Cv disease and MI

Acute coronary syndrome

Acute chest pain due to

• Unstable angina (temporary considered ACS cause it’s unstable)

• Acute myocardial infarction (permanent scar tissue, no electrical conduction)

  • Non-STEMI

  • STEMI

Cardiovascular disease statistics in the united states

Leading cause of death for men and women and most racial and ethnic groups

Life’s essential 8

Sleep, healthy food/diet, exercise, normal blood sugar for people with diabetes, good weight, normal lipid levels (this lowers plaque build up in the arteries), good bp, no smoking

Disparities

Non-white individuals receive less guideline related care and have higher adverse outcome compared with white individuals

Sexual minorities have higher rate of CV disease than cisgender individuals

Modifiable risk factors

Hyperlipidemia, cigarette smoking, hypertension, diabetes, metabolic syndrome, obesity, physical inactivity, chronic inflammatory conditions, chronic kidney disease, excessive alcohol use

Non modifiable risk factors

Family history/ genetic profile, age, gender, race

Coronary arteries

Right cornary artery (first, feed) → Distal right coronary artery (long thin branches on bottom of heart)

Left coronary artery (branches quick) → Circumflex coronary artery (circles around) → Left anterior decending coronary artery

Myocardial infarction defintion

Acute onset of myocardial ischemia (not getting enough oxygen) that results in myocardial death (oxygenated blood not getting where it needs to be)

Myocardial infarction pathophysiology

Plaque rupture (bleeding) → Platelet activation (gathers at rupture) → thrombus formation (clot seals off vessel) → complete vessel occlusion (there is likely some amount of dead tissue)

Necrosis of myocardial cells supplied by occluded vessel

Use of aspirin (antiplatelet, breaks down clot a little bit, low dose 81mg, enteric coated: can’t break down in the stomach breaks down later rather them take a chewing aspirin in emergency)

Necrosis is irreversible

• Results in non-functional area of myocardium (not pumping or conducting its just there)

• Infarcted area can longer act as a pump or conduct electricity

If the thrombus completly occludes the vessel, this will likely cause a STEMI

If the clot partially occludes the vessel rhen this is manifested as unstable angina/ NSTEMI

Prolonged ischemia

>20 minutes → cellular death begins

Ischemic tissue

• May not have normal contractility

• Has an increased risk of dysrhythmia formation

Infarction develops over minutes to hours

Enzymes release in cell death

Troponin (big one, if there is damage to the tissue this is released and you can tell days later)

Creatine phosphokinase

Myoglobin

Lactic dehydrogenase

Type of MI

Based on an EKG but it can be a STEMI or NSTEMI

Location of MI

Which part of the heart has been damaged

• Anterior, lateral, inferior, posterior (all in the left ventricle when there is one on the right it will say right ventricle MI)

Point of time MI

Acute, evolving, resolved

• Can tell when its happening on EKG

ST elevation MI

STEMI

Transmural or full thickness

If whole wall is dead when its healing the macrophages come it can cause a rupture

Non ST elevation MI

NSTEMI

Subendocardial- partial thickness

Acute MI - CV signs and symptoms

Chest pain

• Severe, sudden, crushing (pressure like someone is pushing on your chest), unrelieved by rest or nitroglycerin (not relieved because its a vasodilator if given by mouth it’s more a venodilator that decreases the workload of the heart but doesn’t get rid of the clot, when you dialate the veins the blood stays down in the feet decreasing demand

• Often radiates to one or both arms, jaws, neck, and back

New murmur, S3 or S4 heart sounds

If heart failure is present JVD, SOB

Dysrhythmias

BP increases or decreases (pulse up presssure down bad, pulse up pressure up good)

EKG changes

Clinical presentation associated symptoms

SOB/ pulmonary edema, diaphoresis, palpitations, nausea/vomiting, anxiety, feeling of impending doom, skin cool, clammym cardiac arrest, shock, dysrhythmias, low-grade fever- later sign (comes with tissues dying and macrophages come in and clean it up), cardiac enzyme elevation, EKG changes, vital signs

