Cardiac Flashcards
Preload
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.
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.
Afterload
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:
• CO=HRxSV
• 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
VFib
Asystole
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
Nitroglycerin
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.
Aspirin
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 attack). • 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:
WORRY ABOUT THE STEMI CLIENT
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
MAJOR ARRHYTHMIAS
•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.
Fibrinolytic’s
• 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.
