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NURS 487 > cardio > Flashcards

cardio Flashcards

1
Q

objective data when assessing cardiovascular system

A

IPAP-S =
Inspect

Palpate

Ausculate

Percuss

Smell (GI, Integumentary)
Neck Vessels
Assessing Jugular Vein Distention (JVD), volume overload, increased right sided heart pressure 
Blood pressure
May need to do blood pressures on both arms
Pulse 
Apical and Radial
Extremities
Pedal pulses x 2
Post tibial pulses x 2
Precordium (Heart Sounds)
APE To  Men
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2
Q

inspecting overall CV status

A 
Patient’s overall color
Pallor, cyanosis, mottling, glossy 
Neck Veins
Nail beds
Clubbing, splinter hemorrhages
Presence of Edema
You have not palpated to document level of edema (+1 to +4) only that it is present or not and requires further assessment
Overall Skin for CV health
 petechiae, purpura, ecchymosis, bruising breakdown, ulcers (venous or arterial), varicose veins
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3
Q

neck checklist

A

Inspect jugular venous pulse assessing for distention
Carotid pulse—Palpate and Auscultate
If JVD is present, estimate or measure

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4
Q

precordium checklist inspect and palpate

A

Look at your patient’s chest
Any skin blemishes, scars, movement of chest wall, color
Do you see any pulsations
If present, it appears on the 4 or 5th intercostal space
You are looking for a heave or lift
Palpate the apical pulse at the 4th or 5th intercostal space

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5
Q

what is a thrill

A

palpable vibration, like a hum or purring cat, it is turbulent blood flow that goes with murmurs. May also coincide with extra heart sounds.

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6
Q

precordium auscultate

A

Identify anatomical areas where you would listen
Note rate and rhythm of the heart beat
Identify S1 and S2 and note any variation
Listen in systole and diastole for any extra heart sounds
Listen in systole and diastole for any murmurs
Repeat sequence with bell
Listen at the apex with person in left lateral position
Listen at the base with person in sitting position

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7
Q

heart sounds

A

S1 and S2 are best heard with the diaphragm
Aortic and Pulmonic Valves are best heard with the diaphragm
Tricuspid and Mitral Valves are best heard with the diaphragm
Listen to the apical pulse while palpating the radial pulse (A=R) and document

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8
Q

heart sound explanations

A

S1: Is the first heart sound, closure of the Tricuspid and Mitral valves, and is the beginning of systole
S2: is the second heart sound, occurs with the Pulmonic and Aortic valves, and signals the beginning of diastole

When the aortic valve closes significantly earlier then the pulmonic valve, you can hear the two components separately…this is known as a split S2

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9
Q

extra heart sounds

A

S3: low intense vibrations created by ventricular filling. Occurs when ventricles are resistant to filling during the rapid phase. Occurs immediately after S2.
Occurs in patients with left ventricular failure such as volume overload or Heart Failure and mitral valve regurgitation, high Cardiac Output states, hyperthyroidism, anemia and pregnancy
Ausculated after S2 and known as “ventricular gallop”
“Kentucky”
S4: low frequency vibration caused by atrial contraction. The vibrations heard create S4, this occurs just before S1 (end diastole/pre-systole).
Coronary artery disease, cardiomyopathy and with systolic overload (afterload), LV hypertrophy
Outflow obstruction to the ventricle (aortic stenosis), and systemic hypertension.
Ausculated before S1 and known as “atrial gallop”
“Tennessee”
S3 = volume, too much volume in ventricle, heart failure
S4 = end of diastole and just before systole, louder sound after s1 and s2

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10
Q

assess for murmurs

A

Timing. It is crucial to define the murmur by its occurrence in systole or diastole.
Loudness. Describe the intensity in terms of six “grades.” For example, record a grade ii murmur as “II/VI.”
Grade I —barely audible, heard only in a quiet room and then with difficulty
Grade II —clearly audible, but faint
Grade III —moderately loud, easy to hear
Grade IV —loud, associated with a thrill palpable on the chest wall
Grade V —very loud, heard with one corner of the stethoscope lifted off the chest wall
Grade VI —loudest, still heard with entire stethoscope lifted just off the chest wall
Pitch. Describe the pitch as high, medium, or low. The pitch depends on the pressure and the rate of blood flow producing the murmur.
When you get to erbs point, change stethoscope to bell and you’ll be able to hear murmurs easier

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11
Q

cardiovascular check list for infants and children

A

Transition from fetal to pulmonic circulation is immediate
Fetal shunts normally close 10 to 15 hours after birth but up to 48 hours
Assess CV during first 24 hours and then again 2-3 days later to see if there are any differences
Inspect: color is the infant cyanotic?
Palpate: apical impulse to determine size and position of the heart looking for: cardiac enlargement, pneumothorax, diaphragmatic hernia, and dextrocardia
Auscultate: tachycardia, bradycardia  account for variations with activity and rest
Palpate: apical impulses is displaced in certain conditions: cardiac enlargement (to the left), pneumothorax (away from affected side), diaphragmatic hernia (shift to right most hernias occur in the left), dextrocardia (heart is located on the right side of the chest)

Auscultate best heard with diaphragm of the pediatric stethoscope of the bell

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12
Q

normal heart rates for infants and children

A 
newborn = 100-180
1 week-3 months = 80-160
3 months-2 years = 70-150
2-10 years = 60-110
10-adult = 50-100
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13
Q

pitting edema

A

If pitting edema is present, grade it on the following scale:
1+Mild pitting, slight indentation, no perceptible swelling of the leg
2+Moderate pitting, indentation subsides rapidly
3+Deep pitting, indentation remains for a short time, leg looks swollen
4+Very deep pitting, indentation lasts a long time, leg is very swollen

