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NUR2226 > Week 2: Cardiac A > Flashcards

Week 2: Cardiac A Flashcards

1
Q

Define atherosclerosis

A

Characterised by the soft deposits of intra-arterial fat and fibrin along the vessel wall that harden over time.

  • a pathological process not a diagnosis
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2
Q

Define arteriosclerosis

A

Chronic condition related to the thickening and hardening of the walls of the arteries.

  • a pathological process not a diagnosis

arTeria= THICK

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3
Q

Define ischemia

A

a condition in which the blood flow (and thus oxygen) is restricted or reduced in a part of the body.

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4
Q

What can persistent ischemia to the coronary arteries cause?

A

acute coronary syndrome

This can be further divided into infarction and irreversible myocardial damage.

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5
Q

What are the risk factors that for arteriosclerosis?

A
  • old age; normal part of aging

- presence of hypertension (HTN) can exacerbate it

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6
Q

What are the risk factors for atherosclerosis?

A
  • smoking
  • hypertension
  • DM
  • increased levels of low density lipoprotein cholestrol
  • decreased levels of high density lipoprotein (HDL)
  • endothelial damage
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7
Q

What are the risk factors for endothelial damage and why are they important to look out for?

A

Risk factors for endothelial damage to the vessel walls that can precipitate atherosclerosis include;

  • elevated C-reactive protein (CRP)
  • increased serum fibrinogen
  • insulin resistance
  • oxidative stress
  • infection
  • peridontal disease.
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8
Q

What are the clinical manifestation of arteriosclerosis?

A

Chest pain

Atypical presentations may include:

  • Nausea
  • Dyspnea
  • Fatigue
  • Back pain
  • Diaphoresis
  • Syncope

May include clinical manifestations associated with heart failure and low cardiac output

Some populations will present with ‘atypical’ clinical manifestations

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9
Q

What diagnoses hypertension?

A

on repeated blood pressure (BP) measurements at different times:

Systolic blood pressure recorded is >140 mmHg or the diastolic pressure is 90 mmHg or greater.

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10
Q

What causes hypertension?

A

a change in one or more factors affecting peripheral vascular resistance or cardiac output.

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11
Q

Why is hypertension an issue?

A

The consistent elevation of blood pressure considerably increases a person’s risk of developing coronary heart disease, heart failure, kidney disease and stroke.

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12
Q

Explain the relationship between hypertension and atherosclerosis?

A

Hypertension increases the risk of atherosclerosis.

It contributes to endothelial injury and can lead to myocardial hypertrophy, which increases myocardial demand for coronary flow..

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13
Q

Explain the types of hypertension

A

Primary hypertension

  • 90-95% there is no known cure
  • aka BP just keep climbing
  • usually asymptomatic

Secondary hypertension (10%)
- cause can be identified
- low renal blood flow (damages glomerlus’ and renal corpusle while also preventing them from excreting adedquate water therefore increasing BV and BP)
risk factors incude anything that reloeases renin e.g. kidneys or tumor
- symtpoms relate to underlying cause

Hypertensive crisis

Hypertensive urgency: sever BP elevation > 180/110 mmHg; not immediately life-threatening and associated symptom can include a headache.
- hasnt yet been dmaage to end organs (heart, brain, lungs)

Hypertensive emergencies: Severe BP elevation > 220/140 mmHg; associated acute organ failure.
- symptoms= confusion, drowiness, chest pain, breathlessness

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14
Q

List some causes and risk factors for hypertension

A
  • Family history
  • Advancing age
  • Cigarette smoking
  • Obesity
  • Heavy alcohol consumption
  • Gender (males>females under the age of 55; females>males over the age of 55)
  • High dietary sodium intake
  • Low dietary intake of potassium, calcium, magnesium
  • Glucose intolerance
  • Chronic stress/anxiety
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15
Q

What complications can result from hypertension?

A
  • Heart attack
  • stroke
  • aneurysm
  • heart failure
  • kidney damage/renal impairment or failure
  • Dementia
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16
Q

What causes hypertension?

