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NUSC 2P14 > Week 7: Cardiovascular Disorders > Flashcards

Week 7: Cardiovascular Disorders Flashcards

1
Q

The Cardiovascular System

A

Consists of the: Blood, Heart, Blood vessels
-Carries nutrients & oxygen to cells throughout the body
-Increases blood flow to meet energy demands (i.e. physical activity)
-Stops bleeding & promotes healing (i.e. site of injury or bleeding)
-Produces & carries white blood cells & antibodies (defense)
-Regulates body temperature:
(Heat from muscles carried through body)
(Blood vessels dilate to cool body or constrict to conserve heat)

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2
Q

Heart- Great Vessels

A

Vena Cava
Pulmonary Arteries: to the lungs
Pulmonary Veins: to the heart
Aorta: pumps blood, oxygen, nutrients to where it needs to go

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3
Q

Heart- Pump

A

Heart –> double pump
-Pulmonary circulation: to the lungs
-Systemic circulation: to the body

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4
Q

Heart- 3 Layers

A

Endocardium
-Inner layer
-Continuous with vessels
Myocardium
-Middle layer
-Thick and muscular
-Cardiac muscle
Epicardium
-Outer layer
-Forms pericardium
Pericardium
-Sling like membrane
-Supports the heart by attaching it to other structures (diaphragm, large blood vessels)

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5
Q

Blood Flow Through the Heart

A

Deoxygenated Blood:
Right atrium
-Receives blood from body (vena cava)
Right Ventricle
* receives blood from right atrium
* pumps to lungs via pulmonary artery
Oxygenated Blood
Left Atrium
-Receives blood from lungs (pulmonary veins)
Left Ventricle
-Receives blood from left atrium
-Pumps to body via aorta

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6
Q

Cardiac Cycle: One Heartbeat

A

Systole (contraction) & diastole (relaxation) act in coordination

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7
Q

Cardiac Conduction System

A

Cardiac Impulse (action potential) spreads throughout the heart
-Specialized conduction tissue
Arises in the SA node (pacemaker of the heart)
and spreads over the atria
-SA node originates the cardiac impulse
-Atria contract
Goes to the AV node and spreads over the ventricles
-AV node slows cardiac impulse and sends it to bundle of His
-Bundle of His send the cardiac impulse to Purkinje fibers through the ventricles
-Ventricles contract

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8
Q

Cardiac Conduction System- ECG

A

Waves
P = atrial depolarization
QRS = depolarization of the ventricles
T = repolarization of the ventricles
U = repolarization of the purkinje fibres or might be hypokalemia

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9
Q

Cardiac Mechanical System

A

-Depolarization triggers mechanical activity

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10
Q

Systole

A

-Contraction of the myocardium
-Results in ejection of blood from the cardiac chamber

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11
Q

Diastole

A

-Relaxation of the myocardium
-Allows for filling of the chamber

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12
Q

Cardiac Output (CO)

A

-Measurement of the heart’s mechanical efficiency
-Amount of blood pumped by each ventricle in 1 minute
Stroke Volume (SV)= the amount of blood ejected from the ventricle with the heartbeat

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13
Q

Factors Affecting Cardiac Output (CO)

A

The HR is regulated primarily by the autonomic nervous system
Factors Affecting the SV:
-Preload
-Contractility
-Afterload
Increases in preload, contractility, and afterload (increases workload of the myocardium), results in increased oxygen demand

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14
Q

Cardiac Reserve

A

Ability of the heart to respond to stress by increasing CO as much as three-fold or four-fold. Can increase HR to 180 bpm for short periods without hard

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15
Q

Blood Vessels- Function

A

-Act as a delivery system
-Regulate blood pressure
-Exchange nutrients and waste between the capillaries and cells
-Redistribute blood in response to changes in body needs
-Helps regulate body temperature

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16
Q

Types of Blood Vessels

A

-Arteries: thick surrounding for pumping blood
(arterioles)
-Capillaries: thin surrounding for gas exchange
-Veins
(Venules)

