lOMoARcPSD|69074652
MED SURG 2 EXAM 1
Ch. 25 – ASSESSMENT OF CARDIOVASCULAR FUNCTION
Conduction System
Automaticity = ability to initiate an electrical impulse
Excitability = ability to respond to an electrical impulse
Conductivity = ability to transmit an electrical impulse from one cell to another
SA node à AV node à bundle of his right bundle branch à left bundle branch à
purkinje fibers
*SA node is the primary pacemaker of the heart
Depolarization: electrical activation of cell caused by influx of sodium into cell while
potassium exits cell
Repolarization: return of cell to resting state caused by re-entry of potassium into
cell while sodium exits
Refractory periods
Effective refractory period: phase in which cells are incapable of depolarizing
Relative refractory period: phase in which cells require stronger-than-normal
stimulus to depolarize
Cardiac Action Potential Phases (won’t ask but understand)
Phase 0 = Na comes into the actual cell (RAPID depolarization, SODIUM IN)
Phase 1 = early cell repolarization – K+ coming out of the cell (POTASSIUM OUT)
Phase 2 = plateau phase (rate of repolarization slows); Ca+ ENTER CELL
Phase 3 = complete repolarization (return of cell to resting state)
Phase 4 = resting phase before the next depolarization
Aorta has the highest pressure (biggest) high force…pressure in left ventricle + aorta
highest pressure is higher pressure in the cardiac system
** Majority of MI occurs in left ventricle!
CO = HR x SV
Cardiac output = total amt. of blood ejected by one of the ventricles in L/min (in resting
adult about 4-6 L/min)
Stroke volume = amount of blood ejected from one of the ventricles per heartbeat
(average = 60-130 mL)
Changes in HR are due to inhibition or stimulation of the SA node by the
parasympathetic and sympathetic divisions.
PNS travels to SA node through vagus nerve vagal stimulation = slows the HR
, lOMoARcPSD|69074652
SNS increases HR by innervation of the beta-1 receptors located within SA node (occurs
through an increase in circulation catecholamines (secreted by the adrenal gland) and by
excess thyroid hormone, which produces a catecholamine-like effect
HR also affected by CNS and baroreceptor activity (sensitive to changes in BP) when
BP is high – baroreceptors stimulate PNS activity, lowering HR. When BP is low they
stimulate SNS activity, raising HR.
SV is determined by preload, afterload, and contractility.
Preload = how much blood is within the ventricle before you pump it out (at the end of
diastole right before systole occurs)
Afterload = the resistance of ejection of blood from the ventricle
Contractility = the force generated by the contracting myocardium
Women usually develop CAD 10 years later than men b/c they benefit from female
hormone estrogen and its cardioprotective effects
1. Increase in HDL (transports cholesterol out of arteries
2. Reduction in LDL (deposits cholesterol in the artery)
3. Dilation of the blood vessels (enhances blood flow to the heart)
*post-menopausal women = higher risk of CAD b/c estrogen levels slowly disappear
COMMON SYMPTOMS of CVD
Chest pain
Dyspnea
Peripheral edema, weight gain, abdominal distention
Palpitations
Fatigue
Dizziness, syncope, changes in level of consciousness
Chest pain – identify quantity (0-10), location, and quality. Radiation of pain?
Associated S/S like sweating or nausea; duration? Assess for other cardiac conditions;
assess for other significant conditions
Pneumonia, pulmonary embolism
Hiatal hernia, GERD
Costochondritis
Vascular
“Costochondritis – inflammation process in the cartilage (pain can be so severe that
they think they’re having a heart attack); TX would be rest… would still do an EKG”
ASSESSMENT:
Medications – aspirin = common OTC med that improves outcomes in CAD pts
Nutrition – nut. risk factors = hyperlipidemia, HTN, diabetes
Height + weight
BMI ** (assessment for obesity)
Lab results – glucose, glycosylated Hb (diabetes), cholesterol, HDL, LDL,
triglyceride level
, lOMoARcPSD|69074652
Diet & eating habits (commercially prepared foods, high-sodium, etc)
Elimination – nocturia = common in pts with HF **
Screen for bloody urine or stools in pts taking platelet-inhibiting meds
(ex. aspirin, Plavix; platelet aggregation inhibitors, or anticoagulants (ex.
heparin, warfarin (Coumadin), Lovenox, etc.
