2) Cardiology (Part 1) Flashcards
Non-modifiable coronary heart disease risk factors
- Age
- Male sex
- Family history
Modifiable coronary heart disease risk factors
- Hyperlipidemia
- Hypertension
- Diabetes mellitus
- Metabolic syndrome
- Cigarette smoking
- Obesity
- Sedentary lifestyle
- Heavy alcohol intake
Markers for CHD
- Elevated lipoprotein (a)
- Hyperhomocysteinemia
- Elevated high-sensitivity C-reactive protein (hsCRP)
- Coronary arterial calcification detected by CT (CAC)
Atherosclerosis
- Pathological process in which coronary arteries become narrowed by the buildup of fatty material in their walls
Atherosclerotic plaques
- Lead to narrowing of the artery lumen
- Decrease blood flow and oxygen delivery to the coronary arteries
CAD diagnosis
- Cardiac catheterization (often after an abnormal cardiac stress test)
Or
- CT angiography
CAD treatment
- Treat Modifiable Risk Factors (Hyperlipidemia, Hypertension, Diabetes mellitus, Metabolic Syndrome, Cigarette Smoking, Obesity, Sedentary Lifestyle, Heavy Alcohol Intake)
- Low-dose aspirin 75-100mg/daily for secondary prevention
Primary prevention (preventing 1st heart attack)
- Mostly don’t prescribe low-dose aspirin
- Sometimes used in select adults aged 40-70 years who have a higher risk of developing ischemic heart disease but not an increased bleeding risk
Angina
- Limitation of Coronary Blood Flow
- Decreased Oxygen supply to the heart muscle
- Pt. develops chest pain
Classic history of angina
- Chest discomfort, usually described as “heaviness” “pressure” “squeezing” “smothering” or “choking”
Levine’s sign (pt making fist over sternum describing pressure)
- Can radiate to either shoulder and to both arms (especially the ulnar surfaces of the forearm and hand)
- Can arise in or radiate to the back, interscapular region, root of the neck, jaw, teeth, and epigastrium
- Angina is rarely localized below the umbilicus or above the mandible
Anginal “equivalents” symptoms
- Dyspnea
- Nausea
- Fatigue
- Faintness
- More common in elderly and diabetic patients
Types of angina
- Prinzmetal’s Variant Angina/Vasospastic Angina
- Stable Angina
- Unstable Angina
Prinzmetal’s Variant Angina
- Caused by coronary artery vasospasm resulting in transmural ischemia
- Severe ischemic pain that usually occurs at rest and is associated with transient ST-segment elevation
- Diagnosed with coronary angiography demonstrating transient coronary spasm
Stable angina
- Transient myocardial ischemia
- Caused by exertion typically is relieved in 1–5 min by slowing or ceasing activities and even more rapidly by rest and sublingual nitroglycerin
Unstable angina
- Part of “Acute Coronary Syndrome”
- Has at least one of three symptoms
- Can have ECG changes, but has negative troponins
Symptoms indicative of unstable angina
- Ooccurrence at rest (or with minimal exertion) lasting >10 min (usually more than 20 min)
- Relatively recent onset (i.e., within the prior 2 weeks)
- Crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previous episodes)
Stable angina Tx
- Treat modifiable risk factors
- Nitrates
- Beta or Calcium Channel Blockers, Ranolazine
Prinzmetal’s Variant Angina Tx
- Nitrates
- Calcium channel blockers
Unstable angina Tx
- Admission
- Dual antiplatelet therapy + glycoprotein IIb/IIIa inhibitor + anticoagulation with heparin +/- statin +/- cardiac cath
Unstable Angina (UA) ischemic symptoms
- Rest angina usually more than 20 minutes, new onset angina that limits physical activity, increasing angina that is more frequent, longer, and occurs with less exertion than previously
- With or without EKG changes in contiguous leads (ie T wave inversions, ST segment depressions)
- NO elevation of troponin
Non-STEMI ACS symptoms
- Same as unstable angina, but troponin is elevated
STEMI ACS symptoms
- ST segment elevations of 1 mm (0.1 mV) in 2 anatomically contiguous leads or 2 mm (0.2 mV) in 2 contiguous precordial leads
- OR new left bundle branch block and presentation consistent with ACS
Plaque rupture in ACS
- Rupture of the fibrous cap of an atheromatous plaque
- Exposure of highly thrombogenic, necrotic core material rich in red cells
ACS occlusion status
- Unstable angina = partial obstruction
- Non-STEMI = larger obstruction with occlusion of lumen
- STEMI = complete occlusion of lumen
Diagnosis of ACS
- ECG is the best initial test
At least 2 of the following
- History (angina or angina equivalent)
- Acute ischemic ECG changes
- Typical rise and fall of cardiac markers
- Absence of another identifiable etiology
Patient history indicating ACS
- Chest discomfort (pain, tightness, dull, heaviness, etc.)
