Complex exam 1

• Vagal stimulation causes bradycardia, hypotension, heart block, or other dysrhythmias

• Can be used to decrease heart rate in something like SVT

Vagal maneuvers like the Valsalva maneuver

• bearing down

• blowing into a straw

• carotid massage (but that is only for a doctor to do)

• face in ice cold water

• educate the patient on vagal stimulation maneuvers like the Valsalva maneuver if they need to bring down a rapid heartrate

• this should also be documented and reported to the physician if used in emergent scenarios like SVT

• the nurse cannot preform a vagal maneuver like the carotid massage

Adenosine, beta blockers, statins, and ace inhibitors

Atropine, scopolamine, anticholinergic drugs

The superimposition of an ectopic beat on the T wave of a preceding beat

What is the significance?

pt has Vtach and it becomes unstable

can go into VFib

• Before the procedure the nurse will assess the patient’s physical and psychosocial readiness for the procedure

  • they will give information about what it will feel like and what will be happening during the procedure

• after the procedure the nurse should restrict the patient to bedrest, the insertion site must be kept straight

• vitals should be monitored every 15 min For 1 hour, then every 30 min. For 2 hours or until stable and then every 4hr

• Assess insertion site for drainage, assess peripheral pulses,

• Positive ionotropic- increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the heart

• Negative chronotropic- stimulates the PSNS, which slows electrical conduction, and decreases HR

• assess apical HR before administration

• teach patient to report signs of dig toxicity

Signs of dig toxicity

• nausea

• vomiting

• diarrhea

• paresthesia

• confusion

• visual disturbance

Common side effects

• facial flushing

• SOB

• chest pain

Antacids interfere with the absorption

• Lots of medications will be administered: immunosuppressants, anti-proliferatives, 

• Education on risk of rejection, increased risk of cancer

• myocardial muscle protein released into bloodstream with injury to myocardial muscle

• Troponin T <0.1ng/mL

• Troponin I <0.03ng/mL

• Elevation indicates myocardial injury or infarction

• When muscle tissue is damaged, CPK leaks into your blood

• before providers used Trops to assess for HF, this was used

• it is not reliable because it does not apply specifically to cardiac muscle

Peptide produced and released by the ventricles when they stretch when the patient has fluid overload as a result of HF

• <100 pg/mL

• increase indicates HF

Measures the activity of prothrombin, fibrinogen, and factors V, VII, and X

• most reliable way to monitor anticoagulant status in warfarin therapy

• 0.8-1.1 if they are not using anticoagulants

• Increase indicates that Warfarin therapy is successful and there is a risk for prolonged bleeding

• Decrease indicates that blood is clotting quicker and the pt is at risk for thrombi/emboli

• measures how well blood is coagulating

• used during heparin therapy, aPTT must remain in therapeutic range

• usually 1.5-2.5x normal control levels

the arterial BP necessary to maintain perfusion of major body organs, such as the kidneys and brain

• at least 60 mm Hg

• usually 60-70 mm Hg

• pericardiocentesis to remove fluid and relieve pressure on the heart

• antibiotics

• pericardial drainage

• NSAIDs for pain

• Corticosteroids when NSAIDs don’t work

• Colchicine twice a day for 3 months to prevent pericarditis recurrence

Inflammation or alteration of the pericardium, the membranous sac that encloses the heart

Symptoms

• substernal precordial pain that radiates to the left side of the neck, shoulder, or back

  • aggravated by inspiration, coughing, and swallowing

• pericardial rub

• ST elevation

Sitting upright and leaning forward will help with the pain

Diuretics and Nitrates

ACEIs, ARBs, and ARNI (Sacubitril/Valsartan)

Digoxin, Milrinone, and Beta blockers

• IV drugs use

• Valve replacement

• Systemic alterations in immunity

• Structural cardiac defects

Microbial infection of the endocardium

Symptoms

• fever associated with chills, night sweats, malaise, and fatigue

• anorexia and weight loss

• cardiac murmur

• petechiae

• splinter hemorrhages

• Osler nodes (on palms of hands and soles of feet)

