA, vision changes, nausea r/t brain swelling)

• Bleeding/infection

Peritoneal Dialysis

Uses patient’s perineum as a filter - works via gradient system from solute solution

Stable patients, can be done at home (over 8 hours) slowly!

Sterile procedure

Watch for infection/peritonitis - pain, drainage

• Keep overflow bag below abd

• Warm dialysate prior to instillation

• Color should be light yellow/clear

Continuous Renal Replacement Therapy (CRRT)

For the most unstable patients - ICU patients that can’t handle large fluid shifts

• Continuous, gentle filtration 24/7

• Not as effective

• Slowest form of dialysis

• Via CVC (needs big vein, jugular, subclavian, femoral)

Watch for:

• Filter clotting (anticoagulation therapy prophylaxis)

Nursing Interventions for Dialysis

Assess fistula (joined artery and vein) for thrill (feel) and bruit (sound) of whooshing

• Don’t use fistula arm for BP, venipuncture

• Don’t sleep or put pressure on site

Watch for infection at CVC catheter sites (kidneys play a large role in immunity)

Assess baseline vitals and weight before dialysis - reassess after

Hold dialyzable meds

Monitor B/P during

Monitor CBG (dialysate contains glucose)

No NSAIDs for AKI patients

Ischemic Stroke

Inadequate blood flow

Can be a thrombus (formed in brain)or embolus (traveling clot)

• May be preceded by TIA

Facial drooping is hallmark

Hemmoragic Stroke

Bleeding into brain tissue

1. Intracerebral hemorrhage - sudden onset “worst headache of life” - HTN is most common cause

2. Subarachnoid hemorrhage- bleeding into CSF filled space - trauma, aneurysm burst

• Keep MAP >70 for first 14 days s/p subarachnoid hemorrhage

Causes displacement of tissues - causes herniation and death if not treatment

Hemorrhagic type stroke usually has more loss of LOC

TIA

Usually lasts <60 min and resolves completely with no deficits

• Hx of TIA is associated with increased risk of stroke later on (highest risk within 48 hours)

• Ischemia without infarction

Treatment:

• Antiplatelet - ASA, clopidogrel

• Antihypertensives if indicated (HTN is common cause)

• Afib meds as indicated (a-fib is common cause)

Stroke Localization Deficits

Right sided damage:

• Left sided hemiplegia, neglect

• Impulsivity, impaired judgment

• Deficits begin at the nose level - eyebrows are spared but mouth droop occurs

Left sided damage:

• Right sided hemiplegia

• Aphasia/language impairment

• Receptive aphasia (can’t understand you)

• Expressive aphasia

• Slower and more cautious

Diagnosis of Stroke

1. Non contrast CT within 25 min of ED arrival - shows hemorrhagic stroke w/o contrast but not ischemia

2. CT with contrast if no hemorrhage on initial NoCo CT to look for ischemia

3. Hx if able - onset, duration, progression - ‘last known well’ is hour 0

4. NIH stroke scale

Nursing Interventions for Stroke/S/P

• Draw labs - coag studies

• CBG (hypoglycemia can mimic stroke)

• CT scanner ASAP

• Last known well assessment

• Airway protection

• Careful fluid management

• NPO with swallow eval before oral feedings - aspiration pneumonia is big risk after stroke

• Tx fever quickly - can raise ICP

• Have suction ready during mealtimes

• Place food on unaffected side

• Dress affected side first

• Support limp extremities to prevent dislocation

• Swallow with neck flexed forward

• Teach scanning side-side if patient has homonymous hemianopsia

Acute Care for Ischemic Stroke

Goal: preserve life - prevent further brain damage and reduce disability

• ABCs

• Baseline neuro assessment - patients may worsen in 24-48 hours

• Thrombolytic therapy - tPA - must be given within 3-4.5 hours of symptom onset

• Monitor for conversion (switch between ischemic to hemorrhagic stroke r/t tPA)

After stabilization:

• Antiplatelets

• Anticoagulants (for life if patient has stent placed)

• Stains

• Nimodipine to prevent vasospasm

Keep BP a little higher to increase perfusion

Acute Care for Hemorrhagic Stroke

Tx based on cause of bleed - evacuation of hematomas, AVM resection, catheter embolization, clipping/coiling of aneurysm

• No anticoags or antiplatelets - admin antidote if patient has taken any

• Nicardipine for hypertension management (keep BP in lower range to reduce bleeding)

• Seizure prophylaxis - suction setup - keppra admin ?

tPA Notes

• Do not administer with antiplatelets or anticoagulants within 24 hours

• Monitor for hypotension

• Monitor for intracranial hemorrhage and bleeding

Arterial vs Venous Thrombosis

Arterial thrombosis:

• Blood can’t go to extremities

• Absent pulses

• More uncommon r/t fast arterial blood flow

• atherosclerosis, tissue ischemia, polycythemia and A-fib are causes

Venous thrombosis:

• Blood can’t get OUT of extremities

• Superficial and deep

• Virchow’s Triad

Virchow’s Triad:

Virchow’s Triad:

1. Endothelial damage (smoking, HTN)

2. Hypercoagulability (hereditary, cancer, chemo, pregnancy, obesity)

3. Stasis (immobility, polycythemia)

A risk factor for increased clotting/venous thrombosis

Clotting Lab Tests

Prothrombin time (PT)

• How long blood takes to clot via the extrinsic and common pathways (clotting factors I,II,V,VII and X)

• Timed study - how long to clot (in seconds)

International normalized ratio (INR)

• Clotting time compared to normal average

• Warfarin needs INR between 2-3

Partial thromboplastin time (pTT)/(aPTT)

• How long blood takes to clot via the intrinsic and common pathways (clotting factors VIII, IX, XI, XII)

• Timed study - how long to clot (in seconds)

• Prolonged time indicates problem in secondary hemostasis

Venous Thrombosis

Superficial: not as concerning

• May extend deeper if untreated

• Cord-like to the touch

• rendess, pain warmth (usually no edema)

• Confirmed via duplex ultrasound

• Tx with compression stockings/bandages, elevation, mild exercise/walking, NSAIDs

Deep VTE:

• Tenderness, redness, edema, fast cap refill

• Confirmed with duplex ultrasound and increased D-dimer

• Can cause PE, post thrombotic syndrome (chronic inflammation)

• Heparin

Pulmonary Embolism

Blockage of one or more pulmonary arteries by thrombus, fat or air embolus that obstructs alveolar perfusion

• Dyspnea

• Chest pain

• Tachycardia/tachypnea

• Crackles, wheezing, pleural friction rub

• Change in LOC

• Cough with hemoptysis (r/t blood in alveolar space)

• Refractory hypoxia (O2 application not working)

Can cause

• Pulmonary infarction

• Abscess secondary to infection

• Pleural effusion

• Pulmonary HTN r/t hypoxemia

Diagnosis of PE

• D-dimer

• CT scan WITH contrast

• Ventilation perfusion (V/Q) study if contrast is contraindicated

Nursing Management of PE

• Oxygen support - mechanical ventilaltion if indicated

• Fluids and vasopressors

• Diuretics

• Analgesics

• Surgery for massive PE

• Apixaban, alteplase

DIC

Widespread, uncontrolled clotting that consumes all clotting factors and platelets - leads to uncontrolled bleeding

• Never a primary dx, always secondary to underlying problem

1. Triggering event/cause - sepsis, trauma, OB emergency

2. Thrombin overproduced - coagulation cascade activated systemically

3. Microvascular clots - organ ischemia leading to MODS

4. Factors and platelets depleted - consumed by widespread clotting - UNCONTROLLED HEMMORAGE :(

DIC Clinical Manifestations

Thrombotic Manifestations:

• Cyanosis, mottling

• Gangrene of fingers and toes

• Oliguria/anuria (AKI)

• Decreased LOC

• Stroke

Bleeding Manifestations:

• Petechiae, purpura

• Oozing from IV sites, wounds, gums

• Hematemesis, melena, hematuria

• Intracranial hemorrhage

• Hemoptysis

Diagnostic Studies for DIC

• D dimer elevated

• Fibrinogen decreased

• Platelets decreased

• PT/PTT prolonged

• RBC, Hgb, Hct decreased

Treatment of DIC

Treat underlying cause - DIC will not resolve until trigger is eliminated

Thrombosis dominant DIC:

• anticoagulation with heparin

• antithrombin 3 concentrate

• monitor PTT

Bleeding dominant DIC:

• Cryoprecipitate (replaces fibrinogen and factor VIII)

• FFP (replaces all clotting factors)

• Plt transfusion if <50,000 or active bleed

• PRBCs for significant anemia/hemorrhage

Usually FFP, fluids and heparin all done at the same time

Nursing Interventions for DIC

• O2 therapy/mechanical ventilation

• Large bore IV access

• Fluids/pressors for shock

• Cardiac, o2 UOP monitoring

• Inspect all skin for petechiae, purpura and ecchymosis

• Check all IV sites for oozing

• Assess neuro status

• Avoid unnecessary injections

• Pressure >5min to all sites

• Soft mouth care, electric razor only

• No rectal temps, smallest gauge needles

Heparin Induced Thrombocytopenia (HIT)

Similar presentation to DIC- autoimmune reaction to heparin

• Usually occurs 5-10 days after heparin admin

Platelet drop >50% from baseline

• Thrombosis despite low platelets

• DVT, PE and arterial clots

STOP heparin and never give again

• switch to argatroban or bivalirudin for anticoagulation

• monitor platelets until >150,000

Protamine sulfate is heparin antidote