CVS Flashcards
AORTIC STENOSIS
MURMUR: systolic crescendo-decrescendo w/ ejection click
L&R: upper sternal border -> radiates to carotids
OTHER FINDINGS:
paradoxical S2 split
S4
narrow pulse pressure
AORTIC INSUFFIECIENCY
MURMUR: early decrescendo diastolic
L&R: left lower sternal border
OTHER FINDINGS:
de Musset sign
Quincke’s sign
MITRAL INSUFFICIENCY
MURMUR: holosystolic murmur
L&R: apex; radiates to back or clavicular area
OTHER FINDINGS:
diminished S1
wide S2
S3 gallop
MITRAL STENOSIS
MURMUR: S2 w/ opening snap then low pitched diastolic rumble
L&R: left lateral decubitus position with bell
OTHER FINDINGS:
high left atrium pressure
MITRAL VALVE PROLAPSE
MURMUR: midsystolic click -> systolic murmur
L&R: apex
OTHER FINDINGS:
standing: inc murmur
Squattinf: dec murmur
PULMONARY INSUFFICIENCY
MURMUR: crescendo-decrescendo
L&R: Left upper sternal border
PULMONARY STENOSIS
MURMUR: diastolic crescendo-decrescendo
L&R: Right upper sternal border
OTHER FINDINGS:
ejection click
TRICUSPID INSUFFICIENCY
MURMUR: blowing holosystolic murmur
L&R: Left lower sternal border
OTHER FINDINGS:
Carvallo’s sign
S3 & S4
TRICUSPID STENOSIS
MURMUR: diastolic rumble
L&R: Left lower sternal border
OTHER FINDINGS:
ejection click
SYSTOLIC MURMURS
Aortic stenosis
Pulmonary stenosis
Tricuspid regurgitation
Mitral regurgitation
DIASTOLIC MURMURS
Aortic regurgitation
Pulmonary regurgitation
Tricuspid stenosis
Mitral stenosis
FINDINGS THAT SUGGEST A LARGE INFARCT IN NSTEMI
Diaphoresis
Sinus tachycardia
3rd or 4th heart sounds
Bibasilar rales
Hypotension
RUPTURED PLAQUE HAS _____
Thin fibrous cap
Collagen poor fibrous cap
Large lipid core
Many macrophages
Fibrin rich thrombus
MAJOR DETERMINANTS OF MYOCARDIAL O2 DEMAND
Heart rate
Myocardial contractility
Myocardial wall tension
DETERMINANTS OF ADEQUATE SUPPLY OF O2
Level of O2 carrying capacity of blood determined by inspired O2, pulmonary function, and Hgb concentration, & level of coronary flow
Histology findings in simulant induced cardiomyopathy (due to cocaine or amphetamine use)
Microinfarcts and thrombus secondary to endothelial dysfunction
Histology findings in acute viral myocarditis
Massive myocardial lymphocytic infiltration with clear myocyte damage
Histology findings in alcoholic cardiomyopathy
Cardiomyocyte atrophy with interstitial and perivascular fibrosis and hyperplasia of small mitochondria
Histology findings in amyloidosis
Birefringence pattern of congo red staining between myocardial fubers under polarized light
Pericarditis that happens after myocardial infarction
Dressler’s syndrome
Diagnosed when a typical viral syndrome occurs without cardiac symptoms but with elevated biomarkers
Possible subclinical myocarditis
Diagnosed when there is histologic or immunohistologival evidence of inflammation on endomyocardial biopsy
Definite myocarditis
Risk factors for peripartum cardiomyopathy
Increased maternal age
Incresed parity
Twin pregnancy
Malnutrition
Use of tocolytic therapy for premature labor
Preeclampsia or toxemia of pregnancy
Alternating strong and weak pulse resulting from variations in left ventricular stroke volume with every cardiac cycle because of incomplete LV recovery
Pulsus alternans
Exaggerated fall in a patient’s BP during inspiration by >10mmHg; seen in cardiac tamponade and constrictive pericarditis
Pulsus paradoxus
Weak pulse seen in patients with aortic stenosis
Pulsus parvus et taedus
Increased pulse with double systolic peak seen in AR
Pulsus bisferiens
