AMBOSS SHIT

CARDIO
Block 1
 Premature ventricular contractions (PVCs) – asymptomatic skipped beats
o Palpitations, lightheadedness, dizziness, irregular heartbeat
o EKG – intermittent doublets of broad monomorphic QRS
o Triggered by lack of sleep & stress in young healthy pt.
o Tx. Observation and rest
o If frequent or long episodes of PVCs  echocardiography
 V tach – unstable  synchronized cardioversion
 Cardiac tamponade – patient unstable – FIRST pericardiocentesis to stabilize & then
treat underlying condition
 Strep. Gallolyticus (bovis) – colonoscopy
 Acute rheumatic fever – GAS infection – Tx. Penicillin V
o Prophylaxis with IM penicillin G benzathine every 4 weeks
 Alternative: oral penicillin V
 Penicillin allergy: sulfadiazine
 RF without carditis – 5 years or until 21 y/o
 RF with carditis – 10 years or until 21 y/o
 RF with carditis + permanent valvular heart defects – 10 years or until 40
y/o
 ARF – previously pharyngitis/tonsillitis without Abx. Tx. (GAS) + carditis + erythema
marginatum
o JONES – major / minor (high fever, elevated acute phase reactants, arthralgias)
 2 major or 1 major + 2 minor
o Carditis – dyspnea, JVD, b/l ankle edema, S3 gallop + enlarged cardiac silhouette
& prominent vascular markings
o Erythema marginatum – ring-shaped macules & patches
 Myocarditis – signs of CHF + recent URTI
o Viral infections (coxsackie B, parvovirus B19, HHV-6 infection)
o ECG & echocardiography – assess severity of cardiac dysfunction
 Myocarditis – presents with acute decompensated CHF complicated with dilated
cardiomyopathy
o Echocardiography – ventricular dilation & global ventricular hypokinesis
 Mediastinitis – due to perforation of mediastinal organs (ex. Esophagus) or by extension
of retropharyngeal infections
 Acute pericarditis – complications: cardiac tamponade or constrictive pericarditis
 Abx. Ppx. – prosthetic heart valves, hx. of IE, unrepaired cyanotic CHD
o Oral amoxicillin 1 hr. before procedure
 Infectious endocarditis – prosthetic heart valves
o S. epidermidis (early-onset IE)
 o S. viridians (late-onset IE) > 1 year after valve replacement
 Also preexisting damaged native heart valves (ex. Bicuspid)
 Prosthetic valve IE due to MSS (methicillin-susceptible staph)
o Tx. Nafcillin + rifampin for 6 weeks + gentamicin for 2 weeks
 Prosthetic valve IE due to MRS (methicillin-resistant staph)
o Tx. Vancomycin + rifampin + gentamicin
 Right sided IE – TR – complication: septic pulmonary embolism
o IVDU & indwelling intravascular devices
 IE - HACEK – 3rd generation cephalosporins – gram (-) bacteria
o Haemophilus species
o Aggregatibacter actinomycetemcomitans
o Cardiobacterium hominis
o Eikenella corrodens
o Kingella kingae
 IE with native heart valves – Tx. Empiric with IV vancomycin (includes MRSA)
o 3 blood cultures
 IE – neurologic complications due to septic emboli to brain
o Ischemic stroke, intracerebral hemorrhage, cerebral microabscesses
o Tx. Empiric Abx. & noncontrast CT of brain
 IE – new conduction abnormality (ex. AV block) – perivalvular abscess – perivalvular
thickening with an echolucent cavity
 Biological valves (bovine & porcine) – preferred in patients > 65 yrs., patients with high-
risk bleeding & women with desire to have children
o If Hx. of intracranial hemorrhage, coagulopathy
o If severe thrombocytopenia (< 50,000)
o Short lifespan – sclerotic degeneration of valves
 IE surgical indications – mechanical valve replacement – < 65 y/o without CI for
anticoagulation
o Uncontrolled infection
o Systemic embolization
o Prosthetic valve endocarditis
o Fungal endocarditis
 Cardiac tamponade – pulsus paradoxus – SBP drop > 10mmHg during inspiration
 Thoracic aortic rupture – high velocity blunt chest wall trauma
o Widened mediastinum
o Esophageal deviation (deviation of NG tube)
o Depression of left main bronchus
o Hemothorax
 Can’t exercise – pharmacological stress test – adenosine, regadenoson, dobutamine or
dipyridamole
 Acute mesenteric ischemia (AMI) – hemodynamically stable – Tx. Endovascular
revascularization
  MVP – high-frequency mid-to-late systolic murmur at apex + midsystolic click
 Cardiac myxomas – LA – position-dependent symptoms – early diastolic “plop” + mid-
diastolic rumbling murmur at apex  echocardiography  surgical resection
 Blunt force aortic injuries
o If stable – contrast-enhanced CT angiography
o If unstable – TEE
 MI  cardiogenic shock
o Tachycardia, hypotension, pulmonary edema, JVD, cold & clammy skin
 Aortic dissection – unstable & patients with renal insufficiency – TEE
 Mitral stenosis – opening snap + low-pitched diastolic murmur – if symptomatic –
Percutaneous mitral balloon commissurotomy
 Acute limb ischemia (due to Afib) – if threatened extremity – IV heparin + emergency
revascularization (within 6 hours) – balloon catheter embolectomy & catheter-directed
thrombolysis
 Surgical bypass – Tx. For chronic LE ischemia due to PAD
 Leriche syndrome – aortoiliac occlusive disease
o Buttock, hip, or thigh claudication