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14
Q

subjective data collection for CV system

A 
Chest pain: onset, location, character, pain brought on by, any associated symptoms (PQRST)
Dyspnea
Orthopnea
Cough
Fatigue
Edema
Nocturia
Cardiac history
Family history
Personal habits (cardiac risk factors)
Cyanosis or pallor
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15
Q

cardiac output

A

the amount of blood pumped by each ventricle per minute

Variables that affect CO:
Heart Rate (increased or decreased)
Stroke volume (preload, afterload and contractility)
Metabolic rate and O2 demand
Females< males
Larger body requires > CO
Decreases with age
Decreased from supine to upright
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16
Q

heart rate

A

controlled by autonomic nervous system, neural reflexes, atrial receptors, and hormones
> 100 beats per minute considered tachycardia
60-100 beats per minute considered normal heart rate *
< 60 beats per minute considered bradycardia
Centers of the brain: medulla and pons areas of the brainstem, as well as hypothalamus, cerebral cortex and thalamus
Neural Reflexes: Baroreceptors respond to BP and HR which is mediated by tissue pressure receptors found in the aortic arch and carotid sinus
Hormones
Adrenocortical hormones
Thyroid hormones
Decrease in growth hormones
Neurotransmitters
Norepinephrine (causes constriction)
Epinephrine (increases flow)

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17
Q

stroke volume

A

the volume of blood ejected per beat during systole

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18
Q

preload

A

the amount of stretch on the myocardial fibers (pressure) at end- diastole which is determined by the ventricular filling (end diastolic) volume
 filling volume  stretch

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19
Q

factors that affect preload

A

Slower HR prolongs diastole allowing longer filling time
Total blood volume- Increased volume Increased myocardial stretch
Distribution of Blood- supine/ Trendelenburg, increased arterial/venous tone
Atrial kick
Compliance

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20
Q

afterload

A

ventricular force or pressure required to overcome impedance to ejection
Left Ventricular Outflow Resistance- aortic diastolic pressure, Systemic Vascular Resistance (SVR), aortic valve resistance
Right Ventricular Outflow Resistance- pulmonary artery diastolic pressure, Pulmonary Vascular Resistance (PVR), pulmonic valve resistance

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21
Q

SVRI

A

resistance of blood flow throughout systemic circulation (left ventricle has to work harder to overcome resistance)

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22
Q

PVRI

A

resistance of blood flow throughout pulmonary circulation (right ventricle has to work harder to overcome the resistance) right ventricle hypertrophy, right ventricle heart failure

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23
Q

increase in afterload

A 
(decrease SV):
Increased ventricular work
Increased myocardial O2
Hypertension (HTN)
Aortic/pulmonic stenosis
Vasoconstriction
High body mass index
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24
Q

decrease in afterload

A

(increase SV):
Decrease ventricular work
Decrease myocardial work
Vasodilation

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25
Q

contractility

A

the ability of the myocardium to increase the extent and force of muscle fiber shortening independent of preload/afterload
Force of contraction depends on:
Change in stretching of the ventricular myocardium caused by preload
Alterations in the inotropic stimuli of the ventricles
Adequacy of myocardial oxygen supply

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26
Q

ejection fraction

A

amount of blood ejected from the ventricle/beat compared with end-diastolic volume
- Normal EF of LV is > 65%, below 40% is evidence of decreased contractility and heart failure

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27
Q

factors affecting blood pressure

A 
Is directly proportional to the cardiac output and the amount of peripheral resistance in the arteriolesFactors that increase BP:
Increase sympathetic activity
Abnormal renin theory (RAAS)
Increased blood volume
Aortic impedance
Genetic predisposition
Sensitivity of baroreceptors
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28
Q

hypertension (HTN)

A

Consistent elevation of systemic arterial blood pressure
Isolated HTN is defined as sustained systolic blood pressure accompanied by normal diastolic blood pressure < 90 mmHg
Classified as either Primary or Secondary Hypertension
Primary: elevated BP with no specific cause of HTN
Secondary: elevated BP with specific underlying disorder

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29
Q

primary hypertension

A

(around 90-95% of all cases)
Increased SNS activity, over production of sodium-retaining hormones and vasoconstrictors, increased sodium intake, greater than ideal body weight, excessive alcohol intake, hormones, and inflammation

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30
Q

secondary hypertension

A

(5-10% in adults and 80% in children)
Coarctation or congenital narrowing of the aorta, renal disease, endocrine disorders, neurological disorders, sleep apnea, medications

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31
Q

complicated hypertension

A

Chronic hypertension that damages the walls of the systemic blood vessels
Walls lead to hypertrophy and hyperplasia with fibrosis leading to vascular remodelling
Contributing factors of this include: endothelial dysfunction, angiotensin II, catecholamines, insulin resistance, and inflammation
Leads to target organ damage such as the kidney, heart, extremities, and eyes

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32
Q

hypertensive crisis pathophysiology

A

Severe and abrupt elevation in BP with a diastolic > 120-130 mmHg
High arterial pressures prevent the regulation of blood flow to cerebral capillary beds
High hydrostatic pressures in the capillaries cause vascular fluid to exude into the interstitial space
If BP not reduced, cerebral edema and cerebral dysfunction (encephalopathy) increased until death
Organ damage can occur such as intracranial or subarachnoid hemorrhage, acute left ventricular failure with pulmonary edema, myocardial infarction, kidney failure, dissecting aortic aneurysm, papilledema, cardiac failure, uremia, retinopathy

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33
Q

hypertensive emergency

A

develops over hours to days where there is evidence of acute target-organ damage

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34
Q

hypertensive urgency

A

develops over days to weeks where there is no clinical evidence of target-organ damage

