Transcript lec. 2 ( heart assessment part 1)

King Saud university
college of nursing
critical care nursing
lecture2
Cardiovascular assessment
4/8/2016
1
General Heart
Anatomy
• Blood vessels can be divided into a pulmonary circuit (between
the heart and the gas exchange surfaces of the lungs) and a
systemic circuit (between the heart and the rest of the body)
• Heart contains 4 muscular chambers, 2 associated with each
circuit
– Right atrium receives deO2 blood from the systemic circuit and passes it to
the right ventricle which discharges it into the pulmonary circuit.
– Left atrium receives O2 blood from the pulmonary circuit and passes it to the
left ventricle which discharges it into the systemic circuit
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• Atria have thin flaccid walls corresponding to their light
workload. Why is it light?
• Right and left atria are separated by the interatrial
septum..
• The thick interventricular septum separates the LV and
RV.
• LV is 2-4x as thick as the RV because of its large
workload.
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Valves
• Necessary to ensure oneway flow.
• Each consists of 2-3 flaps of connective tissue covered by
endothelium
• 1)Atrioventricular Valves
– Tricuspid Valve  Btwn RA and RV
– Bicuspid Valve  Btwn LA and LV. k.a. mitral valve
2) Semilunar valves
(aortic valva and pulmonic valva)
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Basic Pathway of Blood Flow
CS
SVC
IVC
Right
Atrium
Tricuspid
Valve
Right
Ventricle
Systemic
Capillaries
Pulmonary
Semilunar
Valve
Pulmonary
Trunk
Aorta
Pulmonary
Arteries
Aortic Semilunar Valve
Left
Ventricle
Pulmonary
Capillaries
Bicuspid
Valve
Left Atrium
Pulmonary
Veins
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Coronary Circulation
• Cardiac muscle is not nourished to any extent
by the blood flowing thru its chambers, so it has
its own network of arteries, capillaries, and veins –
the coronary circulation
• 5% of circulating blood is delivered to the heart
After the aorta emerges from the LV it gives off
2 branches, the left & right coronary arteries
• The coronary circulation has many anastomoses –
where 2 arteries come together and combine
their blood flow.
– What is the advantage to this?
• Blockage of coronary arteries causes ischemia
• a loss of blood flow. Temporary and reversible ischemia produces a
sense of pain known as angina pectoris.
• Prolonged coronary blockage can lead to myocardial cell death
myocardial infarction
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Cardiac Conduction
System
– Sinoatrial Node → Adjacent to
the SVC opening in the RA
– Atrioventricular Node → Near
the right AV valve at the bottom
of the interatrial septum
– Atrioventricular Bundle →
Inferior interatrial septum
– Right & Left Bundle Branches
→ Interventricular septum
– Purkinje Fibers → Distributed
throughout the LV and RV
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• the heartbeat originates
at the SA node. For this
reason, it is known as the
heart’s pacemaker and
its rhythm (sinus rhythm)
determines heart rate.
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• At the AV node, the impulse is delayed momentarily to
allow the atria to complete their contraction before the
ventricles contract
• From the AV node, the impulse travels to the AV bundle.
•
The AV bundle is the ONLY electrical connection btwn
the atria and the ventricles.
• The impulse travels on to the L&R bundle branches and
onward to the Purkinje fibers which begin at the heart
apex and extend upward thru the ventricles
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Extrinsic Control of Heart
Rate
• Sympathetic nerve input increases both the rate and the
force of the heartbeat while parasympathetic input
decreases the heart rate.
• Parasympathetic fibers project via the vagus nerve
(CN10) to the SA and AV nodes.
• Various hormones (epinephrine, thyroxine) also affect
the heart’s rhythm.
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Conduction Pathologies
• Arrhythmia → Irregular heart rhythm
• Fibrillation → Condition of rapid and out-of-phase
contractions. Why are fibrillating ventricles useless as
pumps?
• Ectopic Focus → A region of the heart becomes
hyperexcitable and generates impulses faster than the
SA node. Can also lead to premature contractions or
extrasystole (e.g., premature ventricular contraction
(PVC)
• Heart Block → Any damage to the AV node. Interferes
with the transmission of impulses to the ventricles. Can
very in severity.
