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NUR ADN 35 > Wk 1-2 Cardiac Problems > Flashcards

Wk 1-2 Cardiac Problems Flashcards

1
Q

What is Heart Failure?

A

Slide:
•An abnormal condition involving impaired cardiac pumping/filling
• Heart is unable to produce an adequate cardiac output (CO) to meet metabolic needs.

Miller: “not necessarily a disease itself but more of a syndrome” (this is the take away she wants us to understand)*

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2
Q

What are the characteristics of the syndrome heart failure (HF)?

A

Characterized by:
• Ventricular dysfunction
• Reduced exercise tolerance (SOB @ rest)
• Diminished quality of life
• Shortened life expectancy (less than 6 mo, hospice)

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3
Q

3 vessels/Components of circulation

A

•Arteries carry oxygen-rich blood away from your heart.

•Capillaries are tiny, thin blood vessels that connect veins and arteries.

•Veins carry oxygen-poor blood from your body’s tissues back to your heart.

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4
Q

Where does blood back up in R & L sided heart failure?

A

•Right sided heart failure backs up into body
•Left sided heart failure backs up into lungs

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5
Q

Cardiac circulation route

A

On the right side:
1. Oxygen-poor blood from all over your body enters your right atrium through two large veins, your inferior vena cava and superior vena cava.

  1. Your tricuspid valve opens to let blood travel from your right atrium to your right ventricle.
  2. When your right ventricle is full, it squeezes, which closes your tricuspid valve and opens your pulmonary valve.

4.Blood flows through your pulmonary artery to your lungs, where it gets oxygen.

On the left side:

5.Oxygen-rich blood travels from your lungs to your left atrium through large veins called pulmonary veins.

6.Your mitral valve opens to send blood from your left atrium to your left ventricle.

7.When your left ventricle is full it squeezes, which closes your mitral valve and opens your aortic valve.

8.Your heart sends blood through your aortic valve to your aorta, where it flows to the rest of your body.

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6
Q

Explain systole and diastole (simple)

A

•Systole (squeezing) the heart is contracting

•Diastole the heart is relaxing between contractions

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7
Q

Explain Systole & Diastole (technical)

A

Cardiac cycle:
1.Diastole - atria fill, all valves are closed
2.Diastole - increased atrial pressure opens AV valves, ventricles fill
3. SYSTOLE BEGINS: atria contract & empty, ventricles are full.
4. SYSTOLE: ventricles begin contraction, pressure closes AV valves, atria relax
5. SYSTOLE: ventricles contract, increased pressure in ventricles, aortic & pulmonary valves open, blood ejected into aorta & pulmonary artery
6. DIASTOLE: ventricles empty, ventricles relax, aortic & pulmonary valves close

Starts all over at 1. Again

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8
Q

Stroke volume

A

1539 Lewis*

•Stroke volume is the amount of blood ejected with each ventricular contraction
•it is always* presented in a %

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9
Q

How is stroke volume measured?

A

•Volume of blood in ventricle prior to ejection is the end diastolic volume (EDV)

•Amount of blood that remains in the ventricle after ejection is the end systolic volume, (ESV)

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10
Q

Stroke volume calculation ex:

Stroke volume 70%
Heart rate = 70
What is the CO?

A

Change to decimal: 70% = 0.70

0.70 SV X 70 HR = 49% CO

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11
Q

Look up cardiac output range in book

A
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12
Q

What organs are directly effected by the heart?

A

•Brain
•Lungs
•kidneys (and heart are in a relationship, if one is off the other tries to regulate, but the heart needs to perfuse the kidneys to make that happen)

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13
Q

3 Factors that impact heart workload

A

•Preload
•Afterload
•Contractility

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14
Q

Explain Preload

A

volume of blood present in a ventricle of the heart just before ventricular contraction

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15
Q

Explain Afterload

A

Miller: “Resistance the heart must overcome in order to pass through one cardiac cycle and perfuse the body. Afterload is almost in correlation with the diastolic phase of the heart” (ejection of blood from ventricles)

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16
Q

Explain contractility

A

•max force of cardiac contraction.
Miller: *when the heart starts to fail and the muscle/ventricles become enlarged the forceful contraction is not happening. The heart is not able to effectively squeeze & produce enough blood volume to complete cardiac output.”

