Cardiac Flashcards

1
Q

Pathogenesis of atherosclerosis:

A
  1. Chronic endothelial injury - hypertension, tobacco use, hyperlipidaemia, diabetes
  2. Fatty streak - lipids accumulate at the place of injury and migrate into smooth muscle cells
  3. Fibrous plaque - collagen covers the fatty streak, narrowing the vessel lumen and reducing blood flow
  4. Complicated lesion - plaque rupture and thrombus formation, further narrowing or total occlusion of the vessel
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2
Q

Management of CAD:

A
  • Controlling cholesterol abnormalities
  • Managing hypertension
  • Promoting cessation of tobacco use
  • Maintaining exercise and healthy diet
  • Reducing stress
  • Controlling diabetes
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3
Q

Unmodifiable risk factors for CAD:

A
  • Genetic predisposition
  • Age
  • Gender
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4
Q

Modifiable risk factors for CAD:

A
  • gout
  • cigarette smoking
  • sedentary lifestyle
  • high stress levels
  • hypertension
  • obesity
  • diabetes
  • untreated bacterial infections
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5
Q

What is angina caused by?

A

Insufficient coronary blood flow, hence, a disruption in the balance between oxygen supply and oxygen demand

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6
Q

Stable angina:

A
  • Angina symptoms during moderate physical activity or when you are pushing yourself physically
  • symptoms go away with rest/medication
  • atheroma narrows the vessel and still allows blood to flow
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7
Q

Unstable angina

A
  • Angina symptoms while doing very little or resting
  • Thombus occluding the vessel
  • increasingly severe and frequent chest pain associated with ST segment depression
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8
Q

Define:
- Atheromas
- Atherosclerosis
- Myocardial infarction

A
  • Atheroma: fatty deposits in the intima of the heart vessels
  • Atherosclerosis: narrowing of the heart vessels
  • Myocardial infarction: cells in the myocardium become necrotic and die
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9
Q

What is acute coronary syndrome?

A
  • Culmination of atherosclerosis and angina and NSTEMI/STEMI
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10
Q

Unstable angina

A

Ischaemia without infarction
ECG changes: Normal or transient ST depression
Cardiac troponin: normal or slightly elevated
Often precedes MI

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11
Q

NSTEMI

A

Non-ST elevated MI
No ECG changes
Cardiac marker (troponin) levels are elevated (cell death)

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12
Q

STEMI

A

ST elevated MI
Complete occlusion of coronary artery
Cardiac markers elevated
ECG changes: ST segment elevation

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13
Q

Treatment for ACS

A
  • Antiplatelets (aspirin), angina meds (nitroglycerin), O2 therapy
  • Confirmed ACS treatment = anticoags, beta blockers, ACE inhibitors, statins
  • STEMI patients (emergency): cardiac catheterisation –> PCI (stent) or fibrinolytic therapy if PCI N/A + aspirin
  • Unstable angina/NSTEMI: angiography, fibrinolytic therapy not indicated
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14
Q

Surgical interventions for CAD and ACS

A
  • PCI = percutaneous coronary intervention (angioplasty with a stent)
  • CABG = coronary artery bypass graft - take veins from leg or mammary artery and connect to coronary arteries in order to bypass a blockage
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15
Q

Conduction pathway of the heart:

A
  1. Sinoatrial (SA) node
  2. Atrioventricular (AV) node
  3. Bundle of His
  4. Left and right bundle branches
  5. Purkinje fibres
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16
Q

How to calculate rate in bpm?

A

Count number of P waves (atrial rate) or QRS complexes (ventricular rate) in 30 square (6 seconds)

Multiply number by 10 (1min)

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17
Q

Clinical manifestations associated with angina:

A

Signs: SOB, sweating, vomiting
Symptoms: fatigue, crushing chest pain (burning, squeezing), dizziness, nausea, pain in the arms, shoulder, neck, back or jaw

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18
Q

Abnormal findings expected with atherosclerosis and angina:

A
  • Low O2 sats
  • irregular pulse/palpitations
  • rapid heartbeat
  • increased RR, SOB
  • chest pain
  • nausea
  • fatigue/weakness
  • pallow
19
Q

Angina nursing interventions

A
  • Administer analgesia when required
  • Bed rest to reduce O2 demand
  • Deep breathing, tripodding, semi-fowlers
  • administering O2 therapy if required
  • reducing anxiety through education & distraction
  • monitor vital signs
20
Q

Priority nursing interventions in AMI?

