What are the signs and symptoms of left heart fail?
Will see progressive dysnpea and orthopnea (cough when lying down)
CXR: Cardiomegaly, blunting of costophrenic angle (pleural effusion) and batwing in the peri-hilum area, Kerley B lines and increased vasdcular shadowing.
Caused by Left ventricle failure leading to increased left atrial pressure and increased ventricle filling pressure (or preload). This increased pressure transmists back to pulmonary capillaries==> fluid transudation into pulmonary interstial and alveolar spaces
When would you see the AV node take over to pace the heart? What would this look like on ECG?
If conduction between SA and AV node is impaired; may be d/t 3rd degree heart block
Changes will be bradycardia (SA has much higher firing rate, AV has slow firing rate at 45 bpm) and will see atria and ventricle depolarize ind of each other = AV dissocation
the QRS complexes will still be narrow bc ventricle depolarization is occuring normally.
Bacterial endocarditis FROM JANE
Bacteria FROM JANE ♥:
Janeway lesions Anemia
Nail-bed hemorrhage Embol
What bacteria are implicated in Acute Bacterial Endocarditis?
Acute—S. aureus (high virulence).
Large vegetations on previously normal valves with rapid onset.
Pt comes to clinic with fever he's had for the past several days. During your PE you notice he has conjuctival pallor and small erythematous lesions on his hands and soles. You ask if they hurt and he states mostly not, except for a raised one on the pad of his thumb. While gathering history on the patient, he admits he has a pretty dangerous drug habit.
What abnromatility would you expect to see in his heart?
BActerial endocarditis: signs of fever, anemia, Osler and Janeway lesions
IV drug use history: (Tricuspid valve implicated in IV drug use)
Think Acute and Staph Aureus; there will be large vegitaitons on previously normal valves
What type of bacterial endocarditis would you expect in a pts that has had recent dental procedures?
What would the vegitations in his heart look like?
(low virulence). Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. Gradual onset.
Most commonly implicated bacteria in culture negative bacterial endocartditis?
What about if the patient also has colon cancer?
What about a pt with prosthetic valves?
Culture Negs: Coxiella burnetii, Bartonella spp., HACEK (Haemophilus,
Actinobacillus, Cardiobacterium, Eikenella, Kingella)
Colon cancer + endocarditis = S. Bovis
Prosthetic vavle + endocarditis = S. Epidermidis
Little girl shows up to the ER with her mother. This little girl has a fever of 102 and crys every time she tries to walk or lift her arms but she doesn't keep still and keeps moving and shifting. The mom states she would like you to avoid putting anything with preservitives in her daughter, that she and her husband are trying to raise them 'holistically'. What is the most immediate concern for this girl?
Child has Acute Rheumatic Fever = Group A B-hemolytic Strep.
Fever, Erhythma marginatum, Vavlular damage, ESR, Red hot joints, SubQ nodules, Syndham chorea
Death from Myocarditis is most concerning.
What late sequale are seen in Rheumatic Fever?
What is the pathology for such complicated heart involvement seen in this diesase?
Late sequelae include rheumatic heart disease, which affects heart valves—mitral > aortic >> tricuspid (high-pressure valves affected most).
Early lesion is mitral valve regurgitation;l ate lesion is mitral stenosis.
Immune mediated (type II hypersensitivity); not a direct effect of bacteria. Antibodies to M protein cross-react with self antigens (molecular mimicry).
What are Antisckow cells and Aschoff bodies?
Associated with Aschoff bodies (granuloma with giant cells ), Anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus), anti- streptolysin O (ASO) titers.
seen in Acute Rheumatic fever
Beck triad (hypotension, distended neck veins, distant heart sounds), Increased HR, pulsus paradoxus. ECG shows low-voltage QRS and electrical alternans
Cardiac Tamponade: Compression of heart by fluid (e.g., blood, effusions) in pericardial space--> Decreased CO.
Equilibration of diastolic pressures in all 4 chambers.
What is Pulsus Parvus and when do you see it?
DECREASE in amplitude of systolic BP by > 10 mmHg during inspiration.
Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup.
