heart failure Flashcards
what is hemodynamics
what controls most of it
the fluid dynamics of blood flow.
the sns controls it primarily
in the book this is…affected by?? everything from CO, SV, preload, afterload, contractility, heart rate
how can you nonivasively assess cardiac hemodynamics
• Estimated by measuring jugular venous distention
Invasive assessment of cardiac hemodynamics (done on hemodynamically unstable pt)
• Pulmonary artery catheter
this is usually in a critical care setting
what is heart failure (HF)?
• Inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients
indicates myocardial disease in which there is a problem with the contraction of the heart or filling of it
used to be called CHF
how is HF characterized
it is recognized as a clinical syndrome characterized by S/S of fluid oveload or inadequate tissue perfusion d/t the heart not being able to produce CO sufficient for demands
is HF acute or chronic, reversible?
either.
can be reversed but its usually progressive and lifelong
where are rates of HF high (what populations)
in rural settings
in older adults
etiology of HF
most prevalent
-ischemic heart disease,->hypoxia->acidosis
-hypertension (systemic or pulmonary)->inc afterload->hypertrophy->inc contractility and is compensatory but may dec space for filling
-diabetes melliutus,
metabolic syndrome,
hyperlipidemia,
smoking
also cardiomyopathy inc metabolic rate eg fever iron overload hypoxia severe anemia (HCt less than 25%) acidosis Worsened by:electrlyte imbalances antiarrythmic meds dysrhythmias
why is HF and the compensatory mechanisms surrounded it termed a “vicious cycle”
the heart cant pump sufficient blood to body so the body stim the heart to work harder but it cant respond so the failure becomes worse
how are systolic and diastolic HF develop
diastolic is d/t hypertrophy (cant fill)
systolic is d/t other factors
HF isnt differentiated by systolic or diastolic as their symptoms are too similar. how is it classified instead
R and L sided HF
or R and L ventricular failure
what causes the S3
aka ventricular gallop-caused by lg volume of fluid entering the V at beginning of diastole
what causes S4
aka atrial gallop. when atrium contracts into stiff V eg s in systolic failure post MI
how does L sided HF affect the lungs/breathing
- Pulmonary congestion occurs when the left ventricle cannot pump effectively
- Pulmonary edema is caused by a backup in the pumping system
- Dyspnea or SOB may be precipitated by activity
- May have orthopnea
- May have sudden attacks of dyspnea at night called paroxysmal nocturnal dyspnea
- Cough associated with left ventricular failure is dry and nonproductive initially will later on be wet with frothy sputum indicating pulmonary edema
- O2 saturation will decrease due to failed pumping ability
- Adventitious sounds. Crackles in lung in early LV failure
how does the dec perfusion affect the rest of the body other than the lungs (from L sided HF)
- Decreased blood flow to kidneys causes reduced urine output (Oligura)
- As it progresses GI symptoms will appear due to lack of O2 perfusion.
- Dec perfusion->dizziness , light headedness, restlessness, anxiety( leads to dyspnea->anxiety=another vicious cycle
- Cyanosis may appear, skin is cool
- -tachycardia, -dysrhythmias->Palpitations may be felt
- Patient becomes increasingly fatigued
what will cause RVF according to ppt
RVF
Acute
Inferior MI
Pulmonary embolus
Chronic
Cor pulmonale
LVF
what will cause LVF according to ppt
LVF
Acute
Anterior MI
Hypertensive crisis
Chronic
Hypertension
clinical mnfts of R sided HF in relation to congestion/edema
- Congestion in the peripheral tissues and viscera is evident
- Increased venous pressure leads to JVD and inc hydrostatic P throughout venous system
- Fluid retention in the lower extremities. Dependent edema, pleural effusion, ascites, anorexia and nausea (congestion in gut), weakness, weight gain
- Edema is usually in ankles-. Can be in sacrum if bedbound. Pitting edema is obvious only after retention of at least 4.5kg of fluid. May occur solely in abdomen,
how does R sided HF affect GI tract/appetite etc
- Anorexia, nausea or abdominal pain result from venous engorgement and venous stasis in abd organs. Cachexia is a potential complication.
how is liver affected by R-sided HF
- Enlargement of the liver (dt venous engorgement) may-> secondary liver dysfx-> fluid forced into the abdominal cavity=ascites. Ascites may->GI distress
how is HF usually Diagnosed
what other info can this diagnositc give
other diagnostics used
echocardiogram
-helps identify cause, ejection fraction
also chest xray
angiogram
ECG
labs performed for HF
- BNP- high levels are sign of high cardiac filling P and can aid in dx of HF. THis is important for diagnosing
- electrolytes
- BUn
- creatinine
- TSH
- CBC
- routine urinalysis
- exercise testing may be done to det if CAD and cardiac ischemia are causing it
class notes add:
- RBC, HCt, Hgb
- GFR
goal of mgmt of HF
- elinate the etiologic factors eg a. fib., excess alcohol, HTN, ischemia
- reduce the workload ont he heart by dec after/preload
- optimize all therapeutic regimens
- prevent exacerbations of HF
how would the ejection fraction be if a pt has diastolic heart failure
it could still be high but the volume (CO) would be lower than normal
what is cor pulmonale. which side of the heart does this cause to fail
enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance or high blood pressure in the lungs (pulmonary hypertension).
