Cardiovascular System

Assessment

By:Omar AL-Rawajfah, RN, PhD

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Lecture Outlines • Review of anatomy of the heart

– Heart champers – Valves – Coronary arteries – Vascular system – Conductive system

• Review of the related physiology – Cardiac cycle – Conduction system

• Assessment of Cardiovascular System – Health history – Diagnostic tests

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Review of Anatomy of The Heart • About 250 – 400g • About 12 cm long & 9 cm wide • Four distinct layers of the heart muscle

– Pericardium: • Fibroserous sac encases the heart • contains about 15 to 50 mL of pericardial fluid • A pericardial effusion is the presence of excessive

pericardial fluid • Cardiac tamponade, a life-threatening complication, that

puts pressure on the heart preventing the ventricles from filling correctly

The Sw

inging Heart

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Review of Anatomy of The Heart

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Valves • Atrioventricular (AV) valves:

– Tricuspid – Mitral

• Semilunar Valves: – Pulmonic – Aortic

• Each valve is composed of flexible fibrous tissue and fibrous supporting ring (Annulus)

• Mitral valve has 2 cups that are more thicker and stronger than the 3 cusps of the tricuspid valve

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Valves of the Heart

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Annuloplasty Ring

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Coronary artery dominance • The artery that supplies the Posterior Descending Artery

(PDA) and the Posterolateral Artery (PLA) determines the coronary dominance.

• If the Right Coronary Artery (RCA) supplies both these arteries, the circulation can be classified as "right-dominant".

• If the Circumflex Artery (CX), a branch of the left artery, supplies both these arteries, the circulation can be classified as "left-dominant".

• If the RCA supplies the PDA and the CX supplies the PLA, the circulation is known as "co-dominant".

• Approximately 60% of the general population are right-dominant, 25% are co-dominant, and 15% are left-dominant

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Coronary Blood Supply (check the textbook

Coronary artery

Cardiac muscle supplied Conducting tissue

Left Main LAD Anterior ventricular septum

Anterior wall of LTV Apex

CLX

Lt atrium Rt ventricle LtV posterior wall

SA node 45% of hearts AV node 10% of hearts

RCA RT atrium RT ventricle Posterior ventricular septum Inferior wall of the LTV

SA node 55% of hearts AV node 90%

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Vascular System

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Electrical Conduction System

• Sinoatrial Node (Sinus Node or SA Node) – “Normal pacemaker” of the heart

• Internodal Atrial Pathways • Atrioventricular Junction (AV junction)

– AV node • “Gatekeeper” • slows conduction to the ventricles allowing time for ventricles to

fill – Bundle of His

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Conduction System/Action Potential

• Phase 0: Rapid depolarization – Opening of fast Na

+ channels

– Rapid influx of Na+ into the cell

– Correspond with ventricular depolarization • Phase 1: Early repolarization

– Inactivation of fast Na+ channels

– Influx of Cl-

• Phase 2: Plateau phase of repolarization – Slow inward flow of Ca

+ +

• Phase 3: Late repolarization – Slow Ca

+ + channel inactivated

– K + leaves the cell

– Cell return into its resting state • Phase 4: Refractory period

– Membrane fully recover before accepting new stimulus – Associated with ventricular diastole

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Cardiac cell depolarization & repolarization

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Cardiac Cycle • Diastole:

– Comprises 60% of the cardiac cycle – 4 components:

• Isovolumetric relaxation: closure of all valves • Rapid filling: tricuspid & mitral opening • Slow filling: low pressure gradient • Atrial contraction: atrial kick → add 30% of CO

– Closure of tricuspid occurs slightly after mitral valve

– Coronary blood flow occurs during diastole

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Cardiac Cycle • Systole:

– Comprises 40% of the cardiac cycle – 4 components:

• Isovolumetric contraction: contraction of ventricles + opening of aortic & pulmonic valves

• Rapid ventricular ejection: tricuspid & mitral opening

• Reduced ventricular ejection:↓ intraventricular pressure

• Protodiastole: closure of aortic & pulmonic valves – Ejection Fraction normally greater than 50%

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Events in the Cardiac Cycle

• Diastole: period of ventricular relaxation – Pressure decreases to about 5 mm Hg – Aortic valve is closed – Mitral valve is opened

