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NUR 120 > Unit 4 > Flashcards

Unit 4 Flashcards

1
Q

Which part of the heart has thinner walls? Why? Which is the thickest? WHy?

A

Atria
Less resistance

L ventricle-must overcome resistance of high aortic pressure.

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2
Q

What are the important coronary arteries?

A

L coronary artery-3 branches:Left main, LAD, circumflex
R-Inferior wall of heart
Posterior-posterior wall

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3
Q

What are the 3 physiologic characteristics of the nodal and purkinje cells for synchronization.

A

Automaticity: ability to initiate electrical impulse
Excitability:ability to respond to an electrical impulse
Conductivity: ability to transmit an electrical impulse from on cell to another.

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4
Q

Where are the SA and AV nodes located and what are there normal firing rates?

A

SA-SVC and R atria-60-100/min

AV-R atria and tricuspid valve 40-60

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5
Q

What is depolarization/depolarization, what ions are involved, and what is this known as?

A

The rapid entry of sodium or slow entry of calcium into the cell while potassium exits creating a pos Extracellular space-depolar. Once complete, ions revert back-repolar.

Cardiac action potential.

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6
Q

What is the refractory period? What are the 2 phases?

A

The requirement of completing repolarization before being able to depolarize again.

Effective (absolute)-unresponsive to electrical stimulus.
Relative-may depolar prematurely if stimulus is stronger than normal.(dysrhythmias)

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7
Q

What occurs in S1 S2 S3 S4

A

S1-AV valves close (heard at apex)
S2- SL valves close (heard at base)
S3-ventricular spilling (common in children)
S4-enlarged chambers (CAD, HTN)

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8
Q

What is a murmur? What are some common causes?

A

Turbulent blood flow through valve, closing too fast or slow (regurgitation).

Pregnancy (inc blood volume), fever (inc metab needs)

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9
Q

What controls the heart rate?

A

ANS
Para-slows by vagal nerve
Sym-speeds by beta 1 receptors in SA node (circulating catecholamines by adrenal gland.

All stimulated by baroreceptors in carotid artery. Inc BP stims ans to use para by vagal nerve to slow. VISA versa.

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10
Q

What is preload and after load?

A

Pre-amount of blood filling ventricle end of diastole. Greatest stretch. (Effects SV)

After-resistance to ejection of blood from ventricle (inverse relationship to SV. So: vasoconstriction inc pressure inc after load. Dilation-less pressure-less after load-inc SV)

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11
Q

What factors can increase and decrease contractility?

A

inc-catecholamines, sns, meds:dig, dopamine. = inc SV

Dec-hypoxemia, acidosis, meds:beta adrenergic blockers (atenolol).

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12
Q

So ultimately, what 3 things can increase SV?

A

Inc preload (increase venous return)

Inc contractility (sns)

Dec after load (periph vasodilation=dec aortic pressure)

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13
Q

What is ejection fraction?

What can result from a severely low EF?

A

The percentage of end-diastolic blood volume that is ejected with each beat. L ventricle is normal at 55-65%.

HF (stroke, coma, death)

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14
Q

In the assessment of the cardiac patient, what information will need to be obtained for history?

A

Family (renal, Diab, HTN, CA, heart)
Past surgeries, meds, allergies, reproductive, alcohol/tobacco, diagnoses, dz’s
Education level
Religion/culture practices
Height/weight (gain or lost in past year)
Exercise levels
Stress changes/relationships/depression/anxiety
Diagnostic testing (recent)
Chief complaint-any tx used?
Fainting/dizziness, unusual fatigue, chest pain/discomfort (better, worse, when)

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15
Q

What consist of the physical assessment of the cardiac patient?

A 
Overall appearance/posture/gait
Clubbing(can be hereditary)
Skin turgor
Bruising/wounds
Jugular
Ortho. Hypo
Pulse, heart inspection, palp, ausc. (Sitting and supine) Look for:thrill (purring), murmur, friction rub, opening snaps/systolic kicks
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16
Q

Specify the pulse amplitudes.

A 
0-not palpable/absent
1-diminished:weak, diff to palate, obliterated w/pressure
2-normal:cannot be obliterated
3-mod inc:easy to palpate
4-increased:strong, Bounding
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17
Q

What differences occur in the cardiac patient in aging, and gender?

A

As aging (or chronic HTN) occurs ventricular chambers thicken (dec compliance). Valves more rigid/thick and vessel dec in elasticity, stiffening.

Men generally have heart dz more often, also AA.

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18
Q

How are cardiac bio markers used in analysis of the cardiac pt?

A

Damaged (necrotic) myocardial cells release enzymes CK (brain), CKMB (myocard muscle) and proteins troponin (card muscle), myoglobin (early ind of MI). These leak into interstitial space and travel into circulation via lymphatic system.

LDH also but not reliable (coats inside of cells)

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19
Q

How does the lipid profile become useful in the cardiac pt?