o Erectile dysfunction
o Absent or diminished femoral pulses

Block 2
 Cardiac contusion – after MVA – from asymptomatic arrhythmias to cardiac rupture
o Hypotension + tachycardia refractive to fluid resuscitation, including vasopressors
o Atrial fibrillation
o (-) FAST
o Cardiogenic shock (decreased CO)
 Chronic venous disease
o Pruritic dermatitis or a venous ulcer  advanced CVD  Tx. Endovenous thermal
ablation (if no CI like DVT or PAD)
o Varicose veins or edema only  mild CVD  Tx. Compression therapy
o Duplex US before any treatment
o Daily exercise & leg elevation
 DVT – CI of anticoagulation – recent surgery, intracranial hemorrhage, or active bleeding
– IVC filter – prevent pulmonary embolism
 Femoral artery catheterization – complication: femoral artery pseudoaneurysm – duplex
US (nonhomogeneous hypoechoic mass connected to a femoral vessel)
o AV fistula – limb edema, venous dilation of lower limb & symptoms of limb
ischemia, HOHF
o Tx. For symptomatic iatrogenic AV fistulas  US-guided compression
 Uncomplicated post-catheterization pseudoaneurysms /> 3cm  Tx. US-guided
thrombin injection (formation of fibrin clot – stops blood flow to the hematoma)
 DVT – Dx. Compression US
 o D-dimer used to r/o DVT when pretest probability is low (Well’s criteria)
 DVT  pulmonary embolism  if stable start anticoagulation (LMWH)  CT pulmonary
angiography
o If unstable  echocardiography  RV dysfunction = PE
 PAD – Tx. Exercise – IF conservative fails then – cilostazol – if both fail to provide
symptomatic relief then – percutaneous transluminal angioplasty with stenting
 Acute limb ischemia – 6 Ps
o Pain, pallor, pulselessness, paralysis, paresthesia, poikilothermy
o Confirmatory test – Digital subtraction angiography
 Identifies arterial occlusions or dissections
 Differentiates between arterial thrombus or embolus
 AAA rupture – emergency surgery
o Alternative – endovascular aneurysm repair
 PVC (premature ventricular contraction) –
o Tall wide QRS
o By electrolyte imbalances, drugs, reduced ventilation
o Asymptomatic & treatment not needed
 MS  increased LAP  LA dilation  atrial fibrillation & increased pulmonary arterial
pressure (to overcome pressure in LA)  increased PVR  right ventricular hypertrophy
(right axis deviation) to compensate  RV failure  JVD & pitting edema
 Constrictive pericarditis – pericardial calcifications
o Fatigue, dyspnea, JVD, edema, kussmaul sing, pulsus paradoxus & pericardial
knock (high-pitched early diastolic)
o Tx. Pericardiectomy
 Aortic coarctation – delayed manifestation – rib notching (after 5 y/o) & left ventricular
hypertrophy
 Paradoxical emboli – through PFO or ASD (right to left shunt) – stroke + DVT
o Noncontrast CT
o Anticoagulant therapy once cerebral hemorrhage r/o
o PFO – confirmed with echocardiography
 VSD – progressive decrease in PVR first few weeks of life  decrease RV pressure 
increased left to right blood flow across VSD  increased overall volume of blood in
pulmonary circulation  increased lung perfusion (increased pulmonary vascular
markings)  increased pulmonary VR to LA  LV volume overload  LV hypertrophy
(left axis deviation)
 DiGeorge syndrome – chromosome 22
o Facial – micrognathia, cleft palate, broad nasal bridge, short philtrum, low-set
ears
o Cardiac defects (truncus arteriosus)
o Impaired development of parathyroid glands – hypocalcemia – tetany & seizures
o Absent thymic shadow
 Lithium pregnancy – Ebstein anomaly – holosystolic murmur at LSB & RA enlargement
with elongation of tricuspid valve leaflets & TR
  PFO – right to left interatrial shunt that opens during coughing (transiently increased
pressure in the pulmonary circulation  increased RA pressure)
o Asymptomatic – no intervention
 Venous hum – benign – continuous murmur at either side of the neck – louder during
diastole & MC on the right
o Murmur disappears o softer in supine position or flexion of the head
(compression of the internal jugular vein)
 Tetralogy of Fallot – RVOT determines severity of cyanosis
o RV hypertrophy  right axis deviation
o Overriding aorta, VSD & pulmonary stenosis
o Boot-shaped heart
 Tricuspid valve atresia – imperforated atrioventricular septum of the right side
o Venous blood from the RA via ASD to LA  mixes with oxygenated blood from
the lungs  pumped from LV into systemic circulation & pulmonary circulation
 cyanosis
o LV hypertrophy – left axis deviation
 VSD not fixed  Eisenmenger reaction (shunt reversal)  becomes cyanotic  chronic
hypoxemia  increased EPO  polycythemia
 Transposition of the great arteries – cyanotic heart condition
o Cyanosis shortly after birth that does not improve with O2
o CXR – egg-on-a-string (enlarged heart with narrowed mediastinum)
o Maternal diabetes
 Cyanotic congenital heart defects
o TOF – DiGeorge, Down, Mom drinking alcohol, PKU, diabetes
o Transposition of great vessels – mom with diabetes
o Tricuspid valve atresia – down syndrome
o Ebstein – lithium
o Total anomalous pulmonary venous return – heterotaxy syndromes
