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BOARDS! > Cardio > Flashcards

Cardio Flashcards

1
Q

A. What is the cause of acute coronary syndromes?

B. Differentiate between the two ends of the spectrum.

A

A. acute coronary syndromes (unstable angina, MI, and sudden death) result from acute plaque change often superimposed with thrombosis.

B.

ulcerated therosclerotic plaque with a partially obtructive thrombus is associated with unstable angin or subendocardial infarction.

a rupture atherosclerotic laque with a fully obstructive thrombus is associated with transmural MI

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2
Q

Differentiate between TRANSudate and EXudate

A

TRANSudate=an ultrafiltrate of plasma caused by hemodynamic changes

EXudate=an extravasation of 1. plasma water, 2. small ions, 3. plasma protein components, and 4. circulating leukocytes as seen in inflammatory states

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3
Q

A1. Define acute pericarditis

A2. what is the most common form?

A3. what is the most striking physical finding?

B1. Define characteristics/physical findings on chronic pericarditis

B2. how long does it take to develop chronic pericarditis?

A

A1. Acute pericarditis: acute-onset, mid-chest pleuritic pain that decreases on sitting up and leaning forward

A2. most common form: fibrinous or serofibrinous pericarditis

A3. most strking physical finding: pericardial friction rub

B1.

Chronic pericarditis: can hear a pericardial knock that is a bief, high frequency, precordial sound heard in early diastole (shortly after S2).

B2. takes months/yrs to develop

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4
Q

What are the major assoiations of autosomal and sex chromosomal-inherited disorders that are associated with developmental cardiac and/or aortic defects or cardiac pathology?

A
  1. Down syndrome: endocardial cushion defects (ostium primum ASD, regurgitant AV valves)
  2. DiGeorge syndrome: tetralogy of Fallot and aortic arch anomalies

>>T-lymphocyte immunodeficiency that results from maldevelopment of the 3rd and 4th branchial (pharyngeal) pouches due to deletion on chromosome 22.

>>clinical associations: absence of a thymic shadow on neonatal x-ray, hypocalcemic tetany (from absence of the parathyroids), cleft palate, mandibular deformity, low-set ears, and aortic arch abnormalities

  1. Friedrich’s ataxia: hypertrophic cardiomyopathy
  2. Marfan syndrome: cystic medial necrosis of the aorta (aortic dissection and aneurysm), MVP
  3. Tuberous sclerosis: valvular obstruction due to cardiac rhabdomyomas
  4. Turner’s syndrome: coarctation of the aorta

>>short stature, short and thick neck, broad chest, shortened 4th metacarpals

>>bicuspid aortic valve=most common congenital cardiac malformation-can occur with aortic coarctation

>>>>pts susceptible to infectious endocarditis due to abnml leaflet structure and turbulent flow

>>CP: aortic ejection sound, early systolic, high-frequency cick heard over right second interspace

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5
Q

Describe the Tetralogy of Fallot (congenital defect)

A

Characterized by:

  1. stenosis of the RV outflow tract
  2. RV hypertrophy
  3. VSD
  4. aorta that overrides the VSD

>>R-to-L shunt leads to early cyanosis; degree of stenosis determines the extent of shunting and cyanosis

>>patients learn to squat in response to a cyanotic spell; increased arterial resistance decreases shunting and allows for more blood to reach the lungs

>>boot-shaped heart on x-ray

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6
Q

Differentiate between slow and fast response tissues

A

Slow response tissues: SA and AV node

fast response: cardiomyocytes

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7
Q

What is the most common cause of aortic stenosis in elderly patients (>70)?

A

degenerative calcification of the aortic valve leaflets

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8
Q

What causes QT prolongation?

A

Decreased outward K+ current during repolarization phase of the cardiac AP results in QT prolongation.