A
  • increased sympathetic activity= increases HR and vasoconstriction= increased BP
  • RAAS system
  • natriuretic peptides
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17
Q

List some clinical manifestations of hypertension

A
  • Can be asymptomatic
  • Headache
  • dizziness
  • fatigue
  • Retinal changes
  • Papilloedema
  • Coronary artery disease/angina/AMI
  • Left ventricular hypertrophy
  • CKD
  • TIA
  • stroke

Secondary hypertension symptoms
- Frequent headaches, sweating, palpitations

Sleep apnoea: obesity, snoring, daytime sleepiness

Complementary and/recreational drug intake

Hypokalemia: muscle weakness, hypotonia, muscle tetany, cramps, cardiac arrhythmias

Symptoms suggestive of thyroid disease

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18
Q

Explain some treatments for hypertension

A
  • diet
  • exercise
  • stress reduction
  • antihypertensive medication
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19
Q

Explain the stages f hypertension

A

Normal= <120/<80
Elevated= <129/<80
Stage 1= <139/<89
Stage 2= >140/>90

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20
Q

Define angina

A

pain or other sensation caused by myocardial ischemia. (lack of oxygen to the heart)

Often described as sever, crushing, behind the sternum pain.

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21
Q

What cause of angina

A

When the demand for myocardial oxygen exceeds the supply of oxygen from the coronary arteries, myocardial ischaemia occurs.

Pain is likley caused due to lactic acid and/or abnormal stretching of nerve fibres.

Angina is the resulting chest pain experienced by the patient due to this lack of oxygen.

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22
Q

What are the two types of angina?

A

Stabe and unstable angina

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23
Q

Explain stable angina

A
  • often a coronary heart disease
  • a brief episode of chest pain or chest tightness.

SUBSIDES WITH MEDICATION AND REST

Often associated with

  • exertion and activity
  • cold weather
  • eating large meals

Occurs due to= accumulated deposites, narrowing the pathway for blood flow.
- This makes sense it would subside with rest as there is less pressure on it.

The pain or tightness can be a sign the arteries supplying blood to the heart are narrowing and there is an increased risk of an acute cardiac event.

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24
Q

Explain unstable angina

A
  • presents as either new-onset angina, angina occuring at rest or angina that is increasing.
  • a form of acute coronary syndroms that results from myocardial ischaemia that is reversible.
  • sudden pain
  • caused by blocking
  • usually reversible myocardial ischemia signaling that the atherosclerotic plaque has become complicated and a can be a strong indicator of acute myocardial infarction (AMI).
  • can be a sign infarction is impending (if atherosclerotic plaque has become complicated)
  • A small fissure or erosion of the plaque can lead to transient episodes of thrombotic vessel occulsion and vasoconstriction.
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25
Q

What are some causes and risk factors of angina?

A
  • Increasing age
  • Smoking
  • High cholesterol
  • Hypertension
  • Uncontrolled diabetes
  • Lifestyle factors such as unhealthy eating, overweight/obesity and insufficient physical activity.
  • sedentary lifestyle
  • history of heart disease
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26
Q

What are some complications of angina?

A
  • Acute myocardial infarction
  • Acute coronary syndrome
  • Arrhythmia
  • Death
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27
Q

What is the pathophysiology of angina?

A
  • occurs when oxygen demand out weights oxygen available
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28
Q

What factors can impact supply of oxygen that can then lead to angina?

A
  • physical exertion
  • emotional stress
  • atherosclerosis

Can all impact oxygen supply

  • narrowing of coronary arteries by atherosclerosis. Usually the coronary artery needs to be blocked (stenosed) by 75% or more for ischaemia secondary to atherosclerosis to occur.
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29
Q

What can a traveling clot/thrombus cause?

A

a myocardial infarction (heart attack) because of further reduced flow, leading to inadequate perfusion and oxygenation to the distal tissues.

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30
Q

What can initiate angina?

A

exercise (due to increased demand on heart and therfore O2 demands increase)

Coronary arteries that are

  • inflamed
  • infected
  • injured
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31
Q

How can angina be diagnosed?

A

ECG- records electrical signals of heart

Stress tests- BP and ECG is watched while exercising.

Echo-cardio gram- produces images of the heart to identify angina related problems (damaged heart muscle due to lack of oxygen)

Nuclear stress- measures blood flow to your heart muscle at rest and during stress. Looks for enlarged heart.