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17
Q

Regulation- Autonomic Nervous System

A

Sympathetic (stress)
-Fight or flight
-SA node activity and heart rate
-Speed of cardiac impulse through conduction system
-Force of myocardial contraction
Parasympathetic (peace)
-SA node activity and heart rate
-Speed of cardiac impulse from SA to AV node
-No effect on strength of contraction

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18
Q

Blood Pressure

A

Arterial BP: measure of the pressure exerted by blood against the walls of the arterial system

Systolic BP: the peak pressure exerted against the arteries when the heart contracts

Diastolic BP: the residual pressure of the arterial system during ventricular relaxation

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19
Q

Age Related Considerations

A

-Age is the greatest risk factor for CV disease
-Most common cause of hospitalization and second leading cause of death in adults < 85
-Cardiac Valves: thicker and stiffer
-Decreased # pacemaker cells (dysrhythmias)
-Arterial and venous blood vessels thicken and become less elastic
-Valves in the veins in the lower extremities
(reduced ability to return blood to the heart)
(often results in dependent edema)

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20
Q

Assessment- Subjective Data

A

History:
-Chest pain
-SOB
-Hypertension
-Stroke
-Smoking
-Edema
Medications
-OTC
-Prescription
-ASA (aspirin)
-NSAIDs
-Blood Thinners
Surgery or other treatments
-related to CV problems

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21
Q

Assessment- Objective Data

A

Measures: general appearance, vital signs
Inspection: skin, extremities (edema, lesions) neck veins, capillary refill
Palpation: bilateral and carotid pulses 2+, (symmetry, quality, rhythm,) lower extremities (edema)
Auscultation: carotid and femoral arteries, abdominal aorta, heart (extra sounds, murmurs)

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22
Q

Assessment- Pulses

A

0: absent
1+: weak, thready
2+: normal
3+: full, bounding

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23
Q

Assessment: Cardiac Auscultation

A

-The movement of the cardiac valves creates some turbulence in the blood flow, the resulting heart sounds are normal
S1: closure of the tricuspid and mitral valves, soft “lubb” (beginning of systole)
S2: closure of the aortic and pulmonic valves, sharp “dupp” (beginning of diastole)

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24
Q

Invasive Diagnostics

A

Cardiac catheterization
Coronary angiography
Intravascular ultrasonography
Hemodynamic monitoring

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25
Q

Noninvasive Diagnostics

A

Chest x-ray
Electrocardiography
(Electrocardiogram (ECG))
(Stress testing)
(Echocardiography)
Nuclear cardiography
Cardiovascular MRI (CMRI)
Cardiac CT
Blood studies

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26
Q

Common Medications

A

Atenolol: hypertension
Nitroglycerin: angina
Furosemide: heart failure
Alteplase: myocardial infarction

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27
Q

Hypertension

A

-Persistent BP measurements above the normal systolic/diastolic pressures 120/80
-Must occur on 2 consecutive occasions
-Persistent systolic BP > 140 mmHg or
-Persistent diastolic BP > 90 mmHg
*Most significant modifiable risk factor for cardiovascular disease and mortality in Canada
-Responsible for up to 50% of deaths due to heart disease & stroke
~20% of Canadian adults have hypertension

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28
Q

Hypertension

A

Even small incremental changes in systolic and diastolic pressures have a direct effect on mortality:
-For every 20-mm Hg increase in systolic BP or a 10-mm Hg increase in diastolic BP, the risk for cardiovascular mortality doubles
As blood pressure increases, so does risk for:
-MI
-Heart failure
-Stroke
-Renal Disease

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29
Q

Subtype of Hypertension

A

Isolated Systolic Hypertension (ISH)
-Sustained elevation of SBP ≥ 140 mm Hg and a DBP < 90 mm Hg
-Common in older adults related to loss of elasticity in large arteries

30
Q

Hypertension Classifications

A

Primary (essential) hypertension:
-Elevated BP without an identified cause
-Does not have a single known cause, but certain risk factors
-90% to 95% of clients
Secondary Hypertension
-Elevated BP with a specific cause
-5% to 10% in adults; >80% in children
-Many causes; treatment aimed at eliminating the underlying cause