Brief physical exam

ABCs, vital signs, general observation

Neuro

• Stroke symptoms, restlessness, lightheaded, anxiety

Cardiac

• Chest pain, EKG changes, JVD, murmurs, S3, S4, pulses

Pulmonary

• Crackles, resp distress, tachypnea, pulmonary edema

GI

• Nausea/vomiting

GU

• Urine output

Skin

• Cool, clammy, diaphoresis, pale

Psychosocial

• Feeling of impending doom, fear, denial

Aortic dissection

Layers ripping apart often related to increase BP

Pulmonary emoblism

People who are on bed rest, afib, post-surgical, long plane flights, cancer pt, birth control pills

Esophageal rupture

Varocies, getting stuff in throat, dilation

Pneumothorax

We put in a chest tube to prevent dying

Special consideration - atypical considerations

Women

Elderly (decreases ability to deceive things)

Diabetes (nerve damage)

Transplanted heart (Nerve damage)

Diagnosis

History and physical

12 lead EKG

Serum enzymes (primarily focus on troponin)

Diagnosis - EKG

Ischemia (temporary, can fix if you get rid of it try to decrease the workload/demand)

• ST segment depression (goes down below baseline, electrolyte abnormalities can cause this)

• T wave inversion

Injury (tissue starting to die, move to MI

• ST segment elevation

Infarction

• Pathologic Q waves (dead tissue, >1 box deep and wide, not conducting electricity moves away) develop permanently with STEMI

• Irreversible damage

EKG

Pathologic Q wave is a deep initial deflection and is permanent on the EKG

Goes down 5 tiny boxes

If you get to the hospital during the acute phase it can be reversed

Q waves develop over time and stays

ST and T will change but then go back to normal

Inferior wall MI

Looking from the bottom up: 2,3, and avf

All have ST elevation and hyperacute MI (starting right now)

Others have ST depression, if something changes you’ll see the mirror of that ST depression

ST segment elevation

Seen on a 12 lead

V3, 4, 5, 6 ST elevation lateral wall Mi

First 6 showing picture from front of the heart it lost electricity in QRS can’t really see it

Diagnosis - enzymes

Serum enzymes

Enzymes are released as cellular necrosis occurs

Troponin

• Very specific for cardiac cellular death (look at all the time starts like an hour or two behind but stays in the bloodstream for 1-2 weeks)

• rises 3-6 hours after injury

• Peaks 12-18 hours

• Stays elevated for 1-2 weeks

Other enzymes that rise

• creatine phosphokinase CPK

• Lactic dehydrogenase LDH

• Myoglobin (MD portion specific to the heart)

Goals of therapy

Relieve symptoms

Prevent or minimize myocardial tissue death (quicker you come in the quicker we can save cells)

Prevent complications

Guidelines for treatment of a STEMI

Rapid transport to the hospital- activate EMS

History/physical exam

12 lead EKG- to be read within 10 minutes

Obtain blood for cardiac biomarker- troponin

Routine medical interventions

• Aspirin- chewable 162mg to 325mg (2-4 baby aspirin or 1 adult aspirin)

• Oral beta blockers- intiated in the 1st 24 hours

• Renin- angiotensin- aldosterone system inhibitors- for all patients with an anterior wall MI, with an EF <40, HF or DM

• Anticoagulation

  • P2y12 inhibitor (clopidogrel), heparin (doesn’t break up the clot just prevents it from moving), glycoprotein IIb/IIIa agents (epitifibatide/Integrilin), direct thrombin inhibitors (Argatroban, bivalirudin)

Evaluate for reperfusion therapy

Reprefusion- for eligible patients with symptoms within the past 12 hours

• PCI (percutaneous coronary intervention) capable facility- door to balloon time 90 minutes

• Non-PCI capable facility - transfer to PCI capable facility if <120 minutes to balloon time

Pokes a hole in coronary artery puts a cactheter in with balloon on end and fixes blood vessel

Biggest complications is breaking the vessel

If PCI cannot be done in <120 minutes, in the absence of contraindications, administer fibrinolytics

If fibrinolytics are given, they should be administered within 30 minutes of arrival to hospital (door to needle time)

You don’t do both fibrinolytics and PCI you do one or the other

Nursing considerations

IV access

Monitoring vital signs/hemodynamic stability

Continuous cardiac monitoring

Labs

• Troponin

• Electrolytes, BUN, Creat, CBC with platelets ct, INR, Magnesium (mag of 2 and potassium is prone to arrythmias), glucose, serum lipids, aPTT

