Cardiac Flashcards Preview

HURST > Cardiac > Flashcards

Flashcards in Cardiac Deck (50):

Normal blood flow thru heart.

The two major veins that bring blood to the right side of the heart are the superior and inferior vena cava (This blood is deoxygenated)→The blood enters the right atrium→ Then the right ventricle→ From the RV the blood is pumped into the pulmonary artery (this artery carries deoxygenated blood) → Then the blood goes to the lungs where it is oxygenated→ Next through the pulmonary veins (they carry oxygenated blood)→ It then goes to the left atrium → to the left ventricle (the big bad pump)→ It is then pumped into the aorta→ And finally this oxygenated blood is delivered throughout the body through the arterial system where it eventually ties back into the venous system.



Preload is the amount of blood returning to the right side of the heart and the muscle stretch that the volume causes . ANP is released when we have this stretch.



Afterload is the pressure in the aorta and *peripheral arteries* that the left ventricle has to pump against to get the blood out.
• This pressure is referred to as resistance.
• With hypertension there’s even more pressure for the left ventricle to pump against. That’s why HTN can eventually lead to HF and pulmonary edema, because high afterload decreases output and decreases forward flow. Plus, it wears your heart out.


Stroke volume

Stroke volume is the amount of blood pumped out of the ventricles with each beat.


Cardiac output

Cardiac Output:
• Tissue perfusion is dependent on an adequate cardiac output.
• Cardiac output changes according to the body’s needs.


Factors that affect cardiac output

a. Heart rate and certain arrhythmias
b. Blood volume
1) Less volume = less CO
2) More volume = more CO
c. decreased contractility
• MI, medication, muscle disease


Patho of decreased CO

L/ventricle=cardiac output

• If your CO is decreased, will you perfuse properly? no
a. Brain: LOC will go down
b. Heart: Client complains of chest pain
c. Lungs: Short of breath, lungs sound wet
d. Skin: cold and clammy
e. Kidneys: UO goes down
f. Peripheral pulses: weak
Arrhythmias are no big deal UNTIL they affect your cardiac output.
3 Arrhythmias that are always a big deal:
Pulseless Vtach


CAD. Coronary Artery Disease

Coronary artery disease is the most common type of cardiovascular disease and the single largest killer of Americans.
• Coronary artery disease is a broad term that includes chronic stable angina and acute coronary syndrome.


Patho of chronic stable angina

1) Decreased blood flow to the myocardium→ ischemia → temporary pain/pressure in chest.
2) What brings this pain on? Low oxygen usually due to exertion.
3) What relieves the pain? rest and/or nitro SL



Used for angina.
a) Nitroglycerin (Nitrostat®): Sublingual
• Causes venous and arterial vasodilation
• This result will cause decrease preload and afterload.
• Also causes dilation of coronary arteries which will increase blood flow to the actual heart muscle (myocardium)
• Take 1 every 5 min x 3 doses.
• Okay to swallow? No
• Keep in dark, glass bottle; dry, cool
• May or may not burn or fizz
• The client will get a headache.
• Renew how often? An average of every 3-5 months. Spray - 2years
• After Nitroglycerin (Nitrostat®), what do you expect the BP to do? Drop. (Stay with the patient)

American Heart Association Algorithm for NTG: Take one NTG SL, after 5 minutes if chest pain/discomfort is unimproved or worsened, activate EMS by calling 911 immediately.


Beta blockers for prevention of angina

Examples: Propranolol (Inderal®), Metoprolol (Lopressor®/Toprol XL®),
Atenolol (Tenormin®), Carvedilol (Coreg®)
• Decreases BP, P, and myocardial contractility
• Decreases the workload of the heart?
Beta blockers block the beta cells... These are the receptor sites for catecholamines- the epi and norepi. So we just decreased the contractility... So we decreased CO. So we have decreased the workload on my heart.

This is a good thing to a certain point, because we decrease the work on the heart the need for oxygen is decreased and that decreases angina. But could we decrease the client’s cardiac output (HR and BP) too much with these drugs? Yes


Calcium channel blockers for prevention of angina

• Examples: Nifedipine (Procardia XL®), Verapamil (Calan®), Amlodipine
(Norvasc®), Diltiazem(Cardizem®)
• Decreases BP
• Calcium channel blockers cause vasodilation of the arterial system.
• They dilate coronary arteries.
• Two benefits of calcium channel blockers are they decrease afterload and increase oxygen to the heart muscle.



