Medsurg Exam 1: Cardiovascular Disorders Flashcards
What side does Heart Failure (CHF) occur on?
Can be left sided / right sided and deals with the pump failing
What are the 4 contributions to Left Side HR
- Hypertension
- Coronary Artery Disease
- MI Cardinal Infractions
- Structure Heart Changes
How does Hypertension contribute to LS CHF?
Pumping out against high pressure
Heart that is already working hard and now its pumping against a close door with hypertension in arterioles
How does Coronary artery disease contribute to LS CHF?
if not perfusing the heart muscle, the heart is going to fail
Vessels that go around heart
Not enough circulation to heart itself
How does MI Cardinal Infractions contribute to LS CHF?
left sided heart failure = tissue damage
Trigger by hypertension
Infract a huge percentage of the heart, and involves a huge part of left
Area of infarction tissue, a huge part of the wall, the heart will balloon out and have no integrity to muscle, it is working against the heart
How does Structure Heart Changes contribute to LS CHF?
Valvular issues
Papillary muscle
Aortic or mitral valve issues
What is the result of LS CHF = Systolic Failure
THINK: FORWARD FLOW
Inadequate pumping (to get that forward flow needed) Not enough force, not enough full volume forward, increasing preload (blood in the atrium)
Preload = volume of blood that is left in the ventricle after contraction due to issues with not ejecting all the blood
If you have a lot of preload it is telling you that the heart isn’t getting it out
Increase afterload = increases peripheral vascular resistance
Arteriole system is compensating for it with increase afterload because they are clamping down to control the lack of blood
Volume low and CO low
Heart failure with an ejection fraction of less than 45 percent
Results of LS CHF on distolic Failure
THINK: Back up of blood
The left ventricle cannot relax
It is working so hard = leads to stiffness
Stiff = issues with filling properly
Left ventricle not relaxed = leads to back flow of blood into the lungs
What are the S/S of LHF
Decreased cardiac output
likely will hear a third heart sound (S3 tells you increased left ventricular pumping) and fourth heart sound (indicates decreased left ventricular compliance), fatigue
Pulmonary cardiac congestion = think the blood is going back into the lungs
tend to get crackles and frothy pink sputum due to the volume not going forward finding itself back in lungs, paranormal nocturnal dyspnea (PND)
What are the three main causes of RS CHF?
LVF
Right Ventricular MI
Pulmonary Hypertension
How does LVF cause RS CHF
usually seen when left side fails leads to right side failure → and the left side usually fails first BUT can make many excuses as to why right failed first
How does Right ventricular MI cause RS CHF
coronary artery disease and can lead to massive right sided MI which leads to decreased wall
How does Pulmonary Hypertension cause RS CHF
a pre existing condition, a right ventricular high afterload → think the right side of the heart has to push against the high pressure system that is the pulmonary tree
What are the results of RS CHF?
Cannot empty the right side ventricle fully
Increased volume in the systemic circulation (right side pumps to the lungs to oxygenate so if they can do this there will be increase in systemic)
S/S of RS CHF
Edema and weight gain = edema is the most directly observable Blood pressure (poor indicator since affected by so many things) JVD = backing up from right side GI and GU issues = increased thirst, oliguria during the day, anorexia and nausea, could see an enlarged spleen/ live
LOOK AT DAILEY WEIGHTS
What is the syndrome called high out put and what are the contributors?
High output = a syndrome of high metabolic function that means the heart cannot meet the demands of the this extreme huper metabolic condition
Contributors
Sepsis = increase metabolic demands, because of high metabolic need
Hyperthyroidism = ramp up the metabolism and the heart struggles to keep up
HF Development from lead to most impaired patients
A = patient with risk factors but no LV impairment B = asymptomatic with LV hypertrophy and/ or LV function C = current or past symptoms of HF D = refractory HF eligible for heart transplant, technical support
How does the body compensate for a failing heart?