affects R side
JVD is an indicator of _____ fx
preload on right side. (R V fx)
what can be used as an indicator of LV afterload
MAP
its an approximate indicator
modifiable risk factors for HF
risk factors from in class
ischemic heart disease (such as cardiomyopathy), HTN, DM, metabolic syndrome, hyperlipidemia, smoking
in class: Risk factors: - Hypertension - Diabetes - Smoking - CAD – atherosclerosis
how can pts modify lifestyle for HF
reduce salt, avoid excessive fluid intake, alcohol, smoking, weight reduction, exercise,
what are the general methods of Tx for HF
- Oral + IV drugs, O2, implantation of assistive devices, surgical approaches (incl transplant)
- Lifestyle
what are the general classes of medications used to Tx HF and how do their actions assist the heart
- ACE inhibitors- promote vasodilation and diuresis by decreasing afterload and preload, decrease the secretion of aldosterone
- Angiotensin II Receptor blockers-similar efects ro Ace Inhibitors. (Result in dec BP, dec systemic vascular resistance and improved CO)
- Beta blockers- reduce mortality and morbidity by reducing the adverse effects from the constant stimulation of the sympathetic nervous system
- Diuretics- prescribed to remove excess fluid, and decrease vascular volume and edema
- Vasodilators- decreases resistance
- Digoxin- increases force of myocardial contraction
- Supplemental O2
- End stage or severe require transplants or VADs
common meds for systolic HF
diastolic HF
ACE I
B-Blockers
diuretics
vasodilators
diastolic failure Tx depends ont he cause. after contributing causes eg HTN and ischemic heart disease are Tx the pt may be started on ACE I and diuretics. May use CCB.
what drug is contraindicated in systolic HF but is ok for diastolic HF
calcium channel blockers
what food could have serious interactions w HF pts drugs
grapefruit
other than pharmacologic interventions what can be done for HF
-supplemental 02
Sx
implantable devices
cardiac transplant
considerations for supplemental 02 in HF
use caution as it may inc afterload and titrated to oxygen sat of>90%
- used for hypoxemic pts
- some pts require supplemental 02 only during activity
how can dysrhythmias in HF pts be addressed
ventricular dysrhythmias can be prevented by placement of
-implantable cardioverter defibrillator (ICD)
how can conduction problems be addressed in pts w HF
• CRT = cardiac resynchronization therapy: biventricular pacemaker to treat conduction deficits
when is a ventricular assist device (VAD) used
it offers mechanical circulatory assistance and is a bridge therapy for cardiac transplantation
nursing interventions for mgmt of HF
o Give meds + monitor
o Assess Na, K, and lfuid balance – intake/output
o Eval pt + family understanding of lifestyle changes, signs + symptoms
o Weigh pt at same time on same scale risk if 1-1.5kg gain/day or 2.25kg gain/week
o Auscultate lungs sounds
o Determine degree of JVD
o Eval edema
o Examine skin turgor + mucous membranes for signs of dehydration; pulse, BP, postural hypotension
o Assess symptoms of fluid overload: orthopnea, PND, DOE
o Med side effects
o Discuss goals, education, etc.
