1
Q
heart failure
A
- the clinical syndrome described as the inability of the heart to pump an adequate amount of oxygenated blood to meet the body’s demands
- inadequate CO
2
Q
heart failure is either
A
a filling problem (poor compliance or lack of space to fill)
OR
-a contracting problem (poor contractility)
3
Q
HF stats
A
- over 5.8 million people in the US have heart failure
- most common reason for hospitalization in adults >65
- number one cause of readmission
- there is no cure for heart failure, only preventative measures and treatment of symptoms is available at this time
4
Q
Etiology: who gets HF?
A
- primary risk factors: coronary artery disease(CAD); advancing age
- contributing risk factors: hypertension, diabetes, tobacco use, obesity, high serum cholesterol, African-American decent
5
Q
The goal is to…
A
Improve cardiac output
6
Q
cardiac output
A
the amount of blood ejected out of the ventricles each minute
7
Q
cardiac index
A
-CO adjusted for body size
-CI=CO X BSA
BSA=body surface area. -calculated with height and weight
[height(cm) X weight (kg)] / 3600^1/2
8
Q
stroke volume
A
the amount of blood ejected from the ventricles with each ventricular systole (contraction)
CO=HR*SV
9
Q
preload
A
-measurement of volume
-the amount of blood in the heart at the end diastole
-increased with volume replacement (IV fluids, etc)
-decreased by blood loss and diuretics
lower preload= lower CO
-atria
10
Q
afterload
A
- resistance heart has to overcome to get blood out of heart
- measurement of resistance
- influenced by vascular resistance, blood pressure, blood viscosity, and aortic/pulmonary stenosis
11
Q
contractility
A
- cannot directly measure but can be seen with echocardiogram
- the strength of myocardial contraction
- influenced by preload (Frank starlings law)
12
Q
Frank Starlings law (or curs)
A
-as you increase preload, contractility will improve, to a point. too much preoad can overstretch the heart and weaken the cardiac muscle causing worsening contractility
13
Q
hemodynamics principle review
A
CO=HR*SV
preload dumps blood into heart
-contractility forces the blood out of the heart
-afterload is the resistance the heart must work against
14
Q
What causes the heart to fail?
A
1) impaired myocardial function: CAD, rheumatic fever, endocarditis, cardiomyopathy
2) increased cardiac workload: hypertension, valve disorders, anemia, congenital heart defects
3) non-cardiac conditions: volume overload, hyperthyroidism, massive PE
15
Q
compensatory mechanisms in HF
A
- when the heart begins to fail the body attempts to compensate
- initially these compensatory mechanisms are helpful, but ultimately they harm the pt only worsening the HF
16
Q
HF affects every body system
A
- respiratory: fluid overload —> pulmonary edema
- neuro: poor CO –> confusion
- integumentary: poor perfusion and edema puts pts at risk for skin breakdown. (cyanosis, edema)
- GI: liver congestion and enlargement, ascites, malnutrition
- urinary: poor renal perfusion
17
Q
The kidneys role in HF
A
1- decreased renal perfusion ( low CO)
2- angiotensin 2 and aldosterone are released
3- causes increased anti-diuretic hormone (ADH)
4- ADH causes kidneys to absorb more water
5-this combo of increased sodium & water leads to a further increased preload
6- the weak heart cannot handle the excess in fluid (preload) and congestion worsens, heart becomes more dilated and CO drops even more
18
Q
systolic HF
A
- decrease in the amount of blood ejected from the ventricle
- -less blood pumoed out of the ventrices, weakened heart muscle can’t squeeze as well.