• Systole: period of ventricular contraction – Pressure peaks to about 120 mm Hg – Aortic valve is opened – Mitral valve is closed

• Possible explanation of heart sounds include – Closure of valve leaflets – Tensing of related structure – Leaflet positions and pressure gradients – Effects of columns of blood

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Hearst Sound • During systole

– LtV starts to contract → pressure rapidly increase → closure of mitral valve → produce first heart sound S1

– LtV pressure continue to rise exceeds the pressure in the aorta → open of aortic valve → early systolic ejection sound (Ej)

– LtV ejects most of its blood → pressure begins to fall → aortic valve close → produce second heart sound S2

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Hearst Sound

• During Diastole – After mitral valve opening → blood flows from LtA

to LtV → this event may produce S3 in children → in adult if herd termed and S3 gallop → change in ventricular compliance

– Atrial contraction produce no audible sound in adult if herd termed and S4 → change in ventricular compliance → it immediately precedes S1

• During Diastole – LtV pressure continue to drop →

mitral valve open → this is usually is a silent event → opening snap (OS) → mitral stenosis

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The splitting of Heart Sounds • Pressure in the Rt side is significantly lower then

the Lt side • Rt-sided events usually occur slightly later then

those of the Lt • Physiologic split

– Second heart sound is composed of 2 components → A2 & P2

• During inspiration: A2 & P2 separate slightly • During expiration: they fused into single sound S2 • Ejection of blood from LtV is shorter than RtV → A2 occurs

slightly earlier

• Pathologic split • A bundle branch block. • If splitting does not vary with inspiration, it is termed a

"fixed split S2" and is usually due to an atrial septal defect (ASD) or ventricular septal defect (VSD).

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The splitting of Heart Sounds • S1, is composed of components M1 & T1. • S1split is also occurs because of the same

reasons • Principle component is the mitral → best

herd on the apex • The softer tricuspid is best herd at lower

left steral border

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Cardiac Output • Index of heart’s overall performance • CO = HR x SV • SV: normally 60 – 80 mL per beat • 3 determinates of SV 1. Preload:

– “volume and pressure generated within the ventricle at the end of diastole”

– Reduced with rapid HR and condition associated with decreased volume

– Increased with reduced pumping ability – Starling’s Law: “the more myocardial fiber stretch during

diastole, the more it shortens in systole and the greater the force of contraction”

– Rt Atrial Pressure (RAP) and Central Venous Pressure (CVP) reflect preload in the Rt side

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Cardiac Output 2. Afterload – force and resistance against which the heart

has to pump to eject the blood during systole – ↑ afterload result in ↓ SV and CO – Pulmonary vascular resistance (PVR): RtV

afterload – Systemic ventricular resistance (SVR): LtV

afterload 3. Contractility or Intropy – Level of catecholamines, sympathetic neuronal activity – Drugs

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Cardiovascular Assessment • Health History

– Chief complain – Present illness – Past history – Advance directive decision

• Risk factors – Modifiable – Nonmodifiable

• Congenital Defects • Rheumatic Disease

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Sings and Symptoms

• Dyspnea – evidence of heart failure

• Syncope – Hypotension Inadequate CO

• Chest pain or discomfort – Location, Radiation, Nature, Other features

include duration, aggravating and relieving factors, and associated symptoms eg nausea and/or vomiting, sweating, dizziness, and palpitations.

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Sings and Symptoms

• Cyanosis • Dependent edema • Fatigue • Hemoptysis • Palpitation

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Physical Examination • General appearance

– obesity or wasting – SOB – Cyanosis

• Vital sings – BP in both arms → difference

more than 15 mm Hg may suggest aortic dissection or atherosclerosis

– Orthostatic hypotension

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Physical Examination • Head and Neck

– Distended neck veins

• Skin – Central Cyanosis – Clubbing

• Heart – Inspection – Palpation – Percussion – Auscultation

• Extremities

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Cardiovascular Laboratory & Diagnostic Test