Patient support and education

Myocardial reperfusion

Percutaneous coronary intervention

Fibrinolytics

Invasive coronary intervention

Percutaneous Coronary intervention (PCI)

Invasive procedure used to assess coronary arteries

It is done in the acute setting as well as on an elective basis

PCI stent insertion

Invasive procedures

• Coronary stent placement

• Done during the cardiac catherization

Cardiac catherization/PCI post procedure care

Monitor for dysrhythmias, chest pain, neurologic changes (if plaque breaks off and goes to the brain)

Bedrest for at least 4 hours (if they went through the femoral artery)

HOB no higher than 30 degrees

Frequent VS check every 15 min x’s 4, every 30 minutes x’s 4, and every hour x’s 4 (pulse up pressure down means bleeding, any angiography)

Assess distal pulses with each VS check

Assess for bleeding or hematoma with each VS check (look for oozing under bandage not gonna spurt up)

Monitor I/O

• Increase fluid intake or IV fluids to prevent contrast induced nephropathy (we want to flush out the kidneys)

• Acetylcysteine- Mucomyst

Complications of a PCI

Hematoma

Vascular complications (careful breaking vessels, plaque ruptures)

Embolism (plaque embolism bad no way to fix)

Hypersensitivity to contrast dye (treating with benadryl)

Dysrhythmias

Bleeding

Restenosis

Stroke

Contrast induced nephropathy

Fibrinolytics

Activate the body’s own fibrinolytic system to lyse coronary clots

Diagnosis of STEMI must be confirmed

Done if PCI connot be done within 120 minutes

Damaged tissues (can happen anywhere), blood vessels or organ stimulate platelet aggregation

A platelet plug forms over damage vessel

Clotting cascade is intiated

Vasconstriction occurs

Fibrin surrounds platelets to form a clot

Fibrinolytics- absolute contraindications

Prior intracranial hemorrhage/hemorrhagic stroke

Known cerebral vascular lesion or neoplasm (cancer)

Ischemic stroke within the last 3 months (embolic strokes can lead to bleeding 3 months later)

Suspected aortic dissection

Active bleeding

Recent major surgery or trauma

Severe uncontrolled hypertension (unresponsive to emergency therapy)

Known bleeding disorders

Pregnancy

Intracranial hemorrhage

The most feared complication of fibriniolysis (head bleed we don’t have a good treatment)

Fatal in 80% of cases

Usually occurs within the first 24 hours

Incidence 0.5-1%

Risk factors for intracranial hemmorrhage

Age >65 years

Weight >70Kg

Female gender

HTN on admission

(if you have bad blood vessels in the legs you probably have bad one is the heart and head)

Risk is similar to different agents

Evidence of reperfusion

Reperfusion dysrhythmias (PVCs, accelerated idioventricular rhythm)

Abrupt cessation of chest pain

• Though may not be a reliable indicator especially when morphine us used

• Pain is subjective

Rapid return of St segment to baseline

• Very good indicator of reperfusion

Best predictor of reperfusion is the cessation of chest pain coupled with ST segment return to baseline

After fibrinolytic therapy

Indications for transfer to PCI-capable hospital after fibrinolytic therapy

• Development of cardiogenic shock

• Urgent transfer for failed reperfusion

• Instable patients between 3 and 24 hours after successful fibrinolysis

Fibrinolytics. have no effect on the underlying atherosclerosis lesion

Nursing care of a patient recieving fibrinolytics - post infusion care

Frequent assessment of VS

Continuous EKG monitoring

Observe for evidence of bleeding- decreased BP and increase HR

• Assess body fluids for evidence of bleeding

• Flank pain/back pain- may indicate retroperitoneal bleeding

• Assess LOC - intracranial bleeding

• Assess puncture sites for bleeding

• Anticipate the need to apply additional pressure at puncture sites

Evaluate response therapy

Report manifestations of re-occlusions

Minimal handling of the patient

• Bedrest for 6 hours

Avoid injections

Best to insert 2 IV’s prior to administration

Prophylactic H-2 blockers

Anticoagulation may be recommended after fibrin therapy to improve vessel patency and prevent re-occlusion

