CVS Flashcards by BP Iv

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

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AORTIC INSUFFIECIENCY

MURMUR: early decrescendo diastolic

L&R: left lower sternal border

OTHER FINDINGS:
de Musset sign
Quincke’s sign

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MITRAL INSUFFICIENCY

MURMUR: holosystolic murmur

L&R: apex; radiates to back or clavicular area

OTHER FINDINGS:
diminished S1
wide S2
S3 gallop

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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

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MITRAL VALVE PROLAPSE

MURMUR: midsystolic click -> systolic murmur

L&R: apex

OTHER FINDINGS:
standing: inc murmur
Squattinf: dec murmur

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PULMONARY INSUFFICIENCY

MURMUR: crescendo-decrescendo

L&R: Left upper sternal border

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PULMONARY STENOSIS

MURMUR: diastolic crescendo-decrescendo

L&R: Right upper sternal border

OTHER FINDINGS:
ejection click

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TRICUSPID INSUFFICIENCY

MURMUR: blowing holosystolic murmur

L&R: Left lower sternal border

OTHER FINDINGS:
Carvallo’s sign
S3 & S4

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TRICUSPID STENOSIS

MURMUR: diastolic rumble

L&R: Left lower sternal border

OTHER FINDINGS:
ejection click

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SYSTOLIC MURMURS

Aortic stenosis
Pulmonary stenosis
Tricuspid regurgitation
Mitral regurgitation

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DIASTOLIC MURMURS

Aortic regurgitation
Pulmonary regurgitation
Tricuspid stenosis
Mitral stenosis

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FINDINGS THAT SUGGEST A LARGE INFARCT IN NSTEMI

Diaphoresis
Sinus tachycardia
3rd or 4th heart sounds
Bibasilar rales
Hypotension

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RUPTURED PLAQUE HAS _____

Thin fibrous cap
Collagen poor fibrous cap
Large lipid core
Many macrophages
Fibrin rich thrombus

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MAJOR DETERMINANTS OF MYOCARDIAL O2 DEMAND

Heart rate
Myocardial contractility
Myocardial wall tension

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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

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Histology findings in simulant induced cardiomyopathy (due to cocaine or amphetamine use)

Microinfarcts and thrombus secondary to endothelial dysfunction

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Histology findings in acute viral myocarditis

Massive myocardial lymphocytic infiltration with clear myocyte damage

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Histology findings in alcoholic cardiomyopathy

Cardiomyocyte atrophy with interstitial and perivascular fibrosis and hyperplasia of small mitochondria

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Histology findings in amyloidosis

Birefringence pattern of congo red staining between myocardial fubers under polarized light

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Pericarditis that happens after myocardial infarction

Dressler’s syndrome

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Diagnosed when a typical viral syndrome occurs without cardiac symptoms but with elevated biomarkers

Possible subclinical myocarditis

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Diagnosed when there is histologic or immunohistologival evidence of inflammation on endomyocardial biopsy

Definite myocarditis

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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

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Alternating strong and weak pulse resulting from variations in left ventricular stroke volume with every cardiac cycle because of incomplete LV recovery

Pulsus alternans

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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

1. Current use of anticoagulants (INR >/=2) 2. Recent (<2 weeks) invasive or surgical procedure 3. Prolonged (>10 min) CPR 4. Known bleeding diathesis 5. Pregnancy 6. Hemorrhagic ophthalmic condition (e.g. hemorrhagic diabetic retinopathy) 7. Active PUD 8. Hx of severe HPN that is currently controlled

ABSOLUTE CI TO FIBRINOLYTICS AMONG PX WITH STEMI

1. History of cerebrovascular hemorrhage at any time 2. Non-hemorrhagic stroke or other cerebrovascular event within the past year 3. Marked hypertension (reliably determined systolic AP >180 mmHg and/or a diastolic pressure >110mmHg) at any time during acute presentation 4. 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

1. Inadequate responsiveness to the combination of BB and nitrates 2. AE/SE to BB (eg. depression, sexual disturbances, and fatigue) 3. Angina and hx of asthma or COPD 4. Sick sinus syndrome or significant atrioventricular conduction distubrances 5. Prinzmetal angina 6. 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