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King Saud university college of nursing

critical care nursing lecture2

Cardiovascular assessment

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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 one-way 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

SVC

IVC

CS

Right Atrium

Tricuspid Valve

Right Ventricle

Pulmonary Semilunar

Valve

Pulmonary Trunk

Pulmonary Arteries

Pulmonary Capillaries

Pulmonary Veins

Left AtriumBicuspid

Valve

Left Ventricle

Aorta

Aortic Semilunar Valve

Systemic Capillaries

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Coronary Circulation• Cardiac muscle is not nourished to any extentby 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 heartAfter the aorta emerges from the LV it gives off2 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 Strip1. 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)