this is the inability of theart ot pump efficiently to circulate adequate blood around the body to meet metabolic needs

muscle is worn out or injured

pump is failing

• forward movement of blood is restruicted, resulting in congestion and edema in pulmonary (left, going to back up into the lungs) or right, peripheral tissues
• when blood is no goin gto the kidneys they sense not enough fluid so there is a increase production of medulla, aldosterone kicks in

this is the ability of the heart to increase cardiac output in time of incrased metabolic activity. normally maintained via some compensatory mechanism

5-6 times

• Dilation of heart chambers occurs when pressure in heart chambers is elevated over time
• muscle fibers stretch in response to volume of blood in heart at end of diastole

*the degree of stretch is directry related to the force of contraction*

• eventrually the elastic elements of the muscle fubers become overstretched and can no longer contract effectively resulting in decreased CO

• As CO and SV become inadequate, SNS activiation occurs resulting in incrased release of epinephrine and norepinephrine which cause an increase in HR, contractility, and vasoconstriction.

• as CO falls, kidney perfusion decreases
• inresponse the kidneys release renin which activated the RAAS
• angiotensin II causes aldosterone release and increases vasoconstriction to increase BP
• REsult- blood volume is increased in a person who already is volume overloaded.

*this is an increase in the muscle mass and cardiac wall thickness in respnse to overwork and strain

over time this make the heart muscle have poor contractility, requiring more O2 to perform and leads to poor coronary artery perfusion making the individual prone to venrticlar dysrhythmias

systolic- cant contract, decrease in perfusion, cynosis, and increase in heart rate

diastolic- no passive filling, bacerialendocarditis in which the heart muscle remains dialated.

• this is the most common cause of HR
• inability of heart to pump blood due to a defect in the ability of the ventricles to contract or pump
• LV cannont generate enough pressure to eject blood foraward
• LV becomes thin, dilated and hypertrophied.

Systolic failure

cause:

MI, hypertension, cardiomyopthy

hallmark is decrease in left ventriclar ejection fraction

• this is a measurement of contractility of the ventricles
• the percent of total ventricular filling volume that is ejected during each ventricular contraction
• normal is >55%
• decrease in this is ventricular failure

• this is impaired ability of the ventircles to relax and fillduring diastole
• decrease filling on ventricels results in decrease stoke volume and CO
• 20-40 percent of patients wil have this failure with a normal EF and systolic function

cause: HTN, aortic stenosis, hypertrophic cardomyopathy

• poor systolic function is further compromised by dilated left ventricular walls that are unable to relax
• patient usually have EFs 35%, highpulmonary pressure, and biventricular failure
• low bp, co, poor renal perfusion, poor exercise tolerance

cause of this:

• blood arrives at R atrium and R ventricle to be pumped into lungs if this fails blood backs up into right side of heart increased pressure in systemic circulation
• due to pulmonary diseases like: COPD, cystic fibrosis, ARDS, pulmonary HTN

signs of right sided HF

(increased fatigue)

  excess fluid accumulation, reduced CO, early symptoms

signs of right sided HF

(altered renal function)

• Reduced CO due to fluid collection in dependent areas
• impaired circulation secondary to fluid inadequate removal of waste products
• renin system might be triggered

Signs of right sided HF

(distended neck veins)

JVD- secondary to increased venous pressure throughout the venous system blood takes the path of least resistance backs up into jugular veins

should disappear at a 45 degree angle, but RHF there is JVD and tye are short of breath

Signs of right sided HF

(liver enlargement)

• Results of venous engorgement of liver
• increased pressure may interfere with livers ability to function as this progresses may force fluid into abdominal cavity(ascites)
• may also increase presssure on diaphragm causing respiratory distress

Signs of Right sided HF

(cynosis)

• this is the most common form of heart failure
• results from LV dysfunction, causing blood to back up through the left atrium into the pulmonary veins
• results in decreased CO
• causes pulmonary congrestion and edema

