Cardiac Path- Wittrack Flashcards
Dilated cardiomyopathy
Dilation of all four chambers of the heart Impaired contractility of one or both ventricles = systolic disfunction (decreased LV ejection fraction)
Common causes of dilated cardiomyopathy
Alcohol abuse Beriberi Coxsackie B Cocaine Chagas Doxorubicin Pregnancy!
Hypertrophic Cardiomyopathy
Massive hypertrophy of the left ventricle Usually due to a genetic mutation in sarcromere proteins Autosomal dominant
What is the most common cause of sudden death in young athletes?
Hypertrophic Cardiomyopathy
Restrictive Cardiomyopathy
Decreased compliance of the ventricular endomyocardium that restricts filling during diastole
What are some causes of restrictive cardiomyopathy?
Amyloidosis, sarcoidosis, endocardial fibroelastosis, Loeffler syndrome Presents as congestive heart failure Classic finding is low voltage EKG with diminished QRS amplitude
Difference between primary and secondary cardiomyopathy?
Primary = disease limited to heart Secondary = associated with systemic disorders
In what cardiac disease would you see impaired LV filling/relaxation with a preserved LVEF Thickened LV Normal to reduced LV chamber size
Hypertrophic cardiomyopathy
In what cardiac disease would you see usually non-dilated, non-hypertrophic ventricles but still have a diastolic LV dysfunction?
Restrictive cardiomyopathy
What are common sources of clinically significant valve disease in developed countries?
Calcific aortic stenosis Mitral valve prolapse
What are common sources of clinically significant valve disease in developing countries?
Rheumatic fever valvulitis (with multiple valve involvement)
What are almost all cases of mitral stenosis due to?
Rheumatic Fever
What is systolic click murmur syndrome?
Due to mitral valve prolaspe
What is mitral valve prolapse?
Ballooning of mitral valve into left atrium during systole Due to myxoid degeneration (accumulation of ground substance) of the valve making it floppy
What is calcific aortic stenosis?
Narrowing of aortic valve orifice Aging-related atherosclerosis of aortic valve cusps with secondary nodular calcification
What is a major cause of human mortality in developed countries?
Acquired heart disease -dominated by atherosclerotic coronary artery disease associated with ischemic heart effects
What >95% of ischemic heart disease due to?
Coronary atherosclerosis
NON-STEMI
Subendocardial infarction
STEMI
transmural infarction
What does the extend of infarction depend on?
The amount of collateral circulation
Which site is a most likely site for visceral cancer metastases?
Pericardium
What are primary tumors of the heart?
RARE! Atria myxomas (left atrium) Rhabdomyomas Cardia Sarcomas
Troponin
Elevated in MI with-in 2-4 hours Peaks at 48 hours Persists 7-10 days
CK-MB
elevated in myocardial necrosis but less specific than troponin
D-dimer
Produced by fibrinolysis/clot dissolution Markedly elevated in pulmonary embolism. deep venous thrombosis (DVT)
Hemoglobin Level
Severe anemia (especially if due to acute hemorrhage or hemolysis) can precipitate dyspnea or aggravate underlying CAD or heart failure
BNP
Secreted by ventricles in response to ventricular failure/ excess myocardial stretching Heart failure
What is Dressler’s Syndrome
Autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post MI)
What is your first consideration of bloody pericaridal fluid?
Malignancy (Per witrack)
Fibrinous pericarditis
Dressler syndrome Uremia Radiation LOUD friction rub
Serous Pericarditis
usual viral pericarditis Often resolves spontaneously Non-infectious inflammatory diseases like RA or SLE
Suppurative/purulent pericarditis
Bacterial infections: Staph Aureus Strep pneumonia H. influenza N. meningitidis Rare now with antibiotics Usually concurrent infection like meningitis
How much fluid in the pericardial sac would indicate large risk for tamponade?
200-300 cc acutely or >1000 cc chronically Increases pressure on heart and impairs cardiac filling/flow
What circumstances are likely to cause FATAL cardiac tamponade?
Retrograde AORTIC DISSECTION with intrapericardial rupture Rupture AMI Penetrating chest wounds
What are symptoms for cardiac tamponade?
Hypotension Soft or absent heart sounds Jugular venous distension Maybe other signs of HF
Treatment for cardiac tamponade?
Pericardiocentesis
What is constrictive pericarditis? Symptoms? Treatment?
