• Electrical signals generated by pacemaker cells
• Cells can generate stimulus w/out outside stimulation- it called automaticity

1. Electrical (caused by automaticity)
2. Mechanical (muscular) known as a contraction

Contraction

pulse

Depolarization= active

Repolarization= resting

Systole

Diastole

diastolic / systolic

systole = contraction

diastole = resting or filling phase

mechanical activity

cardiac contraction

cardiac action potential

• Cardiac muscle cells generate an electrical current = cardiac action potential
• Sinoatrial node (SA node)
• Exchange of electrolytes
• Depolarization
• Repolarization begins

Depolarization:

• Na outside cell; K inside the cell
• Change cell permeability
• Na enters cells; K leaves cells
• Ca slowly enter cells
• ATP (adenosine phosphate) needed to move electrolytes back to resting state

outside

inside

slowly enters

ATP (adenosine phosphate)

• Depolarization leads to contraction
• Repolarization leads to resting & fill of ventricles from atria
• ECG is evidence of electrical activity, not contraction!

• SA node
  Intraatrial & intermodal pathways to AV node
• AV node
• Bundle of His
• Left & right bundle branches; fascicles
• Purkinje fibers

• Depolarization begins- atria fills
• Atrial contraction or atrial kick

• Delays impulse to ventricles; allows for filling
• Back-up pacemaker- hopeful to get if sinus node goes out.

A. Fib

60-100 beats/min

40-60 beats/min

15 to 40 beats/min

* Positive QRS complex

* Negative QRS complex

three-lead or five-lead systems- not a 12 lead EKG

• Record & interpret 6-second strip every 4hrs
• Monitor ST segment
• Monitor dysrhythmias
• Daily 12-lead ECG for cardiac patients- this is not always true...

1. Used to standardize tracings
2. Vertical boxes measure voltage/amplitude
3. Horizontal boxes measure time

0.2

0.4

Atrial depolarization

• Normally indicates firing of the sinoatrial node
• Not to exceed 3 boxes high

-Ventricular depolarization

• Q wave first negative deflection after P wave
• R wave first positive deflection after P wave
• S wave negative waveform after R wave

-Not everyone has a traditional QRS- doesn't mean anything is wrong.

• 0.04 seconds in width
• More than one fourth of the R-wave amplitude
• Indication of a MI

• Atrial depolarization/delay in AV node
• Beginning of P wave to beginning of QRS complex
• 0.12 to 0.20 seconds
• Shorter interval= impulse from AV junction
• Longer interval = 1st° AV block

PR interval

1st° AV block

• Ventricular depolarization
• 0.06 to 0.10 seconds
• Various configurations
• Wide: slowed conduction
  • Bundle branch block (BBB)
  • Ventricular rhythm

Slowed conduction:

- Bundle Branch Block (BBB)

- Ventricular rhythm

0.06-0.10 seconds

Look for depression or elevation:

• ST elevation= Myocardial injury
• ST depression= reciprocal changes- digoxin, and ischemia

The time that it is fixed

• Follows a QRS complex
• Bigger than a P wave
• No greater than 5 small boxes high
• Inversion indicates ischemia to myocardium

Ischemia to myocardium

No greater than 5 small boxes high

-Beginning of QRS complex to end of T wave

-0.32 to 0.50 seconds

-Varies w/heart rate

QT interval

0.32-0.50

• Sometimes seen after T wave
• Unknown origin
  • May be normal
  • May indicate hyopkalemia

Hypokalemia

After the T wave (sometimes)

• Regularity or pattern of heart beats
• PP intervals (atrial)
  • Is regular when distance between PP intervals is equal
• RR intervals (Ventricles)
  • Is regular when distance between RR intervals is equal

Ventricular

Atrial

When the distance between PP intervals is equal

When the distance between RR intervals is equal

-Irregular- count for a full minute

-Calculate atrial PP and Ventricular rates RR

• Regular rhythm
• Rate 60-100 beats/min
• Normal P wave in lead II
• P wave before each QRS
• Normal PR, QRS, and QT intervals