• Janeway lesions (flat, reddened macular on hands and feet)

• Roth spots (hemorrhagic lesions that appear as round or oval spots on the retina)

Nonsurgical

• IV antimicrobials for 4-6 weeks

Surgical

• removing infected valve

• repairing or removing congenital shunts

• repairing injured valves and chordae tendineae

• draining abscesses in the heart

Precautions

• Standard precautions

• Contact with infected person’s blood should be avoided

Thickening of the mitral valve due to fibrosis and calcification, the valve leaflets fuse and become stiff

• valve opening narrows, preventing normal blood flow from the LA and LV

Symptoms

• mild stenosis pts are asymptomatic

• with progression…

  • dyspnea on exertion

  • orthopnea

  • PND

  • palpitations

  • dry cough

  • hemoptysis

  • pulmonary edema

  • apical diastolic murmur

  • symptoms of RVF

• Thromboembolism - anticoagulant therapy 

• Structural valve dysfunction - repair or replacement of the valve

• Endocarditis - most commonly treated with antibiotics, sometimes surgery is needed

Inability of the mitral valve to close completely during systole, which allows the backflow of blood into the LA when the ventricle contracts

• LA and LV dilate and hypertrophy

Symptoms

• fatigue and chronic weakness

• anxiety

• atypical chest pain

• palpitations

Later Symptoms

• dyspnea on exertion

• orthopnea

• high pitched murmur at the apex, with radiation to the left axilla

• S3

Heart failure

Most common type of cardiomyopathy, inability of the heart to pump effectively due to enlargement (dilation) and weakening of the ventricles

Symptoms caused by decreased CO

• dyspnea on exertion

• decreased exercise capacity

• fatigue

• palpitations

• dysrhythmias or heart block

• S3 and S4 gallops

• moderate to severe cardiomegaly

• alcohol abuse

• chemotherapy

• infection

• inflammation

• poor nutrition

Inability of the heart to pump blood effectively due to asymmetric thickening (hypertrophy) of the ventricles and disarray of the myocardial fibers

• some die with no symptoms

• athletes who die suddenly probably had this

Symptoms

• syncope

• dyspnea on exertion

• dizziness

• palpitations

• angina

• mild cardiomegaly

• S4 gallop

• mitral valve structural abnormalities

• Autosomal dominant gene

Rarest types of cardiomyopathy, inability of the heart to pump effectively due to restrictive filling of the ventricles because they are stiff

Symptoms

• symptoms of LVF

• symptoms of RVF

• or symptoms of both

• primary disease

• endocardial disease

• myocardial disease

  • sarcoidosis

  • amyloidosis

• EKG

• echo to look at overall heart function

• cardiac catheterization (biopsy)

• X-ray

Increase CO with

• diuretics

• vasodilating agents

• cardiac glycosides

• medications

  • diuretics

  • Ace inhibitors

• medications

  • ACEI

  • Beta blockers

  • Calcium channel blockers

Causes- hypertension, CAD, valvular disease

Symptoms-

Dyspnea

Rales

Orthopnea

Weakness

Nocturnal paroxysmal dyspnea

Increased HR

Nagging cough

Gaining weight (2-3lb/day or 5lb/week)

Systolic HF- heart failure that results when the heart is unable to contract forcefully enough during systole to eject adequate amounts of blood into circulation

• Ejection fraction <40%

• preload increases with decreased contractility, and afterload increases as a result of increased peripheral resistance

Diastolic HF- heart failure that occurs when the left ventricle is unable to relax adequately during diastole (due to stiffening), which prevents the ventricle from filling with enough blood to ensure adequate CO

• ventricles become less compliant over time because more pressure is needed to move the same amount of volume compared with a healthy heart