Blood test- tested for troponins

Coronary angiography-

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32
Q

Treatment of angina

A
  • exercise
  • medications (nitrates, aspirin, clot-preventing drugs, beta blockers, statins, calcium channel blockers, bP lowering medication )
  • stenting (ballon that widens artery)
  • by pass surgery (artery or vein is attached around the blood vessel)
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33
Q

Define acute coronary syndrome

A

The culmination of angina and atherosclerosis.

These cause myocardial infarction

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34
Q

What is the key to preventing myocardial infarction?

A
  • prevention
  • early recognition
  • early intervention

this will reduce

35
Q

What are the two types of ACS?

A
  • unstable angina

- acute myocardial infarction

36
Q

What are the risk factors/causes of acute coronary syndrome?

A
  • atherosclerosis
  • hypertension
  • increasing age
  • family history
  • Dyslipidaemia (abnormal amount of lipids in the blood)
  • smoking
    lifestyle factrs: overweight/obesity, lack of physical activity
  • DM

PMHx

  • hypertension
  • preeclampsia
  • GDM
37
Q

What complications are associated with acute coronary syndrome?

A
  • inadequate coronary oxygen
  • cellular and systemic events occurring after AMI (acute myocardial infarction)
  • electrical dysfunction
  • mechanical dysfunction (heart failure, myocardial rupture, papillary muscle dysfunction)
  • Thrombotic complications (recurrent coronary ischemia)
  • Inflammatory complications (pericarditis, post-myocardial infarction syndrome)
  • Death
38
Q

What are the clinical manifestations of ACS- AMI

A
  • pain (pressing, neck, jaw, back, shoulder or left arm pain)
  • nausea and vomiting
  • BP initially drop then sympathetic nervous system may activate to temporarily increase BP and HR
  • Peripherial vasoconstriction
  • Diaphoresis
  • Abnormal heart sounds from ventricular dysfuntion
  • Dullness in lung percussion and inspiratory crackles from pulmonary congestion
  • arrhythmias
  • cardiac arrest
  • sudden death
39
Q

What is an important note regarding certain groups with ACS or AMI?

A

some populations (e.g. elderly or with diabetes mellitus) will present with ‘atypical’ clinical manifestations and this may include ‘silent’ infarctions.

Clinical manifestations and complications are often related to the site and severity of necrosis and co-morbidities.

40
Q

Explain the relationship between ACS and myocardial infarction

A

Acute Coronary Syndromes (ACS) can be viewed as the acute process of myocardial ischemia after the often long term, chronic pathological conditions.

Long term myocardial infarction leads to acute coronary syndrome

41
Q

Explain the pathophysiology behind ACS?

A

When blood flow is reduced to the myocardium, it becomes damaged.

Myocardial cell death occurs after approx. 20 minutes of reduced oxygen.

Here is a breakdown of the processes that occurs:

  • After 1 minute of hypoxia, ECG changes are evident (covered in cardiac B)
  • Anaerobic metabolism begins
  • Glycolysis occurs
  • Hydrogen ions and lactic acid accumulate (acid-base imbalance)
  • Electrolyte imbalance
  • Reduction in myocardial contractility
  • Catecholamine release and hyperglycaemia
  • Angiotensin II is activated causing vasoconstriction and fluid retention
  • Ventricular remodelling occurs
42
Q

If a thrombus blocks blood flow in a coronary artery and myocardial ischemia will progress to either;

A

Subendocardial infarction

Transmural infarction

43
Q

Explain subendocardial infarction

A

the thrombus blocking coronary blood flow breaks up before distal tissue necrosis has occurred and only the myocardium directly beneath the endocardium is involved

44
Q

Explain transmural infarction

A

the thrombus permanently blocks the blood flow through the vessel and the necrosis extends through the myocardium, to the endocardium and pericardium resulting in cardiac dysfunction.

45
Q

How long can cells withstand a lack of oxygen?