Sinus rhythm

• Sinus rhythm w/a rate of 100-150 beats/min

*Normal P wave, P before each QRS & normal PR, QRS, QT intervals- sinus

Stimulants, exercise, fever & alterations

Symptoms of low cardiac output:

1. Hypotension
2. ↓ urine output
3. Chest pain
4. Confusion
5. Edema
6. Weakness & fatigue
7. Rapid breathing-> abnormal ABGs
8. ECG changes- abnormal hear rhythm

* These are just to name a few, there are plenty more

• Sinus rhythm w/rate less than 60 beats/min

*Vagal, drugs, ischemia, ICP, and normal in athletes.

* Various hemodynamic responses

NO, do not treat unless patient is symptomatic

2- Chest pain

• Syncope
• Hypotension
• ↓ urinary output

This is just to name a few :)

Tachy causes ↓ cardiac output

Sinus rhythm

Rate varies w/respirations

Rarely affects hemodynamic status

Rate varies w/respirations:

• Inspire= increase
• Expire= decrease

decreases

It increases

• Sinoatrial node fails to initiate impulse
• Causes: vagal, heart disease, and drugs that slow heart rate
• Heart rate can be normal to slow
• Irregular rhythm
• Can decrease cardiac output

Sinoatrial node fails to initiate impulse

Vagal, heart disease, and drugs that slow heart rate

Can be normal or slow

Increased automaticity in the atrium

Generally have P-wave changes

• Stress
• Digitalis toxicity
• Alcohol

1. Electrolyte imbalances
2. Hypoxia
3. Atrial injury
4. Hypothermia
5. Hyperthyroidism
6. Pericarditis

• Early beats initiated by atrium
• P waves and PR interval may vary
• Noncompensatory pause
• P wave may be found in T wave

* Narrow QRS

* Has a P wave

* Compensatory pause after a PAC

Pause noted on rhythm strip

Premature P wave

May alter cardiac output

A nonconducted premature atrial contraction

• Varying configurations of P waves
• At least 3 different P-wave shapes must be seen
• Heart rate not >100
• PR interval varies
• Irregular rhythm

Wandering atrial pacemaker

• Almost identical to wandering atrial pacemaker
• Heart rate exceeds 100 beats/min
• Common in COPD patients

Multifocal atrial tachycardia

P waves/faster

1. Ectopic foci in atria, heart disease
2. Classic "sawtooth" pattern in leads II, III, and aVF
3. Atrial rate fast & regular (250-350 beats/min) with AV block
4. Degree of conduction varies; may be 1:3 or 1:4, etc

Erratic impulse formation in atria

No discemible P wave

Irregular ventricular rate

Aberrant (abnormal) ventricular conductions can occur

Results in loss of atrial kick

High risk for pulmonary or systemic emboli

• Heart rate
• Strength of contraction
• Blood vessels diameter
• Degree of turbulence
• Pressure

flow / resistance

Force exerted on the liquid

* mm Hg

Flow: amount of fluid moved over time

* L/min or mL/min

Resistance: Opposition to flow

Volume of blood ejected from heart/min

HR / Stroke volume (volume of blood ejected w/each beat)

* 4 to 8 L/min

Fraction of blood ejected w/each beat

* Normal 60% to 70%

Degree of muscle fibers stretch before systole

* Volume of blood in ventricle prior to contraction (LVEDV/LVEDP)

* Increased stretch = volume

* Stretch is within physiological limits

- Example= balloon

• Pressure or resistance against flow
• Related to lumen size & viscosity

- Example: Opening a door against wind

Systemic vascular resistance

- Force overcome by the left ventricle upon contraction

Pulmonary vascular resistance

- Force overcome by the right ventricle upon contraction

Force of ventricular contraction

How well the heart is pumping

• Peripheral vascular resistance
• Diameter of blood vessels

Arterial BP= CO x SVR

• Index is better assessment; based on body size
• CI= CO ÷ body surface area
• Calculated on the computer after entering patient's height & weight.