• Hematology – CBC: Hb, WBC, HTC

• Serum electrolytes & glucose level – Na, K, Ca

• Thyroid function (TSH, T4, T3) • Lipid profile

– Cholesterol → less than 200mg/dl – LDL → less than 130 mg/dl – HDL → more than 35mg/dl – Triglycerides → less than 200mg/dl – Cholesterol: HDL ratio → less than 4

• Note: make sure your patient is fasted for about 14 hours before the test

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Cardiovascular Laboratory & Diagnostic Test

• Coagulation studies – Prothrombin time (PT) → 11-13 sec → warfarin → 1.5-2

times the control – International Normalized Ratio (INR) → 1.3 – 1.6 – Partial thromoplastin time (PTT) → 30-45 sec → Heparin

• Cardiac markers: – CK-MB

• High specificity for cardiac tissue • The preferred marker for cardiac injury for many years • Begins to rise 4-6 hours after infarction but can take up

to 12 hours to become elevated in all patients with infarction

• Elevations return to baseline within 36-48 hours, in contrast to troponins

• CK-MB is the marker of choice for diagnosis of reinfarction after CABG because of rapid washout

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Cardiovascular Laboratory & Diagnostic Test

• Cardiac markers: – Cardiac Troponin I (cTnl):

• Serum increase is found between 2-8 hours and returns to normal 7~10 days after AMI.

– Cardiac Troponin T (cTnT) • Peak between 12~96 hours and return to normal 14 days after AMI. • 4-6 hours to rise post-infarct, similar to CKMB • 6-9 hours to detect pathologic elevations in all patients with infarct • Elevated levels can persist in blood for weeks; the cardiac specificity

of troponins thus make them the ideal marker for retrospective diagnosis of infarction

– Myoglobin • The major protein responsible for O2 supply of striated muscle. • It is released into blood rapidly (as early as 1 hour) after damage to

muscle cell. • Early detectable, more sensitive but non-cardiospecific. • High negative predictive value. • Myoglobin is more suitable for the detection of reinfarction.

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Cardiovascular Laboratory & Diagnostic Test

• Chest Radiograph

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Echocardiogram & Transesophageal Echocardiography

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Myocardial Perfusion Scan • Thallium-201 and Technetium 99m

– Keep patient NPO 4hrs before test – Teaching – Procedure takes about 1-4 hrs – Encourage fluid intake after the procedure if allowed

• Indications for a myocardial perfusion test – Diagnosis of CAD and various cardiac abnormalities. – Identifying location and degree of CAD in patients with a history

of CAD. – Prognosis of patients who are at risk of having a myocardial or

coronary incident (i.e. myocardial infarction, myocardial ischemia, coronary aneurysm, wall motion abnormalities).

– Post intervention revascularization (coronary artery bypass graft, angioplasty) evaluation of heart.

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Myocardial Perfusion Scan

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Pharmacologic stress test • Indications: the same as for an exercise stress test

– Inability to perform adequate exercise due to non-cardiac physical limitations or lack of motivation

– Baseline electrocardiographic abnormalities such as left bundle branch block (LBBB), ventricular pre-excitation (Wolff-Parkinson-White syndrome), or permanent ventricular pacing

– Risk stratification of clinically stable patients after acute myocardial infarction (≥ 1 day) or following presentation to the emergency department with a presumptive acute coronary syndrome

• Drugs – Adenosine – Dobutamine

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Exercise stress test • Indications

– Chest pain (equivalent) evaluation – Assess CAD risk (two or more risk factors)* – Pre non cardiac surgery – Post MI – CHF/cardiomyopathy evaluation – Arrhythmia evaluation – Pre exercise program – Post cath assessment of ischemia – Abnormal ECG

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Exercise stress test

• Absolute contraindications: – Acute myocardial infarction within 48 hours – Unstable angina not yet stabilized with medical therapy – Uncontrolled cardiac arrhythmia, which may have significant

hemodynamic responses (e.g. ventricular tachycardia) – Severe symptomatic aortic stenosis, aortic dissection, pulmonary

embolism, and pericarditis – Multivessel coronary artery diseases that have a high risk of

producing an acute myocardial infarction – Decompensated or inadequately controlled congestive heart failure – Uncontrolled hypertension (blood pressure>200/110mm Hg) – Severe pulmonary hypertension – Acute aortic dissection – Acutely ill for any reasons