Signs of L sided heart failure

(shortness of breath)

Signs of L sided HF

(Orthopnea)

• difficulty breathing when lying flat
• fluid in legs now returns to heart and the heart is unable to pump if effciently, lungs become congested and patient develops SOB

Signs of L sided HF

(Nocturia)

Signs of L sided HF

(Decreased urine output)

• Blood flow to kidneys is dereased causing decreased perfusion
• when perfusion falls, renin is released leading to aldosterone secretion which causes Na+ and H2 and increased intravascular volume

Signs of L sided HF

(caugh and blood tinged sputum)

• initial cough is dry, nonproductive 
• will become moist over time
• frothy, pink, blood tinged sputum is an indicator of severe pulmonary congestion (edema)

Signs of L sided HF

(abnormal lung sounds)

Bibasilar crackles not clear by cough, usually early phase of failure

as failure worsens and pulmonary congestion increases, crackles may be auscultated throughout all lung fields

Signs of L sided HF

(Pallor or cyanosis)

• As peripheral blood vessels constrict, the skin appears pale and feels cool and clammy
• cyanosis is secondary to pulmonary congestion and impaired gas exchange

Signs of L sided HF

(fatigue)

Collaborative treatment of CHF

waht can a nurse do?

the nurse can:

• put patient in high fowlers postion
• OX by mask or nasal cannula- but not good if COPD
• cardiac monitor
• oximetry
• monitor VS
• Low sodium diet

Treatment

Digitalis (lanoxin)

• this is used to decrease force of contraction
• improve cardiac contractility
• decrease heart rate

treatment CHF

(diuretics)

used to:

• mobilize edematous fluid by pulling fluid out of circulation so the heart has less blood it has to pump
• reduce preload
• if the excess fluid is excreted, the blood volume returning to the heart can be reduced imporving cardiac funciton.

Treatment

(oxygen administration)

used to:

increase oxygenation of myocaridial tissue

prevent tissue damage

want to keep level <90%

treatment of CHF

(morphine)

used to:

reduce preload

reduce myocardial oxygen consumption- how much oxygen does it take for the heart to do what it needs to do

acts as analgesic and sedative to relax

used to:

• reduces systemic vascular resistance thus, increasing CO
• lower BP while maintaining tissue perfusion
• reduce pulmonary artery pressure
• reduce righ arterial pressure
• reduce LV filling pressure

how it works:

• ACE inhibitors block angiotensin converting enzyme
• so angiotensin I cannot convert to angiotensin II
• remember Angiotensin II released aldosterone (causing reabsorption of sodium and water)so this release is also reduced

this is abnormal accuulation of fluid in the alveoli and interstitial spaces of the lungs

interferes with gas exchange

causes of Pulmonary Edema

most common: left ventriclular failure secondary to CAD albumine is hypertonic

• heart failure
• hypoalbuminemia
• altered capillar permeability of lungs
• lymph system malignancies
• respriatory distress syndorme

• with in the capillary beds there is a balance between hydrostatic and colloidal pressure in the pulmonary capillaries
• pulmonary venous pressure increases due to decreased efficiency of the LV leading to pulmonary vascular engorgement
• as the pressure continues to increase the increased intravascular pressure causes fluid to leave the pulmonary capilaries and enter interstitial spces

• increased RR>30 bpm
• decreased oxygen saturation
• orthopena
• wheezing, crackles, rhonchi
• coughing
• frothy, blood tinged sputum
• tachypnea
• anxious
• pale
• skin clammy and cold

ABGs high CO2, pH is gong to be low, acidosis

BNP level - increase blood level

LFTs- liver cells are going to break down

23 lead ECG

echocardiogram- gel on probe and can measure CO

• high fowlers positing
• o2 by mask or nasal cannula
• monitor VS every hour
• continuous ECG and pulse oximertry
• daily weight
• drug therapy: diuretics nitroglycerin, morphine all IV