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35
Q

hypertensive crisis nursing assessment

A

Monitor signs of neurological dysfunction, retinal damage, heart failure, pulmonary edema and renal failure
Monitor for white coat syndrome
Complete medical history and assessment of lifestyle
Physical exam should include: check eyes, calculate BMI, Neuro: monitoring LOC, mental status, and confusion CV: auscultate carotid, abdominal and femoral areas (for bruits), assess for JVD, assess lower extremity pulses and edema RESP: auscultate for crackles, pulmonary edema, poor oxygen exchange RENAL: monitor urine output, color, frequency, dehydration

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36
Q

hypertensive crisis clinical manifestations

A

Neuro: Headache, nausea, vomiting, seizures, confusion, stupor, coma, encephalopathy, blurred vision and transient blindness
CV: Cardiac instability such as unstable angina to myocardial infarction, pulmonary edema, and aortic dissection
Renal: Renal insufficiency ranging from decreased urine output to complete renal shut down

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37
Q

hypotension pathophysiology

A

In a nut shell, it’s low blood pressure (< 100/60 mmHg)
Due to:
Inadequate tissue perfusion due to a compromised cardiac output
Shifts in intravascular volume
Postural Hypotension
A drop in blood pressure when a person changes position from lying or sitting to standing
Baroreceptors are unable to regulate the heart rate in response to change in position quick enough

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38
Q

hypotension clinical manifestations

A

Patients feel dizzy or faint as a response to postural hypotension

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39
Q

hypotension nursing assessment

A

Neuro: LOC, mental status, oxygenation to the brain, lethargic, stupor
CV: monitoring perfusion is the primary goal, color, pulses, capillary refill, skin cool to touch, goosebumps, tachycardia or bradycardia
RESP: tachypnea, oxygenation status sp02,
RENAL: urine output (due to flow to reduced flow to the kidneys)

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40
Q

hypotension shock

A

Blood pressure falls dangerously low that decreases perfusion to all tissues within the body, compromising the normal physiological response
3 primary types of shock:
Cardiogenic ( inability of the heart to pump effectively)
Hypovolemic (significantly reduced intravascular volume)
Distributive (inability of the vasculature to compensate for hemodynamic changes)
Septic
Anaphylactic
Neurogenic

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41
Q

shock summary

A

Hypovolemic Shock
Blood VOLUME problem

Cardiogenic Problem
Blood PUMP problem

Distributive Shock
Blood VESSEL problem

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42
Q

angina pathophysiology

A

Diminished blood flow and lack of oxygen in the arteries in the heart leading to myocardial ischemia
Clinical Manifestations:
Patient develops chest pain that may or may not go away with rest
Often occurs during increased activity or exercise
Important to Note:
Precursor to myocardial infarction
May be stable or unstable or variant

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43
Q

stable angina pectoris (exertional)

A

effort induced chest pain

- lasts few seconds to 15 minutes
- relieved by rest, removal of provoking factors, or  NTG
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44
Q

unstable angina pectoris

A
  • lasts longer and occurs more frequently
    • may be exertional or occurs at rest
    • often referred to as crescendo angina, pre-infarction angina, nocturnal angina
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45
Q

variant (prinzmental) angina

A

chest pain that occurs at rest in early hours of the morning

- is often associated with ST segment elevations
- often cyclical
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46
Q

acute myocardial infarction pathophysiology

A

Complete interruption of blood supply to the cardiac muscle
Occurs as a result of sustained ischemia leading to myocardial cell death
Location of the infarction correlates with the involved coronary circulation
The longer the area is deprived of oxygen the greater chance of cell death
Inferior MI = top of the heart problem, right side of heart
Anterior MI = bottom of the heart, left ventricles, LAD or circumflex
Lateral = on left the side
LAD = left anterior descending artery
Anterior MI is worse because it affects the left side that has a greater workload

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47
Q

causes of acute myocardial infarction

A 
Plaque rupture
 Thrombus formation
 Coronary artery embolism
 Coronary spasm (cocaine)
 Hypotension
 Decrease in O2 delivery to tissues (anemia, shock, hypoxemia)
 Post procedure
 Spontaneous Coronary Artery Dissection
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48
Q

type 1 myocardial infarction

A

Myocardial infarction where there is a thrombosis of the coronary artery or a plaque rupture.
Spontaneous symptoms
Typically occurs more with men than women (because their hearts typically are bigger) bigger coronary arteries

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49
Q

type 2 myocardial infarction

A

Disruption in the myocardial oxygen supply and/or demand in the absence of any acute atherothrombosis (essentially nothing blocking the artery)
Typically more women present with type 2 MI’s
Patients present with less chest pain and dyspnea as well as other atypical presentations
May or may not present with ischemic events on the ECG

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50
Q

angina vs acute myocardial infarction

A

angina: discomfort = Chest pain, pressure, squeezing, tightness
location and radiation = Midsternal, neck, jaw, arms, back
intensity = mild to moderate
duration = 3-15 min
precipitating factors = exercise, weather, large meal, sex and stress
associated signs and symptoms = none
lab values = none
acute myocardial infarction:
discomfort = Same, abdominal pain, Shortness of breath (SOB)
location and radiation = Same, increased pain associated with radiation
intensity = more intense, silent and severe
duration = >20-30 min
precipitating factors = same but may occur at rest or during sleep
associated signs and symptoms = Diaphoresis, SOB, abdominal pain, indigestion, fatigue, not feeling well, pale, tachycardia, palpitations
lab values = Troponin (high sensitivity troponin), CKMB
magic number for troponin = 50

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51
Q

acute myocardial infarction clinical manifestations

A

Pain
Skin may be ashen, clammy, and cool to touch
If LV dysfunction, may auscultate crackles in the lungs
JVD, hepatic engorgement, and peripheral edema may be associated with RV dysfunction
Abnormal Heart sounds like S3 or S4
Nausea, vomiting
Fever