- Fatigue
- Weakness
- SOB
- Activity at onset
- Risk factors
5 most important history-related factors (in order of importance)
1) Nature of the chest pain
2) History of Coronary Heart Disease
3) Sex/gender
4) Age
5) Number of traditional risk factors
Physical examination
- Vital signs
- Skin color/diaphoretic
- Neck
- Lung sounds
- Heart sounds
- Lower extremity exam
- In considering thrombolytics (“clot busters”), cursory neuro exam
Lung sounds to look for in ACS physical examination
- Rales/crackles = fluid out of the capillaries into the alveoli
Heart sounds to look for in ACS physical examination
- Friction rub
- New murmur
- Acute mitral valve regurgitation or a VSD
- Pericardial effusion/tamponade
ECG in ACS
- Tool for looking at acute ischemia to the coronary arteries that supply areas of the heart
- REMEMBER about 50% may be initially normal, but then develop ST changes
Unstable angina and non-STEMI ECG in ACS
- May be normal or abnormal
STEMI ECG in ACS
- By definition, ST segment elevation in contiguous leads (or new LBBB) in the setting of ischemic symptoms
Troponin I or T (cTnI or cTnT)
- Cardiac biomarkers/enzymes
- The time of presentation and every 3-6 hours for 6-12 hours
High-sensitivity Troponin (hs-cTn) I or T
- Cardiac biomarkers/enzymes
- The time of presentation and every hour x 1-3 hours
False positives in cardiac biomarker testing
- Pulmonary embolism
- Myocarditis
- TYakotsubo cardiomyopathy
- Chronic kidney disease
- Rare analytical problem (heterophile antibodies)
False negatives in cardiac biomarker testing
- Excessive biotin use
Initial interventions with ACS
- Assess and stabilize airway, breathing, and circulation
- Provide Oxygen (ONLY IF O2 Sat is <90% patients in respiratory distress
- Establish IV access
- Treat sustained ventricular arrhythmia rapidly according to ACLS protocols
- Vitals, history, labs
- Portable CXR
Labs ordered in suspected ACS
- Cardiac biomarkers x3
- CBC
- CMP
- PT/INR
- PTT
Initial medications for ACS
- Aspirin
- Nitroglycerin
- Beta Blockers
- Morphine
- Statin
STEMI management
- Immediate reperfusion therapy
- Do not wait for troponin results
- Straight to cath lab if there are ST segment elevations in EKG in contiguous leads
Immediate reperfusion therapy
- Most common is immediate cardiac cath (angioplasty/percutaneous intervention)
- Goal: door to balloon 90 minutes
Non-STEMI and unstable angina management
- Admission, cardiac monitoring, serial ECGs
Plus
- Anti-platelet medications (Aspirin + GP IIB/IIIA INHIBITORS(Integrilin/ReoPro) + Adenosine diphosphate (ADP) receptor antagonists(Ticagrelor/Brilinta or prasugrel/Effient or clopidogrel/Plavix)
Plus
- Anticoagulation (UF Heparin or LMWH)
Plus
- Cardiology Consult (Usually get a Cardiac cath)
Long term management of ACS after hospital discharge
- Dual antiplatelet therapy x 12 months at least (Aspirin + ADP inhibitor)
- Statin
- ACE-I or ARB
- Beta Blocker
Acute pericarditis
- Inflammatory process involving pericardium
- Can occur as acute, sub-acute or chronic form
- Most common of all disease processes involving the pericardium
Acute pericarditis causes
- Variety of etiologies (most commonly post infectious)
- May be associated with a pericardial effusion & even tamponade
- Can become chronic or recurrent
- Can develop into constrictive pericarditis
Symptoms of pericarditis
- Chest pain is usually presenting symptom
- Often sharp, typically retrosternal piercing, & pleuritic in nature with radiation to left shoulder
- Pain aggravated by deep breathing & lying supine
- Pain is non-exertion & may be steady or even crushing in nature & may mimic acute MI
- Pain may also be in epigastric area & increased with swallowing
- If acute infectious etiology, patient is most comfortable sitting up & leaning forward
- Fever usually follows onset of CP
PE findings in pericarditis
- Pericardial friction rub
- Scratchy, rough, gritty sound
- Best heard using diaphragm applied firmly along lower LSB with patient sitting upright & leaning forward
- May be accentuated in inspiration
Pericarditis treatment
- NSAIDs + Cholchicine
Aortic dissection
- Much less common than an MI
- Extreme emergency & can lead to death in minutes
- Blood can dissect up or down aorta
- Blood dissecting up around great vessels can close off carotids
- Blood can dissect down to coronaries & shut them off
Risk factors for ascending aortic dissection
- HTN
- Cystic medial necrosis
- Marfan’s syndrome
Risk factors for descending aortic dissection
- Atherosclerosis
- HTN
- Increased incidence
- Coarctation of aorta; Bicuspid AV,AS, 3rd trimester of pregnancy in otherwise normal women (rare), Rarely traumatic
Symptoms of aortic dissection
- Sudden onset of severe sharp anterior or posterior chest pain with “ripping” or tearing quality
PE findings of aortic dissection
- Unequal Blood pressure readings in the RUE and LUE
- Asymmetry of carotid or brachial pulses
- New onset of Aortic Regurgitation murmur
- Neurologic abnormalities if there is interruption of carotid artery flow
Aortic dissection diagnosis
- “90% will have an abnormal CXR, Mediastinal widening
- CT Angiogram (fast & sensitive)
- Echocardiogram (evaluates aortic valve)
Aortic dissection Tx
- ICU monitoring
- Antihypertensive therapy to maintain systolic BP below 120 mm Hg, using IV agents, followed by oral therapy
Descending aortic dissection Tx
- Stabilized medically with antihypertensives
Ascending aortic dissection Tx
- Immediate surgical repair