31
Q

Primary Hypertension Risk Factors

A

Advancing Age: 50% of people >65
Heavy alcohol use
Smoking > 15 cigarettes / day
Diabetes
Elevated serum lipids
High dietary sodium
Gender: < 55 (men) > 55 (women)
Family history
Obesity
Ethnicity: black and south asian
Sedentary Lifestyle
Socioeconomic Status: low income
Psychosocial stress

32
Q

Secondary Hypertension- Causes

A
  • Coarctation or congenital narrowing of the aorta
    -Renal disease (renal artery stenosis and parenchymal disease)
    -Endocrine disorders (cushing syndrome and hyperaldosteronism)
    -Neurological disorders (brain tumours, quadriplegia, head injury)
    -Pregnancy induced hypertension
    -Sleep apnea
    -Medications
33
Q

Signs & Symptoms

A

None initially “silent killer”
Usually found during check-ups
Severe Hypertension: related effects on blood vessels or increase workload of the heart:
Fatigue, decreased activity tolerance, dizziness, palpitations, angina, dyspnea

34
Q

Complications

A

The most common complications of hypertension are target-organ diseases occuring in the
HEART (hypertensive heart disease)
BRAIN (cerebrovascular disease)
PERIPHERAL VASCULATURE (PAD)
KIDNEYS (nephrosclerosis)
EYES (retinal damage)
-CAD related to atherosclerosis
-Left ventricular hypertrophy related to increased cardiac workload
-Heart failure related to inability to pump enough blood to meet demands
-Stroke related to atherosclerosis
-Intermittent claudication related to atherosclerosis
-Ischemia related to narrowed intrarenal blood vessels
-Blurring, vision loss

35
Q

Hypertension- Diagnostics

A

-Blood pressure monitoring
-Urinalysis
-Blood chemistry
-Fasting blood glucose
-Fasting total cholesterol & high- density lipoprotein, low-density lipoprotein, and triglycerides
-Standard 12-lead electrocardiography
-Assess urinary albumin excretion in clients with diabetes
-All clients with treated hypertension need to be monitored for the appearance of diabetes

36
Q

Hypertension Collaborative Care

A

Lifestyle Modifications
-Nutritional therapy: Dietary Approaches to Stop Hypertension (DASH) diet
-Decreased salt intake: most cost-effective measure to improve health outcomes
-Weight reduction
-Limit alcohol consumption
-Physical activity
-Avoidance of tobacco products – CV benefits seen within 1 year
-Stress management

37
Q

Hypertension Collaborative Care

A

Drug therapy- goal is to achieve a BP of <140/90 mmHg
Current drugs have two main actions:
-To reduce SVR, and
-To decrease the volume of circulating blood
Drug Types:
-Diuretics
-Adrenergic (sympathetic) inhibitors
-Direct vasodilators
-Angiotensin inhibitors
-Calcium channel blockers

38
Q

Nursing Management

A

Goals- the patient will:
-Achieve and maintain the determined target BP
-Understand, accept, & implement the therapeutic plan
-Experience minimal or no unpleasant adverse effects of therapy
-Be confident about the ability to manage & cope with this condition
Health Promotion:
-Dietary modifications
-Screening programs in the community
-Cardiovascular risk factor modification
Ambulatory & Home Care:
-Physical activity
-Home blood pressure monitoring
-Client adherence treatment

39
Q

Age-Related Considerations

A

-Hypertension is common in 60+
-Loss of tissue elasticity
-Increased collagen content & stiffness of the myocardium
-Increased peripheral vascular resistance
-Decreased β- adrenergic receptor sensitivity
-Decreased kidney function
-Decreased renin response to sodium & water depletion
-Impaired baroreceptor reflex mechanisms-risk for orthostatic hypotension

40
Q

Hypertensive Crisis

A

Severe, abrupt increase in DBP (defined as >120–130 mm Hg)
Rate of increase in BP is more important than the absolute value
Risk: history of hypertension and failure to comply with treatment
Hypertensive Emergency is evidence of acute target-organ damage
-Hypertensive encephalopathy, cerebral hemorrhage
-Acute renal failure
-Myocardial infarction
-Acute left ventricular failure with pulmonary edema
-Aortic aneurysm

