1. Nursing Assessment of the Cardiovascular System
Keith Rischer RN, MA, CEN
#1 cause of death resulting in 42% of all deaths
1 million in US annually, more than the next 5 causes of death combined

2. Today’s Objectives…
Review the anatomy and physiology of the cardiovascular system.
Describe cardiovascular changes associated with aging.
Identify factors that place patients at risk for cardiovascular problems.
Explain and describe pre- and post-care associated with diagnostic cardiovascular testing.
Explain the purpose of hemodynamic monitoring.

3. Aortic-Pulmonic Mitral-Tricuspid

4. Coronary Arteries
Right Coronary
Left Anterior Descending
Circumflex

5. Cardiac Conduction SA node  Both Atria  AV Node Both Ventricles 
Bundle of His
Bundle Branches-
Perkinje Fibers
Heart muscle unique in that it can generate and rapidly conduct its own action potentials or electrical impulses
Most myocardial cells capable of generating own action potentials do so at various rates-SA AV ventricles 20-40
Heart has 2 conduction systems one for atrial activity and ventricular activity…AV node connects the 2
SA node innervated w/ both parasympathetic/sympathetic nerve fibers…what is the influence of these???
SA node fastest and therefore usually dominant pacemaker
AV node conduction slows slightly through the bundle of his.Delay allows the atria to completely empty w/atrial kick as they depolarize
Bundle branches- divide off the AV node and depolarize at the same time
Purkinje fibers- large fibers that allow for rapid conduction and depolarize ventricles in unison 5

6. Diastole Diastole Lower # in BP (120/80) Ventricles are relaxed
Passively fill from atria
Ventricular volume pressure becomes lower than atrial pressure resulting in passive flow from atria into ventricles
70% volume flows passively into ventricles
Remaining 30% comes from atrial kick from synchronized atrial contraction as the SA node depolarizes the atria to AV node
What rhythm causes a loss of this kick w/resultant loss of SV??? 6

7. Systole Higher # in BP (120/80)
Ventricles are contracting and emptying
SBP accurately reflects afterload
Begins w/closure of AV valves and first heart sound
Ventricles continue to contract until left ventricular pressure higher than aortic pressure & RV pressure higher than PA pressure
60% volume ejected in first quarter of systole and then remaining in next 2 quarters
End of systole ventricles relax causing large drop in ventricular pressure…this causes semilunar valves to snap shut causing second heart sound and onset of diastole
Avg content of LV is 120cc---on average healthy heart able to eject 65-70% this is the EJECTION FRACTION
Decrease in EF classic sx of CHF
Correlates w/AFTERLOAD
Hi Nurse…. Could you tell me what Blood Pressure means ? ? ? I’ve always wanted to know that 7

8. CO = Stroke volume x heart rate SV (80cc) x HR (80)= 6400cc (6.4 lpm)
Cardiac Output
CO = Stroke volume x heart rate
SV (80cc) x HR (80)= 6400cc (6.4 lpm)
Daily pumps 1800 gallons
657,000 gallons every year
Over 80 year lifetime:
52,560,000 gallons
Every 10 days fills a gallon swimming pool
Every year appx 36 pools
Over lifetime appx 3000 pools
Factors that influence CO are preload, afterload, myocardial contractility, and HR 8

9. Preload: Right side of heart
Preload=primarily venous blood return to RA
Right and left side of heart filling pressure (atria>ventricles)
Pressure/Stretch in ventricles end diastole
There are no valves where SVC-IVC empty into RA
Preload is the filling pressure of the RV-LV and is influenced by venous return…higher venous return or blood volume in atria-the higher the SV will be…opposite is also true
What cardiac meds will most strongly influence preload???
How will volume depletion such as by dehydration or blood loss affect preload??? 9

10. Starling’s Law of the Heart
Maximum efficency of CO achieved when myocardium stretched appx 2 ½ times length
Think rubber band
CO decreased with lower preload/filling pressures or too high
HF occurs when it takes higher filling pressures to accomplish normal contractile force
Incr in preload cause a decrease in SV and higher LVEDP
This causes back pressure into lungs causing leakage of fluid into alveoli causing PE 10

11. “AFTER” load: Left side of heart
Force of resistance that the LV must generate to open aortic valve
Correlates w/SBP
Arterial vasodilation will decrease
Important when in AMI we need to decr workload of heart by intentionally lowering afterload
NTG indirectly affects afterload through decreasing preload
What meds??? B-blockers….ACE inhibitors calcium channel blockers and arterial vasodilators such as hydralazine
Epi will do what to afterload???
Go to page 11 of study guide 11

12. Contractility
Ability of heart to change force of contraction without changing resting length
Influenced by Ca++
Inotropic-Influencing contractility independent of Starling mechanism
Positive inotropic
Negative inotropic
Inotropic Sympathetic drugs such as Dopamine-Dobutamine-Epi
Negative-B-blockers
Chronotropic-rate of HR…look at above for same examples 12

13. Assessment Techniques
History
Demographic data
Age
Gender
Pre vs. post menopause
Family history and genetic risk
Personal medical history
DM, HTN
BCP use for women
Diet

14. Modifiable Risk Factors
Cigarette smoking
Physical inactivity
Obesity
Psychological factors
Chronic disease
Cigarette smoking
Most significant risk factor for CV disease
Nicotine and CO most significant
Physical inactivity
Goal is 30” light to moderate exercise daily
Obesity
64% are obese in US w/BMI 25-30
Psychological factors
Highly competive…overly concerned w/meeting deadlines….angry/hostile or type A
Chronic disease