17
Q

Control of the heart

A

•The heart is self-regulated and can beat on its own with its own electrical conduction system.
•cardiac control center in medulla.

Baroreceptors: Detect changes in blood pressure & volume. (Is there stretch happening? Works closely w/kidneys. Located in the aorta & internal carotid arteries.

•Sympathetic stimulation: Increases heart rate (tachycardia) -not sustainable -muscle will weaken from overworking

•Parasympathetic stimulation: Decreases heart rate (bradycardia)

18
Q

Explain Ejection Fraction

A

Normal: 50-65% (pt’s may have other problems but are asymptomatic)

Below normal: 36-49% (symptomatic, based on pt’s pre-existing health conditions, symptoms may be worse)

Low: 35% or less (heart transplant or hospice care)
These Pt’s at risk for sudden cardiac arrest what is their EF?

19
Q

What are the structures controlling heart action?

A

•conduction system:
#1: SA Node (main pacemaker, 60-100 bpm)
#2: AV Node (40-60 Bpm)
#3: Bundle branches/Purkinje(20-40 Bpm)

20
Q

What happens to the electrical system in HF?

A

When the heart fails to contract adequately but beats faster to get more blood to tissues, it leads to the electrical system misfiring which causes dysthymias

21
Q

What is the most common dysrhythmia in HF?

A

A-fib; their main nodes are too tired or have misfired so much that now they’re not able to keep the rate control. There’s a lot of electrical trying to compensate.

22
Q

Myocardium cell info

A

•myocardial cells (nodes) are the only cells in the body that don’t rely on nervous system stimulation

23
Q

Myocardium cell characteristics

A

•Involuntary control (hypothalamus)
•Intrinsic Control (SA, AV)
•striated muscles (branched)
•single nucleated. Cardiac cells don’t fuse.

24
Q

What are the basics of cell firing? 657 Lewis*

A

•cells begin with a negative charge: “resting membrane potential”
•stimulus causes some Na+ channels to open
•Na+ diffuses in, making the cell more positive
•at threshold potential, more Na+ channels open
•Na+ rushes in, making the cell very positive: depolarization
•action potential; cell responds by contracting
•K+ channel opens
•K+ diffuses out, making the cell negative again (repolarization/resting phase)
•Na+/K+ ATPase dependent sodium potassium pump removes the Na+ from the cell & pumps the K+ back in

Sodium & potassium are important for heart function.
* KNOW how sodium/potassium pump works*

25
Q

Explain PQRST

A

P: atrial depolarization
QRS: ventricular depolarization (& atrial repolarization)
T: ventricular repolarization

26
Q

What labs to look for for HF patients

A

Labs that are married together:
•sodium and potassium
•calcium and magnesium
•phosphorus
• HGB & HCT

“Chem 7: basic labs”
“Chem 12: additional labs Like phosphorus & magnesium really wanted if your pt has a dysrhythmia”

27
Q

What are the primary risk factors for heart failure?

A

735 Lewis 34.1 primary and 2nd causes of heart failure

•myocardial insult = decreased O2, CAD, Diabetes, HTN

•risk factors: #1 HTN, #2 CAD, #3 diabetes. Smoking

•culture: familial link, black/Hispanic/Native American

•cost: 40 billion annually for <3 preservation

28
Q

Heart failure overview

A

740 Lewis
•Clinical syndrome: fatigue, dyspnea & edema
•ineffective pump: contraction (systole) filling (Diastole)
•manifestations: exercise tolerance, quality of life, life expectancy.
(Symptoms go unnoticed, pt’s make excuses till symptoms are advanced.)