Impaired ventricular filling caused by thickened/contracted pericardial scar up 1 cm thick Symptoms: RIGHT heart failure Increased JVD Peripheral Edema Abdominal discomfort Weakness/fatigue (may mimic restrictive CM) Requires pericardial resection
Which primary cardiac tumor is associated with syncope due to obstruction of the mitral valve?
Myxoma! Usually found in LEFT ATRIUM attached to the valve of the fossa ovalis
Which primary cardiac tumor is associated with tuberous sclerosis and arises in the ventricle?
Rhabdomyoma Most common primary cardiac tumor in CHILDREN
Are metastasis or primary tumors most common in the heart?
Metastatic! Usually from melanoma or lymphoma
What is the primary cause of a thoracic aortic aneurysm?
Tertiary Syphillis
- Endarteritis of vaso vasorum
- luminal narrowing
- Decreased flow/ 02 to vaso vasorum
- Atrophy of vessel wall
What are the symptoms of an aortic anuerysm rupture?
Rupture > 5 cm
Hypotension
Pulsatile Abdominal Mass
Flank Pain
What is the primary cause of an abdominal aortic aneurysm?
ATHEROSCLEROSIS
- Thickens vessel wall
- Decreased O2 perfursion to media and adventia
- Atrophy of vessel wall
- Dilation
Usually male smokes > age 60 w/ hypertension
Describe the pathology on Aortic Dissection
Intimal tear with dissection of blood through the media of the aortic wall
- Need 2 things
- High Pressure –> proximal 10 cm of the aorta
- Pre-existing weakness in vessel wall
- Hypertension causes hyaline arteriolosclerosis of vaso vasorum
- Decreased blood flow causes atropy
- OR a connective tissue disorder
Why is a Type A aortic dissection more leathal than Type B?
Type A is of the ascending aorta
Blood can flow in the pericardial sac
Increased fluid/blood in pericardial sac
CARDIAC TAMPONADE
SUDDEN DEATH
54 year old female
Headache
Visual Distrubances
Jaw Claudication
Flu-like symptoms
Polymyalgia Rheumatic
Elevated ESR
What is it?
Most likely Giant Cell (Termoral) Arteritis
How do you diagnose and treat Giant Cell (Temporal) Arteritis?
Temporal artery biopsy!
Negative biospy does NOT rule out disease (because it is segmental- could have just gotten a segment w/out disease)
Treat with corticosteroids
Why do you want to treat a patient with corticosteroids AS SOON as you suspect Giant Cell/ Temporal arteritis?
High risk of BLINDNESS w/ out treatment!!!!
What is the most common vasculitis in older adults?
Giant cell/ temporal arteritis
Middle-aged male with sinusitis or nasopharyngeal ulceration, hemoptysis with bilateral nodular lung infiltrates, and hematuria due to rapidly progressive glomerulonephritis
Granulomatosis with polyangitis/ Wegener Granulomatosis
(Small vessel vasculitis)
Differential diagnosis for pulmonary hemorrhage + rapidly progressive glomerulonephritis?
ANCA-associated vasculitis
Goodpasture’s
SLE
What is the number on ecause of morbidity and mortality in developed countries?
Coronary artery disease and stroke
Name 5 mechanisms for vascular disease
- Lumen stenosis = atherosclerosis, HTN, diabetes, vasculitis
- Sudden lumen occlusion = thrombosis, embolism, wall dissection
- Great majority of acute/catastrophic events (MI, Stroke, PE)
- Vascular wall weakening/ Aneurysmal dilation
- Vasculitis
- Extrinisc vascular compression = compartment syndrome
- Vena cava syndrome = SVC compression from surrounding malignant mediatinal adenopathy (usually lung cancer)
Which vein is the source of the majority of the clinically significant/ fatal pulmonary emboli?
iliofemoral veins
What clues might indicate secondary hypertension (as to primary)?
- Severe/resistant hypertension despite multiple antihypertensives
- Acute BP rise in a patient with previously stable BP
- Age < 35 years, non-obese, non-black patient with no apparent risk factors
- Malignant/accelerated hypertension w/end organ damage, retinal heorrhage/papilledema
- Hypertension onset before puberty
What is the most common potentially correctable cause of secondary hypertension?
Renal artery stenosis!
(Probably from atherosclerosis > age 55)
What are two potential causes of secondary hypertension?
Renal artery Stenosis
Fibromuscular Dysplasia (young white women)
CLUES:
Increase creatinine
Proteinuria
Atrophic kidney
Abdominal bruit
What is fibromusclar dysplasia?