o Persistent truncus arteriosus – DiGeorge
o Hypoplastic left heart syndrome – trisomy 13, 18, turner & Jacobsen syndrome
 WPW – short PR & wide QRS with slurred upstroke (delta wave) – Tx. Procainamide

Block 3
 Fibromuscular dysplasia – young patient + HTN emergency + abdominal bruit at CTVA
o Confirming dx. CT angiography – stenoses of renal arteries
o Other imaging – duplex US & MRA
o Tx. Percutaneous transluminal angioplasty
 Venous hum – continuous murmur at right supraclavicular region – turbulent flow in the
internal jugular veins
 Cocaine-induced ACS – Tx. Aspirin, nitrates &/or CCB, benzodiazepines
o CI b-blockers (propranolol) – unopposed alpha-1 receptor activation
 Dilated cardiomyopathy – chronic alcohol use – ventricular dilation & reduced
contractility – abstinence from alcohol leads to reversal
 ESRD – peripheral edema, anemia, increased Cr & BUN, proteinuria & hyperkalemia
o Hypertensive nephrosclerosis – secondary to long-standing arterial HTN
 Sclerosis in capillary tufts & hyaline arteriolosclerosis on kidney biopsy –
caused by chronic damage from increased capillary hydrostatic pressure
in the glomeruli as well as ischemic damage from progressive narrowing
of renal arterioles
 Elevate BP & labs suggesting impaired renal function
 Arterial HTN – MCC of CHF
 TdP – polymorphic ventricular tachycardia – Tx. IV magnesium sulfate
 New-onset symptomatic Afib – measure serum TSH levels
 Acute limb ischemia – can be caused by thromboembolism due to Afib
o Prevented with warfarin (inhibition of the synthesis of vitamin k-dependent
factors)
 Symptomatic unstable bradycardia – Tx. Atropine
o If not improved – IV epinephrine or dopamine
 WPW – accessory atrioventricular pathway – bypasses the AV node
 Atrioventricular nodal reentrant tachycardia (AVNRT) – a supraventricular tachycardia –
reentry circuit in AV node
o Alternative electrical conduction pathways (one fast & one slow) in the AV node
– underlying cause of AVNRT
o Triggered by stress, alcohol & caffeine
 Narrow QRS < 120 ms
 Wide QRS > 120 ms
 Atrial premature beats – asymptomatic – no treatment
o Avoid triggers – caffeine, alcohol, smoking & stress
o Echocardiography or cardiac monitoring (Holter monitor) considered
 Thromboangiitis obliterans – smoking most important risk factor
o Claudication pain, critical limb ischemia, very low ABI & hx. of migratory
superficial thrombophlebitis
o Smoking cessation – prevent gangrene & amputation
 Prinzmetal angina (vasospastic angina) – angina with reversible ST elevations &
negative troponin
o Tx. CCBs (diltiazem, verapamil) – acute attacks & prophylaxis
 Acute coronary syndrome – angina of new-onset, at rest & persistent, worsening or
changing in character
o Tx. Anticoagulant, antiplatelet, beta blocker, statin, ACEI & analgesic
o Cardiac catheterization
 Mobitz type 2 AV block – unstable bradyarrhythmia (constant PR with dropped beats)
o Immediate treatment (can progress to 3rd degree heart block & death)
o Unstable patients – cardiac pacing
o Tx. Atropine & beta-adrenergic agents (dobutamine, dopamine, epinephrine)
  Dyslipidemia – elevated LDL &/or triglycerides
o Caused by familial hypercholesterolemia or related comorbid conditions
o /< 75 y/o + concomitant clinical ASCVD + LDL /> 190 &/or estimated 10-year
ASCVD risk >/ 7.5%  STATIN
o 40 – 75 y/o + DM  STATIN
 Statins – HMG-CoA reductase inhibitor – most effective reducing LDL levels & improving
HDL & triglyceride levels
 LDL = cholesterol – HDL – (triglycerides/5)
 Vasospastic angina – associated to Raynaud phenomenon & migraine
 Pharmacological stress test (ex. Adenosine)
o Adenosine  coronary vasodilation  tissue ischemia distal to the stenosed
coronary artery  new ECG changes  diversion of blood flow from stenotic
coronary arteries  blood diverted to healthier vessels & collaterals  worsens
ischemia  coronary steal syndrome
 Niacin – upregulates prostaglandin synthesis – cutaneous flushing
o Tx. NSAIDS (aspirin, ibuprofen) – 30-60 min before niacin prevent flushing
 Symptomatic high-risk AV blocks – Mobitz 2 or 3rd degree  Tx. Transcutaneous pacing
 PAD – star management of ASCVD (increased risk of MI or stroke)
o Statin – control hyperlipidemia
o Antiplatelet – clopidogrel or aspirin – all symptomatic patients & considered in
asymptomatic patient with ABI < 0.9
 Recurrent malignant pericardial effusion (cardiac tamponade) – Tx. Pericardial window

Block 4
 OSA – Tx. CPAP
o Alternative – oral appliances (mandibular advancement device) and positional
therapy devices (in lateral)
 Polymorphic ventricular tachycardia with cyclic alteration of the QRS – TdP – prolonged
QT
o Acquired – amiodarone, methadone, ondansetron
o Electrolyte imbalances – hypokalemia, hypomagnesemia, hypocalcemia
 AAA
o Asymptomatic – abdominal US
o Symptomatic – CT angiography
o Elective endovascular aneurysm repair
 Asymptomatic >/ 5.5 cm
 Rapid expansion ( > 1cm per year)
 Symptomatic AAA of any size
 Hypertrophic cardiomyopathy (HCM) – echo  systolic anterior motion of the anterior