Dose is determined by the physician (81 mg-325 mg)

Keep platelets from sticking together and keep blood flowing.


Education for chronic stable angina

• Rest frequently
• Avoid overeating
• Avoid excess caffeine or any drugs that increase HR.
• Wait 2 hours after eating to exercise.
• Dress warmly in cold weather (any temperature extreme can precipitate an
• Take nitroglycerin prophylactically.
• Smoking cessation
• Lose weight.
• Avoid isometric exercise
• Reduce stress

** Do everything you can to reduce the workload of the heart


Cardiac catheterization

1) Pre-procedure:
• Ask if they are allergic to shellfish or iodine. Iodine based dye is used during procedure.
• Also we want to check their kidney function because you excrete the dye through the kidneys. Many doctors order Mucomyst (Acetylcysteine) pre-procedure especially if they have kidney problems. Mucomyst helps to protect the kidneys.
• Hot shot. (When injecting dye)
• Palpitations normal
2) Post-procedure:
• Monitor VS.
• Watch puncture site.
What are you watching for bleeding and hematoma formation
• Assess extremity distal to puncture site (5-Ps). Pulselessness Pallor Pain Paresthesia Paralysis, skin temp, cap refill
• Bed rest, flat, leg straight X 4-6 hours
• Major complication post cath? Bleeding
• Report pain ASAP
• If the client is on Glucophage (Metformin) hold this medicine for 48 hours post procedure. We are worried about the kidneys.
Unstable chronic angina= Impending MI


Acute coronary syndrome/M I, unstable angina pathophysiology and signs and symptoms

a. Pathophysiology:
1) Decreased blood flow to myocardium→ ischemia & necrosis.
2) Does the client have to be doing anything to bring this pain on? No
3) Will rest or Nitroglycerin (Nitrostat®) relieve this pain? No

b. S/S:
• Pain
May describe pain as crushing, an elephant sitting on their chest, pressure radiating to the left arm and left jaw, N/V, or pain between their shoulder blades.

Females usually present with GI signs and symptoms, epigastric complaints or pain between the shoulders, an aching jaw or a choking sensation. Chronic fatigue,

What is the #1 sign of an MI in the elderly? SOB

• Cold/clammy/BP drops
• Vomiting
• Cardiac output is going down.
• ECG changes
You may see the following terms in a test question:
STEMI: ST-Segment Elevation Myocardial Infarction-this indicates that the client is having a heart attack and the goal is to get them to the cath lab for PCI in less than 90 minutes.
NSTEMI: Non-Elevation ST Segment Myocardial Infarction-these clients are usually less worrisome.


Lab work for MI

1) CPK-MB:
• Cardiac specific isoenzyme
• increases with damage to cardiac cells
• Elevates in 3-12 hours and peaks in 24 hours
2) Troponin:
• Cardiac biomarker with high specificity to myocardial damage
• Elevates within 3-4 hours and remains for up to 3 weeks
Most sensitive and specific
3) Myoglobin:
• Increases within 1 hour and peaks in 12 hours
• negative results are a good thing.
Not very specific
4) Which cardiac biomarker is the most sensitive indicator for an MI? Troponin
5) Which enzyme or makers are most helpful when the client delays seeking care? Troponin


Complication of an MI

•What untreated arrhythmias will put the client at risk for sudden death? Pulselessness VTach, VFib, Asystole, bradycardia

Priority treatment for V-Fib: Defibrillate them ASAP
If the first shock doesn’t work and client remains in V-Fib, what is the first vasopressor we give? epinephrine or vasopressor, the. Amiodarone
• Amiodarone (Cordarone®) is an anti-arrhythmic and is used when V-Fib and pulseless VT are resistant to treatment, and also for fast arrhythmias.
• What anti-arrhythmic drugs are commonly given to prevent a second episode of V-Fib? Amiodarone and lidocaine.
• Lidocaine toxicity: any CNS/neuro changes
• Amiodarone (Cordarone®) is the first anti-arrhythmic of choice. Important side effect? Hypotension
This hypotension can lead to further arrhythmias.