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Learning outcome 3
• Describe the configuration of the normal
electrocardiogram (ECG).
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•
ECG is Graphical recording of the heart’s electrical activity, measured by
electrodes on the body surface
•
Normally, consists of 3 waves
– P wave = Represents atrial depolarization
• Atria begin contracting about 100msec after P wave begins
– QRS complex = Represents ventricular depolarization
• Why is it a larger signal than the P wave
• Ventricular contraction shortly after the peak of the R wave
– T wave = Indicates ventricular repolarization
• Why do we NOT see a wave corresponding to atrial repolarization?
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Assessing the Rhythm Strip
1. Determine atrial (P-P) and ventricular (R-R) regularity.
2. Determine the atrial (P-P) and ventricular rate (R-R).
– If regular, count number of large boxes between 2
consecutive P waves or 2 consecutive QRS
complexes and divide by 300.
– If irregular, count the number of complexes in 6
seconds and multiply by 10.
3. P waves: present, absent, all look alike or not, ratio of P
waves to QRS complexes
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4. Determine PR interval; normal is 0.12 to 0.20 sec
• Does the interval vary? Is there a pattern?
5. Determine the QRS complex; normal is 0.06 to 0.11 sec
• Do the complexes look the same?
6. Determine if the ST segment is isoelectric, elevated, or
depressed.
7. Determine QT interval.
Normal values
not >0.42 seco
8. Is the patient stable or not stable?
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Valve Pathology
• Murmur
Abnormal
heart sound due to a
malfunctioning heart valve
• Valvular Stenosis Valve
cusps become stiffened
and the opening is
constricted by scar tissue.
How would this effect the
workload of the heart?
•
Valve Prolapse
insufficiency in which one
or both mitral valve flaps
bulge into the atrium
during ventricular systole
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LEARNING out come 4
• Compare and contrast the significance of
cardiovascular assessment findings.
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Biographic and Demographic Data
• Assessment of biographic and
demographic data includes:
– Age
– Race
– Gender
– Ethnicity
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Chief Complaint
• A complete description of the present
illness
• Patients present their symptoms in their
own words
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Cardiovascular Clinical
Manifestations
• Angina
– Pain may be described as:
•
•
•
•
•
Indigestion
Burning
Numbness
Tightness
Pressure in the midchest, or as epigastric or
substernal pain
• Pain can radiate to the shoulder, neck, arms, jaw,
or back
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Cardiovascular Clinical
Manifestations
– Chest pain (angina)
– Changes in the heart rate and rhythm –
palpitations
– Dyspnea, or shortness of breath
– Orthopnea – dyspnea when patient lies flat
– A cough may suggest pulmonary congestion
– Nocturia may indicate heart failure
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Cardiovascular Clinical
Manifestations
– Edema – fluid accumulation manifested by:
•
•
•
•
Weight gain
A feeling of being bloated
Clothes or shoes no longer fit
May correlate with volume overload
– Dizziness, syncope, or light-headedness
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Cardiovascular Clinical
Manifestations
– Fatigue
– Intermittent claudication
• Pain in muscles of lower extremities
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Clinical exam points
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Clinical Reference Points
Figure 37.7 (continued) Clinical reference points for palpation.
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Auscultation of the Precordium
Figure 37.8 Auscultatory areas.
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Auscultation of the Precordium
• Listen for normal S1 and S2 heart sounds
at each site
– Note the intensity
• Presence of split sounds
– Respiratory cycle affects regularity of the
sounds
– Time between the S1 and S2 for regularity
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Auscultation of the Precordium
• Extra heart sounds and abnormal heart
sounds
– S3 or S4 often signify cardiac disorders
– Pericardial friction rub
– Murmurs and bruits
• Valve abnormalities of stenosis or regurgitation
• Systolic, diastolic, innocent
– If heard, note the timing, pitch, loudness,
duration, and location
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Heart sounds in systole and diastole.
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Cardiac Function
(continued)
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