Cardiology Flashcards
Stable ischemic heart disease (stable angina)
- atherosclerosis of coronary artery
- is the progression of atherosclerosis (a plaque), until it reaches a critical stenosis
- stenosis reaches 70%
- presence of angina by exertion
- no troponin
- no ST elevated segment
Acute coronary syndrome
- rupture & thrombosis of the plaque
- the occlusion of the coronary artery
Types:
1. unstable angina
2. STEMI
3. NSTEMI
Unstable angina
- rupture of thrombosis ( < 100%)
- presence of angina at rest (worst than stable angina)
- absence of troponin & ST elevation
NSTEMI
- rupture of thrombosis ( < 100%)
- Presence of angina at rest
- presence of troponin (myocardial infarction biomarker)
- absence of ST elevation
STEMI
-rupture of thrombosis ( 100%)
- Presence of angina at rest
- presence of troponin & ST elevation
- immediate cardiovascular catheterization (PCI within 90 min ) or ( fibrinolytic within 120 min)
Criteria of ACS
- Substernal crushing chest pain (tightness, heaviness)= angina = anginal equivalent ( if they had it before ?, is it similar to previous pain?)
- Worsen by excertion
- Relieved by nitroglycerin
- Associated symptoms : dyspnea, pre-syncope, N/V
- Risk factors:
- age ( male > 45; Female > 55)
- family history (early atherosclerosis)
- Diabetes, CKD, vasculopathy (atherosclerosis somewhere else)
- HTN, smoking, obesity, dyslipidemia - Physical exam:
- non tender angina
- nonplueritic angina
- non positional angina - Laboratory:
- 12-lead ECG ( rule out STEMI)
- Troponin- I ( Sensitive cardiac troponin, diagnose NSTEMI)
- APPROACH:
- invasive test: PCI
- non-invasive test ( anatomic, functional)—> in outpatient setting (chest pain):- Low risk: no test
- Intermediate/High risk:
- test based on age
- (if patient is < 65 = rule out; coronary CT angiogram (CCTA); anatomic testing)
- CABG + DAPT: if > 3 vessels are obstructed; if left mainstem equivalent; unaccessible
- PCI + DAPT: therapeutic CATH. (Compress plaque) - ( If patient age > 65 = rule in diagnosis; stress test; functional testing= stress the heart, make it work harder or take of blood supply)
- Stress: ( if patient can walk: treadmill) ( if patient cant walk: dobutamine, adenosine, dipyridomole)
- Test: ( ECG = ABNORMAL; use ECHO= wall motion abnormalities during stress= ABNORMAL; use Nuclear test & SPECT). ( MRI ?)
- (if patient is < 65 = rule out; coronary CT angiogram (CCTA); anatomic testing)
- test based on age
- Management:
“ aspirin + statin+ BB + ARB/ACE-I + DAPT (P2Y12) - Aspirin = 81 mg
- P2Y12= clopidogrel, prasugrel, ticagrelor
- Statin = high-potency (atrovastatin, rosuvostatin)
- BB: metoprolol (control HR) ; Carvedilol (control BP)
- ARB or ACE-I (cause angioedema and dry cough):
- Anti-anginal: nitrates (nitroglycerin; isosorbide mononitrate); dihydropyridine CCB (amlodipine, nifedipine), palliative (ranolazine)
NOTE:
- DAPT: Dual anti-platelet therapy ( Aspirin + P2Y12 = clopidogril, prasugrel, ticagrelor)
- CAGB: Coronary artery bypass grafting
- BB: NOT NECESSARY if (no history of infarction, no reduction in EF, Patient didn’t receive CABG)
- IF perform angioplasty alone (without stent)= no duration of DAPT
- IF STENT present = BMS= DAPT (for a month); DES = DAPT ( for a year; aspirin for 6 months; P2Y12 for 3 months)
Acute coronary syndrome
Path:
- rupture & thrombosis
- supply ischemia ( revascularize only way to fix this)
Pt:
- angina @ rest
Diagnosis:
- ECG (rule out ST elevation MI)
-Troponin ( to rule out non- ST elevation MI)
- invasive coronary angiogram (ICA) (CATH; )
12- LEAD ECG anatomic map
I
II
III
Patient with non-ischemic cardiomyopathy treated for atrial fibrillationn
- digoxin toxicity lead to GI symptoms ( anorexia, nausea) + weakness + confusion + lead to life-threatening arrhythmia
- digoxin can interact with amiodarone (or verapamil, quinidine, propafenone) & result in increase digoxin level in blood
- solution:
Decrease digoxin done by 25-50% when initiating amiodarone (or verapamil, quinidine, propafenone therapies)
What conditions lead to atrial fibrillation ?