mitral valve leaflet
o Asymmetric septal hypertrophy
o Increased LVOT pressure
 HCM – systolic ejection murmur that decreases with increased SVR (hand grip) – Tx. B-
blocker
 Thoracic aortic aneurysm (TAA) – CT angiography
 Nitrates – venous dilation  venous pooling  decreased preload  decreased end-
diastolic pressure  reduced myocardial wall tension  decreased myocardial oxygen
demand
 Tachycardia-induced dilated cardiomyopathy – resolves with treatment of arrhythmia
 Hx. of emigration – common rheumatic heart disease – AR
 Unprovoked DVT, DVT in unusual locations or recurrent DVT – limited cancer screening
– screening for colon, prostate, breast & cervical cancer
 Sick sinus syndrome (SSS) – sinus node dysfunction – MC by age-related degeneration &
fibrosis  abnormal automaticity &/or abnormal conduction
o Also exacerbated by beta blockers
o If ECG unrevealing  Holter monitor
o Bradycardia with sinus pause
o Tachycardia-bradycardia syndrome – palpitations, dyspnea, irregular tachycardia
o Tx. Pacemaker
 Chronic uncontrolled HTN – MCC of HFpEF – concentric hypertrophy – LV stiffness –
impaired myocardial relaxation – diastolic heart failure
 Chronic pulmonary HTN  leading to cor pulmonale - RVF
o COPD  hypoxic pulmonary vasoconstriction  pulmonary HTN  if left
untreated  chronically elevated RV AL  RVF
o Doppler echocardiography  estimate of PAP
o Right heart catheterization – to confirm dx.
 Cardiogenic shock – increased PCWP, CVP, SVR ; decreased CO, CI
 Acute radiation-induced pericarditis – adverse effect of radiation therapy of the chest
o High doses of radiation – cellular injury  inflammatory mediators & cytokines
 neutrophilic infiltration of the pericardium
o Constrictive pericarditis – complication of radiation therapy – years after + signs
of fluid overload
 Pulseless electrical activity (PEA) – chest compressions
 Diastolic or holosystolic murmur – considered abnormal so further evaluation
o Best initial test – TTE
 Anthracyclines (ex. Daunorubicin) – chemotherapeutic agents
o Dose-dependent cardiotoxicity – MC left ventricular dysfunction or a new-onset
HF due to dilated cardiomyopathy
o Dexrazoxane – prevent cardiotoxicity
o SE – myelosuppression & alopecia
 Cytarabine – SE: myelosuppression with megaloblastic anemia
 After major orthopedic surgery involving lower limb  increased in pTT is an indicator
of appropriate postoperative management
o Given heparin  heparin-induced thrombocytopenia – 5-14 days after initiation
– thrombotic events
  Atrial fibrillation  stasis of blood & thrombi on atrium  patients undergoing
cardioversion  can get dislodged & cause thromboembolism  anticoagulation with
DOAC (direct oral anticoagulation)  apixaban  prior to cardioversion & continue for
>/ 4 weeks after
 HOCM (hypertrophic obstructive cardiomyopathy) – automated implantable
cardioverter defibrillator – to prevent SCD
 Sustained monomorphic ventricular tachycardia – Tx. Prompt pharmacologic
cardioversion with IV antiarrhythmics (procainamide, sotalol, or amiodarone)
 Malignancy-associated pulmonary embolism  increased PAP & RV AL  right heart
remodeling  RV dysfunction  systemic venous congestion & reduced right heart
output  RH failure  hepatic congestion &/or gastric congestion  decompensated
RH failure
o Tx. O2 therapy, fluid restriction, diuretic

Block 5
 Vascular ring – infants – compressive symptoms of the trachea
o SOB, wheezing, stridor due to tracheal compression; regurgitation of food
o CXR – tracheal bowing & narrowing
 Laryngomalacia – low-pitched inspiratory stridor that worsens in supine position &
during sleeping or feeding
 Afib – symptomatic (palpitations & tachycardia)  NBS is rate control
o Beta-blockers – CI in COPD/asthma
o Verapamil/diltiazem
 MVP – systolic murmur with clicking – myxomatous degeneration – Ehlers-Danlos or
Marfan
 Congenital bicuspid aortic valve – AR in young patients &/or AS
 AR – decrescendo early diastolic murmur
 Dihydropyridine CCBs (“dipine”) – peripheral edema
 Thoracic aortic aneurysm – cystic medial necrosis – back pain & chest pressure
o Marfan, Ehlers-Danlos, HTN, congenital bicuspid aortic valve & cardiovascular
syphilis
 DVT – majority in iliac vein & other proximal deep veins (femoral & popliteal veins)
o Pulmonary embolism – sinus tachycardia & signs of RV pressure overload such
as:
 RBBB
 T-wave inversion in precordial leads &/or inferior leads
 S1Q3T3 pattern (deep S wave in lead I, pathological Q & inverted T wave
in lead III
 Right axis deviation
 STEMI – PCI (percutaneous coronary intervention)
o Door-to-PCI time < 90 min but not exceed 120 minutes
o If PCI cannot be performed within < 120 min – thrombolytic therapy
 Inferior wall infarction (RV) – epigastric pain, bradycardia & hypotension – Tx. NS
 Atrial gallop (S4) – atrial contraction against stiff ventricle – in acute phase of an MI –
cause impaired relaxation of the ischemic LV
 S4 (atrial gallop) in older patients can be normal – ventricular compliance decreases
