midterm #1 Flashcards
systemic inflammatory response system
(SIRS)
- response by a variety including: infection, ischemia, infarction, injury
SIRS is characterized by 2 of the following
- fever
- edema
- hypotension
- tachycardia
- impaired oxygenation
- increased WBC count
septic shock
a subset of sepsis; greater risk of mortality than w/ sepsis alone
- persistent hypotension -> tissue hypoxia -> tissue death
SBP <90 MAP <65
SIRS criteria
- HR >90 bpm
- RR >20
- temp >38 or <36
- WBC >12.0 or <4.0x10^9/L
- altered LOC (GCS)
when is an adult at risk for developing SEPSIS?
if they have a suspected or confirmed source of infection
symptoms:
- OA, pts w/ chronic conditions
(DM, HF, CKD)
- immunosuppressed pts
SEPSIS
- 4 key interventions
1 ) labs & diagnostics
- cultures and lactate
2 ) broad spectrum abx
3 ) IV bolus
4 ) monitoring (VS)
SEPSIS
- monitoring and assessment
VS: SpO2 Q1h x6h -> Q4h x12h
GCS Q1h x6hr
monitor urine output -> 25cc/hr
- minimum urine output 25-30 mL/h
SEPSIS
- call MD for…
RR <10 or >30
O2 sat <90%
P <40 or >140
systolic BP <90 mmHg
sudden change in LOC
urine output <100mL in 4h
OR
hypotension is not resolving even w/ IV bolus fluids
Type 1 (S/S)
polyuria
polydipsia (thirst)
polyphagia
cachexic
Type 1
pathophysiology
DM is a metabolic disorder
B-cells regulate insulin
alpha-cells regulate glucagon
↑glucose → ↑insulin & ↓glucagon
↓glucose → ↓insulin & ↑glucagon
pathophysiology of type 1
lack of insulin secretion
destruction of B-cells
pathophysiology of type 2
insulin resistance
desensitization of B cells to hyperglycemia
diagnosis of type 1 & 2
A1C <6.5%
FBG >7mmol/L
RBG >11.1 mmol/L
goals of care of DM
1 ) reduce sx
2 ) prevent/ manage acute sx
3 ) delay onset + progression chronic complications
4 ) obtain ideal body weight
ABCDESSS of diabetes care
A1C targets (<6.5)
BP targets
Cholesterol targets
Drugs for CV and cardiorenal prot.
Exercise goals and healthy heating
Screening for complication - chronic
Smoking cessation
Self management
sick day management for DM
hold SADMANS
Sulfonylureas & other secretagogues
ACE inhibitors
Diuretics, direct renin-rehibitors
Metformin
Angiotensin receptor blockers
Non-steroidal anti-inflammatory drugs
SGLT2 inhibitors
DKA
hyperglycemia & dehydration
fats metabolized in absence of insulin -> ketosis & acidosis
1 ) illness, infection (stages of stress)
2 ) inadequate insulin dosage or omission
3 ) undiagnosed T1 or poor self management
S/S of DKA
> 14 mmol/L
polyuria, polydipsia
ketones in blood and urine
dehydration, lethargy, weakness, orthostatic hypotension, N/V
HHS
enough insulin to prevent DKA but not enough to prevent severe hyperglycemia
- osmotic diuresis, ECF depletion
S/S >34 mmol/L
somnolence, coma, seizures, hemiparesis, aphasia
chronic complications (DM)
macro:
CAD (atherosclerosis)
hypertension, stroke, PVD
micro:
retinopathy
neuropathy
neuropathy
- sensory: extremities
- autonomic: internally
infections
CAD: atherosclerosis
c-reactive protein CRP inflammation
progression of atherosclerosis
a. fatty streak
b. fibrous plaque
c. complicated lesion
CAD risk factors
non-mod:
age
M>F
ethnicity
family hx
genetics
mod:
hypertension
elevated serum lipids
physical inactivity
smoking cessation
meds
DM management
diet
chronic stable angina
reversible (temporary) myocardial ischemia = angina
primary reason for insufficient blood flow = atherosclerosis
unstable angina
new and onset
