cardiac review

Cardiac Review

Cardiac Monitoring, Leads, Identifying Ischemia, Infarction & Location, ACLS Algorithms,

Other Cardiac Problems

Cardiac Monitoring – Lead I

Lead II

Lead III

MCL1

How it looks on a real chest

12 Lead Electrode Placement

Limb Leads – near ankles and wrists, but may be more proximal- just not on the trunk

aVR should be negative If aVR is upright, check for reversal of

the limb leads.

12 Lead Chest Leads a.k.a. precordial leads V1 – 4th intercostal space to the right of the

sternum V2 – 4th intercostal space to the left of the

sternum V3 – directly between V2 and V4 V4 – 5th intercostal space at left midclavicular

line V5 – level of V4 at left axillary line V6 – level with lead V5 at left midaxillary line

How it looks on paper… plus right precordial leads

The posterior leads

A Normal 12 Lead EKG

St Segment Elevation

Identifying Ischemia and Infarct

Acute Coronary Syndromes

(ACS)

ST Elevation MI(STEMI)

Non-ST Elevation MI

(NSTEMI)

Unstable Angina(USA)

The 3 Is

Ischemia - lack of oxygenation - ST depression or T wave inversionInjury - prolonged ischemia - ST elevationInfarct - death of tissue - may or may not show in Q wave

Ischemia

Inadequate oxygen to tissue Represented by ST depression or T

wave inversion May or may not result in infarct > 1 mm ST depression one small box

to right of J point in 2 or more anatomical leads/ T wave inversion if full thickness of myocardium

Injury

Prolonged ischemia Transmural Represented by ST elevation Usually results in infarct > 1 mm ST elevation one small box to

right of the J point or > 2 mm in the precordial leads in 2 or more anatomical leads

Infarct

Death of tissue Represented by Q wave Not all infarcts develop Q waves Non-Q wave MI looks like ST elevation

and has elevated cardiac enzymes too Q-wave MI indicates dead tissue- if

duration more than one small box and >25% amplitude of R wave

Infarct

EKG includes new or presumed new transient ST deviation ≥ 0.5 mm or T wave inversion ≥ 2 mm with symptoms, fixed Q waves

Cardiac markers include elevated troponin, elevated CK-MB

ACS

All acute coronary syndromes suggest acute myocardial ischemia.

It is often not possible to determine which syndrome is present in the first hours of clinical presentation because they all have the same initiating events:-plaque rupture-thrombus formation-vasoconstriction

Presumed AMI - STEMI

ST elevation of one or more millimeters in two or more contiguous leads

New or presumably new LBBB Strongly suspicious for injury May require repeat 12 leads Treatment may include beta blocker,

clopidogrel, heparin, reperfusion therapy (fibrinolysis or cath), ACE/ARB, statin

Management - NSTEMI

ST depression or dynamic T wave inversion

Strongly suspicious for ischemia High risk unstable angina Treatment: Beta blocker, clopidogrel,

heparin, glycoprotein IIa/IIIb inhibitor, cath within 48 hours, asa, ACE/ARB, statin

Management – Unstable Angina

Normal or non-diagnostic changes in ST segment or T wave

Treatment: serial cardiac markers (including troponin), repeat 12 leads & continuous telemetry monitoring, consider stress test, discharge for follow-up if no evidence of ischemia or infarction

Unstable Angina

Not chronic stable angina if…

-New onset

-Lower exertion threshold

-Change in pattern of relief

-New or different associated symptoms

Management

Story Risk factors EKG Clinical presentation: classical

anginal chest pain, atypical chest pain, anginal equivalents (dyspnea, palpitations, syncope or pre-syncope, general weakness, DKA)

Management

Patients with severe or multiple risk factors should be evaluated with a high index of suspicion for ACS: diabetes, smoking, hypertension, age, family hx, obesity, stress, sedentary

Note re: age- males >35 & females >40; increasing age = increasing risk

ST Elevation

ST Elevation

Evolution of AMI on the 12 Lead

Note Q wave measuring at least 40 ms wide (pathologic associated with cellular necrosis)

When Q waves first form, tissue may not yet be necrotic. Reperfusion may result in Q waves disappearing.

Presence of wide Q and absence of ST segment elevation = previous MI = age undetermined (rather than old MI)

Reciprocal Changes

- Those leads that look at the infarct site from the opposite perspective tend to produce the opposite changes.

- When a lead sees the AMI directly, the ST segment becomes elevated in that lead.

- When a lead sees the infarct from the opposite perspective, the ST segment may be depressed in that lead.

- Reciprocal changes – not necessary to presume infarction, strong confirming evidence when present

Reciprocal Changes

Because of the way the leads are oriented on the patient’s body, II, III, and aVF are on the bottom looking up.

All other leads are on top looking in. Therefore, when AMI produces elevations in II, III, and

aVF, it tends to produce depression in the opposing leads.

II, III, aVF I, aVL, V leads

12 Lead EKG – Related Groups

Each lead has only one positive electrode. The positive electrode is like the eye. The view is from the positive electrode to

the negative electrode. All 6 chest leads are positive electrodes. The 4 limb leads provide another 6 views of

the heart.

Contiguous Leads in the ECGLeads CoronaryArtery Wall Supplied

I, AVL, V5, V6 Left Circumflex Lateral

II, III, aVF Right Coronary Inferior

V1, V2, V3, V4 Left Anterior Descending

Septal

Anterior

Lateral Wall

I, aVL, V5, V6 When ST segment elevation is noted

in Leads I, aVL, V5 and v6 lateral wall infarction should be considered.