Activity, exercise – activity-induced angina or SOB may indicate CAD
Sleep, rest:
orthopnea (need to sit upright or stand to avoid feeling SOB) often occurs in
pts with worsening HF
paroxysmal nocturnal dyspnea – sudden awakening with SOB = another
symptom of worsening HF
Self-perception/concept – quit smoking (to reduce risk of future CV probs)
Roles, relationships – assess the pts support system (esp. bc many invasive
cardiac procedures like cardiac catheterization and percutaneous coronary
intervention (PCI) are being performed as outpatient procedures!
Sexuality, reproduction – impotence may develop in men as a side effect of
cardiac meds (ex. beta blockers) – may cause some men to stop taking it!
Coping, stress tolerance
high levels of anxiety are assoc. with increased incidence of CAD
pts with CAD and HF should be assessed for depression (pts with score of 3
or higher should be referred for further eval.)
social readjustment rating scale – widely used tool to measure life stress
pts with a score less than 150 = slight risk for future illness
score of 150-299 = moderate risk
PHYSICAL ASSESSMENT
(Any deviations from the normal?)
Heart as a pump reduced pulse pressure, displaced PMI from 5th ICS mid-
clavicular line, gallop sounds, murmurs
Atrial/ventricular filling volumes JVD, peripheral edema, ascites, crackles,
postural BP changes
Cardiac output reduced pulse pressure, hypotension, tachycardia, reduced urine
output, lethargy, disorientation
Compensatory mechanisms peripheral vasoconstriction, tachycardia
“Best diagnostic tool – echocardiogram (DX choice to pick up a regurgitation or
stenosis)”
CARDIAC-SPECIFIC
General appearance – changes to LOC, BMI > 30
Assessment of skin/extremities
S/S of acute obstruction of arterial blood flow in extremities = “6 P’s”=
Pain, pallor, pulselessness, paresthesia, poikilothermia (coldness), paralysis
Should be assessed during the first few hours after invasive cardiac
procedures like cardiac catheterization, PCI, or cardiac
electrophysiology testing
Hematoma
Edema (peripheral edema = feet, ankles, or legs common in HF or PVDs
like DVT or chronic venous insufficiency) or pitting edema
Prolonged capillary refill
, lOMoARcPSD|69074652
Clubbing of fingers and toes
Hair loss, brittle nails, dry scaly skin
BP
Pulse pressure = systolic – diastolic! normally 30-40
decreased pulse pressure reflects reduced SV and ejection velocity
(shock, HF, hypovolemia, mitral regurgitation) or obstruction to bloow
flow during systole (mitral or aortic stenosis)
pulse pressure < 30 = serious reduction in CO!!
Postural blood pressure changes postural/ orthostatic hypotension in
pts with CVD most often due to sig. reduction in preload, which compromises
CO. TAKE BP LAYING, SITTING, STANDING!
Arterial pulses
Pulse rate
Pulse rhythm
Pulse amplitude – absent, diminished, normal, bounding
If pulse is absent or hard to palpate = doppler
Jugular venous distention right-sided heart failure, fluid overload
Heart inspection/palpation
Heart auscultation
Normal heart sounds = S1, S2 (AV closure, semilunar closure)
Abnormal heart sounds = S3, S4
Assessment of lungs
hemoptysis pink/frothy = pulmonary edema
cough, crackles, wheezes
Assessment of abdomen distention = ascites, hepatojugular reflex = positive
test confirms DX of HF, bladder distention = urine output is an important indication
of cardiac fxn
*right sided heart failure = ASCITES, HEPATOJUGULAR REFLEX, DISTENTION
“MR. ASS” (systolic) & “MS. ARD” (diastolic) (ACRONYM)
Mitral regurgitation and atrial stenosis = systolic murmurs
Mitral stenosis and aortic regurgitation = diastolic murmurs (not good sign*)
LAB EVALUATION
DX of MI is made by evaluating the HX & physical exam, 12-lead ECG, + labs that
measure cardiac biomarkers.