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52
Q

acute myocardial infarction nursing assessment

A

NEURO: Pain (PQRST) (Table 36-7, pg.823, Lewis et al (2019)), rating the pain, anxiety, LOC, fear, psychosocial, diaphoresis
CV: auscultate apical pulse- tachycardia, bradycardia, pulsus alternans, note any dysrhythmias (especially ventricular- PVC’s, Vtach, VFib), presence of S3 or S4, blood pressure to identify systemic resistance, murmurs, palpate pulses in the extremities, is skin cool to touch, what is the capillary refill time, JVD, peripheral edema
RESP: rate and depth of breath, monitor for signs of LV dysfunction (crackles), oxygenation (associated with LOC)
GI: nausea, vomiting, increased motility, decreased motility
RENAL: urine output (decreased or unchanged), color

Lab Values: Troponin, CK-MB, lipid levels (Total cholesterol, triglycerides, HDL, LDL) increased WBC, sodium, potassium, magnesium, BNP

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53
Q

PQRST meanings

A

P wave = atrium contracting
QRS = ventricle contracting
T wave = preparation for next series of complexes, ventricle relaxing
Flipped/inverted T = ischemia
ST segment depression/elevation, T wave inversion = all equal ischemia

54
Q

NSTEMI

A

non ST elevated MI

55
Q

STEMI

A

ST elevated MI

56
Q

dysrhythmias pathophysiology

A 
Problem with the conduction system of the heart
Can lead to death
Key points to remember:
Is it the top of the heart
Is it the bottom of the heart
57
Q

sinus rhythm

A

Electrical impulse begins in the SA node and travels through the AV node, down the bundle of his and to the ventricles
Normal conduction
HR 60-100 beats per minute

58
Q

bradycardia in the pediatric population

A

Less common in children than adults but can cause significant morbidity and even sudden cardiac death
Guidelines for bradycardia based on a 12-lead ECG
Newborn to 3 years < 100 bpm
3-9 years < 60 bpm
9-16 years < 50 bpm
Guidelines for bradycardia based on a 24 hour holter
Newborn- 2 years < 60 bpm while asleep and < 80 bpm while awake
2-6 years< 60 bpm
6-11 years < 45 bpm
> 11 years  < 40 bpm (unless well trained athletes < 30 bpm)

59
Q

bradycardia in the pediatric population causes and clinical manifestations

A

Sites for issues are from the SA to AV node sinus bradycardia or even heart block
Causes:
Corrective surgery of congenital heart disease
Hypervagotonia and drugs
Clinical Manifestations: (many present asymptomatic)
Dizziness, syncope, poor feeding and lethargy (infants and young children
Fatigue, exercise intolerance, dizziness and/or syncope (children and adolescents

60
Q

bradycardia in the pediatric population diagnosis and management

A

Diagnosis:
ECG and 24 holter monitoring
Management:
Severe symptomatic bradycardia (poor perfusion or shock) require immediate attention (* priority for ABC)
Identify and treat the potential reversible cause including hypoxemia, hypothermia, head injury, toxins and hypervagotonia
Be ready with Epinephrine and Atropine
Consider pacing if required

61
Q

hypoxia vs hypoxemia

A 
Hypoxic = low oxygen to the tissue 
Hypoxemic = low oxygen in the blood
62
Q

heart block

A

The impulse from the SA to the AV node is slowed down delaying conduction or completely fails to initiate conduction
Classified according to degrees of AV block
First degree
Second degree
Type I
Type II
Third degree

Second degree Type II and Third degree are not tolerated well by patients and there is cardiac compromise
First degree = PR interval is longer, P wave is longer, slower than normal impulse from SA to AV node, rest of conduction normal
Second degree type 1 = wenckebach, PR interval gets longer and longer before it drops off at QRS, SA node fires very slowly to AV and then AV node doesn’t fire, ventricle doesn’t beat, no output
Second degree type 2 = no association between SA P wave and QRS complex, conduction takes forever to get down to ventricle, big problem is that it will go into a third degree
Third degree = no QRS complex, very low heartbeat and cardiac output, SA and AV node not even communicating

63
Q

atrial flutter

A

A single irritable focus within the atria producing flutter waves
Constant stimuli to the AV node that cannot conduct all the impulses but allows a few through to the ventricle
Only involves the atria where conduction through to the ventricle is normal
Top of the heart problem, nothing wrong with ventricle, get a re-entry mechanism that causes your SA node to refire

64
Q

atrial fibrillation

A

The atria of the heart quiver
Re-entry mechanism of the conduction pathway
Heart is just quivering, we lose atrial kick, blood starts to pool in atriums, increase in preload, nothing wrong with ventricle, HR is still going to be high enough for cardiac output, GOING TO SEE JUGULAR VENOUS DISTENSION, patients are going to feel like heart is racing or palpitations, short of breath, at risk of developing a pulmonary embolus

65
Q

premature ventricular contractions

A

Extra contraction that originates in the ventricular
Increased excitability of the cardiac cells
Occasional PVC, no issue, three in a row indicates that the patient has increased cardiac irritability, > 10 in a minute may precipitate an MI or Vtach
Extra beat at the bottom of the ventricle

66
Q

ventricular tachycardia

A

Irritable focus of an impulse within the ventricle
Life threatening that leads to Ventricular fibrillation
4 PVCs in a row leads to ventricular tachycardia, decreased preload, no filling, no cardiac output,
Why is V tach worse than sinus tach? No blood getting to the tissues
Prolonged QT interval patient is at risk for V tach and PVCs (watch for with TCA drugs)
Too much potassium could also cause this ^