1. Noninvasive blood pressure
2. Assessment of jugular venous pressure
3. Assessment of serum lactate levels

1. Arterial pressure monitoring
2. Pulmonary artery pressure monitoring
3. Right atrial pressure monitoring

• Invasive catheter
• Noncompliant pressure tubing
• Transducer & stopcocks
• Flush system
• Bedside monitor

Level = phlebostatic axis

* Fourth intercostal space, midaxillary line

* Approx. level of right atrium.

• Negate atmosphere pressure
• Zeroing stopcock is leveled at phlebostatic axis & "zeroed"

Square wave test

Invasive technique to monitor arterial blood pressure

1. Radial artery

* Allen's test prior to insertion to verify collateral circulation in the extremity

* Issues related to predictability of Allen's test

2. Brachial artery

3. Femoral artery

• Pressurized flush solution w/transducer
• Pressure at 300 mm Hg
• Why does this need to by high?
• A-line catheter (angiocath)

Thrombosis
* Clot if flush not used appropriately

Embolism

* Air entering system/clot dislodgment

Hemorrhage

* Loose connections/catheter dislodgement

Infection

Right atrial pressure (RAP)- catheter in right atrium

* Proximal port of pulmonary artery catheter

Central venous pressure (CVP)- catheter in superior or inferior vena cava

* Triple lumen

Values are similar & terms interchanged

• Direct measurement of pressure in right atrium
• Right ventricular preload or right ventricular end diastolic pressure (RVEDP)
• Normal value

- 2 to 6 mm Hg

- Recorded end exhalation as a mean value

• Zero/ balance
• Waveform analysis
• Respiratory variation and PEEP
• Patient position- Head of bed between 0 & 60°
• Correlate values w/assessment
• Monitor for complications

1. Infection
2. Pneumothorax or hemothorax
3. Carotid puncture
4. Heart perforation
5. Dysrhythmias

Flow directed catheter

* Inserted via subclavian, internal jugular, or femoral vein

* Balloon tipped

* Multiple lumens

Variations

* SvO2 catheter

* Continuous cardiac output (CCO)

Proper position of patient

- Trendelenburg common

- Towel roll between shoulder blades

• Inserted w/balloon deflated, selected inflation to "float" catheter into PA
• Waveform changes as catheter progresses
• Check for proper "wedging" for PAOP
• Chest x-ray

• PA systolic
• PA diastolic
• PAOP/PCWP/PAWP

* Inflated balloon flows into wedge position in pulmonary capillary measuring pressure

• Cardiac output/Index

- Thermodilution CO

- Proximal injectate port

• Pulmonary artery occlusive pressure (PAOP) reflects left ventricular end-diastolic pressure

- In many patients the PADP can be substituted for PAOP measurements if values are similar

- Record amount of air to inflate balloon- no more than 1.5 mL

1. Infection
2. Dysrhythmias
3. Air embolus
4. Thromboembolism
5. PA rupture
6. Pulmonary infarction

Procedure:

1. Inject solution within 4secs
2. Increased accuracy at end expiration
3. Check waveform
4. Repeat at least three measurements
5. Average values within 10% of each other
6. Calculate CO and cardiac index (computer does this)

Continuous monitoring via specialized PAC

* Copper filament at distal catheter end

* Pulses of energy at intervals warms blood

Accurate w/head of bed up to 45°

• Calculated values

• Obtained via monitoring catheters

- SvO2- mixed venous oxygen saturation via specialized PAC

- ScvO2- central venous oxygen saturation via specialized central line

• SvO2- 60% to 75%= adequate balance between supply and demand
• ScvO2- 65% to 85%= adequate balance between supply and demand

High values= tissues not able to use oxygen

Low values= oxygen demand exceeds delivery

- Esophageal Doppler

* Thin silicone probe placed in the distal esophagus

* Evaluates descending aortic blood flow

- Pulse contour cardiac output

1. Right atrial pressure variation
2. Systolic pressure variation
3. Arterial pulse pressure variation
4. Stroke volume variation

• Caused by a turbulence of blood flow through the valves
• Rumbling, blowing, harsh, or musical in sound
• Identify location, sound, loudness, and intensity & whether other heart sounds are heard.