Cardiac biomarkers
Creatinine Kinase (CK)
Creatinine Kinase Isoenzymes (CK-MB)
Proteins
Myoglobin
Troponin T and Troponin I “troponin most specific to cardiac”
Lab Tests
Lipid profile – cholesterol, triglycerides, lipoproteins (LDLs and HDLs)
Normal cholesterol = less than 200 mg/dL (elevated cholesterol =
higher risk CAD)
MED SURG 2 EXAM 1
Ch. 25 – ASSESSMENT OF CARDIOVASCULAR FUNCTION
Conduction System
Automaticity = ability to initiate an electrical impulse
Excitability = ability to respond to an electrical impulse
Conductivity = ability to transmit an electrical impulse from one cell to another
SA node à AV node à bundle of his right bundle branch à left bundle branch à
purkinje fibers
*SA node is the primary pacemaker of the heart
Depolarization: electrical activation of cell caused by influx of sodium into cell while
potassium exits cell
Repolarization: return of cell to resting state caused by re-entry of potassium into
cell while sodium exits
Refractory periods
Effective refractory period: phase in which cells are incapable of depolarizing
Relative refractory period: phase in which cells require stronger-than-normal
stimulus to depolarize
Cardiac Action Potential Phases (won’t ask but understand)
Phase 0 = Na comes into the actual cell (RAPID depolarization, SODIUM IN)
Phase 1 = early cell repolarization – K+ coming out of the cell (POTASSIUM OUT)
Phase 2 = plateau phase (rate of repolarization slows); Ca+ ENTER CELL
Phase 3 = complete repolarization (return of cell to resting state)
Phase 4 = resting phase before the next depolarization
Aorta has the highest pressure (biggest) high force…pressure in left ventricle + aorta
highest pressure is higher pressure in the cardiac system
** Majority of MI occurs in left ventricle!
CO = HR x SV
Cardiac output = total amt. of blood ejected by one of the ventricles in L/min (in resting
adult about 4-6 L/min)
Stroke volume = amount of blood ejected from one of the ventricles per heartbeat
(average = 60-130 mL)
Changes in HR are due to inhibition or stimulation of the SA node by the
parasympathetic and sympathetic divisions.
PNS travels to SA node through vagus nerve vagal stimulation = slows the HR
, lOMoARcPSD|69074652
SNS increases HR by innervation of the beta-1 receptors located within SA node (occurs
through an increase in circulation catecholamines (secreted by the adrenal gland) and by
excess thyroid hormone, which produces a catecholamine-like effect
HR also affected by CNS and baroreceptor activity (sensitive to changes in BP) when
BP is high – baroreceptors stimulate PNS activity, lowering HR. When BP is low they
stimulate SNS activity, raising HR.
SV is determined by preload, afterload, and contractility.
Preload = how much blood is within the ventricle before you pump it out (at the end of
diastole right before systole occurs)
Afterload = the resistance of ejection of blood from the ventricle
Contractility = the force generated by the contracting myocardium
Women usually develop CAD 10 years later than men b/c they benefit from female
hormone estrogen and its cardioprotective effects
1. Increase in HDL (transports cholesterol out of arteries
2. Reduction in LDL (deposits cholesterol in the artery)
3. Dilation of the blood vessels (enhances blood flow to the heart)
*post-menopausal women = higher risk of CAD b/c estrogen levels slowly disappear
COMMON SYMPTOMS of CVD
Chest pain
Dyspnea
Peripheral edema, weight gain, abdominal distention
Palpitations
Fatigue
Dizziness, syncope, changes in level of consciousness
Chest pain – identify quantity (0-10), location, and quality. Radiation of pain?
Associated S/S like sweating or nausea; duration? Assess for other cardiac conditions;
assess for other significant conditions
Pneumonia, pulmonary embolism
Hiatal hernia, GERD
Costochondritis
Vascular
“Costochondritis – inflammation process in the cartilage (pain can be so severe that
they think they’re having a heart attack); TX would be rest… would still do an EKG”
ASSESSMENT:
Medications – aspirin = common OTC med that improves outcomes in CAD pts
Nutrition – nut. risk factors = hyperlipidemia, HTN, diabetes
Height + weight
BMI ** (assessment for obesity)
Lab results – glucose, glycosylated Hb (diabetes), cholesterol, HDL, LDL,
triglyceride level
, lOMoARcPSD|69074652
Diet & eating habits (commercially prepared foods, high-sodium, etc)
Elimination – nocturia = common in pts with HF **
Screen for bloody urine or stools in pts taking platelet-inhibiting meds
(ex. aspirin, Plavix; platelet aggregation inhibitors, or anticoagulants (ex.
heparin, warfarin (Coumadin), Lovenox, etc.
