Heart Failure Flashcards
Heart Failure
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
Two problems of Heart failure
- Filling problem
- Contracting problem
Filling problem
poor compliance or lack of space to fill
contracting problem
poor contractility
How many in US have heart failure?
5.8 mil
cure for heart failure
-no cure, only preventative measures and tx of symptoms is available at this time
Primary risk factors for heart failure
- CAD
- Advancing age
Contributing risk factors for heart failure
- HTN
- DM
- Tobacco use
- Obesity
- High serum cholesterol
- AA descent
Path of blood through the heart
- blood from upper and lower body enters the R. Atrium
- moves to the right ventricle
- pumped to the lungs via the pulmonary artery
- returns to the left Atrium
- moves to the left ventricle
- pumped though the body via aorta
Goal for Heart failure patients
improve cardiac output
CO
the amount of blood ejected out of the ventricles each minute
CI
Cardiac Index: CO adjusted for body size
CI= CO/BSA
BSA= ht(cm) x wt(kg)/3600 to the 1/2 power
Stroke Volume
amount of blood ejected from the ventricles with each ventricular systole contraction
CO= HR x SV
CO norm
4-8 L/min
CI norm
2.5 L/min
SV norm
60-130 mls
HR norm
60-100 beats/min
Systemic Vascular Resistance
600-1400
Pulmonary Vascular Resistance
20-130
Preload
- measurement of volume
- amount of blood in the heart at the end of diastole
- increased with volume replacement
- decreased by blood loss and diuretics
Afterload
- measurement of resistance
- influenced by vascular resistance, blood pressure, blood viscosity, and aortic/pulmonic stenosis
Contractility
- cannot directly measure but can be see with echo
- strength of myocardial contraction
- influenced by preload (Frank Starling’s Law)
Frank Starlings Law (or Curve)
As you increase preload, contractility will improve….to a point.
-too much preload can overstretch the heart and weaken the cardiac muscle causing worsened contractility
Hemodynamics prinicipals review
CO = HR x SV
Preload (dumps blood into the heart)….Contractility (forces the blood out of the heart)…..Afterload (the resistance that the heart must work against
According to Frank Starling’s law, when preload is increased, what is the initial response of the heart?
Contractility increased
What causes the heart to fail?
- Impaired myocardial function
- increased cardiac workload
- Non-cardiac conditions
Impaired myocardial function
CAD, rheumatic fever, endocarditis, cardiomyopathy
Increased cardiac workload
HTN, valve disorders, anemia, congenital heart defects
Non-cardiac conditions
volume overload, hyperthyroidism, massive pulmonary embolus
Compensatory Mechanisms in Heart Failure
When the heart begins to fail the body attempts to compensate
- initially these compensatory mechanisms are helpful, but ultimately they harm the patient only worsening their heart failure
- muscle fibers have stretched heart chambers enlarges
Compensatory Mechanisms cascade in heart failure
Decreased CO stimulates the SNS to release Norepinephrine……
Norepinephrine increases HR and contractility but also causes vasoconstriction….
vasoconstriction increases venous return to the heart which increases ventricular filling……
overfilling stretches the heart causing myocardial hypertrophy…..
the hypertrophied ventricle has decreased contractility which in turn decreases CO
HF and Respiratory system
fluid overload
HF and Neuro
poor CO
HF and skin
poor perfusion and edema puts patients at risk for skin breakdown
HF and GI
liver congestion and enlargement, ascites, and malnutrition
HF and urinary
poor renal perfusion
Kidney’s role in HF
- Decreased renal perfusion (low CO)
- Angiotensin II and Aldosterone released
- Causes increased anti-diuretic hormone (ADH)
- ADH causes the kidneys to reabsorb more water
- combination of increased sodium and water leads to a further increased preload
- the weak heart cannot handle the excess fluid (preload) and “congestion” worsens, heart becomes more dilated and CO drops even more
Types of HF
Systolic and Diastolic
Systolic HF
- decrease in the amount of blood ejected from the ventricle
causes: heart attack, increased preload, cardiomyopathy, mechanical abnormalities
Diastolic HF
- when the heart cannot fill effectively, due to increased resistance to filling
causes: left ventricular hypertrophy from chronic HTN, aortic stenosis, hypertrophic cardiomyopathy
Left sided HF
- most common type of HF from left ventricular dysfunction
- the fluid back up reaches the pulmonary bed and causes pulmonary edema
S/S of Left HF
- cap refill > 3 seconds
- Orthopnea
- Dyspnea on exertion
- nocturnal dyspnea
- cough with frothy sputum (indicative of pulmonary edema)
- tachypnea
- diaphoresis
- basilar crackles or rhonchi
- cyanosis
- hypoxia (resp. acidosis)
- elevated pulmonary artery pressures
- elevate pulmonary artery occlusive pressures
- audible S3 and S4 heart tones
- mental confusion
- wt gain
- fatigue/wekaness/lethargy
- murmur or mitral insufficiency
- enlarged left ventricle on xray
- enlarged left atrium on xray
- narrowing pulse pressure
Pulmonary Edema: Medical Emergency
- accumulation of fluid in the interstitial tissue and alveoli of the lungs (pt is literally drowning in their own fluid overload)
- rapid interventions necessary or death is eminent
Tx for pulmonary edema
- diuretics to pull fluid out of the lungs
- nitrates to vasodilate and reduce ststemic vascular resistance
- morphine to reduce anxiety and vasodilate (use sparingly)
Manifestations fo pulmary edema
- cough with frothy, blood-tinged sputum
- breath sounds (crackles, wheezes, rhonchi)
- tachycardia
- hypotension or HTN
- orthopnea
- dyspnea, tachypnea
- use of accessory muscles
- cyanosis
- cool and clammy skin
Right Sided HF
- not as common as left side
- usually caused by left side HF
-other causes: • Coronary artery disease of the vessels that feed the right heart • Tricuspid valve problems • Pulmonic valve problems • Pulmonary hypertension • Pulmonary embolus
Cascade of right sided HF
Increased pressure from the pulmonary vasculature causes the right heart to become distended….