causes: heart attack, increased preload, cariomyopathy, mechanical abnormalities
19
Q
diastolic HF
A
- when the heart cannot fill effectively, due to increased resistance to filling
- less blood fills the ventricles, stiff heart muscle cant relax normally
- causes: left ventricular hypertrophy from chronic HTN; aortic stenosis; hypertrophic cardiomyopathy(thickening of heart muscle)
20
Q
left sided HF
A
- most common type of HF from left ventricular dysfunction
- the fluid back up reaches the pumonary bed and causes pulmonary edema
21
Q
S/S of left sided HF
A
- cap refill >3secs
- orthopnea (SOB when laying flat)
- dyspnea on exertion
- nocturnal dyspnea
- tachypnea
- diaphoresis (sweat)
- basilar crackles or rhonchi
- cyanosis
- hypoxia (resp. acidosis)
- elevated pulmonary artery pressures
- tachycardia (usually)
- cough with frothy sputum (clear or pink, out of lungs, no infection, usually indicative of pulmonary edema)
22
Q
S/S of left sided HF cont
A
- elevated pulmonary artery occlusive pressures
- audibke S3 and S4 heart tones
- mental confusion
- weight gain
- fatigue/weakness/lethargy
- murmur or mitral insufficiency
- enlarged left ventricle on X-ray
- enlarged left atrium on X-ray
- narrowing pulse presure
23
Q
pulmonary edema
A
- a medical emergency
- the accumulation of fluid in the interstitial space tissue and alveoli of the lungs (pt is literally drowning in their own fluid overload)
- rapid interventions necessary or death is eminent
- treat pt with: diuretics to pull fluid out of lungs; nitrates to vasodilate and reduce systemic vascular resistance; morphine to reduce anxiety and vasodilate (sparingly)
24
Q
assessment findings of pulmonary edema
A
- cough w/ frothy, blood-tinged sputum
- breath sounds: crackles, wheezes, rhonchi
- tachycardia
- hypotension or hypertension
- orthopnea
- dyspnea, tachypnea
- use of accessory muscles
- cyanosis
- cool and clammy skin
25
right sided HF causes
-not as common as left sided HF
-usually caused by left sided HF
-other causes include:
CAD of the vessels that feed the right heart
-tricuspid valve problems
-pulmonic valve problems
-pulmonary hypertension
-pulmonary embolus
26
right sided HF
1) increased pressure from the pulmonary vasculature causes the right to become distended
2) the right heart cannot effectively empty and fluids backs up in the systemic circulation
3) abdominal organs become congested and peripheral tissues become edematous
27
S/S of right sided HF
- hepatomegaly
- splenomegaly
- dependant pitting edema
- venous distention
- hepatojugular reflux
- oliguria
- arrythmias
- elevated CVP
- elevated right atrial pressure
- elevated right ventricular pressure
- narrowing pulse pressure
28
S/S right sided HF cont.
- murmur or tricuspid insufficiency
- audible S3 and S4 heart tones
- fatigue/weakness
- abdominal pain
- anorexia
- enlarged right atrium on X-ray
- enlarged right ventricle on X-ray
- ASCITES & MORE EDEMA= MAIN DIFFERENCE
- weight gain
29
diagnosing and monitoring HF
- chest X-ray: cardiomegaly, pleural effusions
- echocardiography (ECHO)- wall motion abnormalities, valvular problems, ejections fraction
- electrocardiogram (ECG)- dysrhthmias (AFib- most common)
- cardiac cath- valves, ejection fraction
- pulmonary artery catheter: response to diuretic therapy pulmonary pressures
30
ejection fraction (EF)
-the amount of blood ejected during systole compared to the amount of blood in the heart at the end of diastole
-normal= 50-70%
2/3 of end diastolic volume is ejected normally
-heart failure EF=
31
diagnostic labs
- beta natriuretic peptide (BNP)
- cardiac enzymes
- alanine-aminotransferase (ALT)
- aspartate aminotransferase (AST)
- arterial blood gases (ABG)
- erythrocyte sedimantation rate (ESR)
- creatinine
- sodium levels
- billirubin
32
BNP
- #1 test done
- normal range 500= heart failure
- a 32-amino acid polypeptide secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells. The release of BNP is modulated by calcium ions.
33
cardiac enzymes
- CKNP
- Triponin
- if elevated=muscle damage
34
AST and ALT
- liver enzymes
- if liver gets edema, could lead to liver damage
- need to monitor for signs of change
35
ESR
measures kidney function
36
creatinine
increases with HF
37
What part do the kidneys play in HF?
