NU 428 Heart Failure
What is heart failure? What is it caused by?
HF is d/t an interference with one of the normal mechanisms regulating cardiac output which lead to ventricular dysfunction & symptoms of HF
SV is affected by preload, contractility, afterload.
HR affected by autonomic NS
Many times, the biggest problem is with the contractility, the strength of the heart pumping muscle to pump blood. Muscles become weak, have problems with stroke volume and CO.
Could be caused by MI, renal problems, etc.
So if they have an MI, tell them about s/s of HF. Teach not just the pt but the patient’s family.
What are the risk factors of heart failure?
1.CAD - lack of blood flow to the heart
3.Diabetes - glucose in the bloodstream, causes blood to be thick and not flow well which causes lack of nutrient transfer
4.Smoking - vasoconstricts and has carcinogens
5.Obesity - increases workload on the heart. Extra tissues need to be fed.
6.Hyperlipidemia - high cholesterol, triglycerides, LDL.
What are the general symptoms of heart failure?
SOB most common --extra pillows, pulmonary congestion from L sided HF.
Abdominal/leg fluid build up (usually one or the other)
Crackles (not necessarily in chronic)
PMI may be displaced (if heart enlarged)
Liver/spleen enlarged – R sided usually
What are the differences between right sided and left sided heart failure?
R sided is more diastolic problem, filling of the heart problem. Get distended neck veins, hepatomegaly, peripheral edema, fatigue, inability to perform ADLs, and weight gain. If you gain 2 pounds within a couple days, call a doctor. *Weight is the best indicator of fluid gain or loss.*
L sided is systolic HF, pumping problem. More pulmonary complications. SOB, crackles, poor O2 sat, activity intolerance, hypoxemia, fatigue, inability to perform ADLs, want to sit up to sleep.
What is the first of the body's compensatory mechanisms triggered by heart failure?
Sympathetic NS Activation:
First mechanism triggered due to low cardiac states (inadequate CO/SV)
But the least effective at solving the problem
Works initially, eventually makes it worse by increasing the O2 demand and workload on a strained heart
Epinephrine and norepinephrine
Overloaded heart tries to maintain CO—which is low---so baroreceptors in carotid sinus, etc are stimulated…which stimulates SNS to release catecholamines, increases heart rate, causes vasoconstriction which causes increased preload on an already volume loaded heart, increases workload of the heart, worsens ventricular performance.
How does the body's hormonal response to symptoms compensate for heart failure?
Hormonal response: BNP is released with any kind of stretching of the heart muscle. Over 100 indicates some degree of heart failure.
Kidneys think there is a decreased volume/fluid.
Release of aldosterone from adrenal cortex: sodium and water retention which causes increased peripheral vasoconstriction (BP).
Secretes ADH (AKA Vasopressin) increases water reabsorption in renal tubules. Kidneys to hold water and increase blood volume. Produces endothelin (also stimulated by catecholamines & ATII), arterial vasoconstriction, increased contractility
Decreased renal perfusion triggers the RAAS cascade. Increase in Renin-angiotensin—aldosterone and increase in ADH (vasopressin). ADH retains fluid and sodium which compounds the problem.
What are two physical changes to the heart caused by heart failure?
From the excessive volume of fluid in the heart.
Enlarged chambers d/t pressure over time
Fibers stretch d/t blood volume @ end diastole.
Frank Starling ’ s Law:
- Initial increase in contractility/CO
- Then becomes overstretched and fails/ decreased CO
Hypertrophy is when the muscle overdevelops when it’s trying to pump against a constricted aorta. Has poor coronary artery circulation (easily becomes ischemic).
SNS + hormonal response = increased cardiac workload, myocardial dysfunction & ventricular remodeling
Remodeling – hypertrophy of myocytes, increased ventricular mass, increased O2 consumption, impaired contractility
Ventricles are larger less efficient pumps - high risk for dysrhytmias & SCD
What are the classifications of heart failure? How does the body respond in both cases?
Left – sided (LV dysfunction)
- Back up into LA/Pulm veins
- Pulmonary edema
- The most common; is a disturbance of the contractile function of the LV; may result from LV MI, mitral/aortic valve disease, HTN.
- S/S: dyspnea (particularly nocturnal); cough and hemoptysis; resp. distress
Right - sided
- Backup into RA/Venous circulation
- JVD, Hepato/Splenomegaly, GI, peripheral edema
- Cor Pulmonale: Vasoconstriction of the pulm. artery, causes R ventricle to enlarge. Usually in COPD patients. High CO2 levels and low O2 causes constriction.