A
  • administer O2 to maintain sats
  • analgesia when required
  • monitor vital signs
  • bed rest to reduce myocardial workload
  • monitor ECG for complications
  • semi-fowlers to assist with dyspnoea
  • assess peripheral oedema/temp/pulses/cap refill to monitor tissue perfusion
  • reduce anxiety through education and distraction therapy
21
Q

Atrial fibrillation pathophysiology

A
  • Multiple ectopic beats cause a loss of organisation of the atrial electrical activity
  • Loss of effective atrial contraction
22
Q

Main complications of persistent HTN:

A
  • Brain: strokes, hypertensive encephalopathy (confusion, headache, convulsion)
  • Blood: elevated sugar levels
  • Retinas: hypertensive retinopathy
  • Heart: MI, cardiomyopathy, HF
  • Kidneys: nephropathy, chronic renal failure
23
Q

Which 4 systems affect BP?

A
  • Nervous
  • Cardiovascular
  • Renal
  • Endocrine
24
Q

Management of HTN:

A

Lifestyle modifications (prior to pharmacological intervention)
- healthy diet
- physical activity
- reduction of alcohol
- smoking cessation
- stress reduction

25
Q

Elements determining BP:

A
  • HR
  • SV (amount of blood pumped with each heartbeat)
  • TPR (total peripheral resistance - resistance of muscles in arteries)
26
Q

Risk for coronary artery disease related to HTN

A
  • Thickening of the heart muscle
  • Increased pressure generated by the muscle on contraction
  • iNcreased workload on the heart
27
Q

Situations in which hypotensive states can occur:

A

a. Haemorrhage
b. Extreme exhaustion when NA is depleted
c. Anaphylactic shock
d. Septic shock
e. Cardiogenic shock
f. Dehydration

28
Q

Heart failure define

A

The pathological process in which the heart’s pumping ability is impaired, causing a decrease in cardiac output, meaning the heart is unable to meet the metabolic demands of the body

29
Q

Precipitating causes of HF

A
  • infection (especially lung infection)
  • arrhythmias (tachycardia, AF, bradycardia)
  • excessive physical activity
  • pregnancy and delivery
  • anaemia
  • administration of inappropriate drugs
  • medication non-compliance
  • excess fluid intake
  • thyrotoxicosis
30
Q

Treatments that lessen the cardiac load:

A
  • rest
  • limitation of salt and water intake
  • diuretics (indicated for fluid retention)
31
Q

Define preload:

A
  • the force that stretches the cardiac muscle prior to contraction
32
Q

Define afterload:

A

The amount of pressure that the heart needs to exert to eject the blood during ventricular contraction

33
Q

Heart failure nursing management:

A
  • Vital signs
  • ECG
  • Diet
  • Fluid restriction
  • monitoring weight
  • Education on medications (difficulties of polypharmacy)
  • Managing stress, anxiety, depression
  • Family involvement for support
  • Changes in level of conscious
    Analgesia
34
Q

Causes of congestive HF

A
  • Coronary artery disease
  • cardiomyopathy
  • hypertension
  • valvular heart disease
34
Q

Pharmacological treatment of HF

A
  • diuretics
  • beta blockers
  • ACE inhibitors
35
Q

Pathophysiology of HF left vs right:

A

Left:
- more affects the lungs
- LV reduced pumping around the body, congestion in pulmonary veins

Right:
- more affects tissues:
- RV reduced pumping to lungs, congestion in peripheral veins

36
Q

Manifestations of HF left vs right:

A

Left: tachypnoea, dyspnoea, orthopnoea, crackles, cardiomegaly, GI upset, nausea, anxiety, pleural effusion

Right: splenomegaly, hepatomegaly, pitting oedema, weakness/fatigue, nocturia

General: confusion/impaired memory, increased urination, fatigue

37
Q

Education points for HF patients:

A
  • medications and how to stick to their regime
  • diet + fluid restriction
  • sleep, relaxation and energy conservation
  • monitoring weight, output/input, oedema
38
Q

Psychosocial considerations for HF patients:

A
  • Referrals to psychologists/counsellors (might not be able to do things they used to, difficulties with polypharmacy)
  • importance of reducing social isolation
  • managing stress, anxiety and depression
39
Q

How does the RAAS system affect BP?

A
  • Responds to renal perfusion and results in salt and water retention to raise BP
40
Q

What do baroreceptors do?

A
  • Sit in the carotid arteries and arch of aorta and respond to changes in pressure exerted by fluid to control BP
41
Q

Manifestations of HTN:

A

a. Usually asymptomatic at first
b. Headache and dizziness (lack of O2 reaching the brain)
c. Chest pain (lack of O2 for heart muscle)
d. Blurred vision (retinopathy)
e. Ischaemic leg pain (decreased blood flow to periphery)

42
Q

Why are HF patients often on fluid restrictions?

A

a. Retention of fluid due to congestion, resulting in oedema and weight gain
b. Excess fluid can sit around the heart (reducing contraction) or sit around the lungs (pleural effusion)
c. The excess fluid also increases totally blood volume, which means the heart has to work harder

43
Q

Nursing strategies to monitor fluid balance:

A
  • use of fluid balance chart
  • educate the patient
  • use pans/bottles (or keep pan in toilet)
  • regular check ins
  • daily weight
  • know measurements of jugs of water/hospital food