What are their normal values?

A

Important for CAD. Risks increase w/ inc of LL or total chol to HDL.
Most useful w/ 12 HR fast.
Cholesterol-less than 200
LDL-less than 160 (transports chol and trig into cell. Deposit subs in arterial walls)
HDL-35-70 (trans chol away from cell of artery to liver to excrete.
TRIG-100-200 (lower better for heart)

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20
Q

Discuss the important electrolytes, normal values, and associated symptoms of imbalance.

A

Sodium-fluid balance, 135-145, dec metal status.
Calcium-neuromuscular/heart automaticity,8.6-10.2, HF, heart block, vent fib.
Potassium-cardiac electrophy function. 3.5-5, dec renal is a problem, pt must be able to void before admin., dysrhythmias.
Mag-help absorp Calcium, pot stores. 1.3-2.3, tachy and heart block.

21
Q

BNT is primary secreted from the ___________ in response to increased ____________. Used for assessment of what dz?

A

Ventricles
Preload
HF

22
Q

What can the EKG/ECG perform?

A

Representation of electrical current from various angles.

Continuous monitoring-Evals segments

23
Q

What are the important electrical segments of the heart?

A 
P wave:atrial muscle depolar
P-R:time between atrial and vent depolar
QRS:vent depolar
T: vent repolar
ST:time after vent depolar to vent repolar (depression=chronic, elevation=acute)
24
Q

What is a echo and what is it able to detect?

What can be performed w/ this imaging?

A 
U/S of heart. (CAD)
Ejection Fraction
Size/shape/motion of structures
Pericardial effusions
Chamber size, cause of murmurs, valve function, vent wall motion.

Stress test (exercise/meds)
Images at rest
Meds/exer given (inc HR)
Images during

25
Q

What is radionuclide imaging?

Specifically myocardial perfusion imaging?

A

Radioisotopes injected can be detected by camera to determine coronary artery perfusion, ischemia, and infarction.

Done w/ stress typically s/p MI to see extent of damage under stress.
Thallium used to show areas of poor perfusion.

26
Q

What is MUGA testing?

A

Records hundreds of heart beats. Sequential images evaluated for L vent function, wall motion and ejection fraction.

27
Q

What are the benefits of the PET scan in the cardiac pt?

A

Shows severity of CAD by viewing myocardial perfusion, L vent function, and damage caused by MI.

28
Q

Discuss cardiac Cath use, purpose, procedure, nursing care.

A

Invasive. Arterial/venous Cath advanced from femoral artery into heart. Best test for CAD. Guided by fluoroscopy. IV sedation.
BUN, PT, PTT, Renal, CBC are done prior to prep for contrast excretion. BP, pulse, pain, and bleeding.
Bed rest 2-6hrs post, pressure on site 30 min.

29
Q

What are the non modifiable and modifiable risk factors for CAD?

A 
Non-
Fam hx
Age (elder)
Gender (males)
Race (AA)
MOD-
Lipid intake (obesity/diet)
Tobacco use
HTN, DM
Sedentary
30
Q

What is considered HTN? And 2 types?

A

Elevated BP over 140/90 (either one or both)
Primary:essential, more common, unknown cause
Secondary:identifiable cause (underlying medical condition:coarctation Narrowing of aorta, hyperaldosteronism retain sodium), med induced

31
Q

What are some suggested causes of HTN?

A 
Inc SNS due to ANS dysfunction.
Inc renal Reabsorption of sod, chl, and water.
Inc renin-angioten-Aldos activity. (Inc vas resis)
Dec vasodilation of Arterioles (vascular endothelial d/o)
Insulin resistance (DM inc blood viscosity, inc Periph resis)
32
Q

Explain the clinical manifestations of HTN.

A

Problem:lack of s/s other than inc BP.

Vision changes
CAD, MI (L vent hyper-due to inc workload pushing against pressure), HF
TIA, stroke
Inc BUN/Creat.(kidney changes)

33
Q

What are the medical managements for the pt w/HTN?

A

Healthy weight/diet/dec sodium:below 2400mg/day or below 1500mg for DM)
Meds:compliance/education
CCB-typically 1st choice for AA and above 80y/o.
Full assessment-baseline data (BP) and trends
Teach DASH diet
BB-dec HR inc CO allowing vents to fill
CCB-dec contraction
Renin inhib-used w/ other meds (diuretics, AI, BB), blocks renin.

34
Q

What is HTN crisis and diff the two types: emergency vs urgency.

A

Pressures above 180/120.

Emergency:
Immed intervention needed
Life threatening
Organ damage (s/s visible)
IV meds, vasodilators, nitrates

Urgency:
High importance, not life threatening
No organ damage
Oral HTN meds

35
Q

What occurs in HTN retinopathy?

A

Narrowing of retinal Arterioles, thickening arteriole walls.