Remember = little compensation can be good, but a lot tends to be bad
Sympathetic nervous system stimulation → will see increase in HR (beta = beta 1 predominates in the heart) and increase in BP (alpha)
Renin-angiotensin-aldosterone system activation → patients will hang onto water
BNP elevation (natriuretic peptide) → released because of the increased amount of stretch on your heart
Myocardial Hypertrophy → anytime you work a muscle harder and harder the heart will get bigger
How to determine heart failure?
Laboratory assessments =electrolytes, BNP, CBC, digoxin level (if one digitalis), ABGS (maybe), thyroid function studies
Radiographic assessment
Pleural effusion = both sides of the heart failing
Electrocardiogram = signs of ischemia, dysrhythmias
Echocardiography
Pulmonary artery catheters → looking at pulmonary tree
What are four ways to decrease CO for patients with HR?
Decrease preload
Decrease after load
Improve contractility
Heart Transplant, LVAD, AICD pacer, resynchronization
How to decrease preload
(amount of blood sitting in heart at end of contraction): get rid of extra salt in their body (salt restricting diet), fluid restrictions (if ordered) , diuretics (potassium sparing and high ceiling loop) and electrolytes, nitrates (venous vasodilation)
How to decrease afterload
ACE inhibitors (arterial dilation)
Suppress RAS and aldosterone secretion → improved SV and arterial dilation aka the prils
A new dry cough or increase in K+ levels means they need to be taken off!
ARBs (arterial dilation0
BLOCKS ANGIOTENSIN 2 RECEPTOR binding site
ARNI
How to improve contractility?
Digitalis = antiarrhythmic which is a +inotrope and a -chronotrope (slow down the heart rate and inotrope deals with force of contraction which we want to increase)
When do you give/ not give → patient need to take their HR for a minute before they administer themselves the digitalis
Need to know the toxic level of digitalis = greater then 2.5 nanograms per liter
Beta blockers: the LOLS
Metoprolol, atenolol, labetalol
Block the sympathetic response and catecholamines
Dobutamine and milrinone
How to help with impaired gas exchange?
Decrease activity
Change positioning
Give supplemental oxygen
Activity intolerance for pts with CHF
Cluster their care, we organize/ plan their care, short burst of care with rest periods in between
What is MWADS = patient teaching?
Medications → what each medication is for, what it does, what are the side effect, take as prescribed and do not run out of them, how medications work synergistically
Do not take NSAIDS
Activity → when at baseline want these patients to be as active as possible, a worsening sign is decreased exercise tolerance
Weight → rapid weight gain (5lbs in a week or 2lbs in a day)
Diet = more restrictive sodium diet
Symptoms → if they have new symptoms == cough more than 3-5 days, dyspnea, increased edema, chest pain
Nursing Interventions and Goals for pts with CHF
Check respirations/ HR/ BP/ breath sounds/ oxygenation Supplemental O2 Positioning → think edema Capillary refill I & O Rest periods Administer medications and monitor effects Diet therapy **daily weights
Essential HPT
no known cause
Can be do to = over 60 or postmenopausal, family history, african american ethnicity, stress, obseisty, smoking, inacvtivity, hyperlipidemia, high salt intake, low potassium intake
Malignant Hypertension
rapidly elevating BP and this needs emergency treatment
Secondary Hypertension
due to some other problem leading to it in addition
usually related to renal dysfunction or endocrine disorders, or even psychiatric disorders
Normal HPT
need to see both systolic and diastolic (120/80 mm hG)
Elevated HTN
120/129 over 80
Stage 1 HTN
130/139 over 90
Stage 2 HTN
140 over 90 (equal or higher then)
Hypertension Crisis
180 over 120 (equal or higher)
Benefits of lowering BP
Decreases stroke incidence by 35-40%
Decreases myocardial infarction by 20-25%
Decreases rate of heart failure by 50%
A sustained reduction of 12 mm HG in SBP over 10 years will prevent 1 death for every 11 patients treated
Lifestyle modification
usually the first suggestions = dietary changes/ alcohol decrease in usage
Medications
Diuretics → furosemide, hCTZ
Calcium channel blockers → amlodipine, diltiazem
ACE inhibitors → lisinopril, captopril, enalapril
ARBS → candesartan, losartan, valsartan
Beta Blockers (the LOLS)→ labetalol, propranolol
