CARDIOVASCULAR DISORDERS STUDY GUIDE
CARDIAC HEMODYNAMICS
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Hemodynamics = is concerned with the forces generated by the heart and the resulting motion of blood through the cardiovascular system
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Resistance = arterioles resistance to ventricular contraction and ejection of blood
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TPR = total peripheral resistance throughout vascular system
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TPR = SVR
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SVR = systemic vascular resistance peripheral to heart and lungs  Arterioles elasticity, diameter of vessels
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Factors that INCREASE SVR  HTN, increases work of heart to eject blood, CO
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Factors that DECREASE SVR  Shock
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Pulse pressure = the difference between SBP & DBP. It is normally about 1/3 of SBP
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INCREASED pulse pressure  during exercise or in individuals with atherosclerosis of the larger arteries as the result of
increased SBP
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Widening pulse pressure is also a sign of increased intracranial pressure.
•
DECREASED pulse pressure  heart failure or hypovolemia
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MAP = CO X SVR = DBP + ((SBP – DBP)/3) = [(2 X DBP) + SBP] / 3]
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MAP is the perfusion pressure seen by organs in the body
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MAP > 60 mm Hg is enough to sustain the organs in the body
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If the MAP is < 60 mm Hg, then the organs are not being adequately perfused & become ischemic, might lead to shock
DEFINITION OF TERMS
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Cardiac output = amount of blood pumped by the ventricle in liters per minute
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Cardiac Output = Stroke Volume X HR
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Normal CO = 5-6 L/min
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Stroke volume = the amount of blood ejected from one ventricle in one contraction; varies with SNS and venous return
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Stroke Volume is determined by Preload, Contractility, and Afterload
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Preload = degree of stretch of the cardiac muscle fibers at the end of diastole
•
Volume returned to heart (Venous Return) creates Preload
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GOOD PRELOAD = GOOD CONTRACTILITY
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Contractility = ability of the cardiac muscle to shorten in response to an electrical impulse
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Afterload = resistance the blood in the ventricle must overcome to force the valves open & eject contents to circulation.
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The force against which the ventricle must eject blood.
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It is determined by PVR or SVR.
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The resistance normally maintained by 1) aortic & pulmonic valves, 2) the condition & tone of aorta, 3) the resistance
offered by systemic & pulmonary arterioles
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Ejection fraction = the percent of end-diastolic volume ejected with each heartbeat
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Low EF  not able to eject adequate amount of blood, may indicate heart failure
FACTORS AFFECTING PRELOAD
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Increased CVP that can result from decreased venous compliance
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Caused by:
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SNS activation of venous smooth muscle
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•
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Increased thoracic blood volume (increased total volume or by venous return augmented by increased respiratory activity, increased skeletal muscle pump activity, or by effects
gravity, e.g. head-down tilt)
Increased atrial force of contraction
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Increased filling of the atria and therefore increased atrial contractile force through the Frank-Staling mechanism.
Increased aortic pressure
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Increases the afterload on the ventricle
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Reduces SV by increasing ESV (End systolic volume), and leads to a secondary increase in ventricular preload
CVP = central venous pressure; pressure of blood in the thoracic aortic near the RA.
- Ventricular systolic failure and valve defects such aortic stenosis, and aortic regurgitation.
- Pulmonary valve stenosis and regurgitation have similar effects on RV preload
-NORMAL CVP = 2 – 8 mmHg
-INCREASE CVP  Indicates HYPERvolemia
-DECREASE CVP  Indicates HYPOvolemia
FRANK STARLING’S LAW OF THE HEART
• Preload = Stretch of ventricular wall. Usually related to volume.
• Frank Starling Law = Increased preload → greater shortening of muscle fibers → increase contractility  increased cardiac output
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When venous return (VR) is increased, there is increased filling of the ventricle leading to an increase in left ventricular end-diastolic volume (LVEDV) that increases left ventricular enddiastolic pressure (LVEDP).
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If the ventricle now contracts at this increased preload, the ventricle empties, thereby increasing its stroke volume & CO.
***ADEQUATE VENOUS RETURN  INCREASE PRELOAD  GREATER SHORTENING OF MUSCLE FIBERS  INCREASE CONTRACTILITY  INCREASE SV  INCREASE CO***
CONGESTIVE HEART FAILURE
Left-Sided Heart Failure (Congestive heart failure)
[L = Lung symptoms]
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Most common form
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Results from left ventricular dysfunction
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Blood backs up into left atrium and pulmonary veins
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 left ventricular end diastolic pressure (LVEDP) & Lt atrial pressure
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 pulmonary pressure causes fluid leakage →→ pulmonary congestion and edema (Lung Crackles)
o S/S:

Orthopnea; DOE; Cough; Crackles

Tachycardia

Confusion

Paroxysmal nocturnal dyspnea (PND)  acute SOB while sleeping due to circulatory
inadequacy and fluid overload

Fatigue

S3 gallop; Mitral Murmur

Diaphoresis

Oliguria
Right-Sided Heart Failure (Cor pulmonale)
[R = Rest of the body symptoms]
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Most commonly caused by left-sided HF
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Right ventricular dysfunction
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Blood backs up into the right atrium and venous circulation
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Increased right ventricular end diastolic pressure (RVEDP) & Rt atrial pressure
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Vascular congestion of GI tract
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Cor pulmonale/ right sided heart failure cause peripheral edema:
o Heart failure → backflow of blood → Increase capillary hydrostatic pressure.
o When capillary hydrostatic pressure exceeds hydrostatic pressure in the interstitial space → fluid moves from capillaries to the cells and tissues causing edema.
•
•
In Heart Failure, assess fluid status
o S/S:

Peripheral edema; Ascites; Weight gain

Hepatomegaly; splenomegaly

Right Upper Quadrant Pain

Tricuspid Murmur

Nausea; Anorexia

Elevated Right Atrial pressure

Elevated Central Venous pressure

Jugular vein distention
Clinical Manifestations and Diagnosis
o Paroxysmal nocturnal dyspnea (PND) usually occurs at night due to HF

The PND may be caused by increased venous return when the pt is lying in bed
o Orthopnea  SOB when lying flat, this is different from PND
o Diagnostics  BNP

B-type Natriuretic Peptide (BNP) found in cardiac ventricle in response to ↑ fluid; secreted by ventricles, increases in CHF
PAROXYSMAL NOCTURNAL DYSPNEA AND ORTHOPNEA
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Paroxysmal nocturnal dyspnea (PND) usually occurs at night due to HF
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The PND may be caused by increased venous return when the pt is lying in bed.
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The sudden awakening of the patient, after a couple of hours of sleep, with a feeling of severe anxiety, breathlessness, and suffocation.
o The patient may bolt upright in bed and gasp for breath.
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Bronchospasm increases ventilatory difficulty & the work of breathing
o Is a common complicating factor of paroxysmal nocturnal dyspnea.
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In contrast to orthopnea (SOB when lying flat), which may be relieved by immediately sitting up in bed, PND may require 30 min or longer in this position for relief.
o Episodes may be so frightening that the patient may be afraid to resume sleeping, even after the symptoms have subsided.
ACUTE DECOMPENSATED HEART FAILURE (ADHF)
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Heart failure is a chronic, progressive condition in which the heart muscle is unable to pump enough blood through to meet the body's needs for blood & O2.
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Clinical Manifestations:
o Early  increased pulmonary venous pressure; Increase RR; Decrease in PaO2
o Later  interstitial edema, Tachypnea
o Further progression  alveolar edema; Can manifest as pulmonary edema
o Life-threatening situation  alveoli fill with fluid; Most commonly associated with left-sided HF

SOB, orthopnea, & edema are EARLY S/S of CHF

Frothy-blood tinged sputum is a late sign of CHF and a sign of Pulmonary Edema
PULMONARY EDEMA
DRUG THERAPY FOR HF
• Diuretics  Decrease volume overload (preload)
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Furosemide (Lasix), Bumetanide (Bumex); Torsemide (Demadex)
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After IV injection of furosemide, diuresis normally begins in about 5 minutes & reaches its peak w/in about 30 minutes
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Med effects last 2 - 4 hours
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Teach patient to take diuretics in A.M. with breakfast due to nocturia
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Make sure to check electrolytes
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When administering a diuretic (e.g. Bumetanide) expected outcomes include:
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Increased urine output
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Decreased crackles
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Decreased weight
• Ace inhibitors (PRILs)  Considered first line therapy for CHF
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ACEI have become the vasodilators of choice in patient w/ mild to severe HF
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ACEIs work by allowing more blood to flow to the heart which decreases the workload of the heart & allows the kidneys to secrete sodium
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Some pts can develop a nagging cough with ACEIs
• Vasodilators  Reduce circulating blood volume & improve coronary artery circulation
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Vasodilator meds are the only class of drugs clearly shown to improve survival in overt CHF
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IV nitroglycerin; Sodium nitroprusside
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Nipride used in hypertensive crisis
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Nitroglycerin transdermal patches
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Nitroglycerin is a coronary vasodilator used for coronary artery disease.
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Pt should apply a new patch each morning & leave it in place for 12 to 14 hours in accordance with health care provider directions.
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This prevents pt from developing tolerance (as happens with 24-hour use).
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The pt does not need to wait to apply a new patch if it falls off because the medication is released continuously in small amounts through the skin.
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The pt should avoid placing the patch in skin folds or excoriated areas.
• Morphine  Reduces preload & afterload
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Morphine is a vasodilator; it decreases BP
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Morphine sulfate reduces anxiety & dyspnea in pts with pulmonary edema
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It also promotes peripheral vasodilation & causes blood to pool in the periphery.
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It decreases pulmonary capillary pressure, which reduces fluid migration into the alveoli.
• Positive inotropes  Inotropic agents are administered to increase the force of the heart's contractions, thereby increasing ventricular contractility & ultimately increasing cardiac output. They
maximize cardiac performance in pts with heart failure by increasing ventricular contractibility.
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β-adrenergic agonists  Dopamine (Intropin)
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 BP, CO & U/O; dose dependent
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Dobutamine (Dobutrex)
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Increase CO
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Phosphodiesterase inhibitors  Milrinone (Primacor)
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Digitalis (Digoxin; Lanoxin)
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POSITIVE inotropic effect as it increases myocardial contraction.
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NEGATIVE chronotropic effect by decreasing the heart rate.
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Indications  Digoxin is indicated to treat CHF and Atrial Fibrillation
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The normal therapeutic range for digoxin is 0.5 to 2 ng/mL (ignore other # values in Saunders or other references and use 0.5-2 for testing purposes)
DIGITALIS (DIGOXIN, LANOXIN)
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Mechanism of Action:
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Increases the force of myocardial contraction
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POSITIVE inotropic action  improves cardiac contractility
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NEGATIVE chronotropic effect  decreases HR
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Increases cardiac output, consequently, increases U/O
Indications: Digoxin is indicated to treat CHF and atrial fibrillation
Normal Therapeutic Range: 0.5 – 2 ng/mL, toxic range is > 2.0 ng/mL
Toxicity:
o The most common early manifestations of digoxin toxicity are:

Gastrointestinal disturbances

Anorexia, nausea, vomiting, diarrhea, abdominal pain

Neurological disturbances

Restlessness, fatigue, headache, weakness, drowsiness, confusion, and nightmares

Visual disturbances

Blurred vision, diplopia “double vision”, photophobia, light flashes, green & yellow halos around bright objects/light

Yellow or green color perception also may occur, seeing spots or halos

Cardiac dysrhythmias bradycardia and other cardiac dysrhythmias

Decreased libido, and impotence
o Toxic levels  When digoxin overdose is suspected, as it would be with a digoxin level of > 2 ng/mL, Fab antibody fragments bind digoxin and prevent it from acting

Antidote = Digibind (Immune Fab)

Hypokalemia and hypomagnesemia potentiate Digoxin toxicity
Nursing considerations:
o Pt teaching should include taking the dose exactly as prescribed each day. If pt misses a dose & more than 12 hours goes by, that dose should be omitted, and only the next scheduled dose
should be taken; the patient should not double dose
o The provider should be consulted before changing brands because the bioavailability of another preparation of the medication may be different
o A daily pulse check is necessary, and the pt should know the parameters for which the HCP should be called
o Clients are advised not to mix digoxin in pill boxes with other medications
o Adjust dose in Renal Failure because Digoxin is excreted by the kidneys
o Check pulse (preferably apical pulse) for one full minute before giving Digoxin
o Hold Digoxin if apical HR < 60 beats /min  Teach pt how to check radial pulse
o When given for CHF, clear lung sounds indicate effectiveness of the medication & the heart failure is being well controlled by the medication (Digoxin).
CIRCULATORY ASSIST DEVICES (CADs)
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Decrease cardiac workload and improve organ perfusion when drug therapy fails
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Provide interim support when  Recovering from acute injury; Stabilizing before surgical repair; or Awaiting cardiac transplant
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Intraaortic Balloon Pump (IABP)
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The most common CAD
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Used in CHF for augmentation (↑) of myocardial blood flow and (↓) the Afterload to enhance coronary artery perfusion during the
diastolic phase of the cardiac cycle.
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Benefits: ↓ventricular workload; ↑myocardial perfusion; Augment circulation; Temporary use only
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Balloon inserted into femoral artery & placed in thoracic aorta. Confirm placement with x-ray
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Inflate balloon with helium in conjunction with ECG
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Complications of IABP therapy
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Vascular injuries
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Thrombus & embolus formation
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Thrombocytopenia
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Peripheral nerve damage
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Ischemia to periphery, kidneys, bowel
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Infection
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Balloon leak
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Malfunction of balloon
CARDIOGENIC SHOCK
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A potential complication of CHF
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Actual heart muscle is unhealthy, and pumping is directly impaired.
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The heart cannot pump sufficient blood to the entire body.
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It commonly occurs due to damage to the Lt ventricle
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Myocardial infarction is the most common cause of direct pump failure.
TREATMENT OF CARDIOGENIC SHOCK
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Oxygen
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Cardiac Monitor
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Pulse Oximeter
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IV Access
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Mobility restricted
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Pedal pulses
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Cardiac Glycoside
o Digitalis: Digoxin (Lanoxin)  exerts a positive inotropic effect on the heart
while slowing the overall rate

Antidote is Immune fab (Digibind)
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-Adrenergic agonists
o
o
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Norepinephrine (Levophed)
Dobutamine (Dobutrex)

Beta 1 agonist, used for short term treatment of HF to increase CO
Dopamine (Intropin)
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Nursing consideration: The client who is receiving dopamine
therapy should be assessed for peripheral vasoconstriction related
to the action of the medication.
INEFFECTIVE ENDOCARDITIS (IE) “ACUTE BACTERIAL ENDOCARDITIS
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Bacterial Infection of inner layer of heart, including the valves
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Occurs in elderly, persons with prosthetic heart valve, injection drug users, & post dental work
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S/S:
o Spiking fever and chills are the most common S/S
o Malaise, fatigue
o Weight loss
o Myalgia
o Profound hypotension
o Conjunctiva petechiae  Roth spots in the eye; retinal hemorrhages with white centers
o Osler's nodes  Tender red lesions as raised papules on hands & feet and palms “fingertips & toes”
o Janeway's lesions  Non-tender flat macular red lesions on palms of the hands & soles of the feet
o Splinter hemorrhages in the fingernails
o Pts with infective endocarditis are at risk for developing STROKE following CNS embolization of the
bacterial vegetation of the affected valve
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Treatment:
o Antibiotic treatment (mainly IV) has improved the prognosis
o Teach pt to take full course and report endocarditis Hx to dentists & providers before any invasive
procedure
PERICARDITIS
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Acute Pericarditis = Acute inflammation of the pericardium
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Causes: Unknown, commonly caused by infection, uremia, neoplasm, MI, surgery or trauma
o Membranes become inflamed and roughened, & exudate may develop
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S/S:
o Sudden onset of severe chest pain that becomes worse with resp. movements and with lying down  Generally
felt in the anterior chest, but pain may radiate to the back

Friction rubs upon auscultation  Sandpaper sound may be heard at cardiac apex & left sternal
border and is diagnostic for pericarditis (but may be intermittent)
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Treatment: Tx symptoms; Look for underlying cause
o Teach pt to stop all antiplatelet & anticoagulant medications
o If pericardial effusion develops, aspirate excess fluid (pericardiocentesis = pericardial tap)
PERICARDIAL EFFUSION
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Accumulation of fluid in the pericardial sac (cavity) which may cause cardiac tamponade
o May be Transudate  extravascular fluid that is low in protein
o Exudate  extravascular fluid seen in inflammation
o Hemorrhagic  when blood leaks into and fills the pericardial sac
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Not clinically significant other than to indicate underlying disorder, unless - Pressure becomes sufficient to cause cardiac
compression
o Cardiac tamponade that ↓ cardiac output  circulatory collapse
o Cardiac Tamponade = pressure on the heart that occurs when blood or fluid builds up in the space between the
heart muscle (myocardium) and the outer covering sac of the heart (pericardium). Blood rapidly collects in
pericardial sac, compresses myocardium because the pericardium does not stretch & prevents ventricles from
filling.
CARDIAC TAMPONADE
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S/S:
o 7 D’s:

Distant (Muffled) heart sounds

Distended jugular veins  INCREASED central venous pressure (CVP)

Decreased BP

Decreased CO

Dyspnea on exertion (DOE)

Dull chest pain

Decreased ECG waveform amplitude
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Other Clinical Manifestations:
o Pulsus paradoxus – Systolic B.P. higher during expiration than inspiration by > 10 mm Hg
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During inspiration intra-thoracic pressure , resulting in an  in venous return.

The subsequent  in blood volume in the right atrium & ventricle causes the intraventricular septum to
bulge into the left ventricle, blocking cardiac output & BP.
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
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Thus SBP  > 10 mm Hg during inspiration.
The right atrium/ventricle cannot bulge outwards (as is normal in response to increased blood flow during inspiration) due to the stiff and/or blood-filled pericardium.
Pericardial effusion can cause cardiac tamponade, but cardiac tamponade does not cause pericardial effusion. Cardiac tamponade can be seen by x-ray or ultrasound
Tx:
o
1) Emergent pericardiocentesis; 2) Tx pain; 3) Surgical repair if cause is aneurysm or trauma

Following pericardiocentesis, the pt usually expresses immediate relief. Heart sounds are no longer muffled or distant & BP increases.

Surgery if cause is aneurysm or trauma.
VALVULAR HEART DISEASE

Heart consists of:
o Two ATRIOVENTRICULAR valves  Mitral & Tricuspid
o Two SEMILUNAR valves  Aortic & Pulmonic

Although all 4 heart valves may be affected, mitral and aortic valves are far more commonly affected than those of the right heart (tricuspid and pulmonic valves).

Types of valvular heart disease depend on:

Valve(s) affected

Type of functional alteration(s)

Stenosis = constriction/narrowing

Valve orifice is smaller

Forward blood flow is impeded

Pressure differences reflect degree of stenosis

Regurgitation = incompetence/insufficiency

Incomplete closure of valve leaflets

“too leaky”

Results in backward flow of blood

Heart Murmur = sound caused by turbulent blood flow through damaged valves.
AORTIC STENOSIS

Develops gradually

Decreased stroke volume

Reduced SBP

Narrowed pulse pressure

Heart rate often slow and pulse faint

Heart murmur

Angina

Dizziness, syncope, fatigue

Can lead to dysrhythmias, MI, and left HF
MITRAL STENOSIS

Results in hypertrophy of LA

Pulmonary congestion → right heart failure

Atrial enlargement can be seen on x-ray
AORTIC REGURGITATION

Reflux of blood from aorta to LV during ventricular relaxation

Widened pulse pressure
MITRAL REGURGITATION

Loud murmur that radiates into the back and axilla

Causes blood to flow simultaneously to the aorta and back to the left atrium (LA)

LV hypertrophy and dilation as compensation
o ↓CO  Heart failure
o Right heart failure
o Edema
o Shock
GENERAL TREATMENT FOR VALVE DISORDERS

Antibiotics for Streptococcal infection

Anti-inflammatories for autoimmune disorder

Analgesics for pain

Restrict physical activity

Valve replacement surgery
DILATED CARDIOMYOPATHY = CONGESTIVE CARDIOMYOPATHY

Cardiomyopathy = Disorders of the heart muscle (myocardium) & valves of the heart; weakening of the heart muscle or change in
the muscle structure due to inadequate pumping
o Heart loses effectiveness as a pump. Results in thickening of myocardial fibers
o Severe dilation of heart chambers without heart valve abnormalities
o The heart has a globular shape (large flabby) & the largest circumference of the LV is not at its base but midway
between the apex and base
o LV is modestly thickened, inadequate contraction
o ↓ C.O., ↓ perfusion to organs, ↑ thrombi formation; ↓ contractility, mitral valve incompetence, arrhythmias
o Treatment: relieve symptoms of HF, ↓ workload, diuretics, beta blockers, ACEI, ARBs, Digoxin, anticoagulants;
Circulatory Assist Devices (CADs), transplants
ANEURYSMS

Outpouching of vessel wall

Atherosclerosis plaque  eroded vessel wall

Emergency
ABDOMINAL AORTIC ANEURYSM (AAA)

Causes: Degenerative; Congenital; Mechanical (Penetrating or blunt trauma); Inflammatory; Infectious
o Most common cause of descending AAA is atherosclerosis
AORTIC ANEURYSM MANIFESTATIONS

Thoracic aorta aneurysms  Often asymptomatic
o S/S:

Deep diffuse chest pain

Pain may extend to the interscapular area

Abdominal Aortic Aneurysm (AAA)  Often asymptomatic
o S/S:

A pulsatile mass in the periumbilical area slightly to the left of the midline may be present

Bruits may be auscultated over the aneurysm

A systolic bruit over the abdomen is a diagnostic indication of an AAA

Rupture  serious complication

Rupture into retroperitoneal space manifested by flank pain and hypotension
o Complications:

Rupture of thinned vessel walls → Massive internal hemorrhage → Flank pain and
hypotension

AAA maybe asymptomatic until it expands/ruptures when pt develops back (flank) pain,
decreased BP and potential abdominal pain due to rupture

Severe back pain

Rupture into thoracic or abdominal cavity  Massive hemorrhage; Most do not survive long enough to get to the hospital

Hypovolemic shock

In this case, simultaneous resuscitation & immediate surgical repair are necessary

AAA pts are at high risk for renal failure because of the anatomical location of the AAA near the renal arteries

Monitor Urine Output
HEMODYNAMIC MONITORING
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Purpose:

Early detection, identification, & Tx of life-threatening conditions such as CHF & cardiac tamponade.