with age
o Hypertrophic cardiomyopathy, AS, or HTN
 S3 (ventricular gallop) can be normal in young adults (< 40 y/o) or pregnant women
o Abnormal in older adults
o Dilated cardiomyopathy, CHF, or chronic mitral or aortic regurgitation
 Elevated JVP – from increased RA pressure – indicative of increased RV pressure
o Right HF, tension pneumothorax, pulmonary artery HTN & constrictive
pericarditis
 Elevated BNP (brain natriuretic peptide) & S3 gallop – indicate increased ventricular
filling pressure – CHF
o BNP released in response to stretching of ventricles
o Sensitive for CHF
o BNP > 400pg/mL in patients with symptoms of CHF  high PPV & have worse
prognosis
 Hepatojugular reflux – pressure to RUQ  jugular veins distended for 15s
o Help distinguish cardiac disease from hepatic disease in patient with b/l LE
edema & ascites
o (+) HJR – impaired relaxation of RV  inability to accommodate increased VR
o MCC are restrictive cardiomyopathy, constrictive pericarditis & RV HF
 Interventricular septum rupture – 3-5 days after MI
o Sudden hemodynamic instability (hypotension, tachycardia, tachypnea)
o Signs of RV failure (JVD, parasternal heave, pedal edema, clear lungs) due to left
to right shunt
o VSD – holosystolic murmur
 TIA + Afib – Tx. Warfarin or DOAC (direct oral anticoagulant) like rivaroxaban
 TIA only – Tx. Antiplatelet therapy (aspirin)
 Stable chest pain in women < 60 y/o or men < 40 y/o without additional risk factors or
concerning findings on initial ECG  low pretest probability of CAD
o No further testing at visit or
o Exercise ECG testing or
o Coronary calcium scoring
 Stable chest pain + intermediate to high PTP of CAD  coronary CT angiography or
cardiac stress testing
 Intermediate to high pretest probability of CAD:
o Advanced age
o Male
o Family hx. of premature cardiovascular disease
o Smoking hx.
o Diabetes
o HTN
 o Obesity
o Dyslipidemia
 Stress testing using adenosine or dipyridamole – CI with reactive airway disease –
asthma – possible bronchospasm (use dobutamine)
 RAS – Dx. Abdominal duplex US
 Aortic coarctation – Dx. Doppler echo
 Chronic thromboembolic pulmonary HTN – can manifest with cor pulmonale
o Can result from single or recurrent episodes of pulmonary embolism & should be
suspected when pulmonary HTN is diagnosed
o Patients with risk factors for venous thromboembolism (malignancy, recent
surgery)
o Westmark sign (associated with pulmonary embolism; high specificity) –
decreased vascular markings on CXR
o Dx. Right heart catheterization + pulmonary angiography to confirm
o Tx. Life-long anticoagulation & pulmonary thromboendarterectomy
 Cause of pulmonary HTN:
o Idiopathy or hereditary
o Left-sided heart disease
o Chronic hypoxic lung disease
o Chronic thromboembolism
o Multifactorial (sarcoidosis, metabolic disease, chronic hemolytic anemia)
 Hypoxic pulmonary vasoconstriction – cause of pulmonary HTN & cor pulmonale in
patient with OSA & COPD & ILD
 Central retinal vein occlusion – does NOT resolve spontaneously
o Massive retinal hemorrhages, dilated tortuous retinal veins, macular edema &
papilledema on fundoscopy
 Central retinal artery occlusion – stenosis of the carotid artery
o Fundoscopy – Hollenhorst plaques (bright yellow refractile bodies at the
bifurcations of the retinal arterioles) – cholesterol crystal embolization
o Carotid duplex US
o Carotid endarterectomy – symptomatic patients with stenosis >/70% or
asymptomatic >/80%
 Patients in shock with severe hemorrhage – initial bolus of IV saline followed by
transfusion of type O Rh (-) packed RBCs
 Acute aortic occlusion – life-threatening vascular event
o Lower limb & mesenteric ischemia symptoms
o Causes: atherothrombosis, occlusion of a stent or vascular graft, aortic dissection
& aortic embolism
 Left ventricular pseudoaneurysm (3-14 days after MI) – mural thromboembolism –
develop acute limb ischemia
o Dx. TTE
o Definitive dx. With angiography
 New-onset Afib – rhythm control with cardioversion or beta blocker (rate control)
  Prolonged episodes of Afib – increased risk of atrial thrombi & dislodgment with
cardioversion
o Afib >/ 48 hours or an unknown period of time – anticoagulation for 3 weeks
prior to cardioversion
o If cardioversion is desired earlier (pregnant or symptomatic) – time to
cardioversion can be shortened by doing TEE – to detect potential thrombi
 Moderate size PDAs – bounding pulses, widened pulse pressure & symptoms of HF
 Hand grip – increase AL – murmur louder
 S4 – decreased compliance of LV – LV hypertrophy – late diastolic contraction of atria
 Splitting S2 during inspiration – physiologic finding
 Superficial thrombophlebitis – NSAIDs, elevation of affected limb & compression
therapy
o Anticoagulation if large segment (>/5cm) or a thrombus near the deep venous
system &/or if risk factors for DVT present
o Duplex US – patients with risk factors for DVT:
 Pregnancy
 Chronic venous insufficiency
 obesity
 Digitalis toxicity – hyperkalemia, GI symptoms, palpitations, blurry vision