A

20 minutes before permanent cellular death occurs

- changes are evident within 20 secs

46
Q

Explain the pathophysiology of myocardial infarction

A
  • Cardiac cells can withstand a lack of oxygen for about 20 minutes before permanent cellular death occurs.
  • Changes are evident within 10 seconds of decreased blood flow.
  • Myocardial oxygen reserves are depleted quickly leading to anaerobic metabolism and a build-up of lactic acid which further compromises the myocardium.
  • Electrolyte disturbances occur resulting in a loss of potassium, calcium and magnesium from within the cell.
  • This has an impact on contractility and the heart’s ability to pump effectively.
  • Catecholamine relase exacerbates the problem by causing coronary artery spasm, peripheral vasoconstriction, fluid retention and hyperglycaemia.
  • After 20 minutes of reduced blood flow, cellular death occurs and this results in the release of intracellular enzymes such as creatine kinase and troponin (which can be measured in blood tests).
47
Q

Explain some structural and functional changes that occur with myocardial infarction

A
  • site and severity of infarction dependant*
  • Myocardial remodelling can occur which causes hypertrophy and loss of contractility and is a process mediated by compensatory mechanisms. The impact of this can be reduced with early restoration of blood flow and the use of medications.

At the time of disruption of coronary blood flow, there can be a reduction of ventricular function. This leads to a drop in the ejection fraction (percentage of blood pumped from the heart: approx. 65%). This impacts the heart’s ability to pump blood throughout the body as effectively as it once may have.

AMIs can be subdivided into non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI). (These concepts are described in Cardiac B).

48
Q

What are the clinical manifestations of ACS?

A

Acute coronary syndrome –> acute myocardial infarction

  • Pain may be similar to angina but more intense (pain radiating to neck, jaw, back, shoulder or left arm)
  • Nausea and vomiting
  • BP may initially drop and then the sympathetic nervous system may activate to temporatily increase BP and HR
  • Peripherial vasoconstriction
  • Diaphoresis
  • Abnormal heart sounds from ventricular dysfuntion
  • Dullness in lung percussion and inspiratory crackles from pulmonary congestion
  • Arrhythmias
  • Cardiac arrest
  • Sudden death

It is important to note that some populations (e.g. elderly or with diabetes mellitus) will present with ‘atypical’ clinical manifestations and this may include ‘silent’ infarctions.

Clinical manifestations and complications are often related to the site and severity of necrosis and co-morbidities.

49
Q

Explain how a MCI occurs?

A

What a plaque deposite breaks away or opens, it misses with the blood and forms a clot, this blocks the vessel and urgent treatment is required to re open vessel.

50
Q

Describe coronary heart disease

A

develops when the coronary artery/arteries clog and narrow due to a buildup of plaque and are not able to deliver enough oxygen to the heart muscle.

Coronary heart disease is an overarching term for the conditions affecting the coronary vessels

Coronary artery disease (CAD) is the damage and disease in the major blood vessels that supply blood to the myocardium.

It is the chronic condition that may have minimal to debilitating symptoms, and the acute condition of acute coronary syndrome with chest pain and myocardial damage/death.

51
Q

What is CHD also known as?

A
  • coronary heart disease
  • ischaemic heart disease
  • coronary artery disease
  • heart disease
52
Q

What are some causes and risk factors for CHD?

A
  • artherosclerosis
  • hypertension
  • high cholesterol
  • Diabetes mellitus
  • Obesity/lack of exercise/sedentary lifestyle
  • Smoking/tobacco use
  • Psychosocial factors - stress
  • Advancing age (men > 45 years; women >55 years (women’s risk increases after menopause)
  • Gender (male or female after meopause)
  • A family history of premature CVD
53
Q

What is metabolic sundrome?

A

The collection of conditions that often occur together and increase risk of DM, stroke and heart disease.

Main conditions=

  • obesity
  • hypertension
  • elevated blood triglycerides
  • low levels of HDL
  • cholesterol and insulin resistance
54
Q

Why is it critical for a nurse to understand the risk factors for coronary heart disease?

A
  • to identify people at risk

- to empower patients to make better choices about their health

55
Q

What are some complications related to coronary heart disease?

A

Cardiac muscle ischemia that can occur due to coronary heart disease can lead to the weakening of the heart and reduced efficiency.

  • Hypertension
  • Angina/chest pain
  • Dysrhythmias
  • Myocardial infarction
  • Heart failure/ischemic cardiomyopathy
  • Sudden cardiac arrest/death
56
Q

List some clinical manifestations of CHD?