- Is a disturbance of the contractile function of the RV; may result from a PE, RV MI, but most commonly from L sided failure
No matter the cause, these pts. will typically have low CO and poor organ perfusion. When pulmonary congestion and edema are present, a diagnosis of HF can be made. The body’s response, whatever the cause, is to mobilize its compensatory mechanisms to maintain CO and BP.
What is the stoplight tool for heart failure?
Green – doing fine; keep taking meds, less than 2 liters of fluid a day, less than 2300 mg of Na a day
Yellow – Little orthopnea, dyspnea, weight gain of 2 pounds in one day or 5 in one week, increase in peripheral swelling, decreased energy; take an extra diuretic, watch Na intake, might give an extra med to take
Red – Indicates immediate need, unstable symptoms, difficulty breathing even at rest, gain more than 4 pounds in a day, wheezing or chest pain, severe weakness, dizziness, or fatigue; Call healthcare provider immediately, maybe 911, do not wait to see if they get better.
What characterizes acute decompensated heart failure?
Early: mild increase in RR, decrease in PaO2
Late: More fluid into interstitial space than lymphatics can handle – interstitial edema
Symptomatic tachypnea (SOB out of proportion to activity)
Pulmonary pressures increase, fluid & RBCs move into alveoli (alveolar edema)
coughing w/ or w/o hemoptysis/frothy sputum
Lung auscultation: crackles and/or wheezing
Further decrease in PaO2 and rise in PaCO2
Clinical findings: anxiety, pale, cyanosis
SNS symptoms: cool/clammy, tachycardia, BP (up then down w/severity)
Resp symptoms: orthopnea, wheezing, cough, hemoptysis, accessory muscle use
When HF progresses to the point where there is inadequate tissue perfusion, this is known as Cardiogenic Shock. (contractility problem, not a lack of volume)
What does a pulmonary artery catheter measure and what are the normal measurements?
CVP – (Normal 2 – 6 mm Hg) measures R vent. Preload (Right end diastolic pressure). It is used to diagnose fluid volume status and R sided heart dysfunction.
PAS (systolic) – (normal 20 – 30) reflects pressure in the pulmonary vasculature.
PAD (Diastolic) – (normal 5 – 10) measures L vent. Preload
PAWP – (normal 5 – 12) Obtained with balloon inflated and measures Left Ventricular End Diastolic Pressure (LVEDP). Is very close to PAD pressure.
During the insertion procedure, the first waveform will be the right atrial pressure. This wave will resemble a CVP wave. The following waveform will be the right ventricular pressure as the catheter passes through the right ventricle. During this time, the patient may experience some ventricular dysrhythmias that disappear as soon as the catheter exits the right ventricle. The catheter will enter the pulmonary artery and this will be its resting place for the majority of the time. Finally, when the balloon is inflated, the catheter will float into the pulmonary capillary and the resulting waveform will be the wedge pressure.
The pulmonary artery catheter is checking body volume. Checks if they overloaded or if they’re dehydrated.
What are the characteristics of chronic heart failure?
Compensatory mechanisms activated (progressive), can easily progress to acute heart failure
Chronic neurohormonal activation
Remodeling: hypertrophy or dilation
Manifestations depend on age, extent, type
- Fatigue – d/t decreased CO, impaired perfusion, decreased O2, anemia (nutrition, renal, drug)
- Dyspnea – d/t increased PA pressures
- Orthopnea – while recumbent, usually have to lay on multiple pillows when sleeping, dry hacking cough (may be 1st sign)
- Paroxysmal Nocturnal Dyspnea (PND) – asleep, reabsorption of fluid, suffocation, panic
- Tachycardia – early sign (may be blocked by Bblocker)
- Edema – dependent, liver, abdominal (ascites), lungs, pitting
- Nocturia – increased renal perfusion d/t reabsorption while recumbent
- Skin changes – dusky, LE brown/brawny, shiny
- Behavioral changes – d/t decreased CO, restless, confusion, decreased attention
- Chest pain – decreased CO, increased myocardial work
- Weight gain - initially d/t fluid, ascites/pressure causes anorexia/nausea, muscle wasting. Gain 3 pounds within 2 days, call the
What are the complications of heart failure?