occurs at rest
worsening pattern
chest pain isn’t sustained
clinical manifestations of ACS
pain
obj: anxiety, fear, restlessness, cool, clammy skin, diaphoretic, pale/grey, tachy/ bradycardia, dysrhythmias, BP change
goals of care:
1 ) ensure they’re resting
2 ) adding O2
3 ) nitroglycerin
4 ) morphine or analgesic for pain
diagnostic study for ACS
12-lead ECG, chest x-ray, echo, exercise stress test
serial troponins
fasting lipid profile: HDL to LDL
unstable angina/ NSTEMI
ECG
serial troponins
stress test
urgent angiogram/-plasty
STEMI
ECG
serial troponins
emergent angioplasty and stenting
meds for CAD
restrict lipoprotein production
“statin” drugs
systolic HF -> HFrEF
EF<40%
impaired contractile function
increased afterload or hypertension
mechanical abnormalities
inability of heart to pump blood effectively
diastolic -> HFpEF
EF > 50%
LV hypertrophy
myocardial ischemic
valvular disease
cardio myopathy
inability of V to relax and fill during diastole
- decreased SV and CO
compensatory mechanism
- increased SNS stimulation
1st but least effective
increased epinephrine and NE -> ↑ HR, myocardial contractility, peripheral vascular constriction
compensatory mechanism
- neurohormonal responses
activating renin-angiotensin-aldosterone mechanism > vasoconstriction and leads to an increase in aldosterone secretion
-> retention Na + H2O
increase preload
helpful at first but becomes excessive -> systemic venous congestion & peripheral edema
compensatory mechanism
- cardiac decompensation
compensatory mech. no longer maintain adequate CO + insufficient tissue perfusion results
compensatory mechanism
- ventricular remolding
cardiac myocytes > large abnormal cells
increased ventricular mass, changes in ventricular shape, impaired contractility bigger but less effective pump
compensatory mechanism
- ventricular dilation
enlargement of heart chambers due to elevated pressure over time
- ↓ elasticity in the muscle fibers leads to ↓ CO
compensatory mechanism
- ventricular hypertrophy
increased muscle mass and cardiac wall thickness due to overwork and stress
Lt. sided HF
pulmonary edema
severe dyspnea >30
improve LV function by:
1 ) ↓ intravascular volume - diuretics
2 ) ↓venous return (preload) - positioning
3 ) ↓ afterload - managing BP
4 ) improving gas exchange & oxygenation - byPAP
5 ) improving cardiac function - inotropes, infusion, ICU
6 ) reducing anxiety - pain/ perception
O2 administration
self-management teaching
regular exercise & activity /daily weight
medications for HF
- diuretics
loop, thiazide
- reduces preload by ↓ intravascular pressure volume
meds for HF
- ACE inhibitors
ramipril and enalapril
1st line therapy
vasodilator (↓BP), ↓ systemic vascular resistance (afterload), CO
meds for HF
- B-adrenergic blockers
↓ cardiac O2 demand ↓HR + ↓BP
meds for HF
- vasodilators
nitrates
reduces afterload by dilating peripheral blood vessels
↑ myocardial O2 supply by dilating cardiac blood vessels
1st line meds for managing chest pain
meds for HF
- digitalis
↑ CO ( ↓HR -> ↑ ventricular filling and contractility)
apical pulse >60
nursing diagnosis for HF (I)
inadequate CO
nursing diagnosis for HF (II)
reduced gas exchange
strokes incidence + risk factors
non-mod:
- age >65
- gender, race, family hx
mod:
- smoking, alcohol
- obesity, inactivity
- high cholesterol
- illicit drug use
- oral contraceptives, HRT
contributes:
- DM
- hypertension
- heart ( afibb.)
