USMLE (Fach) / Cardiovascular (Lektion)

USMLE First Aid

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• Jugular venous pulse (JVP) a wave – atrial contraction. Absent in atrial fibrillation. c wave – RV contraction (closed tricuspid valve bulging into atrium) x descent – downward displacement of closed tricuspid valve during rapid ventricular ejection phase. Reduced or absent in tricuspid regurgitation and right HF because pressure gradients are reduced. v wave – ↑ right atrial pressure due to filling ("villing") against closed tricuspid valve. y descent – RA emptying into RV. Prominent in constrictive pericarditis, absent in cardiac tamponade.
• Myocardial action potention Also occurs in bundle of His and Purkinje fibers. Phase 0 = rapid upstroke and depolarization – voltage-gated Na+ channels open. Phase 1 = initial repolarization – inactivation of voltage-gated Na+ channels. Voltage-gated K+ channels begin to open. Phase 2 = plateau – Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmatic reticulum and myocyte contraction. Phase 3 = rapid repolarization – massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels. Phase 4 = resting potential – high K+ permeability through K+ channels. In contrast to skeletal muscle:- Cardiac muscle action potential has plateau, which is due to Ca2+ influx and K+ efflux.- Cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from SR (Ca2+-induced Ca2+ release).- Cardiac myocytes are electrically coupled to each other by gap junctions.
• Pacemaker action potential Occurs in the SA and AV nodes. Key differences from the ventricular action potential include: Phase 0 = Upstroke – opening of voltage-gated Ca2+ channels. Fast voltage-gated Na+ channels are permanently inactivated because of the less negative resting potential of these cells. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles. Phase 1 and 2 are absent. Phase 3 = repolarization – inactivation of the Ca2+ channels and ↑ activation of K+ channels → ↑ K+ efflux. Phase 4 = slow spontaneous diastolic depolarization due to If ("funny current"). If channels responsible for a slow, mixed Na+/K+ inward current. Accounts for automaticity of SA and AV nodes. The slope of phase 4 in the SA node determines HR. ACh/adenosine ↓ the rate of diastolic depolarization and ↓ HR, while catecholamines ↑ depolarization and ↑ HR. Sympathetic stimulation ↑ the chance that If channels are open and thus ↑ HR.
• Electrocardiogram Conduction pathway: SA node → atria → AV node → bundle of His → right and left bundle branches → Purkinje fibers → ventricles. Left bundle branch divides into left anterior and posterior fascicles. SA node "pacemaker" inherent dominance with slow phase of upstroke. AV node – located in posteroinferior part of interatrial septum. Blood supply usually from RCA. 100-msec delay allows time for ventricular filling. Pacemaker rates – SA > AV > bundle of His/Purkinje/ventriclesSpeed of conduction – Purkinje > atria > ventricles > AV node P wave – atrial depolarization. Atrial repolarization is masked by QRS complex.PR interval – time from start of atrial depolarization to start of ventricular depolarization (normally <200 msec).QRS complex – ventricular depolarization (normally <120 msec).QT interval – ventricular depolarization, mechanical contraction of the ventricles, ventricular repolarization.T wave – ventricular repolarization. T-wave inversion may indicate ischemia or recent MI.J point – junction between end of QRS complex and start of ST segment.ST segment – isoelectric, ventricles depolarized.U wave – prominent in hypokalemia, bradycardia.
• Ventricular fibrillation A completely erratic rhythms with no identifiable waves. - Fatal arrhythmia without immediate CPR and defibrillation.
• Atrial/brain natriuretic peptide Atrial natriuretic peptide: Released from atrial myocytes in response to ↑ blood volume and atrial pressure. Acts via cGMP.- Causes vasodilation and ↓ Na+ reabsorption at the renal collecting tubule.- Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to "aldosterone escape" mechanism. B-type (brain) natriuretic peptide: Released from ventricular myocytes in response to ↑ tension. Similar physiologic action to ANP, with longer half-life. BNP blood test used for diagnosing HF (very good negative predictive value). Available in recombinant form (nesiritide) for treatment of HF.