Pleural effusion – transudation into pleural space
Dysrhythmia – d/t chamber enlargement, alteration in electrical path (esp atrium/Afib) promotes thrombus; occur bc of lack of oxygen OR from K level being out of whack (kidneys aren’t working well, can’t get rid of K). Afib + HF: anticoag, cardiovert, antidysrhytmics. EF <35%: high risk fatal dysrhytmias (VF), 50% will experience SCD/VF – ICD. May hear S3
Left ventricular thrombus – enlarged LV, decreased CO and contractility
Hepatomegaly – esp w/RV failure, impaired liver function (cell death, fibrosis, cirrhosis), elevated liver enzymes
Renal Failure – Decreased CO = decreased renal perfusion. Messes up electrolytes and volume.
How do you diagnose heart failure?
Echo: LV dysfunction, wall motion abnormalities, EF (may do TEE), tells you how the valves are functioning, can see blood flow through the heart. If TEE is performed, check gag reflex after taking it out.
BNP: 100-500 suspect HF, >500 HF likely
EKG: LBB/LVH common, Afib
Constellation of symptoms
What are the principles of immediate management for heart failure patients including interventions and monitoring?
- High fowlers, feet dangling - increases venous return and thoracic capacity
- Oxygen/positive pressure/ventilate, might intubate
- Fluid restriction to 2-3 liters/day
- Daily weight
- Ultrafiltration: rapidly remove extracellular and intravascular fluid similar to dialysis
- Circulatory assist devices
- IABP: increase coronary blood flow, decreases work (afterload reduction)
- LVAD: maintain pumping ability of failing heart (bridge to healing or transplant)
- Pulse Ox
- Hemodynamics: art line, CBP, PAP, CO (may titrate meds to achieve certain numbers to improve CO)
Assess pulses, lungs
What medicines decrease venous return in heart failure patients?
Diuretics (Lasix/ Bumex )
1.Decreased LV volume reduces venous return (preload)
2.Overfilled LV contracts more efficiently & improves CO
3.Increased LV function decreases pulm . vasc . Pressures
4.Improved gas exchange.
Vasodilators: decrease preload by opening up vessels
- reduces preload and afterload
- dilates the pulmonary & systemic vasculature for the treatment of pulmonary edema
- improves gas exchange
- antianxiety, dyspnea relief
What are some vasodilators used for heart failure patients? What should a nurse know about these drugs?
- decreases preload/afterload (high dose)
- Improves coronary artery circulation by dilating coronaries
- Increased myocardial O2 supply
- Safety – headache, BPs
Nipride – POTENT vasodilator. Opens up vessels quickly and extremely
- Reduced preload/afterload
- Improved myocardial ctx & increased CO
- Reduced pulmonary congestion, DOC for ADHF + pulm edema
- Safety – hypotension, thiocyanate tox (after 48h), ICU
- Very photosensitive, has to be wrapped in a dark bag or covered in foil while hanging.
- If a person is on nipride too long, they can get cyanide poisoning.
- Want them to be sitting up, not flat in bed. It increases the preload when lying flat.
- Recumbinant BNP
- Arterial/Venous dilation
- Reduced PAWP
- Increased CO w/o increasing O1 consumption
- cause diuresis
- Short term in ADHF
- No titration, watch BP
What are drugs for improving contractility in heart failure patients?
Beta adrenergic Agonists
- Dopamine ( Inotropin ): increases contractility AND SVR
- Dobutamine ( Dobutrex ): more specific for CO, not a vasoconstrictive drug, doesn't increase SVR but increases contractility
- Digitalis: increases contractility but also increases O2 consumption
- Norepinephrine ( Levophed )
Hemodynamic monitoring: Monitor BP very closely, likely needs hemodynamic monitoring while on these drugs
Safety: Extravasation cases tissue necrosis, ventricular dysrhythmias
- Inamrinone ( Inocor )
- Milrinone ( Primacor )
Only short term
Safety: Only IV, dysrhythmias, thrombocytopenia, hepatotoxicity
What is cardiogenic shock? How is it managed?
The heart fails to pump effectively (40% less effective) and results in compromised cardiac output (CO).
Cardiogenic shock is a state in which the heart has been damaged so much that it is unable to supply enough blood to the organs of the body.
What is shock? Shock – decreased perfusion and impaired cellular metabolism.