Evaluate the patient's immediate response to treatment such as drugs and mechanical support.

Evaluate the effectiveness of cardiovascular function such as cardiac output, and cardiac index.
•
Indications:

Decreased cardiac output

Shock states, bleeding, cardiac pump failure
FUNCTIONS OF PULMONARY ARTERY CATHETER (SWANGANZ CATHETER)

Allows for continuous bedside monitoring of the following:
o Vascular tone, myocardial contractility, and fluid balance can be correctly assessed and managed
o Measures Pulmonary Artery Wedge Pressure (PAWP), CVP, and allows for hemodynamic calculated values
o Measures Cardiac Output (Thermodilution)
o Fluid administration
ARTERIAL LINE

Line is used to continuously monitor BP and MAP

Also used to draw blood for arterial blood gases (ABGs)
HEMODYNAMIC PARAMETERS
Right atrium P (CVP)
2- 8 mm Hg
Right Ventricle P
40 (sys) / 9 (end diastolic)
Cardiac Output (CO)
4-8 L/min
Pulmonary Artery Wedge Pressure (PAWP)
8-12 mm Hg
Cardiac index
CO/BSA 2.2- 4.2 L/min/m2
Ejection Fraction (EF)
55- 70%
Stroke Volume
55- 100 mL/beat
CARDIAC DYSRHYTHMIAS = CARDIAC ARRHYTHMIA

Dysrhythmia: Disorder of impulse formation, conduction of impulses, or both

SA node normal pacemaker of heart (60–100 beats/minute)

Secondary pacemakers
o AV node (40–60 beats/minute)
o His-Purkinje fibers (20–40 beats/minute)

Indications of obtaining an ECG:
o Monitor a patient's heart rate
o Evaluate effects of disease/injury on heart function
o Evaluate the function of the heart pacemaker
o Evaluate response to meds (e.g., antiarrhythmics)
o Obtain a baseline recording before, during, and after a medical procedure
NORMAL ECG
HESI Hint:

T wave represents REPOLARIZATION of the ventricle, so this is a critical time in the heartbeat.

This action represents a RESTING and regrouping stage so that the next heartbeat can occur.

If defibrillation (electric shock) occurs during this phase, the heart can be thrust into a life-threatening dysrhythmia
o Therefore, avoid giving the defibrillation on the T wave by turning OFF the Synchronized (Synch) button on the defibrillator machine.
o Turn ON the Synch button ONLY in Cardioversion

P wave  represents time for the passage of the electrical impulse through the atrium causing atrial depolarization (contraction).

P-R interval  measured from the beginning of the P wave to the beginning of the QRS complex. It represents the time taken for the
impulse to spread through the atria, AV node, and bundle of His; the bundle branches; and Purkinje fibers to a point immediately preceding
ventricular contraction.

QRS complex  consists of three distinct waves. The Q wave is the first negative (downward) deflection after the P wave, short and
narrow, and not present in several leads. The R wave is the first positive (upward) deflection in the QRS complex, and the S wave is the first
negative (downward) deflection after the R wave. The QRS interval is measured from the beginning to the end of the QRS complex. It
represents the time taken for depolarization (contraction) of both ventricles (systole).

ST segment  measured from the S wave of the QRS complex to the beginning of the T wave. It represents the time between ventricular
depolarization and repolarization (diastole). It should be isoelectric (flat).

T wave  represents the time for ventricular repolarization. It should be upright.

Q-T interval  measured from the beginning of the QRS complex to the end of the T wave. It represents the time taken for entire electrical
depolarization and repolarization of the ventricles.
TELEMETRY MONITORING

Observation of HR and rhythm at a distant site
o Centralized monitoring system
o Remote
o Portable Holter monitor
o Advanced alarm system

First Nursing Action when Monitor is not reading?
o ALWAYS assess the patient NOT the machine
HESI Hint: NCLEX questions are likely to relate to early recognition of abnormalities and associated nursing actions
LIMB LEAD PLACEMENT

How to remember limb lead placement:
o White on the right (RA)
o Smoke over fire (black over red)
o Clouds over grass (white over green)

On R arm, L arm and L leg or on the chest at least 10 cm away from the heart
CHEST LEADS
Leads
Ventricular Region
V1-V2
Anteroseptal
V3-V4
Anteroapical
V5-V6
Anterolateral
ECG PAPER: STRIP VS. 12-LEAD

Strip: Graphic tracing of electrical impulses produced by heart

12-Lead ECG: The standard ECG is the 12-lead ECG, which uses 10 electrodes (4 limb leads + 6 chest leads).
ECG TIME AND VOLTAGE

Each segment between the dark lines (above the monitor strip) represents 3 seconds when the monitor is set at a speed of 25
mm/sec.
o Vertical – Voltage
o Horizontal – Time
METHODS TO CALCULATE HR

6 Second Interval x 10 Method
o Number of QRS complexes in 1 minute
o R-R intervals in 6 seconds interval, and multiply by 10

1500 Method
o Number of small squares between one R-R interval, and divide 1500 by this number
o [1500 small squares = 1 minute]