A

Coronary heart disease is an overarching term for the conditions affecting the coronary vessles that supply blood to the heart, therefore review the clinical manifestations of each of the conditions.

e.g. chest pain, fatigue, pressing heavy feeling

57
Q

Explain the pathophysiology of coronary heart disease.

A

Coronary heart disease (CHD) can be viewed as the diagnosis of the often long term, chronic pathological conditions e.g. ACS (atherosclerosis, )

CHD refers to the disorders that affect the blood flow through the coronary blood vessels that supply the heart with blood to deliver nutrients and oxygen. Some of the contributing conditions, such as atherosclerosis and hypertension, have been discussed in this eBook.

58
Q

Explain the management of coronary heart disease

A
  • treatment to reduce the load on the heart via beta blockers or calcium channel bloclers to stop the heart pumping so hard
  • improve coronary atrey blood flow e.g. by pass surgery
  • slowing or reducing build up of plaque e.g. disolving clot with drugs
  • modifying diet
  • regular exercise
    Can slow or reverse athlersclerosis
59
Q

Explain the diagnostic test- ECG

A

Measures the electrical activity, rate and regularity of the heart beat

60
Q

Explain the diagnostic test- Echocardiogram

A

uses U/S to create an image of the heart.
This is used to see the movement of blood through the heart
- checks for signs of stemi or non stemi

61
Q

Explain the diagnostic test- Exercise stress test

A

measures your heart rate while walking on a treadmill. Determines how well heart works when pumping more blood.

62
Q

Explain the diagnostic test- Chest X-ray

A

pictures heart, lungs and other organs in the chest

- ay see signs of cardiac megaly (enlarged heart)

63
Q

Explain the diagnostic test- cardiac catheterization

A

check inside the heart for blockage by inserting a thin, flexible tube through an artery in the groin, arm or neck to reach heart.

  • measure BP within heart and strength of blood flow though the heart’s chambers while collecting a blood sample from the heart or inject dye into the arteries of the heart (coronary arteries)
64
Q

Explain the diagnostic test- coronary angiogram

A

monitors blockage and flow though the coronary arteries. Use X-rays to detect dye injected via cardiac catheterisation

65
Q

Explain the diagnostic test- coronary artery calcium scan

A

Computed tomography (CT) scan that looks in the coronary arteries for calcium buildup and plaque.

66
Q

Explain some diagnostic pathology tests

A
  • Urea and electrolytes (U&Es)
  • glucose lipid profile
  • Liver function tests (LFTs)
  • Full blood examination (FBE)
  • cardiac enzymes (cardiac markers) e.g. troponin + creatine Kinase

Troponin level
Is a protein found in cardiac muscle that is released into the circulation when there is damage to the myocardium.
Levels can increase within 2-3 hours and remain elevated for 2 weeks.

Three types of troponin:

  • Troponin C (TnC)
  • Troponin T (cTnT)
  • Troponin I (cTnI)
  • Creatine Kinase (CK)
    is an enzyme that is release when there is muscle injury
  • Coagulation profile
67
Q

Explain some treatment and management of coronary heart disease and all other pathological processes

A

Immediate treatment/goals;

  • Relieve pain and distress
  • Improve coronary blood flow
  • Restore heart function

Long-term treatment/goals:

  • Improve overall cardiac and vascular function
  • Manage and reduce cardiovascular risk factors

These treatment/goals are achieved by:

  • Medicines to treat risk factors for CAD e.g. high cholesterol, high blood pressure, or an irregular heartbeat
  • Surgical procedures to help restore blood flow to the heart
  • Lifestyle changes e.g. eating a healthier (lower sodium, lower fat) diet
  • increasing physical activity
  • reaching a healthy weight
  • quitting smoking
68
Q

What is the role of nitrates?

A

dilate blood vessels= to increase supply of oxygen

69
Q

What is the role of beta blockers, calcium channel blockers?

A
  • decrease myocardial workload
70
Q

What is the role of anti platelet medications?

A
  • reduce clotting
71
Q

What pathophysiological process can be corrected with surgery?

A

acute coronary syndrome (STEMI) the aim is to reperfuse the coronary arteries as quickly as possible.