Commonly presents with sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward. Presents with friction rub. ECG changes include widespread ST-segment elevation and/or PR depression.
Most common Primary Heart tumor in adult: Where is it locted and What does it look like?
What is the most common Primary cardiac tumor in children?
Myxoma: 90% in Left Atrium adn often called a "ball valve"--> see mult syncopal episodes
Rhabdomyomas: often assoicated with Tuberous Sclerosis
What is the physiology behind Kussmal breathing?
INCREASE in JVP on inspiration instead of a normal decrease
Inspiration-->negative intrathoracic pressure not transmitted to heart--> impaired filling of right ventricle--> blood backs up into venae cavae--> JVD.
May be seen with constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors.
Difference between Cherry and Strawberry hemangioma?
When do you see a cystic hygroma?
What about a Glomus tumor?
Cherry = adults; benign capillary hemangioma that doesn't regress
Strawberry = bengin in infants, does regress
Cystic = jabba neck; Turners
Glomus = painful red-blue under fingernails from Bartonella Henslae (mistaken for Kaposi)
Old lady, Unilateral headache, hurts to chew food
Dx? Tx? Most common location? Associated findings?
Temporal or Giant cell arteritis
Treat with high dose corticosteroids prior to temporal artery biopsy to prevent vision loss
Most often in the brnches of carotid
see associated with Polymyalgia rheumatica and will see focal granulomatous infiltration
Lovely Asian lady with very weak upper extremity pulses. Complains of fever and night sweats as well as achy joings. You notice nodules on her forearms.
Location of disorder
Usually Asian females < 40 years old. “Pulseless disease” (weak upper extremity
pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances.
Granulomatous thickening and narrowing of aortic arch and proximal great vessels.
Tx with corticosteroids.
Your pt has complaints of abdominal pain, bloody stool and recent weight loss. His BP is 160/90, and has an elevated creatinine
What viral inction often coincides
Polyarteritis Nodosa or PAN:
SEeni n Young adults, often Hepatitis B seropositivity in 30% of patients.
Fever, weight loss, malaise, headache. GI: abdominal pain, melena. Hypertension, neurologic dysfunction, cutaneous eruptions, renal damage.
PAN SPARES THE LUNGS
TX with corticosteroids, Cyclophosphamide.
Pathophysiology of PAN
Typically involves renal and visceral vessels, not pulmonary arteries.
Immune complex mediated with Transmural inflammation of the arterial wall and with fibrinoid necrosis.
Innumerable renal microaneurysms and spasms on arteriogram.
What are the sings and symptoms of Kawasakies and what is a concerning complication?
How do we treat it?
Asian children < 4 years old. CRASH and burn
Conjunctival injection, Rash (polymorphous desquamating), Adenopathy (cervical), Strawberry tongue (oral mucositis) , Hand- foot changes (edema, erythema), fever.
May develop coronary artery aneurysms :thrombosis or rupture can cause death.
Treat with IV immunoglobulin and aspirin.
Vascular disease seen in men that smoke...How will they present, What is the pathology?
Buerger diseae: Thromboangiitis Obliterans
Heavy smokers, males < 40 years old. Intermittent claudication may lead to
gangrene , autoamputation of digits,superficial nodular phlebitis. Raynaud phenomenon is often present as well as segmental thrombosing vasculitis; STOP SMOKING
What organ systems are involved in Granulomatosis with polyangiitis (Wegner)?
Upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis.
Lower respiratory tract: hemoptysis, cough, dyspnea.
Renal: hematuria, red cell casts.
Focal necrotizing vasculitis
Necrotizing granulomas in the lung and upper airway
What auto-antiB are present and how do you Tx the pt?
Triad seen with Wegners
AntiB: PR-3-ANCA/c-ANA + and see large nodular densities on CXR
Tx: Clycophosphamide and corticosteorids
Necrotizing vasculitis commonly involving lung, kidneys, and skin with pauci-immune glomerulonephritis and palpable purpura and NO nasopharyngeal involvement.
Dx, antiB present and Tx?