Treatment of an MI

• What drugs are used for chest pain when they get to the ED? O2, aspirin chewable, nitro, morphine
• Head up position. Why?
Decreases workload on the heart and increases CO.



• Goal: Dissolve the clot that is blocking blood flow to the heart muscle>decreases the size of the infarction.
• Medications: Streptokinase (Streptase®)(trouble with allergies), Alteplase (t-PA®), Tenecteplase (TNKase®) (one time push), Reteplase (Retavase®)
• How soon after the onset of myocardial pain should these drugs be administered? Within 6-8 hours
• Brain attack? TIME IS BRAIN.
• Major complication: bleeding
• Obtain a good bleeding history.
• Absolute contraindications:
Intracranial neoplasm, intracranial bleed, suspected aortic dissection, internal bleeding
• During and after administration we take bleeding precautions.
• Draw blood when starting IVs, decrease the number of puncture sites.
• What about ABGs? No
• Follow-Up Therapy: Antiplatelets are another important component of fibrinolytic therapy.
Acetylsalicylic Acid (Aspirin®), Clopidogrel (Plavix®), Abciximab (ReoPro IV®) (continuous infusion to inhibit platelet aggregation)

Give them in a site you can compress.


Medical interventions for MI

• Includes all interventions such as PTCA (angioplasty) and stents
• Major complication of the angioplasty is a MI.
Don’t forget client may bleed from heart cath site, or they could reocclude.
• If any problems occur→ go to surgery.
Chest pain after procedure: call the physician at once→ re-occluding!
• Anti-platelet medications:
• Aspirin
• Clopidogrel (Plavix®)

• Abciximab (ReoPro IV®)
• Eptifibatide (Integrilin IV®)
Given to high risk clients who have been stented to keep artery open those waiting to go to cath lab



b) Coronary Artery Bypass Graft (CABG)
• Can be scheduled or emergency procedure
• Used with multiple vessel disease or left main artery occlusion.
• The left main coronary artery supplies the entire left ventricle.
• Left main coronary artery occlusion, Think: sudden death or Widow Maker.


Cardiac rehab

• Smoking cessation
• Stepped-care plan (increase activity gradually)
• Diet changes- low fat, low salt, low cholesterol
• No isometric exercises-increase workload of heart
• No Valsalva
• No straining; no suppository; Docusate (Colace®)
• When can sex be resumed? When you can climb a flight of stairs or walk around the block,with no discomfort
• What is the safest time of day for sex? Morning when rested
• Best exercise for MI client? Walking
• Teach S/S of heart failure:
Weight gain
Ankle edema
Shortness of breath


Heart failure causes

• HF is a complication that can result from problems such as cardiomyopathy, valvular heart disease, endocarditis, acute MI, and HTN.


Right sided HF

the blood is not moving forward into the lungs...IF it does not move forwards then it goes backwards into the venous system.
• S/S:
Distended neck veins
Enlarged organs
Weight gain
• Terminology:
Systolic heart failure: heart can’t *contract and eject.
Diastolic heart failure: ventricles can’t *relax and fill.

Causes: pulmonary embolism, COPD (hypoxic),


Left sided HF

the blood is not moving forward into the aorta and out to the body...IF it does not move forward, then it will go backwards into the lungs.
• S/S:
Pulmonary congestion Dyspnea
Blood tinged frothy sputum
Nocturnal dyspnea


Dx of HF

a. BNP: B-type natriuretic peptide:
• Secreted by ventricular tissues in the heart when ventricular volumes and pressures in the heart are increased
• Sensitive indicator
• Can be positive for HF when the CXR does not indicate a problem
• If the client is on Natrecor, turn it off 2 hours prior to drawing a BNP.
b. CXR: enlarged heart, pulmonary infiltrates
c. Echocardiogram-pumping action
d. New York Heart Association Functional Classification of Persons with HF:
• Classes 1-4 (Class 4 being worst)

The Swan-Ganz (Pulmonary Artery) catheter is a balloon flotation catheter that can be floated into the right side of the heart and pulmonary artery. It provides information to rapidly determine hemodynamic pressures, cardiac output and provides access to mixed venous blood sampling.