15. Changes with Aging Calcification in valves
Pacemaker cells decrease in number
Conduction time increases
Left ventricle increases
Aorta and large vessels thicken and become stiffer
Baroreceptors less sensitive

16. Women & CAD Vague-atypical chief c/o Only 53% have CP as chief c/o
Fatigue chief c/o
Typically develop CAD 10+ years later then men
Mortality twice as high
Less likely to have definitive 12 lead EKG
Smaller coronary arteries
Higher prevalence of silent ischemia
CABG higher mortality rate/complications
After first MI-more likely to suffer fatal event
Women > 50 pay must address HTN, high cholesterol, family history, diabetes
#1 cause of death of women
Vague- weakness-SOB-nausea-anorexia-pain in back/epigastric 16

17. Men Women Develop 10-15 years earlier Initial event AMI Classic CP sx
Develop greater collateral circulation compared to women
Influence of menopause…4x risk
Causes more deaths in women than men
Initial event angina
Atypical CP sx…fatigue
Menopause before women have higher HDL cholesterol and lower LDL levels-after menopause LDLlevels increase
Deaths for women CAD causes 10x more deaths than breast CA…only 15% consider CAD their greatest health risk 17

18. Elderly & CAD More likely to have vague, atypical c/o
SOB, fatigue, syncope or falls
Any fall must be investigated for mitigating circumstances
Less likely to have radiation

19. Clinical Manifestations:Dyspnea
Can occur as a result of both cardiac and pulmonary disease
Difficult or labored breathing experienced as uncomfortable breathing or shortness of breath
Dyspnea on exertion (DOE)
Orthopnea
dyspnea when lying flat
Paroxysmal nocturnal dyspnea (PND)
after lying down for several hours

20. Other Clinical Manifestations
Fatigue
Palpitations
Weight gain
Syncope
Extremity pain
Ischemia
Venous insufficiency
Fatigue
Determine timing
Palpitations
From change in heart rate or rhythm
Weight gain
Weight gain is the best indicator of fluid retention
1 liter =2.2 lbs
Syncope
Brief LOC can be near syncopal as well…
Any condition that suddenly reduces CO resulting in decr cerebral blood flow
Extremity pain

21. CV Physical Assessment
General appearance
Integumentary system
Skin color
Skin temperature
Extremities
Blood pressure
Orthostatic
Arterial pulses
Jugular venous distention
General appearance
Skin color…LOC, confusion SOB
Integumentary system
Color and temp of skin…use nail beds and mucous membranes
Skin color
Assess for cool, pale or moist skin
Bluish color to skin is cyanosis….central is oxygenation problem…bluisk tinge mucous membranes and tongue
Peripheral cyanosis-decr blood flow to peripheral extremities due to vasoconstriction
Skin temperature
Touch with back of hands
Extremities
Assess for edema in LE-pitting vs. non-pitting
Blood pressure
HTN 135/85
Why a problem with cardiac pt???
Arterial pulses
Jugular venous distention

22. Precordium Auscultation Normal heart sounds…S1S2 Paradoxical splitting
Gallops S3 S4
Murmurs
Systolic most common
Pericardial friction rub
Assessment of the precordium (area over the heart) involves:

23. Serum Markers of Myocardial Damage
Troponin
B-Natruetic Peptide
Serum lipids
C-reactive protein
Lytes K+
Mg++
Blood coagulation
PT & INR
Troponin
Myocardial muscle protein released with injury

24. Brain Natriuetic Peptide:BNP
95 % of BNP resides in ventricles
As pressure inc in ventricles in HF-BNP is released
Bodies own ACE/B-blocker
Only lab test that measures HF
Normal is less than 100
Elevated
+ for CHF >500
Uses: dx- assess response to tx
Bnp is a peptide released when excessive stretch present in ventricles due to excessive end diastolic filling pressures
Works is bodies own ACE inhibitor-causes rapid diuresis and inhibits aldosterone and renin secretion and works as antagonist to angiotensin II and inhibits release of nor-epinephrine 24

25. Cardiac Catheterization
Client preparation
Possible complications: myocardial infarction, stroke, thromboembolism, arterial bleeding, lethal dysrhythmias, and death
Pre-procedure:
Review procedure (video)
Consent
NPO or light breakfast
Cath site shaved
Premeds - sedative

26. Cardiac Catheterization
Procedure
Pt awake – report any chest pain or symptoms
May proceed to Stent Placement
Follow-up care:
Restricted bedrest, insertion site extremity kept straight
Assess groin site and distal pulses closely
Monitor vital signs
Force fluids
Assess for complications

27. Cardiac Catheterization Report

28. Other Diagnostic Tests
12 lead EKG
Holter monitor (ambulatory)
Electrophysiologic (EP) study
Exercise Stress test
Echocardiography
Pharmacologic stress echocardiogram
Transesophageal echocardiogram
Thallium imaging

29. Hemodynamic Monitoring: Arterial Line
Invasive system used in critical care areas to provide quantitative information about vascular capacity, blood volume, pump effectiveness, and tissue perfusion

30. Hemodynamic Monitoring: Pulmonary Artery catheter

31. Hemodynamic Monitoring Strips