activate the renin-angiotensin-aldosterone-system which causes vasoconstriction
38
goals of treatment for HF
1) slow progression of HF
2) reduce cardiac workload
3) improve cardiac function
4) control fluid retention, esp sodium
39
ACE inhibitors
- block RAAS
- reduce afterload through vasodilation
- reduce ventricular remodeling through suppression of myocyte growth
- decreases preload and eft ventrcular filling pressures which increase cardiac output
* Examples: -pril: enalapril, lisinopril, catopril, ramipril, trandolapril
40
ARBS
- angiotensin 2 receptor blockers
- pharmaceutical affect similar to ACE inhibitors
* examples: -sartan: -irbesartan, losartan, telmisartan, valsartan
41
Diuretics
- inhibit the absorption of sodium and water and promote their excretion
- examples: lasix, bumex, spironolactone, diamox, hydrochlortiazide (HCTZ)
42
Digitalis
-cardiac glycoside inhibits the sodium-potassium pump system and increases cardiac contractility
-increases the refractoriness of AV node which decreases the ventricular response to atrial rate (lowers HR)
-digoxin is used as a first-line drug in pts with CHF who are in AFib
-do dig levels every AM esp if on loop diuretics, possibly need K+ replacement
-loop & K+ wasting diuretics can cause dig toxicity
-toxicity: confusion, hallucination, Irregular pulse, Loss of appetite, Nausea, vomiting, diarrhea, Fast heartbeat.
Vision changes (unusual), including blind spots, blurred vision, changes in how colors look, or seeing spots)
43
beta blockers
-improve left ventricular function by inhibiting the SNS
-anti-arrhythmic properties
-slows HR
-examples: -lo, metoprolol, carvedilol, labetolol, sotolol, atenolol, esmolol
SE: fatigue, weakness, dizziness, diarrhea, headache, blurred vision, impotence, decreased libido, depression
44
Nitrates
- causes vasodilation of the vessels which help to decrease cardiac O2 demand, preload and afterload while increasing cardiac output
- IV drip examples: nipride, NTG
examples: isosorbide dinitrate, hydralazine, amlodipine, prazosin
45
sympathomimetic agents
- stimulate the heart to improve the force of contraction
| - examples: dopamine, dobutamine
46
phosphodiasterase inhibitors
- increases contractility and causes vasodilation resulting in decreased afterload and increase cardiac output
- examples: amrinone, mirinone
47
non-pharmacological treatments for HF
- intra-aortic balloon pump (IABP)
- ventricular assistive device (VAD) implantation
- heart transplant
48
IABP for decompinsated HF
- balloon placed in aorta that inflates during diastole and deflates during systole
- offers afterload reduction through vacuum effect and increases coronary perfusion upon inflation
- temporary solution t improve cardiac output for pts in cardiogenic shock
- multiple risks associated with IABP
49
Ventricular assist device placement
- bridge to transplant or destination therapy
- electromechanical pump that augments or completely replaces the work of the ventricle
- most commonly used in the left ventricle:attaches in the apex of the LV-->blood is redirected through a hose and the pump which allows the blood to bypass the aortic valve--> blood enters system circulation in the ascending aorta
- pts at high risk for bleeding and clots
- risks: it can stop (death), infection, bleeding (on blood thinners)
50
heart transplant
- surgery involves removing the recipients heart, except for the posterior right and left atrial walls and their venous connections
- recipients heart is replaced with the donor heart
- anti rejection medications usually started in OR
- pt is at higher risk for infection (compromised host) for the rest of their lives
51
heart transplant: the list
- placed on list according to severity of HF
- waiting period is long, many die
- candidacy is determined by a multi-interdisiplinary health care team
- pysch evals. done
52
life with heart transplant
- high dose of immunosuppressive medications
- strict regiment
- endomyocardial biopsies
- high risk of infection that lead to complications
- rejection of heart
53
invasive cardiac output monitoring
- Swanz-Ganz catheter
| - baloon tipped swanz-ganz catheter for measuring pulmonary capillary wedge pressure
54
heart failure nursing assessment
- monitor vitals/O2/neuro status
- daily weight
- breath sounds
- cap refill
- assess for signs: peripheral edema/JVD/hepatomegaly/ascites
- evaluate electrolytes
- pain levels
- I&Os
55
basic nursing care for HF pts
- ABC's
- O2 therapy
- continuous pulse ox/ cardiac monitoring
- HOB @ 30degrees
- pharm. therapy
- restrict sodium and fluid intake
- cluster care
- monitor restlessness, pain, anxiety, bowels
56
Pt and family discharge teaching
- medication
- diet/fluid restrictions
- smoking cessation support
- the importance of follow-up Dr.s appointments
- daily weights
- self-monitoring
- community resources
57
HF summary
- heart failure is either a filling or pump problem
- pt will never recover from HF
- some pts may have surical interventions if they are a candidate
58
nurses primary role
- monitor CO
- implement interventions to improve CO
- teach pt how to manage their disease process properly
