Cardiac Exam 1

5 components of heart disease

CAD, valvular disease, cardiomyopathy, arrhythmia, congenital heart disease

chronic coronary disease

progressive buildup of plaque in coronary arteries

• includes both CCS and ACS

chronic coronary syndrome (CCS)

stable presentation of ischemia and angina

• long term diagnosis

acute coronary syndrome (ACS)

unstable or acute presentation of ischemia and angina, may be life threatening (MI)

• short term diagnosis

prevalence of CHD

increases with age, appears midlife (40-50s), more prevalent in males but more females will die from it (diagnosed later)

4 parts of a cardiac assessment

1. complete patient hx

2. identify cardiac risk factors

3. complete physical exam

4. evaluate labs and diagnostic tests

patient hx info to gather

• age, sex

• medical conditions

• medications

• employment

• tobacco/alcohol use

• nutritional status

• activity level

• general family hx

• present illness

common physical complaints to screen for

cough, SOB, dyspnea on exertion, hemotypsis, palpitations, syncope, angina, edema, fatigue, impotence, constipation

pulmonary screening questions

SOB (position, worsen with activity, awaken from sleep, need to prop up with pillows)

Cough (dry or wet, cough of blood)

angina screening questions

• what does it feel like

• where is it located

• how long does it last

• what other sx occur with it (SOB, N/V, sweating)

• what makes it worse/better

genitourinary screening questions

erectile dysfunction (can precede CAD by 2-3 years)

urination (overactive bladder, getting up in middle of night)

age and FH - cardiac risk factors

male >/= 45, female >/= 55

FH of early CV event (male < 55, female < 65)

• primary relative - parents, siblings

cardiac risk factors

• HTN

• Hyperlipidemia

• DM

• metabolic syndrome

• CKD

• tobacco and heavy alcohol use

• COPD

• hx of other CV disease

• obesity

• cancer

• chronic inflammatory dz

• cancer

• HIV

• pregnancy complications

• physical inactivity, poor nutrition

• stress

• depression

4 parts of cardiac physical exam

observation, inspection, palpation, auscultation

observation/inspection (cardiac physical exam)

pt in discomfort (sweating, difficultly breathing)

note scars, chest deformities

look for apical impulse (where apex hits chest wall)

normal HR

60-90 bpm

palpation of pulses

rate AND rhythm

point of maximum impulse (PMI)

contraction of apex of left ventricle

• normally in midclavicular line at fifth intercostal space

• if left ventricle dilated, PMI becomes laterally displaced

systole

contraction of ventricles

• sound from closure of tricuspid and mitral valves

• S1 (lub)

diastole

relaxation of ventricles

• sound from closure of pulmonic and aortic valve

  • S2 (dub)

S3

heard early in diastole after S2

• caused by blood from left atrium colliding with blood in overfilled ventricle during early filling

S3 physiologic

children and adults < 30

• normal

S3 pathologic

associated with increased fluid due to HF

S4

heart late in diastole before S1

• created by blood trying to enter a stiff noncompliant LV during atrial contraction

What is S4 associated with (pathologic)?

associated with LVH secondary to longstanding HTN, CCD, hypertrophic CM

murmur

related to sounds of valves

• scale from 1/6 to 6/6 (quiet to loud)

aorta

brings blood from heart to body

left coronary artery (left main)

supplies blood to left atrium and ventricle

circumflex artery

delivers oxygenated blood to heart’s left chambers

left anterior descending artery

supplies blood to bottom portion of heart

• extends from left main down

right coronary artery

supply blood and oxygen to right side of heart

collaterals

branch off epicardial arteries to form secondary network between heart’s main coronary arteries

pre-arterioles

located on epicardium of heart (outer layer)

important in vasodilation

supply blood during diastole

intramural arterioles

embedded in heart muscle tissue

supply blood during diastole

healthy endothelium function

vasodilation, prevent platelets from sticking to wall, prevent LDL from inserting in lining

causes of damaged endothelium in vessels

increased BP and BG, systemic inflammation, tobacco, increased LDL/TG

therapies that promote endothelial health

ACEi/ARBs, statins

• any antihypertensive, LDL-lowering med, BG lowering med

atherosclerosis

LDL oxidized once in vessel wall → recruits macrophages

foam cells

oxidized LDL is cytotoxic to endothelial cells

fibrous cap function

protects underlying lipid core

maintenance important to prevent rupture and thrombosis

risk factors of fibrous cap rupture

increased BP and BG, systemic inflammation, tobacco, increased LDL/TG, macrophages in lipid core, blood flow (shear force)

4 phases of CCD

asymptomatic

stable angina = CCS

progressive angina

unstable angina or acute MI (ACS)

ischemia

lack of O2 and decreased or no blood flow to tissues

angina

spasmodic cramp-like choking pain in chest, jaw, shoulder, back, or arm

angina pectoris

thoracic pain most commonly caused by MI

plaque relayed obstruction of coronary arteries

presence of severe stenosis (>70% obstruction of R1 artery), R2 arteries cannot dilate further

• ischemia and angina

R1 artery

epicardial artery that typically dilates and offers little resistance to blood flow

R2 artery

pre-arteriole and intramural arterioles

alter vascular tone to decrease resistance to blood flow based on O2 demand

normal blood flow (R1 and R2)

in response to exercise, both dilate but R2 dilate more than R1

atherosclerosis (R1 and R2)

when blockage occurs, R2 arteries dilate when pt at rest

focal or diffuse spasm of normal or plaque-diseased arteries

focal vasospasm of epicardial artery at rest

lasts between 5-30 minutes

risk factors for vasospasm

DM, women > men, migraines (vasospasm dz), tobacco, coke/meth

coronary microvascular dysfunction (microvascular dz)

endothelial dysfunction leading to SMC proliferation and thickening along with impaired vasodilation

pts at risk for microvascular dz

women, DM, CKD, obesity, HFpEF

modifiable O2 availability factors

arterial PaO2 (target artery)

coronary flow and distribution (anemia, give O2)

modifiable O2 demand factors

heart rate (beta blockers, non-DHP CCB)

ventricular wall stress or tension (diuretics)