* Progressive narrowing of coronary arteries by atherosclerosis

- Coronary heart disease

- Atherosclerotic heart disease

1. Injury to epithelial cells in intima

* Platelet aggregation

* Migration of monocytes

* Lipoproteins enter intima

2. Fatter streak

- Monocytes develop into macrophages

- Lipid-rich "foam cells" develop

3. Atheroma

4. Damage to intima- liberates platelet-derived growth factor

5. Proliferation of smooth muscle cells

6. Fibrous cap forms

* From connective tissue & low-density lipoprotein (LDL)

7. Fibrous cap often ruptures

- Thrombus

- Clotting cascade initiated

8. Adhesion: platelets bind to receptors

9. Activation: platelets change shape & activate receptors

- Release: thromboxane A2 & serotonin

- Activate glycoprotein IIb/IIa receptors

10. Aggregation: platelets clump together

1. Aspirin
2. Glycoprotein IIb/IIIa inhibitors
3. Heparin
4. enoxaparin (Lovenox)
5. Warfarin- coumadin

- Age:

* Men > 45

* Women > 55

- Family history

- Cholesterol

* High LDL

* Low levels of HDL

- Smoking

- Hypertension

- Inactivity

- Overweight

* Diabetes

• Risk factors
• Prior hospitalizations
• Shortness of breath, chest pain
• Medications

- Erectile dysfunction meds if considering nitroglycerin

• Psychosocial history

- Include stressors

1. 12 lead ECG
2. Holter monitor
3. Exercise tolerance test (stress test)
4. Chest x-ray
5. Echocardiography
6. Transesophageal echocardiography
7. Diagnostic heart scans
8. Single photon emission computed tomography
9. Magnetic resonance imaging
10. Electrophysiology study

AKA- Exercise tolerance test

• Exercise to increase demand on heart
• Stressed via drugs if patient cannot tolerate exercise (e.g., adenosine)
• Monitoring vital signs, ECG

*Tries to induce symptoms of patients complaints*

Ultrasound to visualize cardiac structures

1. Technetium-99m stannous pyrophosphate
2. Thallium-201
3. Multigated blood pool study

Catheter (Right or Left)

- Heart pressures (similar to PA catheter)

- Cardiac output

Arteriography

- Visualize blood vessels

• Bed rest; head of bed no higher than 30°
• Monitor bleeding; newer collagen agents for hemostasis may be used
• Monitor pulses
• Antiplatelet drugs after the procedure (usually after interventions such as PCI)
• May be discharged in 6 to 8hrs; depends on diagnosis & procedures done in catheterization laboratory.

1. CBC- Hemoglobin & Hematocrit (H&H)
2. Potassium
3. Magnesium
4. Calcium
5. Sodium

* Want labs to be w/in normal ranges, if not must fix!

* CK (total)

2 to 6hrs; peak 18 to 36hrs

* CK-MB (cardiac specific)

4 to 8hrs; peak 18 to 24hrs

* Troponin I and T

As early as 1hr after injury

* Myoglobin

30 to 60 minutes after injury

4 to 8hrs- after injury

peaks: 18 to 24hrs

As early as 1hr after injury

HDL- considered GOOD

LDL- is BAD

* No CHD & fewer than 2 risk factors

- 160 mg/dL

* No CHD & 2 or more risk factors

- 130 mg/dL

* CAD

- <100 mg/dL

1. Diet: Low cholesterol, low salt
2. Exercise: aerobic
3. Medications: Lipid-lowering agents

- Various types: weigh advantages & disadvantages of each

* HmG CoA reductase inhibitors; slow production: most effective:

- Statins

* Bile acid resins bind & are excreted via bowel

- Cholestyramine

- Colestipol

* Nicotinic acid; inhibits LDL synthesis & increases HDL; many side effects

* Fibric acid derivatives; increase VLDL clearance

- Gemfibrozil

- ASA

- Others: dipyridamole, ticlopidine, and clopidogrel

• Classic symptom
• Often midsternal
• May radiate to arms, jaw, or back

Myocardial ischemia: demand higher than supply

Chronic, exertional= Effort, classic

T-wave inversion on ECG

Treatment: rest & nitroglycerin

Crescendo (starts off mild, then increases)

- More often & severe, less relief

* May see ST elevation on ECG

* Treatment: Rest and nitroglycerin; drugs affecting platelets; revascularization

Prinzmetal's (vasospasms)

* ST elevation during pain episodes

* Treatment: Calcium channel blockers

Maintain cardiac output

Pain relief

Self-care; risk-factor modification

C. Assessment & documentation of chest pain episodes

• Ischemia w/myocardial cell death
• Imbalance of oxygen supply & demand
• Causes
  • Atherosclerosis
  • Emboli
  • Blunt trauma
  • Spasm

• Q wave: total occlusion of coronary artery w/ thrombus
• Non Q wave: partial occlusion of coronary artery

Collateral circulaion

~ Midsternal chest pain

- Severe, crushing, and squeezing pressure

- May radiate

- Unrelieved w/nitrates

~ Pale & diaphoretic

~ Dyspnea & tachypnea

~ Syncope

~ Nausea & vomiting

~ Dysrhythmias

1. Severe, crushing, and squeezing pressure
2. May radiate
3. Unrelieved w/nitrates

• Signs & symptoms- often atypical symptoms in women
• 12 lead:

- ST elevation followed by Q wave (Q wave myocardial infarction)

- ST depression (non-Q-wave myocardial infarction)

• Elevated cardiac enzymes

- CPK-MB

• Elevated serum troponin I/T, myoglobin

A. Q waves

• Maintain cardiac output
• Treat pain
• Assess for complications
• Increase activity tolerance
• Relieve anxiety
• Ongoing & discharge teaching

• Dysrhythmias
• Sudden death
• Congestive heart failure, cardiogenic shock
• Ventricular aneurysm or rupture
• Papillary muscle dysfunction
• Pericarditis

* Pain relief: morphine, nitroglycerin

* Oxygen

* Drugs affecting platelets- ASA glycoprotein IIb/IIIa inhibitors

* Beta-blockers

* Nitrates

* ACE inhibitors

* Antidysrhythmics

• Get pt. to catheterization lab for emergent percutaneous intervention or stenting if facilities are available
• Better outcomes than thrombolytics

• Time is muscle; 6hr window
• Several thrombolytic agents available, such as:
• Tissue plasminogen activator (t-PA)
• Streptokinase
• Retaplase
• Heparin & glycoprotein IIb/IIIa inhibitors

* Variety of procedures

- Percutaneous transluminal coronary angioplasty (PTCA)

- Intracoronary stenting

* Drug-eluting stents

To increase blood flow to myocardium

• Uncompromised collateral flow
• Noncalcified lesions
• Lesions not on bifurcations of vessels

* Balloon catheter is inflated

1. Tubes placed in conjunction w/angioplasty to keep vessel patent
2. Help prevent the restenosis associated w/angioplasty
3. Similar procedure as PTCA
4. Anticoagulation therapy

* Excimer laser angioplasty

- Xenon chloride laser

* Radiation therapy

- Beta or gamma radiation

• Coronary artery graft (CABG) surgery
• Minimally invasive direct coronary artery bypass (MIDCAB) surgery
• Transmyocardial revascularization (TMR)

• Provides additional conduits for blood flow
  • Saphenous vein
  • Internal mammary artery
  • Radial artery
• Arteries longer patency

1. Unstable angina
2. AMI
3. Failure of percutaneous interventions

~ Increased mortality associated with:

1. Left ventricle dysfunction
2. Emergency surgery
3. Age
4. Sex (female)
5. Number of diseased vessels
6. Decreased ejection fraction w/congestive heart failure

• Median sternotomy or sternum split
• Excision of pericardium
• Cardiopulmonary bypass
• Myocardial preservation or cardioplegia
• Grafts
• Wean bypass; defibrillate if needed
• Mediastinal and chest tubes
• Epicardial pacing wires
• Wire sternum

