Heart failure, strucuture, and MI complications lecture ❤️

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127 Terms

1
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Atherosclerosis

abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen

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Blockages and narrowing of the coronary vessels reduce blood flow to the

myocardium

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high levels of hs-CRP are indicative of what

early indicator of CVD and athereosclerosis

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clinical manifestations of myocardial ischemia

  • Angina pectoris (most common)

  • Other symptoms: epigastric distress, pain that radiates to jaw or left arm, SOB, atypical symptoms in women

  • Myocardial infarction

  • Heart failure

  • Cardiac arrest

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what is angina pectoris

chest pain caused by insuffiecent coronary blood flow

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stable angina pectoris

stable means there is some narrowing in vessels but patient can do what they need to do. pain on exertion. resting makes it go away

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Unstable angina pectoris

unstable means you cant get pain to go away. usually means pre-infarct

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variant angina pectoris (aka Prinzmetal’s)

coronary artery spasm as propsed to embolism.

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What are the two main angina precipitating events

Decreased oxegyn supply (ex asthma, anemia, thrombosis) or increased demand (ex exercise, HTN, stress)

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when assesing someone with anina what 4 things should you ask about

  • Discomfort?

  • Precipitation?

  • Relief?

  • Duration?

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what does an elevated ST segment mean

heart attack

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unstable angina characteristics

  • Non occlusive thrombus

  • Non specific  ECG changes

  • Normal cardiac enzymes


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NSTEMI characteristics

  • Non-occlusive thrombus sufficient to cause tissue damage & mild necrosis

  • ST depression/T wave inversion on ECG

  • Elevated cardiac enzymes

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STEMI characteristics

  • Complete thrombus occlusion

  • ST elevations on ECG

  • Elevated cardiac enzymes

  • More severe symptoms

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MI interventions include increasing supply and decreasing demand. How can you increase supply

applying oxygen,

vasodilations like nitroglycerin,

break up clot (TPA is clot buster. most with MI dont qualify for TPA bc there is a short window to give it (3-6 hrs) and most patients do not present to ED until later)

anticoagulant therapy is heparin because it prevents clot from getting bigger),

antiplatelet therapy (asprin, clavix), angioplasty/stenting

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MI interventions include increasing supply and decreasing demand. How can you decrease demand

  • limit activity, beta blockers (decrease force of contraction. reduces strain on heart. lets heart rest), ACEi (decrease resistance), stool softeners 

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immediate treatment of a MI

MONA B!!!!

  • Morphine* not always nessesary. reseved for last if other interventions are not enough

  • Oxygen

  • Nitroglycerin*can be problematic if client has right sided MI

  • Aspirin

  • Heparin

  • Beta Blockers

  • Obtain EKG* delegate and get this done ASAP

*you do not have to go in that order

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MI diagnostics

cardiac enzymes, EKG, cardiac stress test, cardiac cath

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when do you draw cardiac enzyme labs

  • draw them three times to see if damage is worsening or improving 

  • draw every 4-8 hrs 

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ST depression and/or T‑wave inversion indicates

presence of ischemia.

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ST‑segment elevation indicates

injury

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abnormal Q‑wave indicates

necrosis.

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inferior infarct is problem in the

Right Coronary Artery

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anterior and/or septal infarct is problem in the

Left Main or Left Anterior Descending artery

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lateral infarct is problem in the

Left Main or Circumflex artery

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severe ST elevations indicates

terrible tissue death

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Core Measures: MI (as outlined by joint commision)

  • Aspirin at arrival

  • PCI accomplished within 90 minutes for STEMI patients**

    • PCI is same as angioplasty

  • ASA prescribed at discharge

  • ACE or ARB for LVSD

  • BB prescribed at discharge

  • Statin prescribed prior to discharge

28
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if you cant fix obstruction with stents, you have to

bypass that obstruction with a vein bypass

29
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are veins or arteries better for a vein bypass

  • veins more commonly used but we prefer artery. swap artery for an artery 

  • veins easier to use. 

  • veins cant withstand pressure of artery so it doesnt last as long 

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three things you always monitor for post op

infection, clotting, bleeding

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it is really important for cardiac surgery post op paitents to

restrict activity and movement and monitor respirotry function

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what is ectopy

ectopy are cranky cells. extra beats. beats that aren't right (PVC and PAC)

usually as a result of right MI

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causes of PVC-

tissue damage, potassium, electrolyte disturbances,

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bradycardia and heart blocks are

A “block” or delay in conduction from SA node to AV node

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bradycardia physical assessment-

poor perfusion, cyanosis, dizziness syncope, tachypnea

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bradycardia medications-

atropine, dopamine

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bradycardia procedure-

pacemaker

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Heart Block: Interventions

meds- atropine, epinipehrine

procedures- pacemaker

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Atrial finbrilation phisiology

increased irritability in cells

atria not completely depolarized witheach impulse so the atria quiver, rather than contract forecfully

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pulse deficit equation

Apical pulse – peripheral pulse

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Manifestations of atrial dysrhythmias, such as atrial fibrillation, include

a sensation of palpitations (a racing, fluttering, or pounding heart), shortness of breath, dizziness or lightheadedness, and extreme fatigue

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ventricular tachycardia pathophysilogy

SA node, other atrial pacemaker sites, AV junction all fail to initiate an electrical impulse 🡪 ventricles take over

Rate of 101 to 250 electrical impulses/minute

CAN BE LIFE THREATEING

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Ventricular fibriliation pathophysilogy

  • Ventricles make ineffective quivering movements, not actual contractions.