67
Q

ventricular fibrillation

A

Quivering of the ventricle
Impedes pumping function of the heart
No cardiac output, if patient is saved they get a pacemaker

68
Q

6 Hs and Ts of asystole and pulseless electrical activity

A 
hyperkalemia
hypoxia
hypothermia
hydrogen ion access (acidosis)
hypovolemia 
hypoglycemia 
tamponade (cardiac)
tension pneumothorax
thrombosis (pulmonary embolus)
thrombosis (myocardial infarction)
toxins
trauma
69
Q

heart failure patho and causes

A 
Pathophysiology:
Impaired cardiac function of the pumping ability of the ventricle
Causes:
Myocardial Infarction
Cardiomyopathy
Ischemic Heart Disease (IHD)
Congenital Heart Defects (pediatric)
Cor Pulmonale
Hepatic dysfunction
70
Q

2 primary types of heart failure

A

Left Sided Heart Failure
Dysfunction of the left ventricle’s ability to pump
Decreased CO and perfusion to vital organs

Right Sided Heart Failure
Dysfunction of the right ventricle
Decreased blood being pumped to lungs

71
Q

left sided heart failure patho

A

Reduced pump due to impaired contractility decreased CO
Caused by any changes in cardiac physiology that reduces the ability of the heart muscle to pump such as MI, cardiomyopathy, increased myocardial workload, untreated HTN
Less contractility, leads to increase in Preload and increase in Afterload to compensate and provide an adequate CO that will perfuse the body
Leads to sustained action of the RAAS and the SNS

72
Q

left sided heart failure characterized by and clinical manifestations

A

Characterized by:
Systolic Heart Failure (contractility)
Diastolic Heart Failure (preload)

Clinical Manifestations:
Pulmonary vascular congestion and inadequate perfusion of the systemic circulation
Shortness of breath (SOB), orthopnea, coughing with or without frothy sputum, fatigue, decreased urine output, and edema

73
Q

left sided heart failure nursing assessment

A

NEURO: LOC, alert, orientated, lethargic, dizziness, light headedness; CV: color, hemodynamic status- is the patient pale, pink, grey, cyanotic, are there any LV heaves present, pulsus alternans, tachycardia, pulses x 6, may have abnormal heart sounds such as S3 and potentially S4, capillary refill; RESP: inspiratory or expiratory crackles in the lungs, where (course, fine), is the patient in pulmonary edema, is gas exchange impaired, is the patient tachypneic, SOB, orthopnea, dry, hacking cough, paroxysmal nocturnal dyspnea- assessing how they sleep at night; RENAL: urine output, > 30 cc/hr, colour, consistency, frequency, 24 hour fluid balance, nocturia, MSK: is the gait steady
LAB Values: All electrolytes with careful attention of sodium, potassium, and BNP levels, creatinine, BUN, GFR

74
Q

right sided heart failure patho and causes

A

Pathophysiology:
Inability of the right ventricle to pump into the pulmonary circulation
May result from:
Left sided Heart Failure
Diffuse hypoxic pulmonary diseases such as COPD, Acute Respiratory Disorder Syndrome (ARDS), Cor Pulmonale
Pulmonic valve dysfunction
Myocardial Infarction
Increased pulmonic vascular resistance (increased afterload in pulmonary system) inhibits RV pump causing it to dilate and fail

75
Q

right sided heart failure clinical manifestations

A

Peripheral edema, increased JVD and hepatomegaly, heaves, murmurs, weight gain, tachycardia, ascites, anasarca, right-sided pleural effusion

76
Q

right sided heart failure nursing assessment

A

NEURO: LOC, alert, orientated, lethargic, dizziness, light headedness; CV: color, hemodynamic status- is the patient pale, pink, grey, cyanotic, are there any RV sided heaves present, JVD, RUQ pain (hepatomegaly), tachycardia, pulses x 6, may have abnormal heart sounds such as S3 and potentially S4, capillary refill; RESP: inspiratory or expiratory crackles in the lungs, where (course, fine), is the patient in pulmonary edema, is gas exchange impaired, is the patient tachypneic; GI: anorexia, nausea, GI bloating, ascites; RENAL: urine output, > 30 cc/hr, colour, consistency, frequency, 24 hour fluid balance
LAB Values: All electrolytes with careful attention of sodium, potassium, and BNP levels, creatinine, BUN, GFR

77
Q

ejection fraction

A

amount pumped out of ventricle over the total amount of blood
HF with preserved ejection fraction (HFpEF): LVEF ≥ 50%;
HF with a mid-range ejection fraction (HFmEF): LVEF 41-49%;
HF with a reduced ejection fraction (HFrEF): LVEF ≤ 40%.

78
Q

acute pericarditis patho

A

Acute inflammation of the pericardium
Causes pericardial membranes to become inflamed and roughened
Caused by idiopathic cause or viral infection
Common occurrence as a complication of HIV, post MI, trauma, neoplasm, surgery, uremia, bacterial infection(especially Tuberculosis), connective tissue disease such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), or radiation therapy
Refer to Table 39-7, Etiologies of Pericarditis, p. 895, Lewis et al, (2019)
if pericardium becomes inflamed the heart doesn’t pump well enough

79
Q

acute pericarditis clinical manifestations

A

Low grade fever (< 38°C)
Sinus tachycardia
Chest pain that radiates to the patient’s back
Dysphagia, restless, irritability, anxiety, weakness and malaise
Hypotension or the presence of pulsus paradoxus (a decrease in systolic blood pressure of > 10 mmHg with inspiration) suggests tamponade
auscultate a pericardial friction rub