72
Q

Explain a Percutaneous Transluminal Coronary Angioplasty (PTCA)

Angioplasty= widen vessel

A
  • a catheter is inserted into the blocked or narrowed part of the coronary artery.
  • a wire with a deflated balloon is passed through the catheter to the narrowed area.
  • the balloon is then inflated, opening the artery by compressing the plaque deposits against the artery walls.
  • a stent is inserted to help keep the artery open.
73
Q

Explain Fibrinolysis: tissue plasminogen activator (tPA)

A
  • administered to dissolve blood clots that may cause serious complications in a timely manner
  • used to maximise tissue reperfusions by restoration of coronary blood flow
  • can improve early and long-term survival
74
Q

Explain Coronary Artery Bypass Graft Surgery (CABGs)

A
  • redirects blood flow around a section of a blocked or partially blocked coronary artery.
  • a healthy blood vessel may be taken such as the internal thoracic artery, saphenous vein or radial artery and used to connect above and below the blocked artery/arteries in your heart.
  • it doesn’t cure atherosclerosis or coronary artery disease. It can reduce symptoms, improve blood flow, oxygenation and function of the heart and reduce the risk of dying of heart disease
75
Q

What lifestyle changes can assist in the management of CHD?

A
  • Quit smoking
  • Healthy diet
  • Moderate alcohol consumption
  • Increase physical activity
  • Maintain a healthy weight
    Reduce stress
76
Q

What is cardiac rehabilitation and what it is purpose?

A
  • a supervised program with a multidisciplinary healthcare team that may include nurses, physiotherapists, nutrionists and mental health professionals and includes the following:
  • Physical activity
  • Education about healthy living, including healthy eating, taking medicine as prescribed, and ways to help you quit smoking
  • Counseling to find ways to relieve stress and improve mental health
  • can help to improve quality of life and reduce the risk of another cardiac event.
77
Q

What are some nursing care considerations for dealing with some with a cardiac complication?

A
  • Vital signs
  • Pain assessment: PQRST/OLDCARTS
  • Signs and symptoms associated with myocardial ischaemia
  • Oxygen administration (SpO2 <94% or patient looks ‘shocked’)
  • ECG

Consider

  • IV cannulation
  • administration of medications
  • reduce anxiety
  • continuous monitoring/re-assessment/emergency trolley
78
Q

What is the outcome of team based care?

A

Team-based health care teams can enhance patient care and improve outcomes. Effective collaboration with healthcare providers to ensure patient education, identification of risk factors and prescription and modification of treatments.

79
Q

What is troponin both a good and bad marker for assessing stemi and non stemi?

A

Good= released when cardiac muscle dies

Bad= peaks 2 days after onset of chest pain (could be to late)

80
Q

What acronym is used for initial ACS management?

A

MOAN

M= morphine (IV opoids) 
O= Oxygen (of less than 94%)
A= asprin (to prevent further damage)
N= nitrates (reduce work load on the heart)
81
Q

Explain the process of emergency reperfusion of a stemi

A

1 preference= primary percutaneous coronary intervention PCI placement (stent then inflate ballon)

2 preference= fibrinolytic therapy (thrombolysis)
Drug is used to break down the thrombosis/atherosclerosis

82
Q

What ais a PCI or primary percutaneous coronary intervention

A

A stent and ballon that is placed into an artery to reopen it

83
Q

Explain the process of emergency reperfusion of a Non- stemi

A

dependant or risk identification!

High risk=

  • commenced on anti platelets, anticolagulants, and beta blockers
  • consider revascularisation via PCI

Low risk=

  • continuous monitoring of cardiac markers and ECG
  • monitor for markers they may be high risk and elevate them to the high risk management
  • if no changes occur follow up with cardiologist is reccomended
84
Q

Follow up management of all coronary syndromes includes;

A

Lifestyle modifications e.g.;

  • quit smoking
  • increased exercise
  • reduce alcohol
  • lose weight
  • eat healthy
Pharaocological therapy (ongoing) 
ABAS 
A= ace inhibitors/ angiotension receptor receptor antagonists
- reduce BP and work load on the heart 
B= beta blockers 
- help BP and HR 
A= aspirin and clopiogrel
- prevent clots from forming 
S= statins 
- reduce cholestrol

NUR2226 (9 decks)

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