Micro aneurism, intraretinal hemmorhage, toruousness (twisting vessels)

36
Q

Explain what atherosclerosis is.

A

Most common cause of cardiovas dz in US.
Abnormal accumulation of lipid/fatty subs in lining of arterial blood vessel walls. Block/narrow coronary vessels reducing blood flow to myocardium.

37
Q

What are s/s of atherosclerosis? Prevention?

A

Angina, epigastric distress, radiating pain to jaw or l arm. Sob

All adults 20 y/o and Oder need fasting lipid profile q 5yrs, and if abnormal q6weeks until optimal then q4-6 months.
Maintain LDL HDL Chol and trig levels, inc activity

38
Q

What are the 2 types and factors that are associated with angina pain?

A

Stable:predictable consistent occurring on exertion, relieved by rest/nitrates
Unstable:symps inc in frequency/severity, not relieved by rest/nitrates.

Physical exertion (inc myocard o2 demand)
Exposure to cold (vasoconstric, inc BP, in o2 demand)
Eating heavy meal (inc blood flow to mesenteric for digestion)
Stress (catecholamines release, inc BP, HR, myocard workload)

39
Q

Angina is typically caused by?

S/S?

A

Artherosclerosis, coronary A blocked.

Varies among pts.
Indigestion. Pain from discomfort-agonizing. Radiated pain to neck, jaw,shoulders, inner upper arm, choking, weak/numb in arms, wrist, hands, sob, pallor, diaphoresis, lightheaded, n/v.

40
Q

What are the 1st and 2nd line dx for angina?

TX?

A

1st: 12lead EKG-shows ischemia, changes in rhythm (ST seg).
Labs:CKMB, CKT, troponin, electrolytes, CBC.

2nd:Echo, stress tests, heart Cath

Dec o2 demand (relieve pain, change activity level), inc o2 supply (atleast 93%), medicate:Nitro (vasodilator, can cause HA), O2, BB (dec HR, don’t use on asthma pt), CCB (dec contract), anti platelet (prevent clots)

41
Q

What is ACS? How does this occur?

A

Acute coronary syndrome-emergent, acute myocardial ischemia resulting in myocardial infarction.

Plaque rupture and this thrombus formation occluded artery leading to necrosis of myocardial area effected.

42
Q

What are s/s of ACS/MI?

A

Diaphoresis
Dec BP, dec CO
Cyanotic
SOB/Tachy
Crackles due to pulm edema (if L vent failure)
Edema (R side heart failure)
Dec urine output (dec blood to kidney, inc BUN/Creat)

43
Q

What is used to dx ACS/MI? Tx?

A

EKG, labs (troponin can be detected w/I hours, peaks at 8hrs), pt assessment

NAOM + BB
(Nitrate, Asa, oxygen, morphine)

44
Q

What are potential complications of ACS/MI?

A

Dysrhythmias-(conduction disruption)
Cardiogenic shock-(L vent die, not pumping efficient, dec BP/perfusion)
Pulm Em-(clot dislodges goes into lungs)
Acute pulm edema- (L vent fail, fluid backing into lungs)
Cardiac failure-(AV block-need pacemaker)
Thromboembolic episodes-(DVT, PE, Stroke)

45
Q

Describe the 2 percutaneous coronary interventions?

A

PTCA-open blocked vessel w/ balloon, resolves ischemia (guided by flouro/angiogram).
Enter through femoral artery by used of hollow Cath, balloon threaded.

Stent-used to prevent re-stenosis (treated artery closes back). Metal mesh providing structural support to prevent closure. Some are drug eluding (with can minimize blood clots or scar tissue)

46
Q

What are risks related to PTCA and nurse care?

A

Bleeding (hematoma at insertion site)-assess extremity for pulse, color, and cap refill, bleeding.
Renal function, contrast allergy
Perforation of artery
Dysrhythmias
Chest pain (temp occluded artery during procedure)
Restenosis if no stent placed
Heparin admin during procedure.
Vascular closure device placed to hold pressure to femoral A.
Remain flat, keep affected leg straight until sheath removed.

47
Q

What is a coronary A revasculariztion? And indications for this surgery?
What is a common adverse effect?

A

BYPASS, CABG-blood vessel grafted (can be A or V) to occluded coronary A to allow blood flow beyond occlusion.

  • angina alleviation
  • L main coronary artery stenosis, multi vessel CAD
  • prevent/tx of MI, dysrhythmias, HF

Lower ext edema where vein is removed.

48
Q

Why is hypothermia maintained during CABG procedure?

What is done with the blood in the heart during procedure?

A

Slows body basal metabolic rate, dec O2 demand.(L disassociation curve)

Due to cooled blood, it is mixed with crystalloid solution, blood rewarmed in CPB circuit.

49
Q

How does increased heart rate effect LAD perfusion?

A

Increased heart rate decreases diastole. The LAD supplies the left ventricle perfusion during diastole.

NUR 120 (6 decks)

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