Transcript 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 inversion
Injury
- prolonged ischemia
- ST elevation
Infarct
- 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 ECG
Leads
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