Activity, exercise – activity-induced angina or SOB may indicate CAD
Sleep, rest:
orthopnea (need to sit upright or stand to avoid feeling SOB) often occurs in
pts with worsening HF
paroxysmal nocturnal dyspnea – sudden awakening with SOB = another
symptom of worsening HF
Self-perception/concept – quit smoking (to reduce risk of future CV probs)
Roles, relationships – assess the pts support system (esp. bc many invasive
cardiac procedures like cardiac catheterization and percutaneous coronary
intervention (PCI) are being performed as outpatient procedures!
Sexuality, reproduction – impotence may develop in men as a side effect of
cardiac meds (ex. beta blockers) – may cause some men to stop taking it!
Coping, stress tolerance
high levels of anxiety are assoc. with increased incidence of CAD
pts with CAD and HF should be assessed for depression (pts with score of 3
or higher should be referred for further eval.)
social readjustment rating scale – widely used tool to measure life stress
pts with a score less than 150 = slight risk for future illness
score of 150-299 = moderate risk
PHYSICAL ASSESSMENT
(Any deviations from the normal?)
Heart as a pump reduced pulse pressure, displaced PMI from 5th ICS mid-
clavicular line, gallop sounds, murmurs
Atrial/ventricular filling volumes JVD, peripheral edema, ascites, crackles,
postural BP changes
Cardiac output reduced pulse pressure, hypotension, tachycardia, reduced urine
output, lethargy, disorientation
Compensatory mechanisms peripheral vasoconstriction, tachycardia
“Best diagnostic tool – echocardiogram (DX choice to pick up a regurgitation or
stenosis)”
CARDIAC-SPECIFIC
General appearance – changes to LOC, BMI > 30
Assessment of skin/extremities
S/S of acute obstruction of arterial blood flow in extremities = “6 P’s”=
Pain, pallor, pulselessness, paresthesia, poikilothermia (coldness), paralysis
Should be assessed during the first few hours after invasive cardiac
procedures like cardiac catheterization, PCI, or cardiac
electrophysiology testing
Hematoma
Edema (peripheral edema = feet, ankles, or legs common in HF or PVDs
like DVT or chronic venous insufficiency) or pitting edema
Prolonged capillary refill
, lOMoARcPSD|69074652
Clubbing of fingers and toes
Hair loss, brittle nails, dry scaly skin
BP
Pulse pressure = systolic – diastolic! normally 30-40
decreased pulse pressure reflects reduced SV and ejection velocity
(shock, HF, hypovolemia, mitral regurgitation) or obstruction to bloow
flow during systole (mitral or aortic stenosis)
pulse pressure < 30 = serious reduction in CO!!
Postural blood pressure changes postural/ orthostatic hypotension in
pts with CVD most often due to sig. reduction in preload, which compromises
CO. TAKE BP LAYING, SITTING, STANDING!
Arterial pulses
Pulse rate
Pulse rhythm
Pulse amplitude – absent, diminished, normal, bounding
If pulse is absent or hard to palpate = doppler
Jugular venous distention right-sided heart failure, fluid overload
Heart inspection/palpation
Heart auscultation
Normal heart sounds = S1, S2 (AV closure, semilunar closure)
Abnormal heart sounds = S3, S4
Assessment of lungs
hemoptysis pink/frothy = pulmonary edema
cough, crackles, wheezes
Assessment of abdomen distention = ascites, hepatojugular reflex = positive
test confirms DX of HF, bladder distention = urine output is an important indication
of cardiac fxn
*right sided heart failure = ASCITES, HEPATOJUGULAR REFLEX, DISTENTION
“MR. ASS” (systolic) & “MS. ARD” (diastolic) (ACRONYM)
Mitral regurgitation and atrial stenosis = systolic murmurs
Mitral stenosis and aortic regurgitation = diastolic murmurs (not good sign*)
LAB EVALUATION
DX of MI is made by evaluating the HX & physical exam, 12-lead ECG, + labs that
measure cardiac biomarkers.
Cardiac biomarkers
Creatinine Kinase (CK)
Creatinine Kinase Isoenzymes (CK-MB)
Proteins
Myoglobin
Troponin T and Troponin I “troponin most specific to cardiac”
Lab Tests
Lipid profile – cholesterol, triglycerides, lipoproteins (LDLs and HDLs)
Normal cholesterol = less than 200 mg/dL (elevated cholesterol =
higher risk CAD)