Conditions that lead to atrial dilation &/or conduction remodeling:
- Advanced age
- Systemic HTN
- Mitral valve dysfunction
- LV failure
- CAD & related factors ( DM, smoking)
- Obesity & obstructive sleep apnea
- Chronic hypoxic lung disease (COPD)
Triggers of increased automaticity:
1. hyperthyroidism
2. excessive alcohol use
3. increased sympathetic tone: acute illness (sepsis, MI, PE), cardiac surgery.
4. sympathomimetic drugs ( cocaine)
Note:
-AF: varying R-R interval (irregularly irregular) + absence of organized P wave
- symptoms: palpitation, SOB, Chest pain, lightheadedness, weakness
- check new onset of AF:
1. Echo: evaluate valve disease, LV dysfunction or RV dilation/strain in PE
2. Serum TSH: evaluate hyperthyroidism
3. CT angio: evaluate PE (SOB, pleuritic chest pain) + ECHO (shows RV dilation or strain
4. Exercise stress testing: evaluate for CAD ( seen in old patients)
PAD ( & risk of CVD)
- intermittent claudication + ABI (< 0.9)
-use Combination of aspirin + statin - heparin used in acute thrombotic occlusion in PAD
- surgical revascularization is reserved for patients with:
1. Limb threatening complication ( unhealed ulcer)
2. limitation in activities of daily living
3. Failure to response to exercise
4. Failure to response to drugs
Infective endocarditis (IE) with IV drug use
Patho:
- injected particles (dirts…) damage the Right valves before going to the lungs
- bacterial growth
- increase risk for HIV
Feature:
- tricuspid valve regurgitation (most common affected)
- holosystolic murmur that increases in intensity with inspiration
- Staph. Aureus (most common organism)
- septic pulmonary emboli ( cough, Chest pain, hemoptysis + round lesions in peripheral lung field)
- peripheral manifestation (splinter hemorrhage, painless janeway lesion)
- heart failure is uncommon
- Septic pulmonary embolism (SPE)—> vegetations on a heart valve or a pacemaker lead or a thrombus in an indwelling vascular catheter or graft.
Aortic regurgitation
- diastolic murmur best heard when patient is sitting up
Infective endocarditis
- lead to tricuspid valve regurgitation + septic pulmonary emboli
Or
- lead to aortic regurgitation + No septic pulmonary emboli
Paradoxical splitting of S2
Seen with
Widened splitting ( on inspiration & expiration)
- Delayed P2:
- pulmonic stenosis
- pulmonic HTN
- ASD (wide & fixed splitting)
-RBBB - Early A2:
-VSD - Narrowed splitting (on inspiration) + paradoxical splitting ( on expiration)
- aortic stenosis
- systemic HTN
- LBBB
-HMC
Audible S4 (when patient is in the left lateral decubitus position)
-heard just before S1
- Caused by: blood striking a stiff LV wall (during atrial contraction)
- normally seen in elderly (> 70)
- abnormally seen in children —> indicated:
1. concentric LV hypertrophy ( associated with aortic stenosis or chronic HTN)
2. Restrictive cardiomyopathy (sarcoidosis, amyloidosis, hemochromatosis, cancer, fibrosis)
3. Acute myocardial infraction (MI)
Hypertrophic cardiomyopathy (HCM)
- Systolic murmur that increase in intensity when standing up or valsalva maneuver
- systolic murmur that decrease in intensity when squatting or handgrip
Audible S3
- heard just after S2
- caused by: reverberant sound as blood fills an enlarged LV cavity during passive diastolic filling
Seen with:
1. HFrEF
2. High-output states ( hyperthyroidism)
3. Mitral or aortic regurgitation
Syncope
- syncope occurs at rest or while sitting & without warning symptoms is suggestive for arrhythmic- cardiac etiology
Pericarditis (pleuritic chest pain, decrease with sitting, increase with laying supine, friction rib)