what is a consideration for angiograms
- Angiogram: die shown in coronary arteries ensure does not have dye allergy MAKE SURE DOES NOT HAVE ALLERGY TO SEAFOOD!!! (Will go into anaphylaxis)
what can cause hypo or hyperkalemia for pt on drugs for HF
diuresis may lead to hypokalemia
hyperkalemia can occur w ACE I, ARBs or spinonolactone (a potassium sparing diuretic)
cardiac glycosides eg
DIGOXIN
MOA of cardiac glycosides
by inhibiting sodium-potassium pumo which results in inc calcium concentration->inc in myocardial contractility (it is a positive inotrope)
aslo augments vagal tone>inc diastolic filling between heartbeats and reduces heart rate(negative chromotropic effect) which inc CO and cardiac eficiency
dec velocity of conduction ( this is a negative dromotopic) the dec conduction slows heart rate(negative chromotropic))
indications of digoxin (cardiac glycosides)
HF and ventricular dysrhythmias
what are the benefits of using digoxin in Tx of HF
inc force of contraction->inc volume of blood ejected->less blood remaining in ventricle->less P which->dec in symptoms of pulm edema, pulm HTN, R sided V failure and an inc in tissue perfusion
-promotes diuresis dt inc blood supply to kidneys
contraindications for cardiac glycosides
allergy second or third degree heart block a. fibrillation V tachycardia HF from diastolic dysfx subaortic stenosis (some of the above may also be indications and it depends on discretion of prescriber)
adverse effects of cardiac glycosides
what is the worst thing that could happen
Increase myocardial workload by increasing oxygen demands
- other negative effects include:
- dysrhythmias
- anorexia, nausea, vomiting, abd pain
- headache, faituge, malaise, confusion, convulsions
- coloured vision, halos
symptoms of dig toxicity
anorexia, nausea, vomiting, fatigue, depression, malaise (all early signs)
- changes in heart rythm or rate, irreg
- ECG changes
how do you treat digoxin toxicity
hold the med while monitoring the pts symptoms and serum levels
-if extreme then give digoxin immune fab (antidote) which binds to digoxin. when meas serum levels after this it will be inaccurate as it can differentiate between bound and unbound
pre assessment for positive inotropic durgs
when dont you give
Most important are: apical pulse for 1 minute. dont give if pulse is less than 60BPM or>120BPM
- check electrolyte levels
- check serum drug levels
- Blood pressure, pulse rate (apical and radial for 1 full minute)
- Heart sounds
- Peripheral pulse location and grading
- Capillary refill
- Presence of edema
- Breath sounds
- Weight
- Intake and output amounts
- Serum lab values such as potassium, sodium, magnesium, and calcium
- Electrocardiogram
- Kidney function lab tests (BUN and creatinine levels)
- Liver function tests
- Medication history
- Dietary habits, recall of all food in past 24 hours
- Intake of bran ( increases drug absorption)
- Smoking history
- Alcohol intake
- Electrolytes dt narrow therapeutic range. Hypokalemia may precipitate its toxicity
- Report edema
- Full Neuro assessment
- GI assessment
- Heart assessment-record pulse of less than 60 or over 100 etc
- Vision and sensory assessment; note any changes such as green or yellow halos surrounding peripheral field of vision
- Assess for complaints of anorexia, nausea, vomiting which indicate cardiac glycoside toxicity
dosing for digoxin
what inc the risks of toxicity
it has a narrow therapeutic window (1-2.5nmol/L) therefore the serum levels must be monitored carefully
-low potassium levels inc the potential for toxicity
whats a life threatenging digoxin OD
> 10mg in adults
>4mg in kids
phosphodiesterase inhibitors have what kind of action
they are referred to as inodilators (inotropes and dilators)
how do phosphodiesterase inhibitors work and whats an example of them
eg Milrinone
they inhibit phosphodiesterase which results in inc in intracellular cAMP with an end result in more calcium for the heart to use for contraction.
-it makes the heart more cmpliant
-it has 10-100x higher affinity for blood vessels than heart and its primary beneficial effect is a reduction in afterload by relaxing the surrounding blood vessels
concerns with phosphodiesterase inhibitors
- ventricular dysrhythmia (in 12% of pts)
- no antidote
- has other adverse effects including HoTN, chest pain, hypokalemia
- when given w diuretics ma cause significant hypovolemia
what kind of diuretic is furosemide (class)
it is a loop diuretic
how are loop diuretics particularly useful in comparison to other diuretics
rapid onset of action and they last at least 2hrs
-effective in single daily dose
effects of loop diuretics
-dec BP
-dec pulm vascular resistance
dec systemic vascular resistance
-dec CVP
-dec LV end diastolic P
how does BNP or ANP affect cardiac output or ejection fraction
what are Anp and BNP
Secreted by the ventricles of the heart in response to excessive stretching of cardiac muscle cells
Decreased systemic vascular resistance
Decrease in afterload (BP)
Natriuetic (decrease blood volume)
Discharge of sodium via urine
Increases EF (therefore…..cardiac output)
JVD >? is conidered abnormal
> 3cm
consderations around bed rest and pt with heart failure
they can rest to promote diuresis but they should exercise at least 30-45 miutes a day
what time of day should diuretics be given and why
in morning so the pt doesnt have to get up in the night and pee
considerations for a patients mood/state of being w heart failure
they may be very anxious d/t breathless ness which inc at night. anxiousness inc cardiac workload
primary disadvantage of diuretic use
when do these usually occur
metabolic adverse effect that can result from excess fluid or electrolyte loss
usually d/t doses (dose size?)