29
Q

Etiology of Heart Failure

A

•Any interference with mechanisms regulating cardiac output (CO)

•Primary causes: Conditions that directly damage the heart (examples: drugs, infection)

•Precipitating causes:
Conditions that increase workload of the heart

30
Q

Types of Heart Failure : Left

A

•Left-sided heart failure is most common.
•Left will back up into lungs (L&L)
•S/S of decreased CO & increased pulmonary Venous pressure
•back up of blood into the left atrium & pulmonary veins
•pulmonary congestion
•Edema

31
Q

Left Ventricle Failure classifications

A

735 Lewis
SYSTOLIC:
•HF W/decreased ejection fraction (inability to pump blood forward)
•Causes: impaired contractile function, inc afterload, cardiomyopathy, mechanical abnormalities.
•Hallmark finding: Decreased LV EF

DIASTOLIC:
•HF W/preserved Ejection Fraction (ventricle can’t relax to fill, not getting enough volume to pump to body)
•Impaired ability of the ventricle to relax and fill during diastole, resulting in dec SV and CO.
•Caused: HTN, old age, female,
DM, obesity
•Hallmark Finding: Normal LV EF

32
Q

Types of Heart Failure: Right

A

•Right-sided HF: from left-sided HF(back up in lungs), cor pulmonale, right ventricular MI, edema/swelling in GI tract/ascites in right-sided HF

•Backup of blood into the right atrium and venous systemic circulation
•Jugular venous distention (blood backs up to R ventricle)
•Hepatomegaly, splenomegaly
•Vascular congestion of Gl tract
•Peripheral edema

33
Q

Pathophysiology of HF: General

A

Ventricular failure leads to: Low blood pressure (BP), Low CO, Poor renal perfusion (RAAS; poor renals = effects urinary output)

•Abrupt or subtle onset
•Compensatory mechanisms mobilized to maintain adequate CO

34
Q

Compensatory Mechanisms in HF

A

737 Lewis
These mechanisms are activated to maintain adequate CO.
•1st response: vasoconstriction of vessels which raises BP, but this can’t compensate forever
•Neurohormonal response - RAAS
-As CO falls, blood flow to kidneys decreased & is sensed as decreased volume
1. SNS is activated to increase BP and HR
2. Release of aldosterone from adrenal cortex results in sodium & water retention
3. Peripheral vasoconstriction & increases BP
4. Pituitary gland releases ADH which results in water reabsorption
-ventricular dilation
-ventricular hypertrophy

35
Q

Other compensatory mechanisms

A
  1. Norepinephrine & epinephrine (fight or flight, raise BP)
  2. Inotropy(control ventricular contractility) & chronotropy (stimulates beta adrenergic receptors controlling HR)
    3.dilation (enlargement of chambers of heart that occurs when pressure in left ventricle is elevated)
  3. Hypertrophy (increase in muscle mass & cardiac wall thickness. Leads to poor squeeze, more o2 needs, poor circulation & dysrhythmias)
36
Q

What part of the heart can enlarge?

A

The entire heart overall
The ventricles

37
Q

Difference between systolic & diastolic failure

A

Systolic: stretched & thin chambers (heart can’t pump)

Diastolic: stiff & thick chambers (heart can’t fill)

Both decrease CO and both are bad outcomes

38
Q

Counter regulatory mechanisms

A

668 Lewis
•Labs: BNP (peptide released when heart damage is occurring) & Triponin (indicates ischemia)

BNP less than 100 (check book)
Triponin less than 0.3

39
Q

What do Natriuretic peptides do?

A

Natriuretic peptides:
Atrial natriuretic peptide (ANP)
b-type natriuretic peptide (BNP)

•Released in response to increased blood volume or stretch in heart

•Promotes Diuresis by increased GFR (reduces preload), vasodilation, and lowered BP by inhibiting aldosterone and renin secretion. Counteracts effects of SNS and RAAS

NUR ADN 35 (1 decks)

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