NURS 444 week 4 heart Flashcards
Cardiac output
Heart rate (HR) x stroke volume (SV)
normal is 4-8 L/min
- preload
- afterload
- contractility
Arterial blood pressure:
BP- cardiac output (CO) x systemic vascular resistance (SVR)
**normal: SBP < 120 mm Hg, DBP < 80
Preload
volume in the ventricles at the end of diastole (end diastole pressure). Amount of blood in the ventricles right before contraction
increased in:
Hypervolemia
Regurgitation of cardiac valves
Afterload
Resistance left. Ventricle must overcome to circulate blood
Increased in:
htn
vasoconstriction
increased afterload
increased cardiac workload
Cardiomyopathy (CMP)
Primary- idiopathic and only heart involved
Secondary-
Major types: dilated, hypertrophic, restrictive
Leads to cardiomegaly and HF
leading cause of heart transplantation
Types of secondary CMP
> dilated- due to too much fluid backing up into the ventricle. think of balloon stretching; alcoholic, CAD, htn, valve disease, pregnancy
MOST COMMON mixed heart failure
> hypertrophic (enlarged vent.)- aortic stenosis, htn
more common in men. dyspnea most common symptom
> restricitve- post-radiation therapy, ventricular thrombus, scarring (not as common)
least common
classic symptoms are fatigue, exercise intolerance, and dyspnea
Management for Dilated
- control HF
- doesn’t respond well to therapy- hospitalized numerous times
- vent. assist device***
- heart resynchronization therapy
- heart tranplantation
Hypertrophic management
- beta or calcium channel blockers
- ICD
- surgical treatment
(ventriculomyotomy and myectomy) - percutaneous transluminal septal myocardial ablation
Restrictive management
- no specific tx exists
- conventional therapy for HF and dysrhythmias
Ejection Fraction
normal: 55- 65%
< 45% = HF
Heart Failure compensatory mechanism
sympathetic nervous system
- Catecholamines: epinephrine and norepinephrine
- detrimental over time. increases O2 demand, increases workload of hert
neurohormonal response
- decreases renal perfusion causes kidney to increase renin
RAAS. results in water retention
may be on ACE inhibitor or ARB
Frank Sterling Law
dilation of heart chambers, muscle fibers stretch in response to volume
hypertrophy follows dilation
Patients who have had an MI
will go on a beta blocker to prevent remodeling of the heart
also on a low dose ACE inhibitor
Monitoring HF patients
weigh: call if more than 1lb/ day
BMP stretching: check labs
Left Sided Heart Failure
Pulmonary congestion:
- cough
- crackles
- wheezes
- blood-tinged sputum
- tachypnea
restlessness
confusion
orthopnea
tachycardia
exertional dyspnea
fatigue
cyanosis
** correct fluid before med. therapy
also systolic HF
Right sided HF
“Cor Pulmonale”
- faitgue
- increased peripheral venous pressure
- Ascites
- enlarged liver/ spleen
- may be secondary to chronic pulmonary problems
- DJV
- anorexia and GI distress
- swelling in hands and fingers
- dependent edema
HF complications
! pleural effusions
! dysrhythmias
! left ventricular thrombus
! hepatomegaly
! renal failure
HF management
Drug therapy:
» diuretics
» ACE inhibitors/ ARBs
» Vasodilators: nitrates, B-adrenergic blockers, positive inotropes (help with contractility)
Nutritional therapy:
» diet education: sodium and occasional fluid restriction
» weight management
!! nitrates used to shunt fluid away from lungs
!! probably 2g or less of sodium diet
UNLOAD FAST
Upright position
Nitrates
Lasix
Oxygen
ACE inhibitors
Digoxin
Fluids (decrease)
Afterload (decrease)
Sodium restriction
Test (dig levels, ABGs, potassium level)
2 different valve diseases
Stenosis
Regurgitation
**commmon valve disorders in older adults
Mitral valve regurgitation
- caused by; MI, rheumatic heart disease, mitral valve prolapse, ischemic papillary dysfunction
- chronic leads to; LA enlargement, LV hypertrophy/ dilation and decrease in cardiac output
manifestations of mitral valve regurgitation
chronic
- weakness, fatigue, palpitations, dyspnea with progressive worsening, peripheral edema
- S3
- holosystolic and pansystolic murmur
Valvular heart disease
Aortic stenosis
- rheumatic fever or age calcification (like CAD)
- causes obstruction of flow from LV to Aorta
- results in LV hypertrophy
*** nitroglycerin used cautiously to treat angina
manifestations
- angina, syncope, and dyspnea on exertion
- prominent S4
- systolic murmur
extra oxygen and pressure is used to open valves
*** think of how meds. affect pressure
PAD
intermittent claudication
- ischemic muscle ache or pain caused by exercise, such as walking
- resolves with rest
parasthesia
- from nerve tissue ischemia
neuropathy
PAD manifestations
skin: shiny, thin, taut, hair loss
popliteal and femoral pulses present
others are diminished
** don’t elevate legs over the heart
** keep warm but don’t apply heat, don’t wear restrictive clothing, don’t cross legs
Care for PAD
- SMOKING CESSATION NECESSARY***
- Antiplatelet therapy is critically important
- trental and pletal treat intermittent claudication
- exercise therapy: walking
- nutritional therapy: low sodium, low cholesterol, low saturated fat. High in fruits, veggies, whole grains
- complementary and alternative therapies
- protect from trauma, infection
- decrease pain
***peripheral artery bypass is most common
Chronic Venous Insufficiency; venous leg ulcers
valves in veins are damaged, which allow retrograde blood flow, pooling of blood in legs
Hydrostatic pressure in vein increases
- fluid and RBCs leak into tissue
- enzymes breakdown RBC causing brownish skin discoloration
- skin and subcutaneous tissue are replaces with fibrous tissue
**ulcers are common
Care for venous insufficiency
compression therapy
- make sure PAD or clots not present
patient/caregiver teaching
- avoid trauma
- proper skin care
- avoid standing or sitting for long periods of time
- moist environment- keep dry
nutritional therapy for ulcers
- protein, calories, and micronutrients
meds. for ulcers
- antibiotics may be necessary
skin grafts for ulcers