80
Q

acute pericarditis nursing assessment

A

NEURO: LOC, alert, orientated, numbness and tingling, fever, anxiety; CV: Vital signs to identify changes from baseline, position patient to auscultate for friction rub, chest pain (PQRST), progressive, sharp, pleuritic CP, identify if there are any hemodynamic changes that decrease CO, ECG may show PR segment depression and diffuse ST-segment elevation without Q waves; RESP: dyspnea due to rapid, shallow breaths, does that affect their gas exchange, sp02 level (is the patient compensating with a high HR)
LABS: WBC (to rule out infection), troponin (to rule out AMI), hs-C Reactive Protein (inflammatory biomarker)

81
Q

pericardial effusion patho

A

Accumulation of fluid in the pericardial cavity that can occur in all forms of pericarditis
If the effusion develops gradually the pericardium is able to stretch and accommodate large quantities without compressing the heart
Although, if the fluid accumulate rapidly (50 to 100ml), sufficient pressure can be created causing cardiac compression, known as Tamponade

82
Q

pericardial effusion clinical manifestations

A

Distant or muffled heart sounds
Poorly palpable apical pulse
Dyspnea on exertion
Dull chest pain
Pulsus parodoxus may indicate cardiac tamponade
pulsus parodoxus = decrease of more than 10 mm Hg for systolic pressure

83
Q

pericardial effusion nursing assessment

A

NEURO: LOC, alert, orientated, numbness and tingling, fever, anxiety; CV Auscultate heart sounds to identify changes in the sound, Auscultate apical pulse and palpate radial pulse to identify differences; RESP: Are there any respiratory changes shortness of breath, cyanosis, changes in perfusion, impaired gas exchange leading to hemodynamic changes

Monitor for acute and significant changes with NEURO, CV, and RESP systems as pericardial effusions can lead to a cardiac tamponade
*preload problem

84
Q

cardiac tamponade patho

A

Acute fluid accumulation in the pericardial space
Serious condition that can lead to the pressure exerted by the pericardial fluid equal to diastolic pressure within the heart chambers leading to impaired right atrial filling during diastole
Decreased right atrial failure leads to decreased ventricular filling, decreased stroke volume and reduced cardiac output….Life threatening circulatory collapse may occur!

85
Q

cardiac tamponade clinical manifestations and nursing assessment

A

Clinical Manifestations:
Dyspnea, tachycardia, JVD, cardiomegaly, and pulsus parodoxus
Nursing Assessment:
NEURO: LOC, alert, orientated, numbness and tingling, fever, anxiety; CV Auscultate heart sounds to identify changes in the sound, Auscultate apical pulse and palpate radial pulse to identify differences, JVD, peripheral edema, pulsus parodoxus; RESP: Are there any respiratory changes shortness of breath, cyanosis, changes in perfusion, impaired gas exchange leading to hemodynamic changes; GI: hepatomegaly,

86
Q

infective endocarditis

A

Inflammation of the endocardium due to bacteria such as strep, staph or enterococci
In order for this to occur you need = endocardial damage, blood borne microorganism, formation of vegetation on your valves

87
Q

risk factors for infective endocarditis

A 
Valve disease
Implanted prosthetic heart valves
Congenital lesions like septal defect
Previous diagnosis of endocarditis
IV drug use
Long term indwelling catheters such as for dialysis, feeding or lines to monitor BO
Implantable cardiac pacemakers
Heart transplant with defective valves
88
Q

infective endocarditis clinical manifestations

A

Fever, new or changed cardiac murmur, and petechial lesions of the skin, conjunctiva, and oral mucosa, splinter hemorrhages, Osler lesions (painful erythematous nodules on the pads of the fingers and toes) and Janeway lesions (non-painful hemorrhagic lesions on the palms and soles), weight loss, back pain, night sweats, and heart failure.

89
Q

infective endocarditis nursing assessment

A

NEURO: LOC, alert, orientated, dizziness, light headedness, fever, numbness, tingling, changes in motor power, signs and symptoms of CVA (facial droop, weakness, changes in vision); CV: color, hemodynamic status- is the patient pale, pink, grey, cyanotic, are there any LV or RV sided heaves present, JVD, RUQ pain (hepatomegaly), tachycardia, pulses x 6, may have abnormal heart sounds such as S3 and potentially S4, capillary refill (looking for both Right and Left sided Heart Failure); RESP: inspiratory or expiratory crackles in the lungs, where (course, fine), is the patient in pulmonary edema, is gas exchange impaired, is the patient tachypneic; GI: anorexia, nausea, GI bloating, ascites; RENAL: urine output, > 30 cc/hr, colour, consistency, frequency, 24 hour fluid balance; SKIN: petechiae, painful or non-painful nodules
LABS: clotting factors- Platelets, INR, PTT, WBC (infection), Hgb (blood volume), BNP, Na+, K+

90
Q

deep vein trhombosis patho

A 
Thrombus: clot attached to the vein wall
Thromboembolus: clot formation(thrombus) detached from vein wall 
DVT formation- Virchow’s Triad:
Venous Stasis
Venous endothelial damage
Hypercoagulable states
91
Q

becks triad vs virchows triad

A

becks triad = hypotension, jugular venous distension, muffled heart sounds (goes with cardiac tamponade)
virchows triad = stasis of blood flow, venous endothelial injury/damage, hypercoagulability (goes with deep vein thrombosis)

92
Q

deep vein thrombosis clinical manifestations

A

Inflammation from the thrombus formation can result in pain and redness…although redness is not always seen
Thrombus formation creates blood flow obstruction and can result edema formation

93
Q

untreated DVT

A

associated with high risk of embolization of part of the clot to the lung resulting in Pulmonary Embolus (P.E.)

