Week 2: Acute Cardiac Conditions

Coronary Artery Disease (CAD)

• chronic stable angina and acute coronary syndromes

• waxy substances (plaque) builds up inside the coronary arteries

  • leading to atherosclerosis

• IS preventable

How is CAD diagnosed?

• cardiac cath

• angiogram

• ECG and Echo are helpful

CAD Non-Modified Risk Factors

• family history

• increasing age

  • >45 males

  • >55 females

• ↑ incidence in African Americans

• premature menopause and pregancy-associated disorders

CAD Modifiable Risk Factors

• hyperlipidema

• tobacco use

  • damages epithelium

• HTN

• Diabetes

• Metabolic Syndrome

• Physical Inactivity

• Chronic inflammatory conditions

  • Rheumatoid arthritis, lupus, HIV

CAD: Hyperlipidemia Risk Factor

• elevated cholesterol levels

• forms plaques

• statins can be used to lower bad cholesterol

Tobacco Use: Hyperlipidemia Risk Factor

• smoking impacts heart health

• damages epithelium

• cessation strategies

HTN: Hyperlipidemia Risk Factor

• endothelial damage (injury to vessels)

• blood pressure management

Diabetes: Hyperlipidemia Risk Factor

• chronic ↑ blood sugar → endothelial damage

  • lifestyle modifications are needed

Metabolic Syndrome: Hyperlipidemia Risk Factor

• assess waist size → adipose tissue in abdomen is more active → release cytokines that induce inflammatory activity in vessels

• inflammation can:

  • damage endothelial damage

  • promote plaque formation

  • increase insulin resistance

  • ↑ risk of HTN, HD, and stroke

Chronic Inflammation Conditions: Hyperlipidemia Risk Factor

• Aortic aneurysm → main cause is atherosclerosis

  • All vessels are linked → disease in one area of vessels may be indicative of disease in other areas

  • Excess circulating lipids

• Chronic kidney disease

  • Impact on cardiovascular health

  • slows down the body’s ability to clear out fats

Peripheral Venous Disease (PVD)

• Dysfunction or damage to one-way venous valves in the lower extremities.

• Prevents efficient blood return to the right side of the heart, leading to venous stasis

  • (pooling in legs).

• Manifests as lower-extremity edema

• increases the risk of DVT

Atherosclerosis

• Abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen

  
  

Atherosclerosis Pathogenesis

1. damaged endothelium

2. fatty streak and lipid core formation

   1. lipids accumulate

3. fibrous plaque

   1. raised plaques are visible

   2. blood flow is reduced

4. complicated lesion: artery blockage that has burst open and formed a blood clot

When does Classic (Stable) Angina Pectoris occur?

• occurs with stress or exertion

Classic (Stable) Angina Pectoris

• chest pain or discomfort

• chest pain resolves in 15 mins

• relieved with nitroglycerin

Unstable (Pre-infarction) Angina Pectoris

• occurs frequently with progressive severity

• does NOT get better with rest

• unrelated to activity (unpredictable)

Why does Stable and Unstable Angina Pectoris occur?

• artery narrowing

• partial occlusion

Variant Angina Pectoris

• occurs DURING rest

• caused by vasospasm

  • can be caused by nicotine or cocaine

Myocardial Infarction (MI)

• Prolonged ischemia of the heart muscles caused by an imbalance between oxygen supply and demand

• increased workload of the heart due to the plaque buildup

What are the causes of MIs?