LCA Occlusions

Consider bundle branches supplied by LCA Serious infranodal heart blocks may occur Proximal occlusions of LCA = “widow maker” –

with evidence in septal, anterior, and lateral leads; complications are common

With normal BP do fibrinolysis, if signs of shock do PTCA or CABG

LCA dominance with 10% of population Inferolateral MI

Left Coronary Artery

Left anterior descending (LAD) = anteroseptal area of heart

Left circumflex (LCX) = lateral wall of heart, supplies posterior descending artery

Left Main (proximal LCA) = anterior wall of heart

Inferior Wall MI

Anterior Wall

V3 and V4 – left anterior chest The positive electrode for these two

leads is on the anterior wall of the left chest.

ST segment elevation in V3 and V4 implies an anterior wall infarction.

Anterior Wall MI

Pacemaker Leads

Ventricular Pacemaker Rhythm

Ventricular Pacer – Demand Mode

Atrial Pacer

AV Sequential Pacer

AV Sequential Pacer

ACLS Algorithms

Bradycardia Tachycardia Ventricular fibrillation/Pulseless VT PEA/ Asystole

CHF

The heart is unable to pump effectively to meet metabolic demands of the body or may require elevated filling pressures to meet this demand.

Systolic dysfunction is most common and occurs when the ejection fraction is less than 50%.

CHF – Systolic Dysfunction Systolic dysfunction is the inability of the right ventricle to

effectively pump blood to the pulmonary bed resulting in right sided heart failure.

Stroke volume decreases and the body compensates by retaining water and sodium.

That leads to an increase in stroke volume and results in pulmonary congestion.

The right ventricle enlarges resulting in peripheral edema and elevated JVD.

If you press on the patient’s right abdomen and see an increase in JVD when the patient is at a 30-45 degree angle, it is positive test for heart failure.

CHF – Diastolic Dysfunction EF is normal or greater than 50-55% The left ventricle is unable to fill because it is unable to

completely relax (stiff or non-compliant)– most commonly as a result of hypertension.

Left sided heart failure is diastolic heart failure that results in inadequate filling pressures and rising diastolic pressures. This results in increased left atrial, pulmonary venous, and pulmonary capillary pressures. Systolic function may be normal or hyperdynamic.

Causes: mitral stenosis, constrictive pericarditis, hypertrophic cardiomyopathy, or restrictive cardiomyopathy.

Causes of Heart Failure

Most common – CAD, hypertension, valvular dysfunction, idiopathic

Least common – viral, anemia, dysrhythmias (atrial fibrillation), peripartum, endocrine (diabetes & thyroid), restrictive (amyloid, sarcoid, hemochromatosis), cardiotoxic (alcohol, chemotherapy, cocaine)

HF Signs & Symptoms

Signs – JVD, rales or crackles, tachypnea, unexplained weight gain, ascites, edema, nocturia, pallor, diminished peripheral pulses, hepatomegaly, extra heart sounds, RUQ tenderness

Symptoms – orthopnea, paroxysmal nocturnal dyspnea, fatigue, DOE, depression, cough, anxiety, palpitations, N/V, abdominal fullness, chesst pain, anorexia

Edema

Increased central venous pressure results in a rise in capillary pressure which causes fluid to move from the intravascular space to the interstitial spaces.

Decreased CO results in decreased BP which activates the RAAS so water and sodium are preserved and predispose the patient to edema.

LVH

Causes: volume overload, systemic hypertension, increased resistance to emptying such as aortic stenosis

Isolated systolic hypertension and widened pulse pressure are cardiac risk factors that prompt search for LVH.

RVH

Causes: pulmonary hypertension

Sick Sinus Syndrome

Sinoatrial dysfunction secondary to hypertension, CAD, rheumatic heart disease

Bacterial Endocarditis

Affects endothelium and valves Thrombotic lesions can form at location of

injury (no anticoagulation- usually) Valves can be destroyed and leaflets can

rupture, become incompetent or rupture. Often left heart valves are affected as a result

of IV drug use. Not infectious TEE may be needed

Cor Pulmonale

RV enlargement secondary to pulmonary disease

Myocarditis

Focal or diffuse inflammation Viral etiologies: influenza, cytomegalovirus,

HIV, viral hepatitis, cocksackie, mumps/rubella Bacterial etiologies: strep, meningococcal,

rickettsia, fungal from aspergillis Myocardial fibers injured, hypertrophy results

causing cellular death. Contractility and CO decrease HF occurs with LV dysfunction

Pericarditis

Often associated with fever, chest pain, pericardial friction rub, diffuse ST elevation, and potential for pericardial effusion causing pericardial tamponade.

Cardiomyopathy

Etiologies: viral infections, auroimmune, CAD, valvular heart disease, hypertension, alcohol abuse

Types: dilated, hypertrophic obstructive cardiomyopathy, and restrictive

Pericardial Effusion

May be created slowly or quickly based on cause

Can lead to cardiac tamponade Decreased heart sounds, sudden increases in

CVP, JVD and pulsus paradoxus (pulse stronger when exhales, weaker when inhales resulting in inspiratory reduction in systolic pressure > 10 mm Hg

If chronic, right heart failure can result.

Cardiac Tamponade The result of effusion of fluid or blood in the

pericardial space that causes increased pressure on the myocardium thus restricting diastolic filling of the ventricles and myocardial contractility.

Etiology: cardiac trauma, iatrogenic contractility (pacer wire perforation or cardiac contusion from cpr), aortic dissection, or acute MI with myocardial rupture

Treatment: pericardiocentesis or surgical pericardial window

Miscellaneous

Septal defects Ventricular aneurysm Papillary muscle rupture