• Baroreceptors and chemoreceptors Receptors:- Aortic arch transmits via vagus nerve to solitary nucleus of medulla (responds to ↓ and ↑ in BP).- Carotid sinus (dilated region at carotid bifurcation) transmits via glossopharyngeal nerve to solitary nucleus of medulla (responds to ↓ and ↑ in BP). Baroreceptors:- Hypotension – ↓ arterial pressure → ↓ stretch → ↓ afferent baroreceptor firing → ↑ efferent sympathetic firing and ↓ efferent parasympathetic stimulation → vasoconstriction, ↑ HR, ↑ contractility, ↑ BP. Important in the response to severe hemorrhage.- Carotid massage – ↑ pressure on carotid sinus → ↑ stretch → ↑ afferent baroreceptor firing → ↑ AV node refractory period → ↓ HF.- Component of Cushing reflex (triad of hypertension, bradycardia, and respiratory depression) – ↑ intracranial pressure constricts arterioles → cerebral ischemia → ↑ pCO2 and ↓ pH → central reflex sympathetic ↑ in perfusion pressure (hypertension) → ↑ stretch → peripheral reflex baroreceptor-induced bradycardia. Chemoreceptors:- Peripheral – carotid and aortic bodies are stimulated by ↓ PO2 (<60 mmHg), ↑ PCO2 and ↓ pH of blood.- Central – are stimulated by changes in pH and PCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2. Do not directly respond to O2.
• Atrial septal defect Defect in interatrial septum.- Wide, fixed split S2. - Ostium secundum defects most common and usually an isolated finding. - Ostium primum defects rarer yet usually occur with other cardiac anomalies. - Symptoms range from none to HF. - Distinct from patent foramen ovale in that septa are missing tissue rather than unfused.  - O2 saturation ↑ in RA, RV, and pulmonary artery. - May lead to paradoxical emboli (systemic venous emboli use ASD to bypass lungs and become systemic arterial emboli). 
• Total anomalous pulmonary venous return Pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc). - Associated with ASD and sometimes PDA to allow for right-to-left shunting to maintain CO.
• Hyperlipidemia signs Xanthomas: Plaques or nodules composed of lipid-laden histiocytes in skin, especially the eyelids (xanthelasma). Tendinous xanthoma: Lipid deposit in tendon, especially Achilles. Corneal arcus: Lipid deposit in cornea. Common in elderly (arcus senilis), but appears earlier in life in hypercholesterolemia.
• Arteriosclerosis Hardening of arteries, with arterial wall thickening and loss of elasticity. Arteriolosclerosis: Affects small arteries and arterioles. Two types: hyaline (thickening of vessel walls in essential hypertension or diabetes mellitus) and hyperplastic ("onion skinning" in severe hypertension with proliferation of smooth muscle cells). Mönckeberg sclerosis (medial calcific sclerosis): Affects medium-sized arteries. Calcification of internal elastic lamina and media of arteries → vascular stiffening without obstruction. "Pipestem" appearance on x-ray. Does not obstruct blood flow; intima not involved.- Example of dystrophic calcification- Often seen in diabetes.
• Atherosclerosis Disease of elastic arteries and large- and medium-sized muscular arteries; a form of arteriosclerosis caused by buildup of cholesterol plaques. Location: Abdominal aorta > coronary artery > popliteal artery > carotid artery Risk factors:- Modifiable: smoking, hypertension, dyslipidemia, diabetes- Nonmodifiable: age, sex (↑ in men and postmenopausal women), family history Symptoms: Angina, claudication Inflammation important in pathogenesis: endothelial cell dysfunction → macrophage and LDL accumulation → foam cell formation → fatty streaks → smooth muscle cell migration (involves PDGF and FGF), proliferation, and extracellular matrix deposition → fibrous plaque → complex atheromas. Complications: Aneurysmas, ischemia, infarcts, peripheral vascular disease, thrombus, emboli.
• Aortic aneurysm Localized pathologic dilatation of the aorta. May cause abdominal and/or back pain, which is a sign of leaking, dissection, or imminent rupture. Abdominal aortic aneurysm: - Associated with atherosclerosis. - Risk factors include history of tobacco use, ↑ age, male sex, family history.- May present as palpable pulsatile abdominal mass.- Most often infrarenal.- Chronic transmural inflammation. Thoracic aortic aneuysm: - Associated with cystic medial degeneration.- Risk factors include hypertension, bicuspid aortic valve, connective tissue disease (eg, Marfan syndrome).- Also associated 3° syphilis (obliterative endarteriitis of the vasa vasorum).- Aortic root dilatation may lead to aortic valve regurgitation.