1. Increases blood flow to myocardium
2. Relieve symptoms
3. Prolong survival
4. Improve quality of life

• Cardiopulmonary bypass
• Incisions (ports)

• No cardiopulmonary bypass
• Heart still beating
• One or two bypasses

* Heart stays beating

• Low cardiac output
  • Renal impairment
  • Gastrointestinal dysfunction
  • Impaired peripheral circulation
• Mediastinal bleeding
  • Infection: very serious if sternal
• Atrial dysrhythmias
• Hypovolemia

1. Dysrhythmias
2. Impaired contractility; low cardiac output
3. Intraoperative myocardial infarction
4. Pericardial tamponade
5. Respiratory insufficiency
6. Pain
7. Emboli; stroke
8. Death

Fluid, pus, blood, clots, or gas accumulates in the pericardium (the sac in which the heart is enclosed), resulting in slow or rapid compression of the heart.

• Laser channels into ventricle
• Goal is to increase perfusion of heart muscle
• Relief of symptoms occurs over time
• Poor candidates for CABG Mixed results from clinical trials

• Radiofrequency catheter ablation
• Permanent pacemakers
• Implantable cardioverter-defibrillator

• Supraventricular tachycardia
• Interrupt electrical conduction or activity
• Radiofrequency used
• Electrophysiology

• Used to treat survivors of sudden cardiac arrest
• Some have built-in pacemakers
• Delivers high-energy shock
• Patient education
• Emergency procedures

• Inability to generate adequate flow
• Systolic (impaired contractility)
• Diastolic (Impaired filling)

• AMI
• Hypertension
• Idiopathic; cardiomyopathy
• Valvular disease

1. Decreased pumping action
2. Back-up of blood from left ventricle
3. Fluid build-up in lungs
4. Backflow leads to right heart failure
5. Fail to meet metabolic demands
6. Compensatory mechanisms

* Renin-angiotensin- aldosterone system

* Sympathetic nervous system

7. Right heart failure

* Leads to system symptoms

Improve pump function

• Diuretics
• ACE inhibitors/angiotensin receptor blockers
• Digoxin
• Beta-blockers (carvedilol [Coreg])
• BNP- nesiritide citrate (Natrecor)

• Intraaortic balloon pump
  Ventricular assist device
• Biventricular pacing
• Nursing interventions

• Airway
• Diuresis
• VTE prophylaxis
• Control sodium & fluid retention

Pulmonary edema

• Dyspnea
• Cyanosis
• Gurgles
• Pink, frothy sputum
• Hypoxemia

Cardiogenic shock

• Pericarditis- inflammation of the pericardium
• Endocarditis- inflammation of the endocardium

• After myocardial infarction
• Uremia
• Cancers

Can lead to infusion, tamponade, and scarring

• Friction rub
• Pulsus paradoxus
• Initial ST elevation

- Pericardiocentesis
- Pericardial window

• Endocardium continuous w/valves
• Vegetation
• Embolization
• Valvular dysfunction

1. Echocardiogram
2. Transesophageal
3. Echocardiography

Antibiotics & rest

Antibiotic prescription before treatments (e.g., dentist)

- Heart valve

- History of endocarditis

- Microvascular pressure w/regurgitation

• Dilation or thinning of wall
• Thoracic aortic
• Thoracoabdominal aortic
• Abdominal aortic
• Treat based on size & symptoms
• False versus true

1. Tear of intimal layer of the vessel
2. Sudden
3. Sharp
4. Shifting pain
5. Marfan syndrome

• Long arms, legs and fingers
• Tall and thin body type
• Curved spine
• Chest sinks in or sticks out
• Flexible joints
• Flat feet
• Crowded teeth
• Stretch marks on the skin that are not related to weight gain or loss

Marfan syndrome is a genetic disorder that affects the body’s connective tissue. Connective tissue holds all the body’s cells, organs and tissue together.

• Open approach
• Endovascular approach