94
Q

untreated and accumulating DVT formation

A

can lead to scarring and permanent vein damage

95
Q

aneurysm patho

A

¾ of aneurysms occur in the abdominal region of the aorta
Atherosclerosis is the most common cause of arterial aneurysms
Hypertension increases stress to the aortic wall and can result in aneurysm formation outpouching of a vessel wall or cardiac chamber
Collagen-vascular disorders(i.e. Marfan’s syndrome), syphilis, and other infections can also lead to aneurysm
True aneurysm involve all three layers of the arterial wall and a False aneurysm, is an extravascular hematoma that communicates with the intravascular space

96
Q

aortic aneurysm clinical manifestations

A

Usually asymptomatic
The most common symptom is deep, diffuse chest pain extending to the interscapular area
If located in the ascending aorta and the aortic arch, patients report hoarseness
Dysphagia
Distended neck veins and edema of the head and arms
Dysrhythmias
Heart Failure
Embolism of clots to the brain or other vital organs
Pain upon rupture
Dyspnea
Upon examination, AAA identified by a pulsatile mass in the periumbilical area slightly to the left of the midline
Bruits may be auscultated
Symptoms may mimic abdominal or back pain
May impair blood flow leading to ischemia

97
Q

aortic aneurysm nursing assessment

A

NEURO: Subjective description of pain in the back or peripherals, inspect the abdominal area; CV: auscultate for bruits along the midline of the abdomen, identify and rule out other causes for dysphagia, pulses, color, capillary refill; GI: upon palpation of abdomen, patient may report pain; RENAL: urine output, monitor for renal failure

98
Q

aortic aneurysm further complication

A

Dissection- occurs when there is a tear in the intima and blood enters the wall of the artery…SURGICAL EMERGENCY!
Thrombus formation- due to turbulent blood flow and possible pooling of blood at the aneurysm site
Typically happens in the arch (type a) or the midline (type b) of the aorta
If it happens in the arch the patient will die if not treated immediately
Back pain is very indicative of an aortic dissection!!

99
Q

what we know about spontaneous coronary artery dissection

A

Rare condition that primarily affects women
Patients present with signs and symptoms of acute MI and cardiogenic shock
Exact etiology and pathophysiology remains unknown may be linked to fibromuscular disease
Triggered by the disruption of the intimal layer, a clot develops in the false lumen eventually occluding the true lumen

100
Q

arterial thrombi

A

Two potential threats to circulation:
Thrombus occludes the artery leading to tissue ischemia
Thrombus dislodgement resulting in a thrombo-embolus occluding blood flow into a distal vascular bed

101
Q

cardiovascular disorders in children are divided into two groups

A

congenital heart disease (CHD)

acquired heart disease

102
Q

cyanotic congenital heart failure

A

shunting of blood = right to left
cyanosis = always “blue babies”
surgery = usually done in several stages-technically complex
prognosis = guarded
types = tetralogy of fallot, transposition of the great arteries (TGA), truncus arteriosus, tricuspid atresia, total anomalous pulmonary venous return

103
Q

acyanotic congenital heart failure

A

shunting of blood = left to right
cyanosis = not usual (unless congestive heart failure)
surgery = usually done in one stage-technically simple
prognosis = very good/excellent
types = atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA), coarctation of the aorta (CoA)

104
Q

acyanotic

A

defects with increased pulmonary blood flow

obstructive defects

105
Q

defects with increased pulmonary blood flow

A

Intra-cardiac communication along the septum or an abnormal connection between the great arteries allows blood to flow from the high-pressure left side of the heart to the low-pressure right side of the heart.

106
Q

ventricular septal defect

A

An opening between the two ventricles allowing for unoxygenated blood to mix with oxygenated blood
Usually associated with other defects, such as pulmonary stenosis, transposition of the great vessels, patent ductus arteriosus (PDA), atrial defects and coarctation of the aorta

107
Q

ventricular septal defect patho

A

Blood flows from left to right side through the pulmonary artery
Flow takes path of least resistance high pressures in the left ventricle move to the right side because there is more resistance to pump against systemic arterial circulation
Increased blood volume is pumped into the lungs with leads to increased pulmonary vascular resistance (PVR)
Left to Right shunting and pulmonary resistance causes the muscle to hypertrophy

108
Q

ventricular septal defect clinical manifestations

A

Heart failure
Murmur
Bacterial endocarditis
Pulmonary obstructive disease

109
Q

obstructive defects

A

Blood exiting a portion of the heart meets an area of anatomical narrowing (stenosis), causing obstruction to blood flow.
The location of narrowing is usually near the valve of the obstructive defect

110
Q

coarctation of the aorta

A

Localized narrowing near the insertion of the ductus arteriosus

111
Q

coarctation of the aorta patho and clinical manifestations

A

Pathophysiology:
Due to the narrowing, there is increased pressure proximal to the defect (upper extremities) and decreased pressure distal to it (lower extremities)
Clinical Manifestations:
Blood pressure is higher in the upper extremities than the lower extremities
Bounding pulses in the arms
Weak or absent femoral pulses
Cooler lower extremities may be present

112
Q

cyanotic

A

defects with decreased pulmonary blood flow

mixed blood flow

113
Q

defects with decreased pulmonary blood flow

A

Obstructed pulmonary blood flow and an anatomical defect (ASD or VSD) between the right and left side of the heart are present.
Pressure on the right side of the heart increases, exceeding pressure on the left side, which allows desaturated blood to shunt right to left, causing desaturation in the left side of the heart and in the systemic circulation.

