HEART FAILURE (or CHF)
Inability of the heart to pump sufficient
blood to meet the needs of the tissues
for oxygen and nutrients
Characterized by s/sx of fluid overload
or of inadequate tissue perfusion
Progressive, life-long condition that is
managed with lifestyle changes and
meds to prevent episodes of acute
decompensated heart failure
Chronic HF most common in people
older than 75
2 major types:
Systolic HF more common; alteration
in ventricular contraction; characterized
by weakened heart muscle
Diastolic
HF
less
common;
characterized by stiff and noncompliant
heart nuscle
Assessment of ejection fraction (EF) is
performed to assist in determining the
type of HF; normal EF is 55%-65% of the
ventricular volume
Results from a variety of cardiovascular
conditions (chronic HPN, CAD, valvular
diseases)
Treatment is aimed at opposing the
current mechanisms of the heart and
relieving symptoms
DM pts are at risk for HF; atherosclerosis
of the coronary arteries is the primary
cause of HF
Left-sided HF pulmonary congestion
happens when the left ventricle cannot
effectively pump blood out of the
ventricle into the aorta and the systemic
circulation; Dyspnea, dry & non-
productive cough, pulmonary crackles,
low
O2
sat
levels,;
orthopneic,
experience
paroxysmal
nocturnal
dyspnea (PND sudden attacks of
dyspnea at night); adventitious breath
sounds
Right-sided HF congestion in the
peripheral tissues and the viscera
predominates;
increased
venous
pressure leads to jugular vein distention
(JVD) and increased capillary hydrostatic
pressure throughout venous system;
dependent
edema,
hepatomegaly,
ascites, anorexia, nausea, weakness,
and weight gain
Restriction of dietary sodium; avoidance
of excessive fluid intake, alcohol,
smoking; weight reduction; regular
exercise (30 minutes every day)
ACE inhibitors; Angiotensin Receptor
Blockers;
-adrenergic
blockers;
diuretics, digitalis (digoxin); calcium
channel blockers
MYOCARDIAL INFARCTION
Irreversible
cardiac
damage
occlusion of one or more arteries
Also
called
coronary
occlusion/thrombosis
from
artery
Chest pain that occurs suddenly and
continuous despite rest and meds
SOB, indigestion, nausea, anxiety, cool,
pale, moist skin
Assessment:
Patient Hx presenting symptoms, Hx
of previous cardiac and other illnesses,
family Hx
ECG, 2D-Echo
Lab tests:
Creatinine kinase CK-MB [heart
muscle] (M = 65-70 mg/dL; F = )
increased levels is indicated in
organ/tissue /cell damage & indicate
possible MI
Myoglobin (heme protein that helps
transport O2) increases in 1-3
hours and peaks @ 12 hours; if
negative, excellent parameter for
ruling out an acute MI
Troponin (helps contractile process)
increased for 3 wks
Analgesics, ACE-inhibitors, thrombolytics
Cardiac Rehab
Phase
1
atherosclerosis
diagnosis
of
Phase 2 after patient has been
discharged
Phase 3 long-term outpatient
program, maintaining CV stability
and long-term conditioning
Phase 4 maintenance out-patient
ACUTE PULMONARY FAILURE
Sudden
and
life-threatening
deterioration of the gas exchange fxn of
the lung and indicates failure of the
lungs to provide adequate oxygenation
PaO2 is less than 50 mmHg (hypoxemia)
and PaCO2 is greater than 50 mmHg
(hyercapnia), arterial pH is less than
7.35
Causes: drug overdose, head, chest, and
spinal
cord
trauma,
infection,
haemorrhage, sleep apnea, GuillainBarre syndrome, myasthenia gravis,
amyotrophic
lateral
sclerosis,
,
kyphoscoliosis,
malnutrition,
COPD,
asthma, cystic fibrosis; pneumonia,
ARDS, COPD, HF, pulmonary embolism,
restrictive lung disease
Early
signs:
restlessness,
headache,
dyspnea,
air
tachycardia, increased BP
fatigue,
hunger,
As hypoxemia progress: inc BP, central
cyanosis, diaphoresis, respi arrest,
confusion, lethargy, tachypnea
Correct
underlying
cause
(restore
adequate gas exchange), intubation,
mech ven (to maintain adequate
ventilation and oxygenation)
Assist with intubation and mech ven,
monitor LOC, ABG, pulse ox,v/s, mouth
care, skin care, ROM
STROKE
Ischemic:
Sudden loss of fxn resulting from lack of
blood supply to a part of the brain
s/sx numbness, weakness of face,
arm , leg, esp on one side of the body;
change in mental status;
trouble
speaking/understanding speech; visual
disturbances, difficulty walking/loss of
balance; sudden, severe headache; FAST
Motor loss hemiplegia (paralysis of one
side
of
the
body);
hemiparesis
(weakness of one side of the body)
Communication
loss
(difficulty
speaking);
dysarthria
dysphasia
(impaired speech); apraxia (inability to
perform a previously learned action)
Perceptual disturbances hemianopsia
(loss of half of the visual field)
Sensory loss loss of proprioception;
agnosias (deficits in ability to recognize
previously familiar objects perceived by
one or more senses)
Cognititve impairment & psychological
effects frontal lobe: learning capacity,
memory,
other
higher
cortical
intellectual fxns may be impaired
Non-contrast CT scan; ECG; carotid UTZ;
MRI; transcranial Doppler flow studies;
tranthoracic/transesophageal
echocardiography; xenon-enhanced CT
scan; single photon emission CT scan
(SPECT)
Warfarin;
aspirin
if
warfarin
is
contraindicated;
clopidogrel;
simvastatin; ACE inhibitors; thiazide
diuretics, mannitol; corticostreiods
Hemorrhagic:
Intracranial/subarachnoid hemorrhage;
bleeding into brain tissue, ventricles,
subarachnoid space
Results
from
ruptured
intracranial
aneurysms (weakening of arterial wall)
Depends on cause and type of brain
attack (CVD)
S/sx severe headache, vomiting, early
sudden change of LOC, possibly focal
seizures, nuchal rigidity (pain & rigidity
of nape); visual disturbances, tinnitus,
dizziness, hemiparesis
CT scan/MRI, cerebral angiography; LP is
performed if there is no evidence of
increased ICP, CT scans are (-),
subarachnoid hemorrhage must be
confirmed; toxicology screen for illicit
drug use
Carotid endarterectomy removal of
plaque form carotid artery
Allow brain to recover from initial insult,
prevent/minimize the risk of rebleeding,
prevent/treat complications; fresh-frozen
plasma and vitamin K; anti-seizure meds
for prophylaxis; provide anti-embolism
stockings, fever should be treated; antiHPN meds
Elevate HOB; possible hemicraneictomy
for increased ICP; intubation with ET
Craniotomy if GCS decreases and
diameter of hematoma exceeds 3 cm
t-PA tissue plasminogen activator