300 Method
o Number of large squares between one R-R interval, and divide 300 by this number
6 SECOND INTERVAL X 10 METHOD
o Number of QRS complexes in 1 minute
o R-R intervals in 6 seconds interval, and multiply by 10
1500 METHOD
o Most accurate method
o 1500 small squares = 1 minute
o Count number of small squares between 2 consecutive R waves
o Divide 1500 by that number
300 Method
o Count the number of large squares between one R-R interval, and divide 300 by this number
REGULARITY

Regular Rhythm
o Consistent times between
o Consecutive P waves: P-P interval

(Regular Atrial Rhythm)
o Consecutive R waves: R-R interval

(Regular Ventricular Rhythm)

Determining Regularity
o Using Calipers
o Paper and Pen Method
PATIENT PREPARATION

Clip excessive hair on chest wall

Rub skin with dry gauze

May need to use alcohol for oily skin

Apply electrode pad

Telemetry Monitoring:
o Observation of HR and rhythm at a distant site. 2 types

Centralized monitoring system

Advanced alarm system alerts when it detects dysrhythmias, ischemia, or infarction
ASSESSMENT OF CARDIAC RHYTHM
P wave
Atrial rate and rhythm
P-R interval
Ventricular rate and rhythm
QRS complex
ST segment
Q-T interval
T wave
ECG RHYTHM ANALYSIS
1. Determine heart rate
2. Determine heart rhythm
3. Analyze P waves
4. Measure PR interval
5. Measure QRS duration
6. Interpret rhythm
7. Assess & Treat the patient, not the monitor (Machine)!
P WAVES, QRS COMPLEX

Normal QRS Complex: Duration: 0.04 to 0.12 seconds

Q Wave: Duration: < 0.04 seconds

R Wave: First positive deflection in the QRS

S Wave: The first negative deflection that extends below the baseline after the R wave
PR INTERVAL

Normal PR Interval
o Location: Starts at the beginning of the P wave and ends at the beginning of the Q wave (or R wave if Q is absent)
o Duration: 0.12 – 0.20 seconds

Prolonged in atrioventricular (AV) Block
o Morphology:

P wave followed by a flat line
QT INTERVAL

Normal QT Interval
o Beginning of QRS complex to end of T wave
o Represents ventricular depolarization and repolarization
o Normal range: 0.36 to 0.44 seconds

Prolonged QT effects
o Predisposed to potentially lethal arrhythmia (Torsade De Pointe), a polymorphic ventricular tachycardia, treated by Magnesium Sulfate.

Shortened QT Causes
o
o
Digitalis (therapeutic doses)
Hypercalcemia
NORMAL SINUS RHYTHM

Rate: 60-100 beats/min (SA node fires 60–100 beats/minute; follows normal conduction pattern)

Rhythm: Regular

P waves: Present, consistent configuration, one P wave before each QRS complex

PR interval: 0.12-0.20 second and constant

QRS duration: 0.04-0.12 second and constant
SINUS BRADYCARDIA

Rate: < 60 bpm

Regularity: regular

P waves: normal, followed by QRS

QRS: normal

PR interval: within normal range

QT interval: within normal range

Causes:
o Normal rhythm in aerobically trained athletes and SB is normal during sleep
o Can occur in response to excessive parasympathetic nerve stimulation & certain drugs & Decreased sympathetic stimulation
o Also associated with some disease states, e.g. Myocardial Infarction

Manifestations: Hypotension; Pale, cool skin; Weakness; Angina; Dizziness or syncope; Confusion or disorientation; SOB

Treatment:
o Atropine (INCREASES HR)
o Pacemaker especially if symptomatic SB (Hypotension, low cardiac output, etc)
o Stop offending drugs
o Avoid Valsalva maneuver (straining with bowel movement)
SINUS TACHYCARDIA

Rate: 100 – 160 bpm

Regularity: Regular

P waves: Normal, followed by normal QRS

PR interval: Within normal range

Etiology: Caused by vagal inhibition or sympathetic stimulation

External influences: Caffeine; Alcohol; Smoking

Internal influences: Fever; Hypovolemia; Hyperthyroidism; Anemia

Manifestations: Dizziness; Dyspnea; Hypotension; Angina in pts with CAD

Treatment: Guided by cause (e.g., treat pain)
o Vagal maneuver; β-adrenergic blockers
ATRIAL FIBRILLATION

Key Characteristics: Atrial rate > 350, atria quiver instead of contract, AV conducts impulses only sporadic & irregularly.
o Totally irregular rhythm
o No discernable P-wave, Fibrillatory waves may mimic P waves leading to misdiagnosis

Atrial quiver ↑ risk of thrombi  Can lead to HF, angina, or syncope. Paroxysmal or persistent

Causes: UNKNOWN

Treatment:
o The rapid and irregular ventricular rate  ventricular filling &  cardiac output, further impairing the heart's perfusion ability. Therefore, give
O2 & metoprolol (to slow the ventricular response)
o An ECG helps to assess heart valve function because mitral valve disease can lead to A-Fib.
o
o



Drugs to control ventricular rate and/or convert to sinus rhythm (amiodarone).
The rapid heart rate in Atrial Fibrillation [and in SVT] can be decreased by carotid sinus massage

Carotid sinus massage is one maneuver used for vagal stimulation to  a rapid heart rate & possibly terminate a tachydysrhythmia.