Arterial lines can be places in multiple arteries, but the most common site is the radial artery. It provides continuous intra-arterial blood pressure monitoring and allows for repeated ABG samples to be collected without injury to the client.


ACE Inhibitors for the treatment of heart failure

1) ACE Inhibitors
• These are the Drug of Choice for HF
• They suppress the Renin Angiotensin System (RAS)
• Prevent conversion of Angiotension I to Angiotension II
• Results in arterial dilation and increased stroke volume.


ARBS For the treatment of heart failure

• Block Angiotensin II receptors, and causes a decrease in arterial resistance and decreased BP.
Ace Inhibitors and ARBS both block aldosterone. When we block aldosterone, we lose na and h2o and retain K+.

It is standard practice (a core measure) that a client with HF will be sent home on an ACE and/or a beta blocker. Why?
Because, these drugs DECREASE the workload on the heart by preventing vasoconstriction (decreasing afterload). This will increase the cardiac output and keep blood moving forward out of the heart. That’s what we want, forward flow.


Digitalis/lanoxin For the treatment of heart failure

Normal level 0.5-2
• Used less today, because of the risk of drug toxicity, especially in the elderly.
• Used with sinus rhythm or atrial fibrillation and accompanying chronic HF
• Often given in combination with an ACE Inhibitor, ARB, Beta Blocker or diuretics.
• Contraction? Make stronger
• Heart rate? Slows down
When the heart rate is slowed this gives the ventricles more time to fill
with blood.
• Cardiac output will go up.
• Kidney perfusion increases.
Nursing Considerations:
• Would diuresis be a good thing or bad thing for this client? Good
• We always want to diurese heart failure clients...they can’t handle
the fluid.
• Digitalizing dose-loading dose
• How do you know the Digoxin is working? Because the cardiac output goes up
• S/S of toxicity:
Early: Anorexia, nausea, and vomiting
Late: Arrhythmias and Vision changes
• Before administering do what? TAKE APICAL PULSE
• Monitor electrolytes
All electrolytes levels must remain normal, but K+ is the one that causes the most trouble.
(Digoxin + hypokalemia = toxicity)
Any electrolyte imbalance can promote Digoxin toxicity..


Diuretics for HF

Examples: Furosemide (Lasix®), Hydrochlorothiazide (HCTZ®), Bumetanide (Bumex®), Hydrochlorothiazide/Triamterene (Dyazide®), Spironolactone (Aldactone®)
• decrease preload
• Nursing Considerations:
When do you give diuretics? In the morning


Non med trtmnt of HF

B. Low Na Diet:
• Decrease fluid retention>preload.
• Watch salt substitutes.
Salt substitutes can contain excessive K+.
• Canned/processed foods & OTCs can contain a lot of Na.
c. Elevate head of bed
d. Weigh daily and report a gain of 2-3 lbs
e. Report signs and symptoms of recurring failure.

Fluid retention-think Heart Problems 1st.



f. Pacemaker:
• Your “natural” pacemaker is the SA node or sinus node.
It sends out impulses that make the heart contract
• If your heart rate drops to 60 or below, cardiac output can decrease.
• Pacemakers are used to increase the heart rate with symptomatic bradycardia.
• Pacemakers depolarize the heart muscle and a contraction will occur
(electricity going through the muscle).
• Repolarization (ventricles are resting and are filling up with blood).
1) Pacemakers may be temporary (invasive or non-invasive) or permanent. Most permanent pacemakers are demand, but you can also see fixed pacemakers.
• Always worry if the heart rate drops below the set rate.
• Any pacemaker will maintain a certain minimal heart rate depending on the
settings, in other words the rate set.
• A demand pacemaker kicks in only when the client needs it to.
• Fixed rate pacemakers fire at a set rate constantly.
• It’s okay for the rate to increase but never decrease.
• Always worry if the rate drops below the set rate.

Post-Procedure Care (for permanent pacemakers):
Monitor the incision.
Most common complication post-op? Electrode displacement.
Immobilize arm.
Assisted Passive Range of Motion to prevent frozen shoulder.
Keep the client from raising their arm higher than shoulder height.