- disease/ CAD
strokes
- factors that affect blood flow
- systemic BP
- high BP
- CO
- blood viscosity
strokes
- etiology + pathophysiology
thrombosis, embolism, hemorrhage
= cerebral ischemia
check notes for diagram lol
strokes
- clinical manifestations
BE FAST
motor function
communication:
- expressive aphasia -> Broca’s
- receptive aphasia
- amnesic aphasia
- global aphasia
affect
intellectual function
spatial-perceptual alterations (rt.)
elimination (incontinence)
strokes
- diagnostics
CT scan = 1st
lumbar puncture RBC in CSF
lab work:
- CBC, platelets, PT, INR, PTT)
- low INR = high risk for stoke
- blood glucose
- renal + hepatic study
- cholesterol
cardiac assessment
- why? embolic stroke from afibb
- ECG
- chest x-ray
- cardiac markers: troponins
- echocardiographs
strokes
- collaborative care
drug therapy
- antiplatelet > aspirin
- statins > lower cholesterol
- oral anticoagulants > apixaban & dabigatran
nutritional therapy
strokes
- acute nursing management
goals:
- preserving life
- prevent further brain damage
- reduce disability
assessment:
- ABCs, VS, LOC, A+O (GCS), PERLLA
- neuro assessment for baseline
strokes
- ICP
S/S of ICP
- N/V > projectile
- headache
- decreasing GCS
- swelling
- cerebral edema
- hemorrhagic stroke
Cushing’s triad:
- ↑ systolic BP, ↓ P, ↓ RR
opposite of Sepsis
- ↓ BP, ↑P, ↑ RR
strokes
- nursing interventions
promote rest
reduce visual overstimulation
avoid straining while pooping ↑ ICP
medical induced coma
- reduce brain activity & swelling
meds
strokes
- rehab
first 3-6 months are where the most relearning happens
baseline
PVD
- PAD risk facors
risk factors
- atherosclerosis
- high BP
- smoking
- high cholesterol
- obesity
- DM
- age
PVD
- PAD complications 6 P’s
Pain
Pallor
Pulselessness
Paresthesia
Paralysis
Perishingly cold
PVD
- PAD complications cont.
continuous pain at rest
gangrene
limb threatening disease
elevating foot = pain
S/S:
- intermittent claudication
- dependent rubour
- skin change: cool to touch, pallor, increased cap refill, loss of hair, taut and thin skin
- decreased circulation signs
PVD
- PAD interventions
femoral popliteal bypass
percutaneous transluminal angioplasty (PTA) of the femoral arteries
endarterectomy
amputation = last resort
PVD
- nursing management of PAD
nutritional therapy:
- low cholesterol
- high fiber
- low glycemic indexic food (DM)
exercise therapy:
- increase blood flow
risk factor modification:
- control BP, weight control
- smoking cessation
- blood glucose control
- similar to stroke
- diet
PVD
- SVT and DVT risk factors
blood clots > Virchow’s Triad
- stasis: afibb, valve dysfunction, obesity
- hypercoagulability: cancer, smoking, dehydration, ↑clotting fac.
- cell wall injury/damage
PVD
- clinical characteristics of SVT
- palpable, firm
- cord-like subq veins w/ surrounding area tender, reddened and warm
- pain / discomfort around area
PVD
- clinical characteristics of DVT
- unilateral leg edema
- extremity pain
- sense of fullness in thigh or calf
- warm skin, erythema, cyanotic
- temp >38
PVD
- nursing management
intervention:
early & aggressive mobilization
- 4-6x/day
bedrest pt
- changing positions, dorsiflex feet, rotate ankles Q2-4h
compression stockings
sequential compression devices
PVD
- anticoagulants + nursing management
warfarin (vit K = antidote)
48-72 hr to work
CHECK INR (high = thinner)
thrombin inhibitor (indirect)
- heparin (HIT)
- LMWH (dataperin/ enoxaparin)
thrombin inhibitor (direct)
- hirudin, orgatroben
- directly inhibit thrombin enzyme
PVD
- nursing diagnosis
ineffective tissue perfusion
1 ) walking, feet down, avoid tight socks/shoes, protective clothing
impaired skin integrity
1 ) turning & repositioning
2 ) prevent damage & injury (roomy shoes)
3 ) check H2O w/ fingers
Acute pain
1 ) effective tissue perfusion: walk
2 ) MEDS
activity tolerance
1 ) staggering exercise program
ineffective therapeutic regimen Mgmt.
1 ) education
2 ) do they know/ understand ??
3 ) can they do it themselves?
- open the bottle