• IV heparin

• Enoxaparin

Non-invasive testing

Echocardiogram

• Ultrasound examination of the heart

• Looks at heart and valvular function (looks at regurgitation and stenotic)

• Done as transthoracic (bouncing soundwaves off chest, thorax) or transesophageal (probe goes down the throat behind the heart)

Thallium testing may also be done (stress echo)

Ejection fraction is how much blood is pumped out with each beat

Complications of acute MI

Cardiogenic shock

Heart failure

Dysrhythmias

• Ventricular

• Slow- bradycardia, AV, heart block

Pericarditis (inflammation of pericardial sack)

Papillary muscle rupture (these hold the AV valves in place and if muscles die they can let go and cause regurgitation)

Wall rupture (very low incidence)

• Septum

• Ventricular free wall

LV aneurysm (weak part of tissue buldges out when rest of heart squeezes)

Bleeding

AKI

Anoxic brain injury if there was a cardiac arrest (best CPR is about 1/3-1/4 as good as their heart before)

Complications of heart failure/pulmonary edema

Infarcted tissue does not pump

Acutely may require vasopressor support and intubation

Treat with medications

• ACE inhibitors (decrease workload of the heart by blocking the renin-angiotensin system)

• Beta blockers (decrease workload of the heart block beta 1 and 2)

• Diuretics (decrease workload of the heart corrects any problems in fluid overload)

• Aldosterone antagonist (Use diuretics w/o wasting potassium and blocking aldosterone, bring sodium back → water follows aldosterone can cause random cell death)

Complications - dysrhythmias

Scar-electrical instability

Ventricular dysrhythmias

• Increased risk - EF 30% or lower ventricular dysrhythmias (lower EF the higher amount of blood that just sits in the ventricles)

• Implantable cardioverter/defibrillator (ICD)

• Anti-dysrhythmic drugs (all have side effects even sudden death)

slow heart rate

• Bradycardia or heart blocks- may require a pacemaker (symptomatic brady you have to start atropine then dopamine, EPI, or pacing)

Complications

Papillary muscle rupture

Mitral valve dysfunction

Right side of tricuspid if they have a rupture

LV aneursym

Wall rupture

Pericarditis

Nursing care cardiac assessment

Vital signs

Evaluation and relief of chest pain

Assessing heart failure

Monitoring dysrhythmias

Nursing care evaluation of adequate perfusion

Level of conciousness

Adequate urine output

Gastrointestinal symptoms

Skin temperature (cool,clammy)

Capillary refill

Nursing care for patients with chest pain

Assess and document CP

Vital signs including heart rhythm

Assess skin temperature

12L EKG

Decrease physical activity

Oxygen, NTG, Morphine if indicated

Provide a restful environment

Small meals

Assist with ADLs

Avoid straining- stool softeners needed

Help patient to relax

Teach patient to recognize symptoms

Interprofessional care

Dietitian (especially on low sodium or diabetes)

Cardiac rehabilitation (can be outpatient programs are really good)

Physical and occupational therapy

Statin therapy

Lowers cholesterol

Provide plaque stabilization

Angiotensin converting enzyme inhibitors

If MI is anterior wall

HF and an EF <40%

Aldosterone antagonist

Spironolactone

EF <40%

Symptoms of HF

Diabetes

Dual antiplatelet therapy (DAPT)

If stent was put in

Aspirin

Clopidogrel (plavix)

Discharge instructions

Call 911 for CP/SOB and associated symptoms

Seek immediate care for

• Unusual fatigue

• Rapid pulse

• Bleeding

  • Urine, stool, nose, etc.

• Low urine output

• New or increased swelling in feet or ankles

Medications

• Take as prescribed

• Notify provider for side effects of medications

• Education on medications

  • Indications

  • Side effects

• Manage other health conditions i.e. diabetes

• Regular checks of BP -120/80 a lot have a high bp

• Annual flu shots

Lipid management

Lifestyle modifications

• Heart healthy diet

• Smoking cessation

• Exercise- cardiac rehab

• Maintain ideal body weight

  • BMI 18.5 - 24.9

• Manage stress

Keep follow up appointments