• Aortic dissection Longitudinal intimal tear forming a false lumen. Etiology:- Hypertension- Trauma (eg, deceleration injury)- Vasculitis (eg, syphilis)- Third-trimester pregnancy- Congenital: bicuspid aortic valve, connective tissue disorders (eg, Marfan syndrome). - Can present with tearing, sudden-onset chest pain, radiating to the back +/- markedly unequal BP in arms.- CXR shows mediastinal widening.- Can result in organ ischemia, aortic rupture, death. Stanford type A (proximal): Involves ascending aorta. May extend to aortic arch or descending aorta. May result in acute aortic regurgitation or cardiac tamponade. Treatment: surgery.Standford type B (distal to subclavian artery): Only involves descending aorta. Treat medically with β-blockers, then vasodilators.
• Traumatic aortic rupture Due to trauma and/or deceleration injury. - Most commonly at aortic isthmus (proximal descending aorta just distal to origin of left subclavian artery).
• Angina Chest pain due to ischemic myocardium 2° to coronary artery narrowing or spasm; no myocyte necrosis. - Stable – usually 2° to atherosclerosis (≥70% occlusion); exertional chest pain in classic distribution (usually with ST depression on ECG), resolving with rest or nitroglycerin. - Vasospastic (also known as Prinzmetal or Variant) – occurs at rest 2° to coronary artery spasm; transient ST elevation on ECG. Smoking is a risk factor, but hypertension and hypercholesterolemia are not. Triggers may include cocain, alcohol, and triptans. Treat with Ca2+ channel blockers, nitrates, and smoking cessation. - Unstable – thrombosis with incomplete coronary artery occlusion; +/- ST depression and/or T-wave inversion on ECG but no cardiac biomarker elevation (unlike NSTEMI); ↑ in frequency or intensity of chest pain or any chest pain at rest.
• Coronary steal syndrome Distal to coronary stenosis, vessels are maximally dilated at baseline. Administration of vasodilators (eg, dipyridamole, regadenoson) dilates normal vessels → blood is shunted toward well-perfused areas → ischemia in myocardium perfused by stenosed vessels. Principle behing pharmacologic stress tests with coronary vasodilators.
• Sudden cardiac death Death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia (eg, VF).  - Associated with CAD (up to 70% of cases), cardiomyopathy (hypertrophic, dilated), and hereditary ion channelopathies (eg, long QT syndrome, Brugada syndrome).  Prevent with implantable cardioverter-defibrillator (ICD).
• Myocardial infarction Most often due to rupture of coronary artery atherosclerotic plaque → acute thrombosis. - ↑ cardiac biomarkers (CK-MB, troponins) are diagnostic. ST-segment elevation MI (STEMI)- Transmural infarcts- Full thickness of myocardial wall involved- ST elevation on ECG, Q waves Non-ST-segment elevation MI (NSTEMI)- Subendocardial infarcts- Subendocardium (inner 1/3) especially vulnerable to ischemia- ST depression on ECG
• Evolution of myocardial infarction Commonly occluded arteries: LAD > RCA > LCX.Symptoms: diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, shortness of breath, fatigue. 0-24 h:- Gross: None. Dark mottling: pale with tetrazolium stain. - Early coagulative necrosis, release of necrotic cell contents into blood; edema, punctate hemorrhage, wavy fibers about 4 hours after event. Neutrophils appear. - Reperfusion injury, associated with generation of free radicals, leads to hypercontraction of myofibrils through ↑ free calcium influx.- Complications: Ventricular arrhythmia, HF, cardiogenic shock. 1-3 days:- Gross: Hyperemia.- Extensive coagulative necrosis.- Tissue surrounding infarct shows acute inflammation with neutrophils.- Complications: Postinfarction fibrinous pericarditis. 3-14 days:- Gross: Hyperemic border; central yellow-brown softening – maximally yellow and soft by 10 days.- Macrophages, then granulation tissue at margins.- Complications: Free wall rupture → tamponade; papillary muscle rupture → mitral regurgitation: intraventricular septal rupture due to macrophage-mediated structural degradation. LV pseudoaneurysm (risk of rupture). 2 weeks to several months:- Gross: Gray-white- Contracted scar complete.- Complications: Dressler syndrome (pericarditis), HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus).