o Cardiac monitoring & ECG
o Blood samples – electrolyte abnormalities & serum digoxin concentration
o Tx. Digoxin-specific antibody fragments
 Stable angina – Tx. Beta 1 selective blocker (atenolol) – improve exercise tolerance &
reduce the frequency of anginal episodes – decreases HR & cardiac contractility 
reduces myocardial oxygen demand
o If CI of beta-blockers – CCBs, isosorbide mononitrate & ranolazine

Block 6
 Enterococci faecalis – infective endocarditis – nosocomial UTIs
o Tx. Ampicillin + gentamycin
 Cardiac catheterization (femoral access) + flank/back pain + suprainguinal fullness –
retroperitoneal bleeding
o Contrast-enhanced CT scan of abdomen & pelvis
o Rate but MCC of mortality after cardiac catheterization
 CHF – dyspnea on exertion + paroxysmal nocturnal dyspnea + bibasilar rales from
pulmonary edema (left-sided HF) + pitting edema (right-sided HF)  reduced CO 
organ hypoperfusion  affects kidneys  reduced renal blood flow  compensatory
activation of RAAS  angiotensin 2  vasoconstriction of afferent & efferent arterioles
(more pronounced in efferent) + aldosterone effects  maintains CO
 CCBs – verapamil – PR prolongation & 1st degree AV block – if asymptomatic –
observation – follow-up ECG
 Afib – ablative procedures in patients who remain symptomatic despite medical therapy
– foci near the pulmonary vein
 Atypical chest pain – gastrointestinal discomfort in absence of retrosternal pain in older
patients with diabetes – cardiac stress test
 SA & AV node – supplied by the RCA – inferior wall infarction – can present atypically
with epigastric pain
o High-degree (3rd) AV block can occur because of SA & AV node supplied by RCA
o Right-sided leads (V4R, V5R, V6R) – obtained to evaluate for RV infarction
 Aortic coarctation – increased risk of intracranial hemorrhage if untreated – cause of
brachiocephalic HTN
o Intracranial aneurysm formation (due to HTN)
o Other complications: aortic arch aneurysm & dissection, CAD, ischemic stroke,
endocarditis, LV hypertrophy & HF
 PDA – blood flow from descending aorta to pulmonary artery (left to right shunt)
o In a large PDA – volume overload of the RV & the lung circuit  pulmonary HTN
 Eisenmenger reaction (shunt reversal)
o Palpable right parasternal heave & pronounced S2  right heart strain
o Differential cyanosis – deoxygenated blood reaches only the lower body with
preserved upper extremity oxygenation
 Brugada syndrome – repolarization abnormality – males of Asian descent
o Usually asymptomatic; can cause palpitations & dizziness
o Triggered by substance abuse or alcohol consumption
o ECG  persistent ST elevations on leads V1-V2 with intact P waves
 Paroxysmal atrial fibrillation – supraventricular tachyarrhythmia
o Usually asymptomatic; can cause palpitations & dizziness
o Acute alcohol consumption triggers it – holiday heart syndrome
o Subsides within 7 days without intervention
o Abstain from alcohol
 Constrictive pericarditis with TB – new-onset dyspnea + orthopnea + fatigue + night
sweats, fever, cough + immigration + CXR with pericardial thickening & calcifications
o Compliance of RV decreased & doesn’t expand during inspiration – JVD
(kussmaul sign)
o Tx. NSAIDs, colchicine, glucocorticoids, pericardiectomy & tx. of underlying
condition
 Tabes dorsalis – degeneration of dorsal columns
o Ataxia + lower extremity pain + impaired sensation in lower extremities & Argyll
Robertson pupil (pupils do not react to light)  3ry syphilis
o Risk of TAA (thoracic aortic aneurysm) from aortitis  aortic root dilation & AR
 Nitrates – vasodilation – migraine-like headaches; cutaneous flushing; hypotension
o Other SE: gastroesophageal reflux or reflex tachycardia (tx. beta blockers)
 Drug-induced lupus
o Hydralazine
o Methyldopa
o TNF-alpha inhibitors (infliximab or etanercept)
o Procainamide
 o Penicillamine
o Isoniazid
o Minocycline
o Phenytoin
 Pericardial knock – high-pitched early diastolic sound
o In constrictive pericarditis – abrupt halting of diastolic ventricular relaxation &
filling by rigid pericardial sac
o Reduced ventricular filling  reduced CO  fluid overload  JVD, kussmaul
sign, hepatomegaly
o Etiologies of constrictive pericarditis: TB, prior cardiac surgery, radiation therapy
to chest, viral infection & connective tissue diseases
 Nitrate tolerance (isosorbide dinitrate) – long-term therapy  decreased effectiveness
o To prevent – intermittent therapy – nitrate-free intervals of at least 8 hours –
avoid taking at night
 First-dose hypotension – if two antihypertensives that work synergistically are given at
the same time
o Thiazide diuretics – inhibition of Na-Cl symporter in DCT  BP reduction – if you
add ACEI  hypotension
 Adenocarcinoma – tumor on descending colon with hepatic metastasis
 Carcinoid tumor – small intestine (terminal ileum) is the MC location
o Pellagra (niacin deficiency) – 3 Ds (dementia, diarrhea, dermatitis)
 African American with isolated HTN – Tx. thiazide diuretics (chlorthalidone)