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Electrophysiologic studies:

Holter (24hr) monitoring: • Non-invasive ECG monitor used to quantify freq and complexity of

cardiac activity that occur during pt. activity • Indicated for: palpitation, syncope, dizziness. • Used for outpatient, useless for infrequent symptoms

Cardiac Catheterization

Indications: • Suspected or known coronary • heart disease • Myodcardial infarction • Sudden cardiovascular death • Valvular heart disease • Congenital heart disease • Aortic dissection • Pericardial constriction • Cardiomyopathy • Initial and follow up

assessment for heart transplant

Contraindications

• Active GI bleed • Renal failure • Recent stroke • Fever from infection • Electrolyte imbalance • Anemia • Short life expectancy • Digitalis intoxication

• PT refusal • Uncontrolled

hypertension • Bleeding disorders • Pulmonary edema • Uncontrolled ventricular

arrhythmias • Aortic valve endocarditiis • Allergic to contrast

Complications and Risks

• Death • Myocardial infarction • CVA • Arrhythmia • Hemorrhage • Contrast • Hemodynamic • Perforation

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Catheters

• For LT cardiac cath similar to those for angio

• RT cath requires specialized catheters – Typically flow directed

catheters – With manifolds

Imaging

• Image chain • Digital Angiography

imaging equipment

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Physiologic Equipment

• Equipment to monitor – ECG – Hemodynamic pressures

• Vital signs to • Record PT function

Other Equipment

• Crash cart • Oxygen and suction • Defibrillator • Temporary pacemaker • Pulse oximeter • Blood pressure cuff • Equipment to perform cardiac output

studies • Activated clotting time (ACT) equipment

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Pre-Catheterization Care

• Informed consent obtained • PT history • Physical exam • CXR • Blood work • ECG • Echocardiogram • Exercise stress test • Nuclear Medicine cardiac perfusion studies

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Pre-Catheterization Care

• IV started – Sedation and nausea

• Nothing to eat 4-6 hours before procedure • Records of procedure

– PT hemodynamic data – Fluoro times – Medications administered – Supplies used – Other pertinent information

Catheter Introduction • Prepare catheter introduction

site with aseptic technique – Shaved and cleaned

• Can be at femoral (most

common), brachial, radial, axillary, jugular and subclavian areas

• Selinger technique used

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Selinger Technique

Needle with cannula inserted

Needle withdrawn until there is blood flow

Inner cannula removed & guidewire inserted

Needle removed Catheter over guidewire Guidewire removed

leaving catheter in artery

Patient Positioning for Cardiac Catheterization

• PT must be positioning so that they will not have to be moved during procedure

• Must be positioned so anatomic structures of interest are demonstrated

• PT is supine with shielding as appropriate

Cath of the LT side of the heart: ADULTS

• Catheter introduced into the radial, brachial or femoral artery to the ascending aorta

• Aortic root angio is performed to document competence of the aortic valve

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LT Ventriculography • Provides info on valvular

competence • Interventricular septal

integrity • Efficiency of the pumping

action of LT ventricle • Pressure measurements

are made • When systolic (LT

ventricle) does not match systolic (aorta)- could mean aortic stenosis

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Coronary Angiography • Allows the extent of intracoronary

stenosis to be evaluated

Coronary Angiography

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Coronary Angiogram: LAD Stenosis

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LAD & LCX stenosis

Post Catheterization Care • Firm pressure is applied to puncture site

for 15-30 minutes • Wound sites are cleaned and dressed • The patient will be observed in recovery

for 4-8 hours • The insertion site will be checked

frequently for signs of bleeding. • Medications and discharge instructions are

given • Lots of fluid should be taken in • Vital signs should be monitored for 24

hours

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Questions and answers

Biochemical Changes in Acute Myocardial Infarction

(mechanism of release of myocardial markers)

ischemia to myocardial muscles (with low O2 supply)

anaerobic glycolysis

increased accumulation of Lactate

decrease in pH

activate lysosomal enzymes

disintegration of myocardial proteins

cell death & necrosis

release of intracellular contents to blood

BIOCHEMICAL MARKERS

clinical manifestations (chest pain)

ECG changes