• ECG localization of STEMI Anteroseptal (LAD): V1-V2 Anteroapical (distal LAD): V3-V4 Anterolateral (LAD or LCX): V5-V6 Lateral (LCX): I, aVL Inferior (RCA): II, III, aVF Posterior: V7-V9, ST depression in V1-V3 with tall R waves
• Acute coronary syndrome treatments Unstable angina/NSTEMI – Anticoagulation (eg, heparin), antiplatelet therapy (eg, aspirin) + ADP receptor inhibitors (eg, clopidogrel), β-blockers, ACE inhibitors, statins. Symptom control with nitroglycerin and morphine. STEMI – In addition to above, reperfusion therapy most important (percutaneous coronary intervention preferred over fibrinolysis).
• Shock Inadequate organ perfusion and delivery of nutrients necessary for normal tissue and cellular function. Hypovolemic:- Caused by: hemorrhage, dehydration, burns- Skin: cold, clammy- PCWP (preload) ↓↓- CO ↓- SVR (afterload) ↑- Treatment: IV fluids Cardiogenic:- Caused by: acute MI, HF, valvular dysfunction, arrythmia- Skin: cold, clammy- PCWP (preload) ↑ or ↓- CO ↓↓- SVR (afterload) ↑- Treatment: inotropes, diuresis (no fluids) Obstructive:- Caused by: cardiac tamponade, pulmonary embolism, tension pneumothorax- Skin: cold, clammy- PCWP (preload) ↑ or ↓- CO ↓↓- SVR (afterload) ↑- Treatment: relieve obstruction Distributive:- Caused by sepsis, anaphylaxis, CNS injury- Skin: warm (sepsis, anaphylaxis), dry (CNS injury)- PCWP (preload) ↓- CO ↑ (sepsis, anaphylaxis), ↓ (CNS injury)- SVR (afterload) ↓↓- Treatment: IV fluids, pressors, epinephring (anaphylaxis)
• Cardiac tumors Most common heart tumor is a metastasis (eg, melanoma). Myxoma: Most common 1° cardiac tumor in adults. 90% occur in the atria (mostly left atrium). Myxomas are usually described as a "ball valve" obstruction in the left atrium (associated with multiple syncopal episodes). May auscultate early diastolic "tumor plop" sound. Can lead to a decrease in cardiac output that manifests as dyspnea, lightheadedness, or syncope. Symptoms may be influenced by position (ie, upright posture exacerbates mitral obstruction, whereas lying down alleviates it). Histology: gelatinous material, myxoma cells immersed in glycosaminoglycans. Rhabdomyomas: Most frequent 1° cardiac tumor in children (associated with tuberous sclerosis). Histology: hamartomatous growths.
• Hereditary hemorrhagic telangiectasia Also known as Osler-Weber-Rendu syndrome. Autosomal-dominant inherited disorder of blood vessels. Findings: blanching skin lesions (telangiectasias) on skin and mucous membranes, recurrent epistaxis, skin discolorations, arteriovenous malformations (AVMs), GI bleeding, hematuria.