    • Blood is not pumped throughout body.

    • Patient does not have a pulse.

  • CPR should begin immediately

  • Death will occur if treatment does not begin!

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cardioversion and defibrillation are both used to

  • Treat tachydysrhythmias by delivering electrical current that depolarizes critical mass of myocardial cells

    • When cells repolarize, sinus node is usually able to recapture role as heart pacemaker  

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cardioversion is different from defibrillation because

  • In cardioversion, current delivery is synchronized with patient’s ECG

  • cardioversion is used when paitent has a pulse

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defibrillation is different from cardioversion because

  • In defibrillation, current delivery is unsynchronized

  • used if paitent does not have a pulse

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pacemakers are often used for clients with what condition

good for those with bradycardia bc it gives chambers impulse to contract

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risks of pacemakers

  • cant do MRI’s with most 

  • activity restrictions 

  • uncontrollable hiccups is sign of  pacemaker displacement 

  • risks- infection, bleeding, displacement, pneumothorax

    • procedure can be risky bc surgeon can clip lung during insertion

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if a client is in complete heart block what should you do first

  • - administer atropine 

    • if you know they are in heart block EKG prolly already done. if you already know rhythm give atropine to increase HR

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  • client with AFIB comes in. they are there for 48 hours and dysrythmia persists. what do you give first

  • - warfarin

    • heparin doesnt give as systemic of effects as warfarin. warfarin more widespread 

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heart failure definition

An inability of the heart to provide sufficient blood flow to meet the needs of the body for oxygenated blood

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heart failure is characterized by

  • Volume overload

  • Dyspnea

  • Activity intolerance

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what peptides are released early in heart failure?

  • Atrial Natrieurtic peptide (ANP)

    • secreted in response to atrial stretch

    • results in salt loss, diuresis, vasodilation, inhibits norepinephrine

  • Brain Natriuetric peptide (BNP)

    • gold standard

    • ventricular stretch

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salt and water retention short term and long term effects

short- augments preload

long- pulmonary congestion, ansarca

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vasoconstriction short term and long term effects

short- maintain BP for perfusion of vital organs

long- exacerbates pump dysfunction (excessive afterload), increases cardiac energy expendeture

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sympathetic stimulation short term and long term effects

short -increase HR and ejection

long- increase energy expenditure

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neurohormones (ANP and BNP) short term and long term effects

short- vasodilation, naturiesis, inhibition of RAAS

long- decreased BP, dehydration

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a BNP above what level indicated there is HF

anything over 100

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systolic dysfunction is

HF with reduced EF

Occurs when the left ventricle is unable to contract well against volume and unable to eject blood volume into the aorta


(impaired contractility and ejection)

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diastolic dysfunction is

HF with preserved EF

Inability of the left ventricle to accommodate blood volume during diastole at low to normal filling pressures.

(impaired filling and relaxtion)

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normal ejection fraction

50-70%

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clinical manifestations of LEFT ventricular dysfunction

  • dyspnea, orthopnea

  • fatigue

  • s3 gallop

  • pulomonary congestion (cough, crackles)

  • frothy sputnum (can be blood tinged)

  • altered mental status

  • manifestations of organ failure ex oliguria

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clinical manifestations of RIGHT ventricular dysfunction

  • jugular vein distention

  • edema

  • abdominal distention, ascites

  • fatigue weakness

  • nausea and anorexia

  • polyuria/nocturia

  • liver enlargement and tenderness

  • weight gain

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what medications improve symptoms of HF?

diuretics, digoxin, vasodilators, morphine

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do diuretics treat systolic or diastolic HF?

both! diuretics appropriate for systolic and diastolic HF. used most often in systolic HF. acute exacerbation of diastolic HF can use diuretics, but dont tolerate as well. give diuretic if symptomatic in diastolic 

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is digoxin used to treat systolic or diastolic HF?

  • digoxin helps heart pump more effectively. best for systolic. positive inotrope to increase contractility.

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do vasodiators treat systolic or diastolic HF?

vasodilators used in systolic dysfunction. decreases preload

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is morphine used to treat systolic or diastolic HF?

used for both. slows heart and helps pain. improves respirtroy symptoms

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what medications can help to increase survival rate in HF?

beta blockers, ACEi, spironolactone, ARBs, entresto(sacubitril/valsartan)

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do beta blockers treat systolic or diastolic HF?

beta for diastolic HF. decrease contractility

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do ACEi treat systolic or diastolic HF?