o Also use dihydropyridine CCBs (dipine) – if concomitant metabolic syndrome
 Cardiogenic pulmonary edema – due to LV failure
o CXR – butterfly-shaped perihilar opacification, Kerley B lines
o Further increase in PCWP  alveolar edema (consolidation with an air
bronchogram) & pleural effusion (blunting of CVA)
 ARF – Sydenham chorea – milkmaid’s grip (alternating squeeze & release grip) – self-
limiting within weeks to months
 Afib can lead to atrial thrombus  emboli into arterial circulation – ischemic events
(splenic infarction)
 Fibromuscular dysplasia – most frequently affected arteries – internal carotid & renal
arteries
o Cerebrovascular FMD (headaches, pulsatile tinnitus, TIA)
o Renal FMD (renal HTN, abdominal bruit, renal atrophy)
o Tx. antihypertensives + antiplatelets + revascularization
 Stokes-Adams attacks – sudden loss of consciousness due to abnormal heart rhythm
(especially complete AV block (3rd degree)
 Statins
o Diabetic patient between 40-75 yrs.
o LDL >/ 190 & ASCVD (atherosclerotic cardiovascular diseases)  CAD, PAD,
previous stroke, or TIA
  After MI – (several weeks to months)  ventricular aneurysms  systolic murmur, an S3
&/or S4 gallop & persistent ST elevations
o Can lead to CHF
o Myocardial wall rupture  cardiac tamponade
o Arrythmias
o Mural thrombus
 Critical limb ischemia – urgent revascularization
o >/ 2 weeks of pain at rest, nonhealing wounds &/or frank tissue loss in one or
both lower extremities
o MR angiography with occlusion needed for Dx.
o Via percutaneous transluminal angioplasty or bypass surgery
o Long-segment &/or multifocal stenoses or occlusions  femorotibial bypass
surgery preferred
 Atheroembolism (cholesterol crystals)  livedo reticularis, blue toe syndrome, GI
ischemia, pancreatitis, TIA, stroke, or AKI
 DVT prophylaxis – LMWH (enoxaparin) within 12 hours of surgery – patients with high
risk
o LMWH – lower incidence of DVT & lower mortality
o Therapy continued for at least 3 weeks after surgery
o LMWH – CI in patients with renal failure
 Venous air embolism
o Mill-wheel murmur – churning sound in precordial region – air in heart chambers
o Sudden hypotension, tachycardia, JVD, respiratory distress
o If mechanically ventilated  a sudden fall in end-tidal carbon dioxide
o Can be due to neurosurgical procedures, insertion/removal of central venous
catheters, penetrating lung injuries & barotrauma
o Management: compression of suspected entry site, correction of hypoxia &
hypotension & placing patient head-down position (Trendelenburg) or in left
lateral decubitus (Durant)  trap air emboli in RV apex

Block 7/8
 Congenital long QT syndrome (Romano-Ward syndrome) – family hx. of sudden death
+ syncope with exercise + prolonged QT > 440ms + no electrolyte abnormalities
o Tx. beta blockers (propranolol)
o If not responsive to beta blockers  left cardiac sympathetic denervation
(stellectomy)
o If recurrent syncope despite medical therapy or survival of cardiac arrest 
implantable cardioverter defibrillator
 Jervell & Lange-Nielsen syndrome (congenital long QT syndrome) – associated with
congenital deafness
 Chronic MR  chronic volume overload of LV  eccentric hypertrophy of LA & LV to
compensate & maintain CO  decompensation of chronic MR (due to progressive LV
 dilation & myocardial dysfunction)  decreased SV  decreased CO  increased LV
end-diastolic pressure & increased pulmonary artery pressure
 HCM – associated with harsh crescendo-decrescendo systolic ejection murmur at LLSB;
accompanying murmur of MR (holosystolic at apex)  caused by systolic anterior
motion of the mitral valve leaflets into the LVOT
o Increases intensity with Valsalva & standing
o Decreases intensity with squatting or passive leg elevation
 AS – early stages asymptomatic but syncope with exertion – delayed peripheral pulses
o TTE – confirmatory test
 AR – early diastolic decrescendo murmur at LSB
o TTE – confirmatory test
 AV fistula – followed by intervention on the femoral artery  cardiac catheterization,
femoral ABG, surgery or trauma (gunshot wound) – edema & varicose veins in affected
limb
 Femoral artery aneurysm – continuous bruit
o Risk factors – age, HTN, hypercholesterolemia & chronic smoking
o Associated with other aneurysms (AAA)
 Carotid stenosis – Tx. statin, antiplatelet drugs & lifestyle modification
o Carotid endarterectomy
 Asymptomatic patient with stenosis >/ 80%
 If life expectancy is >/ 2 years
 MVP – myxomatous degeneration – MR – mid-systolic click
 MS – MC complication is Afib
o Rheumatic fever the MCC of MS
 Acute limb ischemia – commonly caused by thrombosis secondary to PAD
o However in absence of PAD – Afib can cause it  atrial thrombus embolizes 
arterial occlusion (MC location of arterial embolism is femoropopliteal artery)
 Confirm Afib with echo
 Cholesterol embolization syndrome – livedo reticularis & AKI
o Eosinophilia & eosinophiluria
o Kidney biopsy – spindle-shaped vacuoles (intravascular cholesterol deposits) –
confirm dx.