- developed less than 4 days after MI
- patient with delayed coronary perfusion following STEMI ( > 3 hours from symptom onset) are at increased risk of developing —> peri-infarction pericarditis (PIP)
- Sign on ECG: diffused ST elevation + PR depression
- sign on ECHO: pericardial effusion
- treatment:
1. Supportive
2. Avoid: NSAID, GC (increase risk for ventricular wall rupture —> pericardial effusion —> cardiac tamponade)
Acute stabilization of ST- elevation in MI
Initial management:
1. Supplement oxygen (if SaO2 < 90%)
2. Aspirin (full dose, chewable)
3. P2Y12 inhibitor (clopidogrel)
4. Sublingual nitroglycerin ( caution with hypotension or RV infarct)
5. Beta-blocker ( avoid in hypotension, bradycardia, or HF)
6. High potency statin ( atorvastatin)
7. Anticoagulation ( heparin infusion)
Additional stabilization (if needed)
1. Persistent chest pain —> IV NTG or morphine
2. Hypertension —> IV NTG
3. Pulmonary edema —> furosemide +/- NTG
4. Unstable bradycardia —> IV atropine
Emergency re-perfusion:
1. PCI within 90 minutes
2. Thrombolysis within 120 minutes (if PCI is not available)
Ventricular fibrillation or pulseless ventricular tachycardia
Managed with defibrillator
Hemodynamic unstable patient with narrow or wide QRS complex tachycardia ( atrial fibrillation, atrial flutter, ventricular tachycardia with a pulse)
- managed with synchronized cardioeversion
Atrial fibrillation
- absent P-wave & irregularly irregular R-R interval
- located at: pulmonary vein
- managed with: hemodynamic unstable (synchronized cardioeversion)
- can be treated surgically with: catheter-based pulmonary vein ablation ( burn or freeze to break up electrical signals that causes irregular beat)
Sick sinus syndrome (SSS)
- caused by: degeneration of sinus node & replacement with fibrous tissue
- elderly people most commonly affected
- present with bradycardia ( fatigue, dizziness, syncope dyspnea on exertion)
- ECG finding: sinus bradycardia + dropped or delayed P-wave
Morbitz type 1 vs. morbitz type 2
Morbitz type 1
- progressive prolongation in PR interval & a drop in QRS complex
- occurs in AV node
Morbitz type 2
- constant prolongation in PR interval & random drop in QRS complex
- occurs in His-Purkinji system
Digoxin toxicity
- side effects —> lead to cardiac arrhythmia due to increase myocardial conduction or vagal tone—> most specific for toxicity—> atrial tachycardia with AV block
Others:
1. Sinus bradycardia
2. Junctional rhythm
3. Ventricular tachycardia
Diagnosis:
- ECG finding of —> atrial tachycardia with AV block
Systemic vascular resistance
Decreased Systemic vascular resistance —> vasodilation
1. Effect of septic shock
2. Signs:
-
Increased Systemic vascular resistance —> vasoconstriction
1. Effect of norepinephrine
High, low, low, high —> obstructive shock (pre-pulmonary; PE
High, high, low, high
Type of shock
CVP, PCWP, CO, SVR
High, low, low, high —> obstructive shock ( pre-pulmonary) ( PE & pneumothorax)
High, high, low, high —> obstructive shock (post pulmonary) (aortic disection, aortic stenosis)
Low, low, low, high —> hypovulemic shock ( diarrhea, vomiting, diueritcs, dehydration)
Low, low, high, low —> septic shock (distributive) ( peripheral vasodilation) ( reduced vascular tone) (hypotension) ( high mixed venous oxygen saturation)
—> tachycardia, hypotension, tachypnea
High, high, looow, high —> cardiogenic shock ( left ventricular failure; Decrease in left ventricular contractility; Myocardial infarction)
—> chest pain, hypotension, severe dyspnea, hemodynamic instability
Low SVR, bradycardia, low SvO2—> neurogenic (distributive shock)