• ask about activity tolerance and ability to perform ADLs

• Ask about a cough, especially nocturnal

• dyspnea, orthopnea, PND

To increase gas exchange

• ventilation assistance

To increase perfusion

• CPAP

• Cardiac resynchronization therapy (CRT)

• Heart transplant

• Ventricular Assist device

• Heart reduction

Medications

MAWDS

Medications

• take them as prescribed and do not run out

• know the purpose and side effects

• avoid NSAIDs to prevent Na and fluid retention

Activity

• stay as active possible but don’t overdo it

• be able to carry on a conversation while exercising

Weight

• weight each day at the same time on the same scale to monitor for fluid retention

Diet

• limit daily Na intake to 2-3g

• limit daily fluid intake to 2L

Symptoms

• note any new or worsening symptoms and notify HCP immediately

• rapid weight gain (3/week or 1-2/day)

• decrease in exercise tolerance lasting 2-3 days

• cold symptoms lasting more than 3-5 days

• nocturia

• dypsnea or angina at rest

• increased swellin in feet, ankles, or hands

• monitor for signs of acute pulmonary edema

  • crackles in lung bases, dyspnea at rest, disorientation, confusion

• administer medications

• monitor weight gain

• monitor respiratory rate, rhythm, and quality every 1-4 hours

• auscultate breath sounds every 4-8 hours

Causes-

Symptoms- SWELLING

Swelling of hands, legs, and liver

Weight gain

Edema (pitting)

Large neck veins (JVD)

Lethargic

Irregular HR (AFib)

Nocturia

Girth (Ascites)

• lower leg edema that may progress to thighs and abdomen

• tight rings or shoes and weight gain

• nausea and vomiting and increased abdominal girth

• diet habits and extreme thirst due to Na retention

• psychosocial assessment

• Assess apical pulse prior to administration; HR >60 no digoxin

• Monitor for dig toxicity, signs include: nausea, vomiting, diarrhea, paresthesia, confusion, or visual disturbances

• most common cause of dig toxicity is hypokalemia or renal complications

• early symptoms of digoxin toxicity are GI symptoms like nausea and vomiting

• later symptoms include visual disturbances (yellow-green discoloration), palpitations, dyspnea, and syncope

• treatment for dig toxicity includes: Digifab and Digibind

  • an immunoglobulin fragment that binds with digoxin and is considered first line treatment for digoxin toxicity causing significant dysrhythmias (severe bradyarrhythmia, 2nd or 3rd degree heart block, ventricular tachycardia or fibrillation)

• nitroglycerin is converted by mitochondrial aldehyde dehydrogenase in smooth muscle cells to nitric oxide, a potent vasodilator, which activates the enzyme guanylate cyclase which converts guanosine triphosphate (GTP) to cGMP in vascular smooth muscle and other tissue. cGMP is an endogenous vasodilator of vascular smooth muscle.

• it can cause hypotension and this can cause nausea, vomiting, diaphoresis, pallor, and fainting

• patient education includes the risk of orthostatic hypotension and how to get up slowly

• headaches are a common side effect and should decrease with continued drug therapy

• concurrent alcohol use should be avoided

• patient should be educated to inform their doctor if they experience dry mouth or blurred vision.

calcium channel blockers block the inward movement of calcium by binding to the long acting voltage-gated calcium channels in the heart, vascular smooth muscle, and pancreas

• lightheadedness

• flushing

• orthostatic hypotension

• headaches

• peripheral edema

• worsening HF

• patients should be taught not to consume large amounts of grapefruit juice during drug therapy

• how to check their pulse and that they should call their doctor if their HR is less than 50bpm

• that this medication can cause orthostatic hypotension and how to move slowly when going from laying down to sitting to standing

• notify their doctor if they experience rash, irregular heartbeat, dyspnea, swelling of hands or feet, pronounced dizziness, nausea, hypotension, constipation, or severe/persistent headaches.