41
Q

Hypertensive Crisis (Nursing Collaborative Care)

A

BP level alone is a poor indicator of the seriousness of the patient’s condition and is not the major factor in deciding the treatment for
a hypertensive crisis
The association between elevated BP and signs of new or progressive end- organ damage determines the seriousness of the situation.
Nursing / Collaborative Care
-IV drug therapy: decrease mean arterial pressure
-Monitor cardiac & renal function
-Neurological checks
-Determines cause
-Education to avoid future crises

42
Q

Atherosclerosis

A

Chronic Endothelial Injury
-Hypertension
-Tobacco use
-Hyperlipidemia
-Hyperhomocysteinemia
-Diabetes
-Infection
-Toxins
Fatty Streak
-Lipids accumulate and migrate into smooth muscle cells
Fibrous Plaque
-Collagens covers the fatty streak
-Vessel lumen is narrowed
-Blood flow is reduced
-Fissures can develop
Complicated Lesion
-Plaque rupture
-Thrombus formation
-Further narrowing or total occlusion of vessel

43
Q

Acute Coronary Syndrome

A

-Associated with deterioration of an atherosclerotic plaque that was once stable
Unstable Angina (UA)
-Chest pain that is new in onset, occurs at rest, or has worsening pattern
-Unpredictable
-Emergency
-May become an NSTEMI
Myocardial Infarction (MI)
-Results from sustained ischemia, causing irreversible myocardial cell death –EMERGENCY
-80-90% occurs secondary to thrombus formation
-Contractile function of the heart stops in the necrotic areas
-STEMI & NSTEMI

44
Q

MI- NSTEMI

A

Non-ST-segment elevation MI
Partial occlusion
Damage (partial thickness)
Pathological Q waves not usual

45
Q

MI- STEMI

A

ST-segment elevation MI
Total occlusion
More extensive damage (full thickness)
Pathological Q-waves present

46
Q

Pain Associated with the Heart

A

Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration is the hallmark of an MI

47
Q

Atherosclerosis- Stents & Bypass

A

Percutaneous Coronary Intervention (PCI)
Coronary Artery Bypass graft (CABG)

48
Q

Fibrinolytic Therapy

A

Aimed at stopping the infarction process by dissolving the thrombus in the coronary artery and reperfusing the myocardium
-Must be given as soon as possible
-Single IV bolus over 30-90 mins
-Major complication: bleeding

49
Q

Rhythm Identification and Treatment

A

-The ability to recognize normal & abnormal cardiac rhythms is an essential nursing skill
-Prompt assessment of abnormal cardiac rhythms, called dysrhythmias, and of the patient’s response to them is critical

50
Q

Cardiac Cells (Automaticity)

A

Ability to initiate an impulse spontaneously and continuously

51
Q

Cardiac Cells (Contractility)

A

Ability to respond mechanically to an impulse

52
Q

Cardiac Cells (Conductivity)

A

Ability to transmit an impulse along a membrane in an orderly manner

53
Q

Cardiac Cells (Excitability)

A

Ability to be electrically stimulated

54
Q

Electrocardiogram (ECG)

A

-Graphic tracing of electrical impulses produced by the heart
-Waveforms of ECG represent activity of charged ions across membranes of myocardial cells
-Typically, there are 12 recording leads in the ECG
-Six leads (leads I, II, III, aVR, aVL, & aVF) measure electrical forces in the frontal plane
-Six leads (V1–V6) measure electrical forces in the horizontal plane

55
Q

ECG Monitoring

A

-The ECG can be visualized continuously on a monitor oscilloscope
-A recording of the ECG (rhythm strip) is obtained on ECG paper attached to the monitor
-The recording provides documentation of the patient’s rhythm
-It also allows for measurement of complexes and intervals, and for assessment of dysrhythmias

56
Q

12-Lead ECG

A

-A lead is a glimpse of the electrical activity of the heart from a particular angle
(a lead is a perspective)
-There are 10 electrodes providing 12 perspectives of the heart’s activity using different angles through two electrical planes
(vertical and horizontal planes)
-When being continuously monitored, between 1 & 12 ECG leads may be used