Common cause for secondary hypertension
- Narrowing of medium-sized arterial lumens by usually medial fibroplasia of unknown causes
- Usually affects renal and cerebral vessels
- Affects young to middle-aged women
“String of beads” angiographic appearance and bruits over some arterial segments?
Fibromuscular Dysplasia
Common in young white women
Cause for seconary hypertension
TX: revascularization via surgery or angioplasty
Young adult with refractory or malignant hypertension or stroke?
Consider Fibromuscular Dysplasia!!!
What is the most common congenital cardiovascular cause of secondary high blood pressure?
COARTCTATION of aorta!
Associated with Turner Syndrome
Upper extremity high bloodpressure w/ lower extremity hypotension
Rib nothcing on CXR
**Left arm pressure/pulse may be diminished if coarctation proximal to left subclavian artery
Sequelae of chronic hypertension?
High risk for systemic atherosclerosis
Thoracic aortic aneurysms and aortic dissection
Palpable purpura suggests which vasculitis….
Henoch-Schonlein Purpura
or
Microscopic Polyangiitis
Pulmonary/renal syndromes suggest which vasculitis…
(hemoptysis/ pulmonary infiltrates / glomerulonephritis)
Wegener’s granulomatosis (c-ANCA)
Microscopic Polyangiitis (p-ANCA)
Headache, scalp pain, and visual symptoms suggest which vasculitis?
Giant Cell (temporal arteritis)
How do you distinguish Wegener’s Granulmatosis from Microscopic Polyangitis?
Wegeners = cANCA
Micro= pANCA
Both have renal and pulmonary involvement
Micro does NOT have nasopharyngeal involvemnt and NO granulomas present
What is the most common vasculitis in children?
Henoch-Schonlein Purpura
Vasculitis due to IgA immune complex deposition
Disease is self-limited, but may reoccur (steroids if severe)
Churg-Strauss Sydrome
Small vessel vasculitis
p-ANCA many organs (espeically heart and lungs)
Asthma and eosinophilla
What are the four vasculitisis with T-lymphocyte response with granuloma formation?
Giant Cell
Takayasu arteritis
Wegener’s
Churg-Stauss
What is required for diagnosis of most vasculitis types?
Tissue Biopsy!!!!
ERS/C-reactive protein
Serum creatinine/UA
Antibodies
Chest XRAY/CT
Large Vessel vasculitic diseases?
Giant Cell Arteritis
Takaysau’s Artertitis
Elderly female with….
Unilateral headache
Jaw claudication
Scalp pain
Visual Disturbances
Polymyalgia rheumatica
Elevated ESR
Temporal Giant Cell Arteritis
40 year old ASIAN female
Absent pulses in upper extremities
Visual and neurological symptoms
Elevated ESR
Takayasu Arteritis
Large Vessel
Classically involves aortic arch at branch points
Treatment is corticosteroids
A young adult with
Hep B seropositivity
Abdominal pain and GI bleeding
High blood pressure
Skin rash
Polyarteritis Nodosa
Medium arteries
Neutrophilic vasculitis w. aneruysm formation
Positive assoication with Hep B
Treat w/ corticosteroids and cyclophosphamide
4 year old asian child presents with
Hand and foot erythema
Enlarged cervical lymphnodes
Kawaski disease
May develope coronary artery aneurysm, thrombosis that leads to MI and ruputres
Treat with IVIg and Aspirin
Disease is self-limited
What is Virchow’s triad of DVTs?
Impeded venous circulation
Hypercoagulability
Endothelial injury/dysfunction
What virus is Kaposi Sarcoma associated with?
HHV-8
Clinically, how can you differentiate between a hemangioma or a Kaposi sarcoma?
The Hemangioma will blanch (because the blood is contained in blood vessels) and a Kaposi Sarcoma will not blanch because blood is not in a vascular channel
MI complications with in 1 day?
Arrhythmias
Cardiogenic Shock
Heart Failure
Sudden Death
MI complications with-in 1-3 days
Fibrinous Pericarditis
Only in transmural infarct
Caused by neutrophil invasion/ inflammation of necrotic tissue
MI complications 3 days- 2 weeks
Macrophages! Clear debris/structural degredation
Tissue at it’s weakest…..
Ventricular free wall rupture –> cardiac tamponde
Papillary rupture –> mitral insufficiency
Septal rupture –> ventral septal defect
Mural thrombis ( “Plugs” hole in myocardium = time bomb)
MI complications after months?
Scar formation
Dresseler’s syndrome
LV anyuersm
Chronic Heart failure