Beta-1 blockers

decreases HR, decreases myocardial oxygen demad

allows for more time for ventricles to fill

allows more time for oxygen demand to get to tissues

decrease preoad and afterload

decre

• These suppress the RAS

• decrease arterial resistance and arterial dilation as well as preventing sodium and water retention

• adverse effects are hypotension, hyperkalemia (esp in pt with renal dysfunction), and angioedema

• decrease potassium intake

  • spinach

  • avocado

  • potatoes

  • bananas

  • lentils

  • tomatoes

  • beats

  • broccoli

A stopcock is used with two syringes, one with adenosine and one with NS flush

1. Dosing starts at 6 mg IV push followed by 20mL NS

2. If it does not work the next dose is 12 mg IV push followed by 20mL NS

The max dose is 30mg

• a code cart and a physician is also necessary to have present when administering adenosine

1. Start with 1mg

2. Can try again every 5 minutes

3. maximum dose of 3mg

Sinus bradycardia when the underlying cause cannot be determined

• potassium channel-blocking effect results in increased action potential duration and a prolonged effective refractory period in cardiac myocytes

  • Myocyte excitability is reduced, thus hindering the continuation of tachyarrhythmias by preventing reentry mechanisms and ectopic foci

• the drug's electrophysiological effects encompass a decrease in the automaticity of the sinoatrial (SA) node, a reduction in AV node conduction velocity, and the inhibition of ectopic pacemaker automaticity

• continually monitor ECG rhythm during infusion

  • bradycardia and AV block can occur

• the drug can cause serious toxicities (Lung damage and visual impairment) so it is only approved for life threatening arrhythmias

• corneal pigmentation occurs in most patients, but generally does not interfere with vision

• Increases HR, BP, and myocardial contractibility

  • all of which cause increased myocardial oxygen demands

  • also causes reduced myocardial oxygen supply through coronary vasoconstriction

• Increases risk for dysrhythmias

• Synchronized countershock that may be performed with new-onset AFib

• can be scheduled electively for stable AF that is resistant to medical therapy

  • must take anticoagulants for 3 weeks beforehand

• it stops the reentry circuit and allow the sinus node to regain control of the heart

• sometimes used for stable Vtach

• Don’t eat for 6 hours prior to procedure

• Take medication to prevent blood clots for at least three weeks prior to procedure if scheduling it electively

• If the cardioversion is being used to treat A-Fib and the onset of A-fib is uncertain a transesophageal echocardiogram can be preformed to assess for clot formation in the left atrium

Asynchronous countershock, depolarizes a critical mass of myocardium simultaneously to stop the re-entry circuit, allowing the sinus node to regain control of the heart

• pulseless V tach, Vfib

• Do not touch patient when they are receiving the shock

• Do not use alcohol to wipe the patient’s chest before the shock

• loudly and clearly command all personnel to clear contact with the patient and the bed and check to see they are clear before the shock is delivered

• Deliver shock and resume CPR for 2 minutes

• Then reassess the rhythm and charge defibrillator again if indicated

• faint

• immediate loss of consciousness

• pulseless

• apneic

• no BP

• heart sounds are absent

• within minutes

  • pupils become fixed and dilated

  • skin becomes cold and mottled

• defibrillate

• CPR until AED is available

• drug therapy

• conduction disorders that are not temporary

  • complete heart block

  • hypertrophic cardiomyopathy

  • symptomatic sinus bradycardia

  • symptomatic 2nd degree heart block

  • sustained Vtach

  • systolic HF

Transcutaneous or External-temporary pacing that is accomplished through the application of two large external electrodes

Transvenous- pacemaker is placed in a pocket between the layers of muscle and the pacemaker leads are placed in the heart, temporary

Implanted- maybe not temporary?