Concentric hypertrophy
Increased mass is out of proportion to chamber volume
Pressure overload
Increased LV mass
Increase relative wall thickness
Eccentric hypertrophy
Increase in cavity size or volume
Volume overload
Increased LV mass
Normal relative wall thickness
Presents with severe sharp or tearing pain in retrosternal area
Acute aortic dissection
Presents with a few seconds of sharp chest pain reproduced by preaaure on the chest
Costochondritis
Presents with chest discomfort radiating to trapezius
Acute pericarditis
Presents with substernal or epigastric pain sometimes related to food intake
GI disorders (GERD/esophageal spasm)
Contraindications to exercise stress testing
Rest angina within 48 hours
Unstable rhythm
Severe aortic stenosis
Acute myocarditis
Uncontrolled HF
severe pulmonary hypertension
Active infective endicarditis
Indications for revascularization
Unstable phase of disease
Intractable symptoms
High risk coronary anatomy
DM
Impaired LV function
RELATIVE CI TO FIBRINOLYTICS IN PX WITH STEMI
- Current use of anticoagulants (INR >/=2)
- Recent (<2 weeks) invasive or surgical procedure
- Prolonged (>10 min) CPR
- Known bleeding diathesis
- Pregnancy
- Hemorrhagic ophthalmic condition (e.g. hemorrhagic diabetic retinopathy)
- Active PUD
- Hx of severe HPN that is currently controlled
ABSOLUTE CI TO FIBRINOLYTICS AMONG PX WITH STEMI
- History of cerebrovascular hemorrhage at any time
- Non-hemorrhagic stroke or other cerebrovascular event within the past year
- Marked hypertension (reliably determined systolic AP >180 mmHg and/or a diastolic pressure >110mmHg) at any time during acute presentation
- Suspicion of aortic dissection and active internal bleeding (excluding menses)
Raynaud’s Phenomenon
Characterized by:
- Episodic digital ischemia
- Sequential development of digital blanching, cyanosis, and rubor of the fingers after cold exposure and subsequent rewarming
- sensation of cold or numbness or paresthesia of the digits often accompanies the phases of pallor and cyanosis
- occurs in patients whose vocations require the use of vibrating hand tools
Pernio
Vasculitic disorder associated to exposure to cold
Raised erythematous lesions develop most commonly on the toes or fingers in cold weather
Erythromelalgia
Characterized by burning pain and erythema of extremities
Feet are more involved more frequently that the hands
Males affected more frequently females
Acrocyanosis
Arterial vasoconstriction and secindary dilatation of the capillaries and venules with resultung persistent cyanosis of the hands, less frequently the feet
Originates from GIT; associated with colonic polyps and tumors
Streptococcus gallolyticus (S.bovis biotype 1)
Located in the oral cavity, skin, and URT
Viridand streptococci
Staphylococci
HACEK (Haemophilus, Aggregatibacter, Cardiobacterium hominis, Eikenella corrodens, & Kingella kingae)
Isolated from cultures of human rectum, vagina, cervix, urethra, skin, and pharynx
Streptococcus agalactiae (GBS)
Most common bacterial species causing IE
Staphylococcus aureus
Most common bacterial species causing IE
Staphylococcus aureus
Diagnosed when typical viral syndrome occurs without cardiac symptoms, but with elevated biomarkers of cardiac injury, ECG suggestive of acute injury, and/or reduced left ventricular EF or regional wall motion abnormality
Possible subclinical acute myocarditis
Diagnosed when criteria for myocarditis are met and accompanied by cardiac symptoms such as SOB, chest pain, etc.