• Risk factors for coronary heart disease Highest risk factors:- Noncoronary atherosclerotic disease- Diabetes mellitus- Chronic kidney disease Major risk factors:- Hypertension- Hyperlipidemia- Cigarette smoking- Advanced age- Obesity- Physical inactivity
• Resistance, pressure, flow ∆P = Q x RVolumetric flow rate (Q) = flow velocity (v) x cross-sectional area (A)Resistance = 8η (viscosity) x length/πr4 Total resistance of vessels in series: RT = R1 + R2 + R3 ...Total resistance of vessels in parallel: 1/RT = 1/R1 + 1/R2 + 1/R3 ... Capillaries have highest total cross-sectional area and lowest flow velocity.Pressure gradient drives flow from high pressure to low pressure.Arterioles account for most of TPR. Veins provide most of blood storage capacity.Viscosity depends mostly on hematocrit.Viscosity ↑ in hyperproteinemic states (eg, multiple myeloma), polycythemia.Viscosity ↓ in anemia.Compliance = ∆V/∆P
• Auscultation of the heart 2nd right intercostal space: Aortic area- Systolic mumor – Aortic stenosis, flow murmur (eg, physiologic), aortic valve sclerosis 2nd left intercostal space: Pulmonic area- Systolic ejection murmur – Pulmonic stenosis, atrial septal defect, flow murmur Left sternal border: - Diastolic murmur: Aortic regurgitation, pulmonic regurgitation- Systolic murmur: Hypertrophic cardiomyopathy 4th left intercostal space: Tricuspid area- Holosystolic murmur: Tricuspid regurgitation, ventricular septal defect- Diastolic murmur: Tricuspid stenosis 5th left intercostal space: Mitral area (apex)- Holosystolic murmur: Mitral regurgitation- Systolic murmur: Mitral valve prolapse- Diastolic murmur: Mitral stenosis
• Bedside maneuvers Inspiration (↑ venous return to atrium):- ↑ intensity of right heart sounds Hand grip (↑ afterload):- ↑ intensity of MR, AR, and VSD murmurs- ↓ hypertrophic cardiomyopathy and AS murmurs- MVP: later onset of click/murmur Valsalva (phase II), standing up (↓ preload):- ↓ intensity of most murmurs (including AS)- ↑ intensity of hypertrophic cardiomyopathy murmur- MVP: earlier onset of click/murmur Rapid squatting (↑ venous return, ↑ preload, ↑ afterload):- ↓ intensity of hypertrophic cardiomyopathy murmur- ↑ intensity of AS, MR, VSD murmurs- MVP: later onset of click/murmur
• AV block First-degree AV block: The PR interval is prolonged (>200 msec). Benign and asymptomatic. No treatment required. Second-degree AV block:- Mobitz type I (Wenckebach): Progressive lengthening of PR interval until a beat is "dropped" (a P wave not followed by a QRS complex). Usually asymptomatic. Variable RR interval with a pattern (regularly irregular).- Mobitz type II: Dropped beats that are not preceded by a change in the length of the PR interval (as in type I). May progress to 3rd degree block. Often treated with pacemaker. Third-degree (complete) AV block: The atria and ventricles beat independently of each other. P waves and QRS complexes not rhythmically associated. Atrial rate > ventricular rate. Usually treated with pacemaker. Can be caused by Lyme disease.
• Normal cardiac pressures Pulmonary capillary wedge pressure (PCWP; in mmHg) is a good approximation of left atrial pressure.- Normal range = 4-12 mmHg - In mitral stenosis, PCWP > LV end diastolic pressure.  - PCWP is measured with pulmonary artery catheter (Swan-Ganz catheter). Right atrium: <5 mmHgRight ventricle: 25/5 mmHgPulmonary arteries: 25/10 mmHgLeft atrium: <12 mmHgLeft ventricle: 130/10
• Myocarditis Inflammation of myocardium → global enlargement of heart and dilation of all chambers. - Major cause of SCD in adults <40 years old. Presentation highly variable, can include dyspnea, chest pain, fever, arrhythmias (persistent tachycardia out of proportion to fever is characteristic). Causes:- Viral (eg, adenovirus, coxsackie B, parvovirus B19, HIV, HHV-6); lymphocytic infiltrate with focal necrosis highly indicative of viral myocarditis.- Parasitic (eg, Trypanozoma cruzi, Toxoplasma gondii)- Bacterial (eg, Borrelia burgdorferi, Mycoplasma pneumoniae)- Toxins (eg, carbon monoxide, black widow venom)- Rheumatic fever- Drugs (eg, doxorubicin, cocaine)- Autoimmune (eg, Kawasaki disease, sarcoidosis, SLE, polymyositis/dermatomyositis) Complications include sudden death, arrhythmias, heart block, dilated cardiomyopathy, HF, mural thrombus with systemic emboli.