Pacemaker teaching

S/S of Malfunction:
• It’s possible that no contraction will follow the stimulus. This is called. Loss of capture.
• What causes this?
The pacemaker may not be programmed correctly.
Electrodes can displaced.
Battery may be depleted.
• Watch for: Any sign of decreased CO or decreased rate
Client Education/Teaching:
• Check pulse daily.
• ID card or bracelet
• Avoid electromagnetic fields (cell phones, large motors).
• Avoid MRIs.
• They going to set off alarms at airport, wand stay below waist level. Should just go thru pat down.
• Avoid contact sports.



2) ICD – Implantable Cardiac Device/defibrillator
May be used to pace the heart, or it might be used to defibrillate people in V- FIB.
Post-op care for an ICD is the same as for a pacemaker.


Pulmonary edema,
risks, patho, signs and symptoms

Who is at risk?
Any person:
• receiving IV fluids really rapidly,
• the very young and the very old,
• any person who has a history of heart or kidney disease

2. Pathophysiology:
• Fluid is backing up into the lungs. The heart is unable to move the volume forward
• Pulmonary edema usually occurs at night, when the client goes to bed.

3. S/S:
• Sudden onset
• Breathless
• Restless/anxious
* Hypoxia
• Productive cough (pink frothy sputum)


Pulmonary edema non drug trtmnt

a. Oxygen
• The priority nursing action is to administer high flow oxygen. Monitor oxygen sat and titrate to keep above 90%.
c. Positioning:
• upright position, legs down
Improves cardiac output
Promotes pooling of blood in lower extremities
d. Prevention:
• Prevention when possible:
Check lung sounds and Avoid fluid volume excess.


Pulmonary edema diuretics

1) Diuretics
• Furosemide (Lasix®)
• Causes diuresis and vasodilation which traps more blood out in the
arms and legs and reduces preload and Afterload.
• 40 mg IV push slowly over 1-2 minutes to prevent hypotension and ototoxicity
• Bumetanide (Bumex®)
• Can be given IV push or as continuous IV to provide rapid fluid removal
• 1-2 mg IV push given over 1-2 minutes


Pulmonary edema
Nitroglycerin IV

2) Nitroglycerin IV (Nitro-Bid IV®)
• Vasodilation: decrease afterload
• Decreased afterload = increased CO because the heart is pumping against
less pressure and more blood can be moved forward.


Pulmonary edema morphine

3) Morphine (Morphine Sulfate®)
• 2 mg IV push for vasodilation to decrease preload and afterload

Decreased the amount of volume coming into the heart.


Pulmonary edema nasiritide

4) Nesiritide (Natrecor®)
• IV infusion; short term therapy; not to be given more than 48 hours
• Vasodilates veins and arteries and has a diuretic effect

Remember to turn the Natrecor infusion off 2 hours before drawing a BNP level.


Cardiac tamponade

1. Pathophysiology:
• Blood, fluid, or exudates have leaked into the pericardial sac resulting in compression of the heart.
• This can happen if the client has had a motor vehicle collision, right ventricular biopsy, an MI, pericarditis, or hemorrhage post CABG.
2. S/S:
• Decreased cardiac output
• CVP will be HIGH, cuz heart is being squeezed
• BP will be dropping.
• Hallmark signs for Cardiac Tamponade
• Decreased BP
• Heart sounds will be muffled or distant.
• Neck veins distended
• Pressures in all 4 chambers are the same
• Shock
• Narrowed pulse pressure (from the baseline)
What is the pulse pressure? It’s the difference between the systolic and the diastolic pressure.
3. Tx:
• Pericardiocentesis to remove blood from around the heart
• Surgery

Narrowed pulse pressure think: Cardiac Tamponade
Widened pulse pressure think: Increased Intracranial Pressure


Arterial disorders

1. General Information:
a. Pathophysiology:
If you have atherosclerosis in one place you have it everywhere.
It is a medical emergency if you have an acute arterial occlusion (numb, pain, cold, no pulse).
Client will c/o numbness and pain
The extremity will be cold
No palpable pulse
More symptomatic in lower extremities Intermittent claudication- hallmark sign.
Arterial blood isn’t getting to the tissue→coldness, numbness, decreased peripheral pulses, atrophy, bruit, skin/nail changes, and ulcerations, hairless extremity
Pain at rest means severe obstruction.
b. Tx:
• If you elevated the extremity would the pain increase. Dangle
• Arterial disorders of the lower extremities are usually treated with either angioplasty or endarterectomy.