No granulomas. MPO-ANCA/p-ANCA H (anti- myeloperoxidase).
Treat with Cyclophosphamide, Corticosteroids.
Young boy with asthma comes to office with his mother. He has a rash on his legs she hasn't seen before, it's raised and very dark. The boy had a recent sinus infection, but he has gotten 6 others this year and not seen this rash so the mother thought it was something different.
What do antiB do you suspect is present in the pts serum?
What are some other complications with this diseaes?
Eosinophilic granulomatosis with polyangiitis (Churg- Strauss)
MPO-ANCA/p-ANCA, HIGH IgE level.
Granulomatous, necrotizing vasculitis with eosinophilia; can involved the heart, kidneys and GI and causes peripheral neuropathy (foot and wrist drop)
Father brings his daughter to the ER. His daughter has a raised, dark rash on her body and says her hurts everywhere. The father states she has a cold last week but thought it got better, until the rash happened and he noticed blood in her stool. What's the Dx and pathology?
Vasculitis 2° to IgA immune complex deposition.
Associated with IgA nephropathy (Berger disease).
What forms the adult structure of the smooth portion of the right atrium = sinus venarum?
What forms the adult structure of the rought parts of the left and right atria?
What forms the adult structure of the smooth portions of the left and right ventricle?
smooth right atrium = sinus venarum
rough left and right atria= primitive antrum
smooth part of L and R ventricles = bulbus cordis
What is the adult derivative of:
1st, 2nd, 3rd, 4th and 6th aortic arch?
1 = maxilary artery
2. Hyoid and Stapedial artery
3. Common Carotic and proximal internal carotic artery
4. left = aortic arch and right = proximal right subclavian
6. Proximal pulmonary arteries and on left Ductus ateriosus (PDA!)
What effects does Nitroprusside have on the cardiac pressure loop when given to pt with heart fail?
Nitroprusside is a balanced venous and arterial vasodialator: Reduces preload and reduces afterlooad but compliance and contractibilty are left unchanged
Young man comes to office with groin pain and swelling. He stated he had a sore on his penis but didn't think anything of it because it didn't hurt- 3 weeks later he started to have swelling in his inguinal region and inflammation of overlying skin and even draining ulcers. He stated that he had a fever around the same time as the groin pain. Cell scrapings from lesions show Cytoplasmic inculsion bodies.
Chlamydia trachmatis: lymphogranulma venerum
Starts as painless ulcer--> progress to painful lymphadenopahty + ucleration: see small and shallow ulcers that heal rapidly
Intracytoplasmic chlyamydial inclusion bodies seen in epitheilal cells
Pt has a painless lesion on his penis but comes to the doctor anyways, he's concerned. You culture the lesion and see Gram-Neg Spirocetes. Dx?
Treponema pallidum = syphillus
Murmur is heard best at left sternal border when pt is leaning forward at the end of expiration. Described as a diastolic decrescendo murumor and heard in early diastole.
Pt has a peridoxical embolism lodge in their left cerebral artery and die. What sound will you hear on auscultation?
paradoxical implies it went through PDA: machine like murmur
*Atrial L--> R shunts cause WIDE and FIXED splitting of S2 that doesn't not change with respiration
Early diastolic decrescendo murmur is characteristic of this heart pathology.
inhalation of amyly nitrate will reduce systemic arterial pressure and regurgitant glow thus lessening the murmur.
A systolic ejection murumr that increases in intesity with standing can be hear in pts with what pathology?
Hypertrophic cardiomyopathy: from decrease in LV outflow tract
Wide splitting of the S1 that is accentruated with inspiration:
why does this happen?
When do we see it?
Sign of delayed closure of tricuspid valve: seen in pts with complete right bundle branch block or tricuspid stenosis
The following diseases are associated with which heart defects?
Down: Cushion defects: ASD from ostium primum or regurgant AV valves
DiGeorge: Tetralogy of fallot or aortic arch anomalies
Friedrichs ataxia: hypertophic cardiomyopathy
Marfan: cycstic medial necrosis of aorta
Tuberous sclerosis : valve destruction form rhabdomyoma
Turners = coarctation