• Syphilitic heart disease 3° syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of vessel wall and dilatation of aorta and valve ring. May see calcification of aortic root, ascending aortic arch, and thoracic aorta.Leads to "tree bark" appearance of aorta. Can result in aneurysm of ascending orta or aortic arch, aortic insufficiency.
• Giant cell (temporal) arteritis Large-vessel vasculitis Presentation:- Usually elderly females- Unilateral headache (temporal artery), jaw claudication.- May lead to irreversible blindness due to opthalmic artery occlusion (amaurosis fugax).- Associated with polymyalgia rheumatica (~50%). Pathology/labs:- Most commonly affects branches of carotid artery.- Focal granulomatous inflammation with formation of giant cells.- ↑ ESR- Treat with high-dose corticosteroids prior to temporal biopsy to prevent blindness.
• Takayasu arteritis (aortic arch syndrome) Large-vessel vasculitis Presentation: - Usually Asian females <40 years old.- "Pulseless disease" (weak upper extremity pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances. Pathology/labs:- Granulomatous thickening and narrowing of aortic arch and proximal great vessels.- ↑ ESR Treat with corticosteroids.
• Polyarteritis nodosa Medium-vessel vasculitis Presentation:- Usually middle-aged men- Hepatitis B seropositivity in 30% of patients.- Fever, weight loss, malaise, headache- GI: abdominal pain, melena- Hypertension, neurologic dysfunction, cutaneous eruptions, renal damage.- Usually spares the lungs Pathology/labs:- Typically involves renal and visceral vessels, not pulmonary arteries.- Transmural inflammation of the arterial wall with fibrinoid necrosis.- Different stages of inflammation may coexist in different vessels.- Innumerable renal microaneurysms and spasms on arteriogram. Treat with corticosteroids, cyclophosphamide.
• Kawasaki disease (mucocutanous lymph node syndrome) Medium-vessel vasculitis Presentation:- Asian children <4 years old- Conjunctival injection, rash (polymorphous → desquamating), cervical adenopathy, strawberry toungue (oral mucositis), hand-foot changes (edema, erythema), fever.- May develop coronary artery aneurysms; thrombosis or rupture can cause death. - Acute necrotizing Treat with IV immunoglobulin and aspirin.
• Buerger disease (thromboangiitis obliterans) Medium-vessel vasculitis. Presentation:- Heavy smoker, males <40 years old.- Intermittent claudication may lead to gangrene, autoamputation of digits, superficial nodular phlebitis (often migratory).- Raynaud phenomenon is often present. - Segmental thrombosing vasculitis with vein and nerve involvement. Treat with smoking cessation.
• Granulomatosis with polyangiitis (Wegener) Small-vessel vasculitis - Constitutional symptoms: Fever, weight loss, night sweats- Upper respiratory tract: Perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis → saddle nose deformity.- Lower respiratory tract: Hemoptysis, cough, dyspnea.- Renal: Hematuria, red cell casts. Triad:- Focal necrotizing vasculitis- Necrotizing granulomas in the lung and upper airway- Necrotizing glomerulonephritis (pauci-immune, i.e. absence of immune complexes/deposits) Lab findings: PR3-/c-ANCA (anti-proteinase 3)CXR: large nodular densities Treat with cyclophosphamide, corticosteroids.
• Microscopic polyangiitis Small-vessel vasculitis Necrotizing vasculitis commonly involving lung (hemoptysis), kidneys, and skin (palpable purpura) with pauci-immune glomerulonephritis and palpable purpura.Presentation similar to granulomatosis with polyangiitis but without nasopharyngeal involvement.- Associated with antibiotic use. Biopsy: Fibrinoid necrosis with infiltration of neutrophils, no granulomas.Lab findings: MPO-/p-ANCA (anti-myeloperoxidase) Treat with cyclophosphamide, corticosteroids.