Septic shock signs
Low BP (Hypotension)
High HR (tachycardia)
High RR (tachypnea)
Note:
- Peripheral vasodilation —> reduced SVR—> reduced vascular tone —> Hypotension
- CVP (central venous pressure) —> preload
- PCWP (pulmonary capillary wedge pressure) —> left atrial pressure
- CO (cardiac output)
- SVR (systemic vascular resistance)
Scenario
- left-sided heart failure
- pleural effusion, pneumothorax, atelectasis —> decrease breath sound
- electrolyte imbalance
- mitral regurgitation ( pulmonary edema secondary to CHF)
- hematuria + protunuria secondary to AKI
LV & RV failure in association with cardiorenal syndrome
- can lead to cardiogenic shock ( chest pain, dyspnea, hypotension)
- lead to:
1. Low CO —> low renal artery perfusion —> low GFR —> activation of RAAS system & increase H2O & Na reabsorption
2. High CVP & renal venous pressure (RVP) —> low Glomerulus capillary filtration gradient (GCFG) —> low GFR —> activation of RAAS system & increase H2O & Na
Note:
- Glomerular filtration occurs due to the pressure gradient in the glomerulus.
- Increased blood volume and increased blood pressure will increase GFR.
- Constriction in the afferent arterioles going into the glomerulus and dilation of the efferent arterioles coming out of the glomerulus will decrease GFR.
Anti-platelet therapy (aspirin or clopedogril )
- prevent coronary artery disease in patients with ischemia
Dual anti-platelet treatment ( aspirin & clopidogrel)
- recommended for 12 months after MI
- REDUCES THE RISK OF STENT THROMBOSIS FOLLOWING CORONARY STENT PLACEMENT
S4…S1……..S2….S3
S4:
- blood striking a stiff LV wall during atrial contraction
Heard in:
- concentric LV hypertrophy ( HTN, aortic stenosis) (decrease LV compliance )
- restrictive cardiomyopathy
- acute MI
- normal finding in elderly (age-related loss of LV compliance)
S3:
- occur as blood fills a dilated LV cavity during passive diastolic filling
Patient comes with epigastric pain ( differentiate between GI causes or cardiac causes)
Via
- first step:
1. Resting ECG
Symptoms of acute coronary syndrome:
1. Chest pain
2. Dyspnea
3. N/V
4. Epigastric pain
Nonclassic presentation of ACS in women, elderly, diabetic patients —> epigastric pain + N/V
Evaluation of disease
- Serum amylase/lipase —> acute pancreatitis
- ECG —> acute coronary syndrome
- Abdominal U/S —> cholecystitis ( positive murphy sign)
- Upright chest x-ray —> perforated peptic ulcer ( positive air under diaphragm = pneumoperitunium)
- CT angiography —> acute mesenteric ischemia ( positive severe epigastric pain)
Post MI complication
- Arrythmias ( ventricular fibrillation) —> most common cause of death
- Papillary muscle rupture ( Mitral regurgitation) —> new systolic murmur ( 5-7 days after MI)
- Ventricular wall rupture ( pericardial effusion & cardiac tamponade) —> severe hypotension
- Ventricular wall aneurysm —> persistence ST elevation ( 1 month after) + new systolic MR murmur
- Atrial-ventricular dissociation ( ventricular fibrillation or 3rd degree AV block) —> cannon A wave + bounding JVD
- Dressler’s syndrome ( autoimmune pericarditis; treated with NSAIDs + aspirin) —> pleuritic chest pain + fever ( 5-10 weeks after)
LV free wall rupture
- develops 5 days to 2 weeks after acute MI
- lead to sudden onset chest pain + development of cardiac tamponade + obstructive shock + no palpable pulse ( pulseless electrical activity)
Papillary muscle rupture & inter-ventricular septum rupture
- occurs within 5 days
- can cause pulmonary edema ( & palpable pulses)
Ventricular fibrillation
- most common cause of cardiac arrest in patient with acute MI