• plaque rupture

  • protective cap over an atherosclerotic plaque ruptures → blood clot forms to try to heal it →occludes the entire lumen

• spasm

  • muscle severely constricts → blood cannot pass through

• inflammation

  • damage

Ischemia

• blood flow and oxygen to a part of the body are reduced or blocked

EKG Change: Ischemia

• inverted T wave

EKG Change: Injury

• ST elevated

EKG Change: Infarction

• wide Q wave

• delay in depolarization of ventricles → widened Q wave is a sign of irreversible damage to the ventricles

MI Assessment

• chest pain

• HTN (early)

• HoTN (shock)

• ↑ HR

• ↓ HR (damage)

• S3 and S4 heart sounds

• N/V

Chest Pain in MI

• “squeezing, choking, smothering”

• chest pain not relieved by rest or nitro

• women: discomfort in the arms, back, neck, jaw, or stomach

MI: Hypertensive Response

• happens early

• body is responding to pain, anxiety, and decreased O2

• sympathetic nervous system (fight or flight)

• release of epinephrine and norepinephrine → constricts blood vessels → ↑ BP

HoTN during MI

• cardiogenic shock

  • damaged heart cannot pump enough blood/O2 to maintain adequate circulation

• due to blockages

• often MORE concerning

Tachycardia in MI

• The body senses that the heart muscle is not getting enough oxygen and activates the sympathetic nervous system.

• Release of epinephrine and norepinephrine → ↑HR

Bradycardia in MI

• Damage to the heart’s electrical conduction system

• SA/AV node ischemia → HR ^*

• 3rd degree heart block

S3 and S4 Heart Sounds in MI

• S3 and S4 are extra heart sounds

• S1 and S2 are normal

S3 Heart Sounds in MI

• Volume overload, poor ventricular pumping. Damaged ventricle.

• “The ventricle is failing”

• MI Relation: shows heart failure after MI

• S1-S2-S3 (“ken-tuc-ky”)

S4 Heart Sounds in MI

• Atria contract to force blood into a stiff, non-compliant ventricle

• “The ventricle is stiff”

• MI Relation: acute ischemia or recent MI

• S4-S1-S2 (“ten-nes-see”)

Diagnostic Labs: MI

• Troponin T and Troponin I

• Creatine Kinase-MB (CK-MB)

• Myoglobin

• CBC

• 12-lead EKG

• cardiac cath.

• chest x-ray

Troponin T and Troponin I

• GOLD STANDARD for MI marker

• released from heart when there is strain

• NSTEMI = elevated troponin but no ST changes

How long does Troponin T and Troponin I stay elevated for?

• elevated within a few hours of acute MI

• remain elevated for 3 to 6 days

Creatine Kinase-MB (CK-MB) in MI

• creatine kinase isoenzyme found mainly in heart

• begins to increase within a few hours of chest pain

• peaks within about 24 hours

Why is CBC needed in MI?

• anemia can cause MI

• checks for bleeding

• checks coagulation

Emergency Management of the Patient with ACS/MI

• Assess ABCs (Defibrilate)

• O2 sat > 95%

• ECG within 10 mins

• Assess pain

• RRT (rapid response team)

• Vascular access needed

• Aspirin

Why is morphine used during MIs?

• used for pain

• reduces preload

  • workload of heart

• *can cause respiratory depression

Oxygen Saturation with MI

• keep > 95%

• supernormal O2 can be bad

MI: Collaborative Management

• Reperfusion Therapy: Fibrinolytics ("clot-busting" drugs)

  • Door-to-needle goal of 30 minutes

  • Door-to-balloon time is 90 minutes

• Tissue Plasminogen Activator (t-PA)

What is reperfusion therapy (fibrinolytics)?

• Fibrinolytics dissolves thrombi in coronary arteries and restores myocardial blood flow

What is Tissue Plasminogen Activator (t-PA)?

• Powerful "clot-busting" medication

• *Carries a severe risk of dangerous bleeding

MI: Ongoing Management

• continuous EKG

• O2

• pain relief

• prevent complications

• glycemic control

MI: Complications

• dysrhythmias

• HF

• cardiogenic shock

• papillary muscle rupture

• wall rupture

• acute kidney injury

• hyperglycemia

What dysrhythmias occur with MI?

• Vtach, Vfib

• Vtach with pulse → synch cardioversion

Why does HF occur with MI?

• arteries and veins become more sensitive to vasopressors when people age

• the loss of blood flow during an MI deprives the heart muscle (myocardium) of oxygen

Papillary Muscle Rupture in Acute MI: Pathophysiology & Management

Mitral valve damaged → blood back flows → pressure in lungs, low blood flow to body → SOB, hypotensive → emergent valve replacement (surgery)

Why does blood glucose increase with MI?