• Behçet syndrome Small-vessel vasculitis Presentation:- High incidence in Turkish and eastern Mediterranean descent.- Recurrent aphthous ulcers, genital ulcerations, uveitis, erythema nodosum. - Can be precipitated by HSV or parvovirus.- Flares last 1-4 weeks. Pathology:- Immune-complex vasculitis- Associated with HLA-B51 Diagnostics: Positive pathergy test (exaggerated reaction to skin trauma with needle prick)
• Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) Small-vessel vasculitis Presentation:- Asthma, sinusitis, skin nodules or purpura, peripheral neuropathy (eg, wrist/foot drop).- Can also involve heart, GI, kidneys (pauci-immune glomerulonephritis). Pathology:- Granulomatous, necrotizing vasculitis with eosinophilia- MPO-/p-ANCA, ↑ IgE level
• Immunoglobulin A vasculitis Small-vessel vasculitis, also known as Henoch-Schönlein purpura. Presentation:- Most common childhood systemic vasculitis.- Often follows URI.Classic triad:- Skin: palpable purpura on buttocks/legs- Arthralgias- GI: abdominal pain (associated with intussusception) Pathology:- Vasculitis 2° to IgA immune complex deposition- Associated with IgA nephropathy (Berger disease)
• Bicuspid aortic valve Aortic ejection sound, which is an early systolic, high-frequency click heard over the right second interspace
• Systolic and diastolic heart failure Systolic heart failure: - Caused by primary disease in myocardial contractility- Reduced left ventricular ejection fraction (LVEF) <50%- Progressive chamber dilation with increased LV volume- Elevated left ventricular end-diastolic pressure (LVEDF) Diastolic heart failure:- Caused by conditions that decrease LV compliance, such as impaired myocardial relaxation (eg, from ischemia) or increased intrinsic ventricular wall stiffness (eg, from amyloid deposition)- Normal LVEF (>50%)- Normal end-diastolic volume- Increased LV filling pressures
• Third heart sound (S3) - Ventricular gallop sound (after S2).- Heard during rapid passive filling of ventricles in diastole.- Sudden cessation of filling as ventricle reaches its elastic limit. Physiologic in those <40 years and pregnant patients. Sign of left ventricular volume overload/failure. Pathophysiology: In early diastole, the ventricles relax and the atrioventricular valves open, allowing blood to rush in and fill the ventricles. An S3 develops with forceful rapid passive filling that exceeds the expansion capacity of the ventricle, leading to sudden deceleration of the entering blood column and reverberation of the ventricular walls. As a result, S3 is often heard in pathologic settings causing high ventricular filling pressures and/or volume overload, particularly aortic or mitral regurgitation and dilated cardiomyopathy.
• Forth heart sound (S4) - Atrial gallop sound (before S1).- Heard immediately after atrial contraction as blood is forced into a stiff ventricle. Physiologic in healthy older adults. Pathologic in younger adults, children; diastolic dysfunction (eg, LVH)
• Subclavian steal syndrome Typically occurs due to hemodynamically significant stenosis of the subclavian artery proximal to the origin of the vertebral artery. Subclavian stenosis is typically caused by atherosclerosis, although less common etiologies include Takayasu arteritis and complications from heart surgery (eg, aortic coarctation repair).  The lowered distal subclavian arterial pressure leads to reversal in blood flow ("steal") from the contralateral vertebral artery to the ipsilateral vertebral artery, away from the brainstem. Symptoms:- Arm ischemia (eg, exercise-induced fatigue, pain, paresthesias)- Vertebrobasilar insufficiency (eg, dizziness, vertigo, drop attacks)- Significant difference (>15 mmHg) in brachial systolic blood pressure between the affected arm and normal arm
• Pressure-volume loops and cardiac cycle Phases – left ventricle:1. Isovolumetric contraction – period between mitral valve closing and aortic valve opening; period of highest O2 consumption.2. Systolic ejection – period between aortic valve opening and closing.3. Isovolumetric relaxation – period between aortic valve closing and mitral valve opening.4. Rapid filling – period just after mitral valve opening (S3).5. Reduced filling – period just before mitral valve closing (S4).
• Autoregulation Heart: Local metabolites (vasodilatory): adenosine, NO, CO2, ↓ O2 Brain: Local metabolites (vasodilatory): CO2 (pH) Kidneys: Myogenic and tubuloglomerular feedback Lungs: Hypoxia causes vasoconstriction Skeletal muscle: Local metabolites during exercise: CO2, H+, adenosine, lactate, K+. At rest: sympathetic tone. Skin: Sympathetic stimulation most important mechanism for temperature control

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