Pulmonary embolism
-risk factor: prolonged immobilization
Symptoms:
1. Pleuritic chest pain
2. Dyspnea
3. Tachycardia
4. Tachypnea
5. Hypoxemia
6. Unilateral lower extremity edema ***
Diagnosis:
- CT pulmonary angiography
Pericarditis
Signs:
1. Diffused ST segment elevation ( seen in all leads)
2. Pleuritic chest pain ( improves when leaning forward)
Dressler syndrome ( autoimmune-mediated pericarditis) can develop post- cardiac injury ( MI):
- Occurs several weeks to months
2.X-ray: pleural effusion + enlarged cardiac silhouette - Treatment: NSAID (high dose aspirin) + colchicine
- Avoid (anticoagulation—> can lead to development of hemorrhagic pericardial effusion)
Stress-induced cardiomyopathy
(Takotsubo)
Seen in:
1. Post menopausal women
2. Emotional stress or recent physical stress —> causes surge of catecholamine
Symptoms:
1. Chest pain mimicking MI
2. Decompensated heart failure
3. Moderate troponin elevation
4. ECG: ischemic changes ( T-wave inversion) in precordial lead ( V2-V4)
Diagnosis:
1. Catheterization: no obstructive Coronary artery disease
2. Echo: LV apical hypokinesis, basilar hyperkinesis
Treatment:
1. Resolves in several weeks with supportive care
Apical hypokinesis
- marker for early RV dysfunction in pulmonary HTN
- hypokinesis: decrease in the amplitude of LV wall motion
Carbon monoxide poisoning
- disrupt oxygen delivery to the tissue
- can mimic Myocardial ischemia
- diagnosis: elevated carboxyhemoglubin level
- treatment: high flow 100% oxygen or hyperbaric oxygen therapy
Alcoholic cardiomyopathy
-Complete alcohol cessation is the mainstream therapy
- improvement of LV function over time
SLE
- treatment: hydroxychloroquine
- SLE can lead to acute pericarditis:
- Pericarditis: (pleuritic chest pain + fever + pericardial friction rub + diffuse ST segment elevation + PR segment depression + pericardial effusion)
- SLE: ( joint pain + cytopenia + low complement protein + rash)
Acute pericarditis
Causes:
1. Viral or idiopathic
2. Autoimmune disease ( SLE)
3. Uremia ( acute or chronic renal failure)
4. Post- MI: peri-infraction pericarditis ( early), Dressler syndrome ( late)
Symptoms:
1. Pleuritic chest pain ± fever
2. Pericardial Friction rub ( systolic sound between S1 & S2) (Louder at inspiration)
3. ECG: diffused ST segment elevation or PR- segment depression
4. Echo: pericardial effusion
Treatment:
1. NSAIDS ( high dose aspirin) & colchicine
Pleuritic chest pain after 6 weeks of CABG surgery, MI, PCI
( + fever, leukocytosis, elevated inflammatory marker; ESR, CRP)
- acute pericarditis due to post-cardiac injury syndrome
- due to: immune-complex deposition in the pericardium & pleural
—> if it occurs after MI, then it is called Dresssler syndrome
- dyspnea on exertion
- lightheadedness (hypotension, syncope)
- URI recently
- aortic stenosis ( cocentric LV hypertrophy —> S4)
- rapid upstroke of the peripheral pulse
Aortic stenosis
Aortic stenosis:
- Valsalva manuever ( decreases preload) —> decrease murmur intensity
- Handgrip ( increase afterload) —> decrease murmur intensity
- S4 often present
- Ejection click usually present
- Carotid pulses soft & delay
Hypertrophic cardiomyopathy
(Interventricular septal hypertrophy + crescendo-decrescendo heard at left sternal border + rapid upstroke/brisk of the peripheral pulses )
HCM:
- Valsalva manuever ( decreases preload) —> Increase murmur intensity
- Handgrip ( increase afterload) —> decrease murmur intensity
- S4 often present
- Ejection click usually absent
- Carotid pulses brisk
Symptoms:
-LV outflow obstruction—> lead to dyspnea on exertion + lightheadedness/presyncope
- crescendo-decrescendo murmur that increase in intensity with decrease LV blood volume ( decreased preload)
Uremic pericarditis
Can occur in patients with:
1. BUN > 60
Present as other types of pericarditis, except for:
- Absence of classic ECG finding of pericarditis( diffuse ST elevation, or PR depression)
Treatment: dialysis is the best treatment (not the typical pericarditis treatment of NSAID + Colchicine)
Acute aortic dissection
Associated with:
1. chronic systemic HTN ( AGE > 60)
2. Marfan syndrome (AGE < 40)
3. cocaine use
Symptoms:
- severe, sharp, tearing pain ( worst pain ever felt)
- SBP is > 20 mmHg between arms
Signs:
- sudden chest pain & back pain ( shoulder blades)
- blood pressure changes between both arm
- x-ray: widen mediastinum
- ECG: non-specific ST segment & T wave changes
Statin- induced myopathy
(serum creatinine kinase elevated)
(mechanism of action of statin: inhibition of intracellular synthesis pathway)
Function:
- inhibits HMG-COA reductase —> reduce serum LDL
- decrease coenzyme Q10 synthesis
Side effect:
- hepatic dysfunction ( elevated AST & ALT enzymes)
- myalgia ( elevated creatine kinase)
Signs for statin-induced myopathy:
- Acute onset muscle pain
- elevated AST & ALT
- elevated Creatine kinase
Pulsus paradoxus (PP)
- defined as: fall in SBP by more than (> 10 mmHg) during inspiration
- seen with:
1. cardiac tamponade (with pericardial effusion)
2. Severe Asthma
3. COPD
Marfan syndrome is associated with aortic dissection in younger patients ( < 40)
- connective tissue disorder
- associated with:
1. aortic dilation, regurgitation ( early diastolic murmur), dissection
2. Mitral valve prolapse
Chronic aortic regurgitation
( due to congenital bicuspid aortic valve)
signs:
1. Decrescendo early diastolic murmur
- Best heard at left sternal border, when patient is learning forward & hold their breath after expiration
Bicuspid aortic valve
Associated with:
- Aortic stenosis ( crescendo-decrescendo systolic murmur that radiates to the carotid) —> diagnosed < 70
- Aortic regurgitation ( decrescendo early diastolic murmur) —> diagnosed < 40
Most common cause of aortic stenosis (AS)
- Senile calcific aortic stenosis
- Bicuspid aortic valve
- Rheumatic heart disease
Aspirin & beta blocker in asthma
- can trigger bronchoconstriction in asthma patient
Acute mitral regurgitation
- early systolic murmur heard at the apex
- increased LV end diastolic pressure ( elevated left atrial & ventricular filling pressure)—> lead to pulmonary edema & heart failure
- caused by papillary muscle rupture due to MI
Patient with valvular disorders
( assessment for undergoing noncardiac surgery)
- Asymptomatic patients with normal EF & no pulmonary HTN can typically undergo surgery without further intervention
Fibromuscular dysplasia
Women (15-50 years) less than 50 years with 1 of these:
1. Severe or resistance HTN
2. Onset of HTN before age of 35
3. Sudden increase in BP from baseline
4. Increase in creatinine (> 0.5-1) after starting ACE-inhibitor or ARBs (without effect in BP)
5. Systolic-diastolic epigastric bruit
Symptoms:
1. Resistance HTN —> renal artery involvement
2. Symptoms of brain ischemia ( amaurosis fugax, Horner syndrome, TIA, stroke)
3. Non-specific symptoms (headache, pulsatile tinnitus, dizziness) —> carotid/vertebral artery involvement
Diagnosis:
1. CT angiography, duplex ultrasound
Signs:
- FMD—> decrease perfusion to kidney —> increase both renin & aldosterone level ( causing secondary hyperaldosteronism) —> concentration of aldosterone/renin (almost 10)
