CAD, ACS, MI

coronary artery disease

blood vessel disorder

coronary arteries supply your heart with oxygen, blood, and nutrients; specific to the heart

atherosclerosis begins as soft deposits of fat that harden with age, can occur in any artery in the body

when fat deposits form in the coronary arteries it is called CAD

pathophysiology of CAD

lipid deposits within the intima, the innermost layer of the arterial wall

a layer of endothelial cells lines the intima to provide a barrier between blood and the arterial wall

this changes with endothelial inflammation and injury

chronic endothelial injury —> fatty streak (earliest lesions) —> fibrous plaque (beginning of progressive changes in the endothelium of the arterial wall) —> complicated lesion (last stage and most dangerous)

want the LDLs low and the HDLs high

collateral circulation

normally some arterial anastomoses or connections, called collateral circulation, exist within the coronary circulation

two factors exhibit to the growth: inherited predisposition to develop new blood vessels (angiogenesis), and presence of chronic ischemia

risk factors for CAD

increasing age, gender, ethnicity, genetic predisposition and family hx of heart disease

total cholesterol over 200

triglycerides over or equal to 150

LDL cholesterol over 130

HDL cholesterol less than 40 in men and less than 50 in women

HTN, diabetes, tobacco use, physical inactivity, obesity, waist circumference over or equal to 102cm in men and 88cm in women

contributing factors to CAD

psychosocial risk factors

high CRP, lipoprotein, and homocysteine levels

substance abuse

management and tx of CAD

identifying high risk persons

managing high risk patients

physical activity

nutrition

hyperlipidemia drug therapy

restrict lipoprotein production: HMG-CoA reductase inhibitors (statins), niacin, fibric acid derivatives, ATP-citrate lyase inhibitor, omega 3 fatty acid

increase lipoprotein removal: bile acid sequestrants, proprotein convertase/kexin 9 inhibitors

decrease cholesterol absorption

gerontologic considerations

aggressive tx of HTN and hyperlipidemia

tobacco cessation

physical activity

make modest diet changes

acute coronary syndrome

prolonged chest pain from ischemia that is not immediately reversible: unstable angina, NSTEMI, STEMI

caused by atherosclerotic plaque

heart muscle becomes hypoxic within the first 10 seconds of total coronary occlusion

irreversible heart damage starts after 20 minutes if there is no collateral circulation

unstable angina

chest pain that is new in onset, occurs at rest, or occurs with increasing frequency, duration, or less effort than the pt’s chronic stable angina

does not have to have a hx of stable angina

pain usually lasts 10 minutes or more

must be treated immediately

STEMI vs NSTEMI

STEMI:

• emergency!!!

• caused by occlusive thrombus

• ST elevation in the ECG leads facing the area of infarction

• artery must be opened within 90 minutes

• can use PCI or thrombolytic therapy

• 12 lead could give you an idea to where the blockage is

NSTEMI:

• caused by nonocclusive thrombus

• does not cause ST segment elevation on the 12 lead ECG

• do not need emergent cath but usually undergo one within 12-72 hours

• thrombolytic therapy is not an option

• cardiac biomarkers

clinical manifestations of MI

persistent pain —> consistent pain that does not change

heavy, pressure, tight, burning, constricted, or crushing

substernal or epigastric area

pain may radiate to the neck, lower jaw, and arms or to the back

pain often occurs while the pt is active or at rest, asleep, or awake

diaphoresis, skin may be ashen, clammy, or cool to touch

high BP and HR —> if BP drops = cardiogenic shock

may cause decreased renal perfusion and urine output

crackles, JVD, hepatic engorgement, peripheral edema —> going into HF

n/v

fever

complications from MI

dysrhythmias: most common complication after MI

VT and VF are the most common cause of death in pts in the prehospital period

PVCs may precede VT and VF

pt with symptomatic bradycardia may require an external pacemaker or a temporary transvenous pacemaker

HF

cardiogenic shock

papillary muscle dysfunction or rupture

left ventricular aneurysm

ventricular septal wall rupture and left ventricular free wall rupture

pericarditis

dressler syndrome

MI diagnostic studies

ECG 12 lead

serum cardiac markers: proteins released into the blood from necrotic heart muscle after an MI; cardiac specific troponin biomarkers are highly specific indicators of MI

cardiac cath: STEMI must undergo within 90 min of presentation to ED or receive thrombolytic therapy within 30 min in agencies without PCI capability

MI tx

emergent percutaneous coronary intervention

thrombolytic therapy

nutrition: NPO, advance as tolerated, low salt, low fat, low cholesterol

MI drug therapy

IV nitro- initial tx

morphine

beta blockers

ACE inhibitors and ARBs

antidysrhythmic drugs

lipid lowering drugs

aldosterone antagonists

stool softeners

nursing management of MI

acute care: VS, ECG, 12 lead, cardiac biomarkers, maintain bed rest

pain: nitro, morphine, supplemental oxygen

monitoring, rest and comfort, anxiety, emotional behaviors, pt teaching, physical activity, cardiac rehab, resuming sexual activity