• stress of MI can increase cortisol

• high cortisol → increases blood sugar

What is reperfusion therapy?

• critical medical treatment that restores blood flow to blocked blood vessels

• gold-standard reperfusion therapy: Percutaneous Coronary Intervention (PCI)

  • threading a catheter to the blockage

  • inflating a tiny balloon to open the artery, and placing a stent

Reperfusion Therapy Timing

• door-to-needle = 30 minutes

  • start catheter

• door-to-balloon = 90 minutes

  • balloon to open vessel

Reperfusion Therapy: Collaborative Management

• advice pt to stay still

• feeling warm/hot is normal when dye is infused

• HOLD anticoagulants 3 days before cath.

• dual antiplatelet therapy

What is dual antiplatelet therapy used in post reperfusion therapy?

• Aspirin + Clopidogrel (Plavix)

• use for 1 year

• prevents re-stenosis (re-narrowing)

What is Coronary Artery Bypass Graft (CABG)?

• surgeons take a healthy blood vessel from another part of the body and use it to create a detour around blocked or narrowed coronary arteries

The Bypass Machine

• temporarily takes over your heart and lung functions, circulating and oxygenating blood while the surgeon temporarily stops your heart to perform the grafts safely

What is the goal of The Bypass Machine

• maintain cardiac and pulmonary function

Risks of The Bypass Machine

• coagulopathy

• increased bleeding risk

• inflammatory response

  • due to contact with artificial surfaces in bypass machine

Coronary Artery Bypass Graft (CABG): Collaborative Management (before)

• skin prep: clip vs shave

  • shaving can increase infection risk

• medication: surgical antibiotic prophylaxis

Inflammatory & Structural Heart Disease: Regurgitation

• valve does NOT CLOSE properly and blood backflows through the valve

• causes high volume problem

• ex. mitral valve not closing → back flow to left atrium → into lungs

Inflammatory & Structural Heart Disease: Stenosis

• valve does NOT OPEN completely (narrowing) and blood flow through the value is reduced → murmur

• valve is calcified and stiff

  

Valve Prolapse

• stretching of the valve leaflet into the atrium during systole

• mitral has two leaflets

• valve become floppy, weirdly shaped

Causes of Valvular Heart Disease?

• Rheumatic heart disease (RHD)

• Endocarditis

• Marfan’s syndrome (tall, thin)

  • Can cause valve prolapse

• Congenital

• Age-related valve calcification (aortic stenosis)

  • Need valve replacement to maintain CO

• ACS/MI

Valvular Heart Disease: Nursing Priority Problems

• Decreased cardiac output related to valvular incompetence

• Excess fluid volume related to heart failure

• Activity intolerance related to decreased cardiac output

• HF is a concern

  • Check wt, medication management

What is Endocarditis

• An infection of the endocardial surface including valves, caused by bacterial, fungal or viral agents

Endocartditis: Possible Ports of Entry

• Oral cavity

• Skin rash/lesion/abscess

• Surgery or invasive procedure

Endocarditis: Clinical Manifestations

• fever

• new heart murmur

• Osler nodes, Janeway lesions, Roth spots, and splinter hemorrhages in nailbeds

Endocarditis: Osler’s Nodes

• Painful, erythematous or purple, pea-like nodules

• Most commonly found on pads of fingers & toes

Endocarditis: Janeway Lesions

• Nontender, erythematous & nodular or lesions

• Most commonly found on palms & soles

Endocarditis: Roth’s Spots

• Oval-shaped, white-centered hemorrhages

• Present on retina during fundoscopic exam

Endocarditis: Splinter Hemorrhages

• Small, linear hemorrhages under the nails that are usually asymptomatic

Infective Endocarditis: Collaborative Management

• A serious, life-threatening infection of the inner lining of the heart chambers and valves

• Obtain blood cultures BEFORE starting antibiotics.

• Specific type of endocarditis