Medsurg Exam 1: Cardiovascular Disorders Flashcards

1
Q

What side does Heart Failure (CHF) occur on?

A

Can be left sided / right sided and deals with the pump failing

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2
Q

What are the 4 contributions to Left Side HR

A
  1. Hypertension
  2. Coronary Artery Disease
  3. MI Cardinal Infractions
  4. Structure Heart Changes
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3
Q

How does Hypertension contribute to LS CHF?

A

Pumping out against high pressure

Heart that is already working hard and now its pumping against a close door with hypertension in arterioles

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4
Q

How does Coronary artery disease contribute to LS CHF?

A

if not perfusing the heart muscle, the heart is going to fail

Vessels that go around heart

Not enough circulation to heart itself

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5
Q

How does MI Cardinal Infractions contribute to LS CHF?

A

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

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6
Q

How does Structure Heart Changes contribute to LS CHF?

A

Valvular issues
Papillary muscle
Aortic or mitral valve issues

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7
Q

What is the result of LS CHF = Systolic Failure

A

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

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8
Q

Results of LS CHF on distolic Failure

A

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

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9
Q

What are the S/S of LHF

A

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)

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10
Q

What are the three main causes of RS CHF?

A

LVF

Right Ventricular MI

Pulmonary Hypertension

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11
Q

How does LVF cause RS CHF

A

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

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12
Q

How does Right ventricular MI cause RS CHF

A

coronary artery disease and can lead to massive right sided MI which leads to decreased wall

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13
Q

How does Pulmonary Hypertension cause RS CHF

A

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

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14
Q

What are the results of RS CHF?

A

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)

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15
Q

S/S of RS CHF

A
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

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16
Q

What is the syndrome called high out put and what are the contributors?

A

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

17
Q

HF Development from lead to most impaired patients

A
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
18
Q

How does the body compensate for a failing heart?

A

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

19
Q

How to determine heart failure?

A

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

20
Q

What are four ways to decrease CO for patients with HR?

A

Decrease preload

Decrease after load

Improve contractility

Heart Transplant, LVAD, AICD pacer, resynchronization

21
Q

How to decrease preload

A

(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)

22
Q

How to decrease afterload

A

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

23
Q

How to improve contractility?

A

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

24
Q

How to help with impaired gas exchange?

A

Decrease activity
Change positioning
Give supplemental oxygen

25
Q

Activity intolerance for pts with CHF

A

Cluster their care, we organize/ plan their care, short burst of care with rest periods in between

26
Q

What is MWADS = patient teaching?

A

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

27
Q

Nursing Interventions and Goals for pts with CHF

A
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
28
Q

Essential HPT

A

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

29
Q

Malignant Hypertension

A

rapidly elevating BP and this needs emergency treatment

30
Q

Secondary Hypertension

A

due to some other problem leading to it in addition

usually related to renal dysfunction or endocrine disorders, or even psychiatric disorders

31
Q

Normal HPT

A

need to see both systolic and diastolic (120/80 mm hG)

32
Q

Elevated HTN

A

120/129 over 80

33
Q

Stage 1 HTN

A

130/139 over 90

34
Q

Stage 2 HTN

A

140 over 90 (equal or higher then)

35
Q

Hypertension Crisis

A

180 over 120 (equal or higher)

36
Q

Benefits of lowering BP

A

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

37
Q

Lifestyle modification

A

usually the first suggestions = dietary changes/ alcohol decrease in usage

38
Q

Medications

A

Diuretics → furosemide, hCTZ
Calcium channel blockers → amlodipine, diltiazem
ACE inhibitors → lisinopril, captopril, enalapril
ARBS → candesartan, losartan, valsartan
Beta Blockers (the LOLS)→ labetalol, propranolol