1. Pathophysiology:
• Blood stasis, vessel injury, blood coagulation.
• The blood can get to the tissue, it just can’t get away.
2. S/S:
• Edema
• Tenderness
• Warmth
3. Tx:
• Anticoagulant drugs: Heparin, Warfarin (Coumadin®), Enoxaparin (Lovenox®), Pradaxa
These prevent aggregation or prevent the clot from getting bigger.
• While on Coumadin, Limit foods with Vitamin K.
• Bleeding Precautions
• Surgery
• Bed rest
• Elevate- to increase blood return; decrease pooling.
TED hose- to increase venous return; decrease pooling Used with SCD’s many times
With a known clot TEDs or SCDs may not be used on the unaffected extremity or not at all
Warm, moist heat-decreases inflammation Never put cold on a vein= excessive vasoconstriction
Never put hot on a vein= excessive vasodilation
Prevention is the key!
We ambulated and hydrate the client.
Also for prevention we put on SCDs and get the client to do isometric exercises Isometrics decrease stasis.



Clotting lab values

Clotting Studies
Normal Lab Values: (may vary with institutions):
aPTT: 30-40 seconds.
PT: 11.0-12.5 seconds
Therapeutic INR: 1.3-2.0



Blocks conversion of angiotensin I to angiotensin II What they do: promote vasodilation and diuresis, decreases the secretion of aldosterone (so the kidneys will get rid of sodium and water and retain potassium).
Enalapril (Vasotec®) Fosinopril (Monopril®) Captopril (Capoten®)
Hypertension and heart failure
Nursing Observations:
If the drug ends in –pril it is most likely an ACE inhibitor.
Watch for hyperkalemia, orthostatic syncope, hypotension, and renal dysfunction. Angioedema-laryngeal swelling, can be fatal dry, nonproductive cough-reversible when drug stopped.
Fall precautions.



Blocks effects of angiotensin II (a potent vasoconstrictor) at the receptor site (used as an alternative to ACE inhibitors) ACE inhibitors block the conversion of AI to AII but AII can also be formed by other enzymes that are not blocked by ACE Inhibitors
What they do: decrease blood pressure, increase CO
Valsartan (Diovan®)
Losartan (Cozaar®)
Irbesartan (Avapro®)
Hypertension and heart failure.
Nursing Considerations:
If the drug ends in –sartan it is most likely an ARB Watch for hyperkalemia, hypotension, and renal


Beta adrenergic blockers

Block adverse effects from sympathetic nervous stimulation.
What they do: block the receptor sites for epi and they will decrease afterload and a result they decrease the BP and HR.
Propranolol (Inderal®)
Metoprolol (Lopressor®/Toprol XL®) Atenolol (Tenormin®)
Carvedilol (Coreg®)
Angina, chest pain. Hypertension, ventricular dysrhythmias and thyroid storm.
Nursing Consideration:
If the drug ends in–lol it is most likely a Beta Blocker.
Don’t give to asthmatics (some beta blockers also constrict the smooth muscle of the bronchioles) Don’t give to diabetics (block the sympathetic responses seen in hypoglycemia).


Arterial ulcer

Symptom: Chronic Arterial Insufficiency
Pain: Intermittent claudication (progresses to rest pain)
Pulses: Decreased or maybe absent
Color: Pale when elevated, red with lowering of leg
Temperature: Cool
Edema: Absent or mild
Skin Changes: Thin, shiny, loss of hair over foot/toes, nail thickening
Ulceration: If present will involve toes or areas of trauma on feet (painful)
Gangrene: May develop
Compression: Not used


Venous ulcer

Pain: None to aching pain depending on dependency of area
Pulses: Normal (may be difficult to palpate due to edema)
Color: Normal (may see petechiae or brown pigmentation with chronic condition)
Temperature: Normal
Edema: Present
Skin changes: Brown pigmentation around ankles, possible thickening of skin, scarring may develop
Ulceration: If present will be on sides of ankles
Gangrene: Does not develop
Compression: Used