  • ACEi used for both. 

    • everyone on ACEi at discharge. gold standard 

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is spironolactone used to treat systolic or diastolic HF?

both

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what are some complications of HF?

  • hypertrophy

  • pleural effusion

  • thromboembolism

  • dysrrythmias

  • liver enlargment

  • kidney failure

  • electrolyte imbalances

  • cardiogenic shock

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sytolic dysfunction occurs when

Occurs when the left ventricle is unable to contract well against volume and unable to eject blood volume into the aorta

<p><span style="font-family: &quot;Century Gothic&quot;, sans-serif;">Occurs when the left ventricle is unable to contract well against volume and unable to eject blood volume into the aorta</span></p>
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diastolic dysfunction occurs when

Inability of the left ventricle to accommodate blood volume during diastole at low to normal filling pressures.

  • this can occur from the ventricles working too hard and the muscles becoming too large, making the chamber smaller and not able to fill as much

<p><span style="font-family: &quot;Century Gothic&quot;, sans-serif;">Inability of the left ventricle to accommodate blood volume during diastole at low to normal filling pressures.</span></p><ul><li><p>this can occur from the ventricles working too hard and the muscles becoming too large, making the chamber smaller and not able to fill as much</p></li></ul><p></p>
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what is cardiomyopathy and what can it lead to

diseased heart muscles causing impaired CO

  • can lead to heart failure, sudden death, or dysrhythmias.

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idiopathic cardiomyopathy

  • idiopathic= we dont know why it happened

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Dilated Cardiomyopathy

  • Left Ventricle becomes dilated and “floppy”

  • Cannot contract well

  • common in ppl with MI

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Hypertrophic Cardiomyopathy

  • Heart muscle thickening

  • Decreased size of ventricles

  • Decreased volume = decreased CO

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Restrictive Cardiomyopathy

  • Least Common

  • Fibrosis/Scarring of heart tissue

  • Ventricular stiffness results in unable to relax and fill 

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Takotsubo Cardiomyopathy

  • Temporary weakening of left ventricle brought on by extreme stress

  • The ”broken heart” syndrome (can be seen after death of loved one or other periods of extreme stress)

  • Presents like MI with chest pain

  • has EKG and enzymes  of MI but there is no blockage

  • reversible 

  • treated by reducing stress on heart (ex beta blockers)

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downsides of artifical hearts

bridge therapy (buys time, but not permanent for life). expensive and risky

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what is an LVAD? what are the downsides

  • mechanically implant pump to pump for pt 

  • bridge therapy. buys us time but not meant to last forever . does not solve problem 

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heart transplantation pros,cons, and important considerations

  • best solution for failing heart

  • low supply of hearts 

  • key considerations 

    • anti rejection medications and regiment must be adhered to

    • no nerve connection in transplanted heart 

      • poor innervation to heart means they cant feel pain in heart if MI occurs. look for symptoms besides pain 

      • vagus nerve severed so meds that work on vagus nerve (ex atropine) dont work

    • heart transplant maybe last 10-20 years

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s1 heart sounds are caused by

mitral & tricuspid valves closing

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s2 heart sounds are caused by

aortic & pulmonic vlaves closing

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heart sounds are the sound of

valves closing

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when someone has stenosis you will hear

clicking or extra sound

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when someone has regurgitation you will hear

whooshing

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regurgitation

The valve does not close properly, and blood backflows through the valve

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stenosis

The valve does not open completely, and blood flow through the valve is reduced

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valve prolapse

  • The stretching of an atrioventricular valve leaflet into the atrium during diastole

  • pretty similar to regurgitation

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should aortic and pulmonic valves be open or closed during systole? what does it mean if they are not?

OPEN in systole. if hard to do=stenosis

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should mitral and tricuspid valves be open or closed during systole? what does it mean if they are not?

CLOSED. if they dont=regurgitation

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should aortic and pulmonic valves be open or closed during diastole? what does it mean if they are not?

CLOSED. if they arent = regurgitiation

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should mitral and tricuspid valves be open or closed during diastole? what does it mean if they are not?

OPEN. if this is hard to do= stenosis

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mitral valve prolapse. what causes it? what are symptoms? what type of murmur is this?

  • Leaflet(s) buckle back into the left atrium during ventricular systole 

  • systolic murmur often asymptomatic

  • can be inherited or from endocarditis


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mitral regurgitation. what causes it? what type of murmur? what are symptoms?

  • can be from MI, ruptured papillary muscles or endocarditis

  • Valve allows blood to return to left atrium from the left ventricle during systole

  • systolic murmur

  • risk for clots

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mitral stenosis. what causes it? what type of murmur is it? what are symptoms

  • Obstruction of flow from left atrium to left ventricle

  • caused by endocarditis

  • SOB, DOE, pulmonary congestion

  • diastolic murmur

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aortic stenosis. what causes it? what type of murmur? what are symptoms?

  • caused by malformations, age, or endocarditis

  • systolic murmur

  • can cause left ventricle muscle to thicken bc it has to work harder