Others include inducing the gag reflex & asking the pt to strain or bear down.
Decrease in CO, increased risk of stroke; PE; & VTE
Pts with uncontrolled A-Fib with a ventricular rate >100 beats/minute is at risk for low CO
Assess pt for palpitations, chest pain or discomfort, hypotension, pulse deficit, fatigue, weakness, dizziness, syncope, shortness of breath, distended neck
veins
POTASSIUM

Hypokalemia can cause prominent U wave after a T wave on the ECG
o Also, shallow, flat, or inverted T waves, ST segment depression

Hyperkalemia can cause tall, peaked, or tented T waves on the ECG
NCLEX QUESTIONS
1. While calculating the cardiac ejection fraction the nurse determines a client end diastolic volume. What occurs during myocardium diastole?
A. The ventricles refill the atria contract and the myocardium is perfused
B. The ventricles contract and eject blood into the pulmonary and systemic circuits
C. An electrical stimulus is generated that causes myocardial cells to respond
D. The resting membrane potential of cardiac cells spontaneously depolarizes.
Answer A
Rationale: In myocardial diastole, the ventricles refill, the atria contract, and the myocardium is perfused. Choice B described myocardial systole. Choice C describes what occurs immediately prior to
myocardial systole. Choice D describes what occurs in the sinoatrial node to initiate an electrical impulse.
2. The nurse is preparing to administer the alpha-beta blocker labetalol (Normodyne) intravenous push (IVP) to a client diagnosed with hypertensive crisis. Which intervention should the nurse implement?
A. Monitor the client’s labetalol serum drug level
B. Keep the medication covered with tin foil
C. Administer the medication slow IVP over 5 minutes
D. Teach the client signs/symptoms of hypertension
Answer C
Rationale:
A. Labetalol does not have a serum drug level.
B. Only medications that are inactivated or weakened by exposure to light would have to be covered; this medication is not affected by light.
C. Medications that directly affect the cardiac muscle or vasculature are administered slowly over a minimum of 5minutes for safety reasons. Many medications require dilution with normal
saline to have sufficient volume for a smooth equal delivery to prevent cardiac dysrhythmias.
D. The nurse should teach the client about possible signs or symptoms of hypertension, but remember, clients with hypertension are often asymptomatic. Hypertension is the “silent killer.”
3. The nurse is preparing to administer a nitroglycerin patch to a client diagnosed with coronary artery disease. Which interventions should the nurse implement? Rank in order of performance.
A. Date and time the nitroglycerin patch.
B. Remove the old patch.
C. Clean the site of the old patch.
D. Apply the nitroglycerin patch.
E. Check the patch against the MAR.
Answer EABDC
Rationale:
E. The nurse should implement the five rights of medication administration, and the first is to make sure it is the right medication and the right client.
A. Before applying the nitroglycerin paste, the nurse should date and time the application paper prior to putting it on the client so that the nurse is not pressing on the client when writing on the patch.
B. The nurse should have the gloves on when removing the old application paper for the above reason.
D. Last, the nurse should administer the nitro patch application paper in a clean, dry, non-hairy place.
C. The nurse should make sure no medication remains on the client’s skin.
4. The plan of treatment for a client with heart failure includes interventions to reduce afterload and improve coronary artery perfusion. Which action will the nurse prepare to provide to this client?
A. Monitor the results of a beat-adrenergic antagonist
B. Monitor the results of a cardiac glycoside
C. Monitor the results of a diuretic
D. Monitor the intraaortic balloon pump
Answer D
Rationale: The intraaortic balloon pump will mechanically reduce afterload to enhance coronary artery perfusion during the diastolic phase of the cardiac cycle. Choice A will block sympathetic innervation
to reduce cardiac contractility. Choice B will cause a slowing of the heart to reduce the cardiac workload. Choice C will reduce intravascular volume and control excess sodium levels.
5. The client is being prepared for a cardiac catheterization. Which statement by the client would warrant immediate intervention by the nurse?
A. “I took my blood pressure medications yesterday.”
B. “I broke out in an awful rash after eating oysters.”
C. “I have not had my daily aspirin in more than a week.”
D. “I am highly allergic to poison ivy or oak.”
Answer B
Rationale:
A. The client should take his or her blood pressure medication prior to the cardiac catheterization; therefore, this statement does not warrant intervention.
B. This may indicate the client is allergic to iodine, a component of the cardiac catheterization dye, and warrants further assessment by the nurse.
C. The client should stop any medication that interferes with clot formation, so this statement does not require intervention by the nurse.
D. An allergy to poison ivy or oak would not interfere with this procedure
6. When assessing a client with infective endocarditis the nurse notes that the client has reduced strength in the right arm and leg and difficulty speaking. What mechanism is most likely responsible for
these findings?
A. Infection of the meninges
B. Ischemic damage to the left hemisphere
C. Decreased cerebral perfusion due to septicemia and shock
D. Disseminated intravascular coagulation resulting in intracerebral hemorrhage.
Answer B
Rationale: Clients with infective endocarditis are at risk for developing stroke following CNS embolization of the bacterial vegetation of the affected valve. Choices A and C are incorrect because meningitis
and shock do not support diagnosis of stroke. D is incorrect because DIC and hemorrhagic stroke are very rare complications of endocarditis.
7. Which of the following patients are MOST at risk for developing endocarditis? Select-all-that-apply:
A. A 25-year-old male who reports using intravenous drugs on a daily basis.
B. A 55-year-old male who is post-opt from aortic valve replacement.
C. A 63-year-old female who is newly diagnosed with hyperparathyroidism and is taking Aspirin.
D. A 66-year-old female who recently had an invasive dental procedure performed 1 month ago and is having a fever.