o Tx. revascularization – via angioplasty or endovascular grafting
 PAD – stenosis of the femoropopliteal artery – MC site
 Digoxin – increases vagus nerve activity – negative chronotropic effects – leads to PR
prolongation with possible AV block
o Hypokalemia increases risk of digoxin toxicity (ex. Loop diuretics & thiazide
diuretics)  avoided with digoxin
 CHF – hyponatremia – increased mortality
 MS – enlarged LA – compress esophagus – dysphagia megalatriensis
 AS – LV hypertrophy – increased LV oxygen demand – MI (angina) during exercise or
stress
o SAD – syncope, angina, dyspnea
 CCBs (dipine) – peripheral edema – Tx. ACEI & ARBs (vasodilation of postcapillary vessels
 reduction of transcapillary pressure)
 Beta-blocker intoxication – bradycardia + hypotension + wheezing + confusion +
hypoglycemia + prolonged PR
o IV glucagon – in symptomatic patients with no response to IV fluids & atropine
 RAS – reduced blood flow to kidney  unilateral kidney atrophy
o Treatment-resistant HTN; high renin & hypokalemia
 Isolated systolic HTN – decreased arterial elasticity & compliance – with aging
o Elevated SBP & normal DBP  wide pulse pressure
o > 60 y/o
o High risk of renal dysfunction & cardiovascular events
 Newly diagnosed HTN pt. – evaluate for end-organ damage & cardiovascular risk
o ECG
o CBC, fasting glucose
o Lipid profile
o TSH
o Electrolytes
o Renal function (creatinine with eGFR)
o Urinalysis
 Amiodarone – SE: chronic interstitial pneumonitis (inflammation with fibrosis of
interstitium of the lung) – 6 – 12 months after initiation
o Nonproductive cough, dyspnea, weight loss & fatigue
o Bilateral dry crackles during inspiration
o CXR: ground-glass opacifications
 TEE – detect aortic dissection in unstable patients
 TTE – detect pericardial effusion & cardiac tamponade
 Cardiac stress test – withheld medications before test
o Beta blockers
o CCBs (verapamil, diltiazem)
o Nitrates
o Methylxanthines (caffeine, theophylline)
 Aortic dissection
o Elevated BP, asymmetrical BP b/w limbs, diminished distal pulses, syncope,
sweating & confusion
o Extension of dissection into the aortic valve – AR at RSB – high-pitched blowing
diastolic murmur
o Complications of ascending aortic dissection – cardiac tamponade, MI & stroke
 Hereditary hemochromatosis (iron overload) – dilated cardiomyopathy + arthritis +
hepatomegaly + hyperpigmented skin + diabetes  Tx. regular phlebotomy
o Testicular atrophy
o Complications – dilated cardiomyopathy, restrictive cardiomyopathy & CHF
o Iron deposition in cardiac conduction system – lead to conduction abnormalities
  MC arrhythmia  paroxysmal atrial fibrillation
 Sinus node dysfunction
 Complete AV block
 Atrial & ventricular tachyarrhythmias
 Rarely SCD
 Pulmonary HTN - right-sided HF (peripheral edema + JVD + split S2) + pronounced
central pulmonary arteries
o Idiopathic; amphetamine & cocaine associated
o Confirmatory test – Right-heart catheterization
o Dx. made when mean pulmonary artery pressure >/ 20mmHg at rest & no
evidence of underlying pulmonary or left heart conditions
 Mitral murmurs – heard best during expiration & while patient lies on left side
 Pulseless electrical activity – nonshockable rhythm
o Chest compressions & IV epinephrine
 Reinfarction
o Serial measurement of troponin T levels (second measurement 3-6 hrs. later
showing 20% increase indicates reinfarction)
o Creatine kinase MB (CK-MB) – help in the evaluation
o Troponin T – 6 – 14 days to return to normal
o CK-MB – 2 – 3 days to return to normal (not commonly used)
 TRALI (transfusion-related acute lung injury) – within the first 6 hours - hypovolemia
o Dyspnea & diffuse bilateral opacities on CXR
o Hypotension & fever
 TACO (transfusion-associated circulatory overload) – within 12 hours - hypervolemia
o HTN & wide pulse pressure
o Evidence of volume overload (pulmonary edema, S3, JVD)
o Tx. supplemental O2 + diuresis
 Acute STEMI – emergency revascularization
o Percutaneous transluminal coronary angioplasty (PCTA)
o Dual antiplatelet therapy (P2Y12 receptor inhibitor & aspirin) & anticoagulation
therapy (heparin or bivalirudin) also indicated
o Beta blocker initiated within the first 24 hours of admission
o High-intensity statin – regardless of cholesterol levels
 Ambulatory BP measurement – distinguish b/w HTN & white coat HTN