carbonic anhydrase inhibitors are from
derived from sulfonamide antibiotics
cardbonic anhydrase inhibitors (CAI) MOA, indications,
MOA: reduce the formation of hydrogen ions and bicarbonate ions from C02 and H20 and blocks their reabsorption resulting in reduction of avail of these ions
indication: many, mostly open angle glaucoma. used to manage edema secondary to heart failure but they are less potent than loop diuretics or thiazide diuretics
CAI
contraindications, adverse effects
hyponatremia, hypokalemia, severe liver and kindy dysfx etc
adverse: metabolic abn eg acidosis and hypokalemia, inc blood glucose
allergy to what would cause you to refrain from giving your pt loop diuretics
to loop diuretics or to sulfonamide antibiotics
worst side effects of loop diuretics
hypokalemia, dehydration
hyperglycemia, NVD, inc calcium excretion
osmotic diuretics eg
mannitol, urea, organic acids, glucose. mannitol is most common
osmotic diuretics MOA
its nonabsorbable and causes osmotic P in glomerular filtrate which pulls fluid into renal tubules from surrounding tissues
may induce vasodilation
it isnt that good for peripheral edema as it doesnt stimulate enough sodium loss
adverse effects of osmotic diuretics eg mannitol
pulmonary congestion, convulsions, thrombophlebitis
potassium sparing diuretics eg
MOA
spinonalactone
competitivly binds to aldosterone receptors and blocks reabsorption of sodium and water thats induced by aldosterone secretion
strength of potassium sparing diuretics compared to other diuretics
characteristic that makes them good to pair with _____
weak compared to thiazide and loop
as theyre potassium sparing theyre good to pair with the above as they have the opposite effects on potassium and chloride
adverse effects of potassium sparing diuretics
electrolyte imbalance (hyperkalemia) bleeding issues
thiazide diuretics are from
MOA
from sulfonamide antibiotics
inhibit reabsorption of sodium, potassium, chloride in DCT resulting in osmotic water loss AND cause relaxation of arterioles to dec afterload
thiazide diuretics indications
HTN, heart failure, edema
thiazide diuretics toxicity or adverse effects
hypokalemia. Tx involves electrolyte replacement
HoTN
what should be assessed for pts on diuretics
assess fluid volume status (cap refill, skin turgor, mucous membranes) electrolyte status, ph, postural blood pressures, resp rate, temp, SOB
monitoring of pt during diuretic therapy includes
BP, pulse, i&O, daily weight
s/s of hyperkalemia
NVD, abdominal cramping.
pt teaching for pt on diuretics
pay attention to potassium rich foods
- change positions slowly to dec risk of syncope
- may need to force fluids to maint hydration
- keep journal of weight, other factors related to Dx
- may need meas to prevent constipation
- s/s of hypokalemia
- avoid heat to prevent hypovolemia
- pts taking diuretic and digitalis should learn to monitor pulse
- pts w diabetes should be taught to monitor BG levels as the diuretics may inc BG
s/s of hypokalemia
weakness, leg cramps, cramping
which drugs used to treat heart failure are afterload reducers
ACEI:afterload reducer
Drug name:Enalapril
MOA: block conversion of angiotensin 1 to angiotensin 2inhibits vasoconstriction, decrease fluid (Na and H20) reabsorption by inhibiting aldosterone/ADH secretion
Pre/post assessments: Monitor BP and pulse frequently, assess for signs of angioedema (dyspnea). Monitor weight and assess pt routinely for fluid overload; labs (renal, electrolytes?)
Worst side effect: inadequate CO, cough develops from action of vasodilator bradykinin, increased K
ARB:afterload reducer
Drug name:
MOA Primarily effect smooth muscle and adrenal gland by selectively blocking the binding of Angiotensin2block vasoconstriction and the secretion of aldosterone and ADH
Pre/post assessments: BP, labs (renal, electrolytes?)
Worst side effect: hypotension, increased K, cough, inadequate CO from peripheral vasodilation, aggravated HF
Direct vasodilators:afterload reducer
Drug name:
MOA: direct acting peripheral vasodilationdecrease SV
Pre/post assessments: BPq5 min if given IV; Watch for reflex tachycardia
Worst side effect: hypotension, reflex tachy, headache, dizziness, inadequate CO from peripheral vasodilation, aggravated HF
which drugs used to treat HF are preload reducers
diuretics
which drugs are positive inotropes used to treat heart failure
Cardiac glycosides positive inotrope
Drug name: Digoxin
MOA: increased myocardial contractility by inhibiting NaK ATPase pumpincrease in cellular Na and Ca; decrease velocity of electrical conductionprolongs the refractory period
Pre/post: narrow therapeutic window (0.64-1.54 nmol/L), low K levels increase risk of toxicity, dysrhythmia
Worst SE: increase myocardial workload by increasing oxygen demands, digtoxic, hypokalemia
Digoxin Immune FAB- antibody for OD
Phophodiesterase inhibitors: positive inotrope
Drug name: Milrinone
MOA: Milrinone works by selectively inhibiting phosphodiestrease type 3, which results in more calcium for the heart to use in muscle contraction
Pre/post:
Worst SE: increase myocardial workload by increasing oxygen demands