LV contractility (beta-blockers, non DHP CCB)

Hx and physical exam of chest pain

detailed sx hx, focused physical exam, and risk-factor assessment

characteristics of angina

squeezing, grip-like, pressure-like, suffocating, heavy

• pain gradually increases in intensity then gradually fades away

common sx associated with chest pain

SOB, palpitations, lightheadedness, confusion, syncope, upper abdominal pain or heartburn unrelated to meals

angina location and duration

located under sternum, jaw, shoulder, neck

radiation does not equal MI

5-30 min duration

5 E’s of angina

Exercise

Exposure to cold (vasoconstriction)

Emotional stress

Eating large meals

severe anEmia

angina precipitating factors (+ 5 E’s)

effort requiring use of arms above head

walking against wind

sexual activity

sx reproducible after specific amount of exertion

angina relieving factors

rest

nitroglycerin

questions to ask for angina

How many tabs needed to relieve angina?

How quickly does it work?

classification of chest pain (4)

stable

unstable

prinzmetal (vasospasmic)

silent

stable angina classification (3)

1. cardiac

2. possibly cardiac

3. non-cardiac chest pain

cardiac angina

• substernal chest pain with characteristic quality and duration

• provoked by exertion or emotional stress

  • relieved by rest or nitroglycerin (goes away)

possibly cardiac angina

meets 2 characteristics of cardiac classification

• usually different location (women)

non-cardiac chest pain

meets 1 or none of above characteristics

other causes of chest pain

PE, ACS, aortic dissection, esophageal rupture, pneumonia, shingles

aspirin MOA

irreversibly inhibits COX-1 and COX-2, decreasing TXA2 → inhibits platelet aggregation

What does ASA low dose inhibit?

COX-1

anti platelet effect

What does ASA high dose inhibit?

COX-2

pain/inflammation

Aspirin indications

analgesic

Afib (not used)

primary and secondary prevention of CAD

stroke/TIA

PAD

Where is ASA absorbed?

rapidly absorbed in stomach and upper intestine

ASA PK

platelets inhibited for ~10 days

peak plasma concentration is 30 min

ASA side effects

bleeding/bruising

GI toxicity

intracranial hemorrhage (rare)

hypersensitivity

ASA monitoring

CBC, fecal occult blood test

ASA contraindications

children < 16 yo with viral illness

syndrome of asthma, rhinitis, nasal polyps

ASA and ibuprofen interaction

competitive inhibition of COX binding when taken together

• tk ibuprofen 30 min after or more than 8 hours before ASA

ASA drug interactions

antithrombotics

thrombolytics

ibuprofen

ASA use for primary prevention of CVD in guidelines

81 mg chewable considered for primary prevention in ages 40-70 with high ASCVD risk but low bleeding risk

• no if high bleed risk

ASA recommendation for adults 40-59 with 10% or more 10 year CVD risk?

individual decision

• low bleed risk more likely to benefit

thienopyridines

clopidogrel, prasugrel, ticlodipine

ticlodipine

no longer used in US (replaced by clopidogrel)

thrombotic thrombocytopenia purpura (TTP)

clopidogrel pearls

prodrug (CYP2C19)

loading dose then 75 mg daily

with or without food

used alone or with ASA

stop at least 5 days before surgery

clopidogrel interactions

CYP3A4 statins (SLA)

PPIs (omeprazole, esomeprazole)

clopidogrel boxed warning

CYP2C19 metabolism alleles → lack of functional, increased thrombotic risk

prasugrel boxed warning

significant or fatal bleeding

not recommended 75 years or older except if DM or previous MI

do not use if urgent CABG surgery

D/C 7 or more days prior to surgery

contraindication: h/o TIA or stroke and active bleeding

Ticagrelor boxed warning

increased risk of significant/fatal bleeding

ASA doses > 100 mg avoided

contraindications: severe hepatic impairment, hypersensitive, active bleeding

D/C 5 days prior to surgery

PAD

dz of arteries NOT including coronary and cerebral vessels

caused by atherosclerosis and thromboembolism

PAD risk factors

race, gender, age, smoking, diabetes, HTN, dyslipidemia, inflammatory markers, hypercoagulable

>/= 65 yo

50-64 with RFs for atherosclerosis

< 50 with known atherosclerotic dz

4 clinical subsets of PAD

asymptomatic

chronic symptomatic

chronic limb-threatening ischemia (CLTI)

acute limb ischemia (ALI)

asymptomatic PAD

~40 of people

may have functional impairment

chronic symptomatic PAD

most common

claudication exertion leg sx

pain distal to occlusion

chronic limb-threating ischemia (CLTI)

ischemic pain at rest, gangrene, non healing wounds

can result in amputation

ABI scale

less than 0.9 is abnormal

1-1.4 is normal

antiplatelets and symptomatic PAD

single anti platelet therapy recommended (ASA)

• dual (ASA + clopidogrel) maybe after LE revascularization

antiplatelets and asymptomatic PAD

single anti platelet therapy

when should therapeutic anticoagulant be used in PAD?

only if pt has another indication for therapeutic anticoagulant (VTE, Afib)

Dual therapy with ASA and DOAC (PAD)

for symptomatic PAD

low dose rivaroxaban (2.5 mg BID) combined with low-dose ASA