114
Q

tetralogy of fallot patho

A

Includes Four defects: Ventricular Septal Defect (VSD), Pulmonic stenosis, over-riding aorta and right ventricular hypertrophy
Pathophysiology:
Flow of blood depends on the degree of pulmonic stenosis, the size of the ventricular septal defect and the pulmonary and systemic resistance to flow
Pulmonic stenosis decreases blood flow to the lungs and the amount of oxygenated blood that returns to the left side of the heart
Mixing of oxygenated and unoxygenated blood due to ventricular septal defect

115
Q

tetralogy of fallot clinical manifestations

A

Acute cyanosis at birth to mild cyanosis that progresses over the first year of life
Systolic murmur
Episodes of cyanosis and hypoxia called blue spells or tet spells
Anoxic spells occur during crying or after feeding
Patients are at risk for emboli, seizures, and loss of consciousness or sudden death following an anoxic spell
Apnea
Bradycardia
can also have v tach

116
Q

mixed defects

A

Fully saturated systemic blood flow mixes with the desaturated blood flow, causing desaturation of the systemic blood flow.
Pulmonary congestion occurs and cardiac output decreases.

117
Q

transposition of the great arteries patho

A

The pulmonary artery leaves the left ventricle and the aorta exits from the right ventricle, with no communication between the pulmonary and systemic circulation
Pathophysiology:
Septal defects or patent ductus arteriosus must be present to permit blood to enter the systemic circulation or the pulmonary circulation for mixing of saturated and desaturated blood
Most common defect is the patent foramen ovale
Ventricular septal defects increase risk of heart failure because it allows blood to flow from the right to the left ventricle and produces high pulmonary blood flow under high pressure which increased PVR

118
Q

transposition of the great arteries clinical manifestations

A

Newborns are severely cyanotic and have depressed function at birth
Those with large septal defects or patent ductus arteriosus may be less cyanotic
Cardiomegaly

119
Q

assessment of CHD familial history

A

Familial history of CHD, especially in siblings and parents.
Obtain a maternal health history, history during pregnancy, and birth.
Maternal prenatal infection such as Rubella.
Maternal (insulin-dependent) diabetes.
Maternal alcohol or illicit drug use during pregnancy.
Maternal medication use (e.g. Phenytoin (Dilantin).
Maternal age:
< 18 years old
> 40 years old

120
Q

assessment of CHD child related factors

A

Presence of chromosomal abnormalities/syndromes and congenital defects in other body systems (e.g. Down Syndrome).
Difficulty Feeding
Parents need to wake child for feed.
Has a weak suck.
May turn blue when eating.
Infant takes overly long time to feed.
Falls asleep during feeding, without finishing

121
Q

nursing assessment CHD

A 
Abnormal vital signs:
Tachycardia (HR >160 beats/min)
Tachypnea (R > 60 breaths/min)
Changes in BP
Cyanosis due to hypoxia
Failure to grow at a normal rate
Developmental delays
Shortness of breath on exertion
Audible murmurs
Cyanotic heart defects:
“Tet spells”
Clubbing of fingers and toes
Increased red blood cells
122
Q

summary of CHD

A

CHD is the most common form of cardiac disease in children.
Several prenatal factors may predispose a child to CHD (i.e. maternal prenatal infections, drinking during pregnancy, maternal age, and maternal Type 1 Diabetes).
Two major categories of CHD are cyanotic and acyanotic defects.
Major categories to investigate in the cardiac history are poor weight gain, poor feeding habits, fatigue during feeding, and evidence of exercise intolerance.
Most common tests used in assessing cardiac function are radiography, electrocardiogram, echocardiography, and cardiac catheterization.

123
Q

acquired heart defects

A

Acquired heart disease is much more common in adults than in children.
It is usually the result of damage done to the heart by a disease, virus, or bacteria.
The two most common acquired conditions among children are Kawasaki Disease and Rheumatic Fever.

124
Q

kawasaki disease

A

Is an acute, febrile, multisystem disorder believed to be autoimmune in nature.
Affects primarily the skin and mucous membranes of the respiratory tract, lymph nodes, and heart.
The exact cause is unknown.
It occurs in children between the ages of 1-14 years old.
75% of cases occur in children under 5 years old.
Common in children of Japanese or Korean descent.
Spontaneous recovery occurs within 3-4 weeks.

125
Q

kawasaki disease acute stage nursing assessment

A

High fever (38.9°-41°) lasting more than 5 days
Conjunctivitis
Red throat
Swollen hands and feet
Generalized rash on trunk and extremities
Irritability

126
Q

kawasaki disease subacute stage nursing assessment

A 
Dry, red, cracked lips
“Strawberry tongue”
Peeling of the palms of the hands and the soles of the feet
Joint pain
Laboratory Tests:
Elevated: white blood cell count
Elevated: platelet count
127
Q

diagnostic criteria for kawasaki disease

A

Child must have a fever > 5 days along with 4 or 5 clinical criteria:
Changes in extremities
Bilateral conjunctival inflammation without exudation
Changes in oral mucous membranes (i.e. “strawberry tongue”)
Rash
Cervical lymphadenopathy

128
Q

rheumatic fever

A

Is an acute, systemic, inflammatory disease affecting multiple organs and systems:
Heart
Joints
Brain
Skin
Usually seen in school age children (age 5-15 years old).
Caused by untreated Group A β-hemolytic streptococcal pharyngitis.

129
Q

diagnostic evaluation: jones criteria major manifestations

A 
Carditis
Polyarthritis
Erythema marginatum
Subcutaneous nodules
Chorea
130
Q

diagnostic evaluation: jones criteria minor manifestations

A 
Clinical
Joint pain (Arthralgia)
Fever
Laboratory
Increased erythrocyte sedimentation
Positive C-reactive protein
Anemia
Supportive Evidence
Positive throat culture for streptococcus
131
Q

summary of acquired cardiovascular disease

A

The most common acquired cardiovascular diseases are Kawasaki Disease and Rheumatic Fever.
Acute Rheumatic Fever is a systemic inflammatory disease that can damage the cardiac valves.
Kawasaki Disease causes extensive inflammation of small vessels and capillaries that can progress to involve the coronary arteries.

NURS 487 (8 decks)

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