Answer A, B, D
8. The nurse is concerned that a client, recovering from coronary artery bypass graft surgery, is developing cardiac tamponade when what is assessed? (Select all that apply.)
A. Central venous pressure increased from 10 mm Hg to 12 mm Hg
B. Distant heart sounds
C. Thready radial pulse
D. Decreased electrocardiogram waveform amplitude
E. Distended neck veins
Answer A, B, D, E
Rationale: Manifestations of cardiac tamponade include a rising central venous pressure, distant heart sounds, decreased electrocardiogram waveform amplitude, and distended neck veins. These
manifestations are caused by the accumulation of blood or fluid in the pericardium which compresses the atria and ventricles. Choice C is not an indication of cardiac tamponade.
9. A client with pericarditis develops pulsus paradoxus. What mechanism explains this finding?
A. Inspiration decreases intra-thoracic pressure.
B. Inspiration increases intra-thoracic pressure.
C. Expiration decreases intra-thoracic pressure.
D. Expiration increases intra-thoracic pressure.
Answer A
Rationale: Pulsus paradoxus is a decrease in systolic blood pressure > 10 mm Hg during inspiration. In this phenomenon, the heart sounds can be heard upon auscultation but the radial pulse cannot be
palpated. This finding is associated with (restrictive) pericarditis, cardiac tamponade and restrictive cardiomyopathy. During inspiration intra-thoracic pressure decreases, which results in an increase in
venous return. The subsequent increase in blood volume in the right atrium and ventricle causes the intraventricular septum to bulge into the left ventricle, blocking cardiac output and blood pressure.
Note that the right atrium/ventricle cannot bulge outwards (as is normal in response to increased blood flow during inspiration) due to the stiff and/or blood filled pericardium. Choice B is incorrect
because during inspiration the diaphragm contracts and pulls downward. This lowers the pressure in the intra-thoracic cavity (allowing air to flow into the lungs and blood to return to the heart). Choices C
and D are incorrect because during expiration the diaphragm relaxes and moves upward. This increases the intra-thoracic pressure, causing air to be expelled from the lungs and decreasing venous return.
10. A client is diagnosed with cardiac dysrhythmia. How should the nurse explain the normal conduction system of the heart to the client
A. Atrioventricular node
B. Bundle of his
C. Purkinje fiber
D. Intermodal pathways
E. Right and left bundle branches
F. Sinoatrial node right atrium
Answer F, D, A, B, E, C
Rationale: The sinoatrial node is the normal pacemaker of the heart and is located in the right atrium. This impulse travels across intermodal pathways to the atrioventricular node. It then passes through
in the bundle of His and continues down the interventricular septum through the right and left bundle branches and out to the Purkinje fibers.
11. Test Yourself
Answer:
1. P wave
2. P-R interval
3. QRS complex
4. ST segment
5. T wave
6. Q-T interval
12. Regular or Irregular?
Answer:
1. Regular, same distance between Rs
2. Irregular, not same distance between Rs
3. Regular
4. Irregular
5. Irregular
6. Regular
13. A client’s latest electrocardiogram waveform is demonstrating changes in the ST segment. The nurse is concerned that the client will begin to demonstrate.
A. Ventricular dysrhythmias
B. Atrial dysrhythmias
C. Atrioventricular conduction blocks
D. Sinus arrhythmias
Answer A
Rationale: Ventricular dysrhythmias originate in the ventricles. One characteristic of this waveform is an abnormal ST segment. Choice B is incorrect because P wave changes are seen in atrial
dysrhythmias. Choice C is incorrect because changes would be seen in the QRS complex and P waves. Choice D is incorrect because a sinus arrythmia is a sinus rhythm that fluctuates with respirations.
There are no specific waveform changes with arrythmia.
14. A client is diagnosed with atrial fibrillation. For which complication should the nurse instruct the client if this disorder is left untreated?
A. Myocardial infarction
B. Peripheral vascular disease
C. Diabetes mellitus
D. Cerebral vascular accident
Answer D
Rationale: Uncontrolled atrial fibrillation is a common cause of a cerebral vascular accident. Choices A, B, and C are incorrect because uncontrolled atrial fibrillation does
not cause a myocardial infarction, peripheral vascular disease, or diabetes mellitus.
15. The nurse is preparing to administer Digoxin to a client diagnosed with congestive heart failure. Which area should the nurse assess prior to administering the
medication?
A. A
B. B
C. C
D. D
Answer D
Rationale:
A. This is the second intercostal space right sternal notch, which is one of the two areas used to auscultate the aortic valve, but it is not where the apical pulse
is assessed.
B. This is the second intercostal space left sternal notch, which is used to auscultate the pulmonic valve, but it is not where the apical pulse is assessed.
C. This is the fourth and fifth intercostal space to the left of the sternum and is where the tricuspid valve is best heard.
D. The apical pulse located at the fifth intercostal midclavicular space must be assessed for 1 minute prior to administering digoxin. If the apical pulse is less than 60 beats per minute, the nurse should
hold the medication
16. The home health-care nurse is visiting a client diagnosed with deep vein thrombosis who is taking Warfarin (Coumadin). The nurse assesses a large hematoma on the abdomen and multiple small
ecchymotic areas scattered over the body. Which action should the nurse implement?
A. Send the client to the emergency department immediately.
B. Encourage the client to apply ice to the abdominal area.
C. Inform the client that this is expected when taking this medication.
D. Instruct the client to wear a MedicAlert bracelet at all times.
Answer A
Rationale:
A. Abnormal bleeding is a sign of Coumadin overdose; the client needs to be assessed immediately and have a STAT International Normalized Ratio (INR) laboratory test.
B. Ice causes vasoconstriction, but this bleeding is abnormal and will not stop without medical treatment.
C. Abnormal bleeding to this extent is not expected while receiving Coumadin therapy.
D. This is an appropriate teaching intervention for clients receiving Coumadin, but this is not an appropriate action at this time