Decreased perfusion of tissue NOT from hypovolemia, but lack of CO is from LV damage!
As a result of decreased contractility…pt develops elevated left ventricular and RV filling pressures (represented by….PAP and CVP) and low cardiac output.
Other S&S r/t decr CO: hypotension, early indication is narrowing PP (D incr and S decreases …normal around 40--think of PP of 120/80!) Telltale symptom: SBP < 90 and HR > 110 and tachypnea (pain and hypoxia), tachycardia, decreased U/O, rapid, shallow respirations (initially see resp. alk), confusion, cyanosis is late sign
- Cool clammy skin, decreased cap refill, weak pulses, decreased UOP, Confusion.
- Tachycardia, tachypnea, Elevated CVP, Hypotension, Narrow PP
Impaired cellular metabolism
If AMI, reestablish coronary blood flow (angioplasty, thrombolytics); if a failing valve (correct the valve problem); if arrhythmias (correct arrhythmia problem)
Increase O2 supply with supplemental O2
- nitrates – improve coro. blood flow and decr. preload/afterload
- pos. inotropes – improve myocardial contractility
- beta-blockers – decrease HR and contractility
- ace-inhibitors – decreases afterload
- diuretics – decrease preload and afterload (careful if low BP)
Circulatory assist devices (IABP)
Treat the cause
- Increase oxygen supply
- Decrease oxygen demand
What are the goals of chronic heart failure treatment?
Tx cause: rhythm, ischemia, valvular problems
Maximize CO/ Improve Ventricular function: Beta blockers, digoxin, reduce preload/afterload, improve squeeze, PPM (Perm Pacer) usually RA/RV, CRT is BiV to stimulate normal simultaneous conduction, improves CO
Alleviate Sx/ Improve QOL: swelling and SOB can be improved w/ rehab, home health (PT/exercise program), ICDs.
Preserve “ target organ ” function: perfuse kidneys/liver, brain (watch pressures/anticoagulate), provide O2
What are the principles of drug therapy with heart failure?
- Mobilize edema
- Reduce preload & pulm venous pressure
- Thiazide (HCTZ)
- Txs HTN & HF
- Inhibits sodium resorption in distal tubule
- Promotes excretion of Na & H2O
- Loop (Lasix/Bumex)
- Na, Chl, H2O secretion
- Watch K+
Ace Inhibitors (Captopril, Lisinopril, enalapril)
- DOC to block RAAS & ultimately reduce aldosterone (improves diuresis)
- Decrease ventricular remodeling
- Reduces SVR, increasing CO (tissue perfusion)
- Side effects: hypotension, cough, angioedema
Angiotensin receptor blocker (Losartan, valsartan)
- Potassium sparing diuretic
- Block aldosterones effects
Vasodilators (Isosorbide mononitrate/Dinitrate
- Watch w/ED meds (Viagra)
Beta blockers (Coreg, Toprol XL)
- Block negative effects of SNS
- do reduce contractility, start slow
- BP 1h after dose, watch BP, fatigue, bradycardia
Positive Inotropes (digoxin)
- Increase the force of cardiac contraction (inotropic)
- Decrease conduction speed, slow HR (chronotropic)
- More completely empty ventricles
- Toxicity: anorexia/N/V, “yellow” vision, dysrhytmias (Digibind)
- Hypokalemia is most common cause
What are the most common reasons for re-admission due to heart failure complications? What teaching should be provided in these situations?
Usually from not following guidelines for diet, fluid restriction, med routine.
Take meds and stick to the routine
< 2.3 gram Na diet
Fluid restriction w/renal dz.
3 pounds in 2 days or 3-5 pounds in a week, call the doctor!
What are the core measures in treatment of heart failure?
1.Written DC instructions: activity level, DC meds, f/u appt , weight monitoring, what to do if symptoms worsen
2.Documented LV function
3.EF <40% (mod/severe systolic dysfunction) must be discharged on ACE-I or ARB
What are two pneumonics for hospital and self-management of heart failure respectively?
Hospital management: UNLOAD FAST
Aminophylline: increases glomerular filtration rate, improves kidney function, but don't give it much anymore
Digoxin: Know signs of toxicity
Fluids - decrease
Afterload - decrease
Sodium - decrease
Weight - weigh yourself every day at the same time on the same scale
Diet - encourage to lose weight if overweight, less than 2.3 g of Na, limit amount of alcohol consumption