the right heart cannot effectively empty and fluid backs up in the systemic circulation…
Abdominal organs become congested and peripheral tissues become edematous
S/S of Right sided HF
- hepatomegaly
- splenomegaly
- dependent pitting edema
- venous distention
- hepatojugular reflux
- oliguria
- arrhythmias
- elevated CVP
- elevated right atrial pressure
- elevated right ventricular pressure
- narrowing pulse pressure
- murmur or tricuspid insufficiency
- audible S3 and S4 heart tones
- fatigue/weakness
- abdominal pain
- anorexia
- enlarged right atrium on xray
- enlarged right ventricle on xray
- ascites
- wt gain
CXR
cardiomegaly, pleural effusions
ECHO
wall motion abnormalities, valvular problems, ejection fraction
ECG
dysrhythmias
Cardiac Cath
valves, ejection fraction
Pulmonary artery catheter
response to diuretic therapy pulmonary pressures
Ejection Fraction
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
- HF EF is less than 40%
HF Diagnostic Labs
- Beta Natriuretic peptide (BNP)
- Cardiac enzymes
- Alanine- aminotransferase (ALT)
- Aspartate Aminotransferase (AST)
Arterial Blood Gases (ABG)
Erythrocyte sedimentation rate (ESR)
Creatinine Sodium
Levels Bilirubin
Goals of Tx for HF
- Slow the progression of HF
- Reduce cardiac workload
- Improve cardiac function
- Control fluid retention
Pharm Tx for HF
- Ace Inhibitors
- ARBS
- Diuretics
- Digitalis
- BB
- Nitrates
- Sympathomimetic Agents
- Phosphodiesterase Inhibitors
Ace Inhibitors
the “PRILs”
- block the RAAS process
- reduce afterload through vasodilation
- reduce ventricular remodeling through suppression of myocyte growth
- decreases preload and left ventricular filing pressures which increase CO
ARBS
“tans”
- Angiotensin II receptor blockers
- Pharm affect similar to ACE inhibitors
Diuretics
inhibit the absorption of sodium and water and promote their excretion
-Lasix, bumex, spironolactone, diamox, HCTZ
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 patients with CHF who are in a fib
BB
“lols”
- improves left ventricular fx by inhibiting the sympathetic nervous system
- anti-arrhythmic properties
- slows HR
Nitrates
Cause vasodilation of the vessels which help to decrease cardiac oxygen demand, cardiac preload, and afterload while increasing CO
- nipride (IVD)
- NTG (IVD)
- Isosorbide dinitrate
- Hydralizine
- Amlodipine
- Prazosin
Sympathomimetric Agents
stimulate the heart to improve the force of contraction
“mine”
- dopamine
- dobutamine
Phosphodiasterase Inhibitors
increases contractility and causes vasodilation resulting in decreased afterload and increased CO
“none”
- Amrinone
- Milrinone
Non-pharm tx for HF
- IABP placement
- VAD implant
- Heart transplant
IABP for decompensated HF
Intra-Aortic Balloon Pump
- balloon placed in aorta that inflates during diastole and deflates during systole
- offers afterload reduction through vacuum effect and increases coronary perfusion upon inflation
- temporarily solution to improve cardiac output for patients in cardiogenic shock
- multiple risks associated with IABP
Ventricular Assist Device Placement
Electromechanical pump which augments or fully 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 the system circulation in the ascending aorta
- “Bridge to transplant” or “Destination therapy”
- Patients are at high risk for bleeding and clots
Heart Transplant
- Surgery involves removing the recipient’s heart, except for the posterior right and left atrial walls and their venous connections
- Recipient’s heart is replaced with the donor heart
- Anti-rejection medications usually started in the OR
- Patient is at high risk for infection (compromised host) for the rest of their life
List for Heart transplant
- placed on list according to severity of HF
- waiting period is long, many die
- candidacy is determined by multi- interdisciplinary health care team
- psych evals
Life with a Heart Transplant
- High dose of immunosuppressive medications
- Strict regiment
- Endomyocardial biopsies
- High risk of infection that lead to complications
- Rejection of heart
HF nursing assessment
- Monitor vital signs/oxygenation/Neuro status
- Daily weight
- Breath sounds
- Capillary refill
- Assess for signs: peripheral edema/ jugular vein distention/hepatomegaly/ascites
- Evaluate electrolytes
- Pain level
- Intake and Output
Basic Nursing Care for HF
- ABC’s
- Oxygen therapy
- Continuous cardiac/Pulse oximetry monitoring.
- HOB @ 30 degrees
- Pharmaceutical therapy
- Restrict sodium and fluid intake (strict I&O)
- Cluster care
- Monitor restlessness, anxiety, pain. bowels
Patient 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
HF Summary
- Heart Failure is either a filling problem or a pump problem
- Patient will never recover from heart failure
- Some patients may have surgical interventions if they are a candidate
- Nurses primary role is to monitor CO, implement interventions to improve CO, and teach patient how to manage their disease process properly.