Synchronous- demand

Asynchronous- fixed rate

Single chamber- One lead attaches to the upper or lower heart chamber

Biventricular- cardiac resynchronization therapy (CRT) device, has three leads connected to the right atrium and both ventricles. We use the biventricular pacemaker to treat people with arrhythmias caused by advanced heart failure

Dual chamber- Uses two leads, one for the upper and one for the lower chamber

• pacemaker spike before complex

• it shows output failure

• must assess your patient

• report any fever, redness, swelling, or drainage

• avoid tight clothing or belts

• you can take baths and showers

• no sudden jerky movement for 8 weeks to allow the pacemaker to settle in place

• if the surgical incision is near the shoulder, do not lift the arm over the head or lift more than 10lbs for the next 4 weeks

• impulses do not travel from atria to ventricles

• AV dissociation: Ps walk out independently of QRS complexes

• medical emergency

• Pacemaker

Find cause first

• medication

  • if this then discontinue med

• intrinsic factor

  • pacemaker

• PR interval becomes longer then drops a QRS

• will most likely need a pacemaker

• impulses from atria occasionally are blocked in AV node

• PR interval remains constant then drops a QRS

• will most likely need a pacemaker

• impulses from atria often are often blocked in AV node

PR interval >0.20 seconds

• all sinus impulses reach the ventricle

an interruption or delay of electrical conduction from the atria to the ventricles due to conduction system abnormalities in the AV node or the His-Purkinje system

• Unstable tachycardia: when cardiac output is reduced to th epoint of causing serious symptoms such as: chest pain, dyspnea, weakness, syncope

  • Ex: torsades, ventricular tachycardia, SVT, A-Fib, 

• Stable tachycardia: HR within 100-149 without serious signs and symptoms; can turn into unstable tachycardia

Atrial fibrosis and loss of muscle mass

• hypertension

• heart failure

• CAD

• genetic mutations

• Stroke due to the pooling of blood that occurs

• Heart failure due to decreased CO

Face

Arms

Speech

Time

The loss of coordinated atrial contractions can lead to pooling of blood

• this results in clotting

• they are at high risk for PE

• thrombi may form within the RA and move through the RV to the lungs

• they are at high risk for embolic stroke

• clear instructions and education about medications

  • side effects that need to be reported

  • should not be stopped abruptly

• teach pt and family how to take HR and BP

• report signs of a change in HR

  • significant decrease in pulse rate

  • rate >100bpm

  • increased rhythm irregularity

• form of tachycardia that involves the rapid stimulation of atrial tissues at a rate of 100-280 bpm

• Often occurs in healthy young people, especially women

• P wave may not be visible, QRS is normal

• Cause- re-entry mechanism in which one impulse circulates repeatedly throughout the atrial pathway, restimulating the atrial tissue at a rapid rate

Signs and symptoms

• Sustained- palpitations, chest pain, weakness, fatigue, sob, nervousness, anxiety, hypotension, and syncope

• If rate dose not sustain adequate BP- angina, HF, cardiogenic shock

• Nonsustained or slower- asymptomatic

• Only needed if it is sustained

• Adenosine, rapid IV push, never given without a physician being present, need all emergency equipment, basically a reset of the heart

• Preferred treatment is radiofrequency catheter ablation

• Desired outcomes: decrease ventricular response, convert dysrhythmias to a sinus rhythm and treat the cause

• Vagal maneuvers- vagal stimulation of the cardiac conduction system, specifically the SA and AV node, include carotid massage and Valsalva maneuvers

• Drugs: Adenosine, beta blockers, calcium channel blockers

1. Determine the HR

2. Determine the heart rhythm

3. Analyze the P waves

4. Measure the PR interval

5. Measure the QRS duration

6. Examine the ST segment

7. Assess the T wave

8. Measure the QT interval

P- atrial depolarization

PR segment- when electrical impulse is traveling through AV node, where it is delayed

QRS- ventricular depolarization

ST segment- early ventricular repolarization

T- ventricular repolarization

QT interval- total time required for ventricular depolarization and repolarization

Ventricular tachycardia

Ventricular fibrillation

Torsades de Pointes