57
Q

Impulse Formation

A

-Disorders of impulse formation can cause dysrhythmias
-Normally, the main pacemaker of the heart is the SA node, which spontaneously
discharges 60-100x/min
-Secondary pacemakers may originate from the AV node (40 to 60x/min) or the His–Purkinje system (20 to 40x/min)

58
Q

Sinus Bradycardia

A

-SA node fires at a rate <60 bpm
-May be normal in trained athletes
-Tx = atropine or pacemaker

59
Q

Sinus Tachycardia

A

-SA node fires at a rate >100bpm
-Physiological and psychological stressors
-Tx = treat the underlying cause

60
Q

Premature Atrial Contraction (PAC)

A

-Contraction originates in the atrium from a focus other than the SA node, travels in an abnormal way
-Stress, fatigue, substances and other medical conditions
-Tx = withdrawal of sources of stimulation

61
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

A

-Originates in a focus above the bundle of His
-Overexertion, emotional stress, and stimulants
-Tx = vagal stimulation (valsalva & coughing), IV adenosine

62
Q

Atrial Flutter

A

-Atrial tachydysrhythmias: recurring, regular, sawtooth-shaped flutter
-Disease states: CAD, hypertension, cardiomyopathy, etc
-Tx = low ventricular response by calcium channel blockers and β- adrenergic blockers. Convert flutter by amiodarone, propafenone. May need cardioversion (shock)

63
Q

Atrial Fibrillation (A-Fib)

A

-Total disorganization of atrial electrical activity leading to loss of effective atrial contraction
-Underlying heart disease (CAD, HF, pericarditis)
-Tx = decrease ventricular rate by CCB and beta-adrenergic blockers (metoprolol); or anticoagulation therapy

64
Q

Junctional Dysrhythmias

A

-Originate in AV node because SA node failed to fire, AV node becomes pacemaker, safety mechanism when SA fails
-CAD, HP, inferior MI, electrolyte imbalances
-Tx = atropine, beta-adrenergic blockers, CCBs, and amiodarone

65
Q

AV Block- 1st Degree

A

-Duration of AV conduction (PR interval) is prolonged
-MI, CAD, hyperthyroidism, vagal stimulation, some meds
-Tx = none; may need to adjust meds that are causing it

66
Q

Premature Ventricular Contractions (PVCs)

A

-Contractions originating in the ventricles (wide distorted QRS)
-Stimulants (caffeine, nicotine), epinephrine, electrolyte imbalances, MI, HF, CAD
-Tx = based on the cause, O2, or may not be treated

67
Q

Ventricular Tachycardia (V-tach)

A

-When a run of three or more PVCs occurs, ventricles take over as pacemaker
LIFE THREATENING
-MI, CAD, CNS disorders
-Tx = treat the precipitating cause

68
Q

Ventricular Fibrillation (V-fib)

A

-Severe derangement of the heart rhythm: irregular undulations of varying shapes and amplitude on the ECG
-Mechanically, the ventricle is simply “quivering” and no effective contraction: no cardiac output occurs
-MI, myocardial ischemia, CAD
- Tx = assess airway, breathing, pulse
-CPR, Defibrillation

69
Q

Asystole

A

-Total absence of ventricular electrical activity. On occasion, P waves are detected
-No ventricular contraction occurs because depolarization does not occur. Patients are unresponsive, pulseless, and apneic

70
Q

Defibrillation

A

-Most effective method of terminating ventricular fibrillation and pulseless VT
-Accomplished by the passage of a DC electric shock through the heart that is sufficient to depolarize the cells of the myocardium
-The intent is that subsequent repolarization of myocardial cells allows the SA node to resume the role of pacemaker
-Upon defibrillation, the operator calls, “All clear” and looks to see that personnel are not touching the patient or the bed at the time of
defibrillator discharge
-It is essential that the operator ensures that all personnel are clear before the defibrillator is discharged

71
Q

Artificial Cardiac Pacemakers

A

-Electronic device used to pace the heart when the normal conduction pathway is damaged or diseased
-The electrical signal (stimulus) travels from the pacemaker, through the leads, to the wall of the myocardium which then contracts

NUSC 2P14 (7 decks)

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