Probable acute myocarditis
Diagnosed when histologic or immunohistologic evidence of inflammation on endomyocardial biopsy is present
Definite myocarditis
Most commonly diagnosed non-infective inflammatory process affecting the myocardium
Granulomatous myocarditis
Sarcoidosis
Giant Cell Myocarditis
Mechanism of paroxysmal a.fib
Automaticity
Mechanism of Torsades de pointes
Early afterdepolarization
Mechanism of ventricular tachycardia from digoxin toxicity
Delayed afterdepolarizations
Mechanism of atrial flutter
Reentry
Blocks multiple cardiac ionic currentd and has sympatholytic activity; most effevtive anti-arrhythmic for supressing VAs
Amiodarone
Reversal agent of Dabigatran
Idarucizumab
Reversal agent of rivaroxaban, apixaban, edoxaban, & apixaban
Andexanet alfa
Reversal agent of warfarin
FFP, Prothrombin complex concentrate, Vit K
Direct vasodilator that has antioxidant and nitric kxide enhancing actions
Hydralazine
Non-selective aldosterone antagonist; binds progesterone and androgen receptors; SE include gynecomastia, impotence, and menstrual abnormalities
Spironolactone
Newer agent that doesn’t have the same SE as spironolactone; selective aldosterone antagonist
Eplerenone
Indications for using CCB for IHD
- Inadequate responsiveness to the combination of BB and nitrates
- AE/SE to BB (eg. depression, sexual disturbances, and fatigue)
- Angina and hx of asthma or COPD
- Sick sinus syndrome or significant atrioventricular conduction distubrances
- Prinzmetal angina
- Symptimatic PAD
Severe asymptomatic HPN (SBP >180 OR DBP >120)
Hypertensive urgency
BP Parameters similar to HPN urgency + acute target organ damage
Hypertensive emergency
Patients with BP persistently >140/90 despite taking 3 or more anti-hypertensive including a diuretic
Resistant HPN
Associated with abrupt increase in BP in a patient with underlying HPN or related to sudden onset HPN in a previously normotensive individual
Recognized by progressive retinopathy (arteriolar spasm, hemorrhages, exudates, and papilledema), deteriorating renal function with proteinuria, microangiopathic hemolytic anemia, and encephalopathy
Malignant hypertension
Autosomal dominant disorder characterized by elevated plasma levels of LDL-C with relatively normal TG levels; mutation on LDLR gene
Familial hypercholesterolemia
Adipose tissue in certain fat depots is impaired; loss of subcutaneous fat in the extremities and buttocks; accompanied by increased visceral fat; patients described to have muscular appearance
Familial Partial Lipodystrophy
Recessive disorder; mixed hyperlipidrmia (elevated TG and LDL) due to accumulation of remnant lipoprotein particles (chylomicron and VLDL or IDL)
Familial dysbetalioproteinemia
Fasting TGs >150 mg/dl and evidence of elevated cholesterol containing lipoproteins such as LDL-C >130 mg/dl or non-HDL-C >160 mg/dl)
Mixed hyperlipidemia
Most common familial lipid disorder; mixed lipidemia (plasma TG levels bet 150 and 500 mg/dl and total cholesterol bet 200 and 400 mg/dl; usually with HDL-C levels <40 mg/dl in men and <50mg/dl in women) and a family history of mixed dyslipidemia and/or premature CHD
Familial combined hyperlipidemia
Lipids primarily influenced by obesity, insulin resistance, and T2DM
Triglycerides
Lipids primarily influenced by diet that is high in saturated and trans fat
LDL
ABCA1 deficiency or Tangier disease
Extremely low circulating plasma levels of HDL-C <5mg/dl and apoA-I <5 mg/dl
Cholesterol accumulates in the reticuloendothelial system resulting in hepatosplenomegaly and pathognomic enlarged grayish yellow or orange tonsils
Cholesterol absorption inhibitor that binds directly to and inhibits NCP1L1 and blocks intestinal absoprtion of cholesterol
Ezetimibe
dec inhibtion of cholesterol synthesis -> inc hepatic LDL receptors
HMG COA reductase inhibitors
- lovastatin, rosuvastatin, simvastatin, atorvastatin
dec inhibtion of cholesterol synthesis -> inc hepatic LDL receptors
HMG COA reductase inhibitors
- lovastatin, rosuvastatin, simvastatin, atorvastatin
Inc bile acid secretion -> inc LDL receptors
Bile acid sequestrants
- cholestyramine, colestipol, colesevelam
Dec PCSK9 activity due to Ab inhibition -> inc LDL receptors
OR
Dec PCSK9 synthesis due to siRNA silencing -> inc LDL receptors
PCSK9 inhibitors
- evolocumab
- alirocumab
- incilisiran
Dec inhibition of cholesterol synthesis -> inc LDL receptors
ATP citrate lyase inhibitor
- bempedoic acid
MTP inhibition -> dec VLDL assembly and secretion
MTP inhibitor
- lomitapide
Dec ApoB synthesis due to ASO silencing -> dec ApoB/VLDL secretion
ApoB inhibitor
- mipomersan
Dec ANGPTL3 activity due to Ab inhibition -> inc LPL activity, inc LDL catabolism
ANGPTL3 inhibitor
- Evinacumab