>>major cardiac pathophy consequence of QT prolongaion=an increased risk of episodic polymorphic ventricular tachycardia, including torsades de pointes

>>Adenosine and ACh reduce the rate of spontaneous depolarization in cardiac pacemaker cells by prolonging phase 4

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9
Q

Mitral Regurg

  1. location for ausc
  2. major hemodynamic finding:
  3. best indicator
A
  1. most prominently heard over cardiac apex
  2. major hemodynamic finding: abnormally prominent upsloping LA “v wave” during cardiac catheterization (L. atrium line in Wiggers)
  3. best indicator of MR with LV volume overload is the presence of an SR gallop=increased rate of LV filling due to large volume of regurgitant flow re-entering the ventricle during mid diastole
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10
Q

Wiggers Diagram

A
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11
Q

Aortic Regurg

  1. location for ausc/sound characteristic
  2. major hemodynamic finding:
  3. best indicator/Wiggers
A
  1. decrescendo type murmur over the right sternal border
  2. large left ventricular stroke volume-some pt exhibit head bobbing with carotid pulsations (de Musset sign) due to transfer momentum from the large LVSV to the head and neck
  3. large regurgitant SV; large pulse pressure-leads to bounding femoral and carotid pulses marked by abrupt distention and quick collapse (“water-hammer” pulses)

>>LVEDV also increased due to incompetent aortic valve

>>Wiggers: elevated LVDP and decreased aortic diastolic pressure due to regurgitant flow from the aorta to the LV

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12
Q

Mitral Valve Prolapse

A
  • most common cardiac abnormality predisposing to native valve bacterial endocarditis (NVBE)
  • age: 15-60yo (in US)
  • mid-systolic click accompaniedby a late systolic murmur
  • MVP more common in CTD; connective tissue diseases (Marfan, Ehlers-Danlos)
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13
Q

Mitral Stenosis:

  1. location for ausc
  2. major hemodynamic finding:
  3. best indicator/Wiggers
A

>>seen in rheumatic heart disease

>>produces a mid-diastolic, low pitched, rumbling murmur that may begin with an opening snap best heard over the apex of the heart

>>on Ventricular PV loop, MV opening occurs at the point between isovolumetric relxation and diastolic filling

>>LV diastolic pressures usualy near-nml, pressures proximal to stenotc MV typically elevated; SV and pulse pressures usually near nml

>>Wiggers: increased LA pressure during diastole (not systole) due to primary obstruction of LV filling

Epidemiology: Often an immigrant (non-US)

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14
Q

Aortic Stenosis

A
  • harsh crescendo decrescendo systolic ejection murmur
  • hear beat in the right 2nd intercostol space with radiation to the carotids
  • causes delayed, prolonged carotid pulses (pulsus parvus et tardus).
  • systolic vibrations or a carotid shudder (thrill) may also be present
  • Wiggers: LV systolic pressure significantly higher than aortic systolic pressure
  • most common cause in US: bicuspid aortic valves
  • pts with bicuspid aortic valves develop clinically significant AS aroung 50yo. In comparison, senile calcific stenosis of nml aortic valves become symptomatic >65yo
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15
Q

Tricuspid Regurg

A

>>holosystolic murmur that increase in intensity during inspiration (also in MR and ventricular septal defects)

>>loudest near left lower sternal border

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16
Q

What are the different types of heart pigments?

A
  1. Lipofuscin/lipid peroxidation: insoluble pigment composed of lipid polymers and protein-complexed phospholipids, lipofuscin is considered a sign of wear and tear or aging. this ylw-brown, finely granular perinuclear pigment is the product of free radical injury and lipid peroxidation. commonly seen in the heart and liver of aging or cachectic, malnourished pts
  2. Hemosiderin-during iron overload there is deposition of iron-contained brown pigmented granules
  3. Melanin-oxidation product of tyrosine metabolism and typically appears as dark brown to black pigmented granules
  4. Glycogen-glucose polymerization product that typically appears as clear vacuoles within the cytoplasm
  5. Hyaline-form of protein accumulation typically appearing as a glassy, homogenous pink deposit
  6. exogenous pigment endocytosis:

>>common ex: when urban residing individuals inhale carbon or coal dust that is taken up by macrophages within the lung parenchyma (anthracosis)

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17
Q

(Adult type) Aortic coarctation

  1. TRIAD
  2. pre v. post ductal
  3. clincal a, b, c
  4. RF
  5. radiographic exam
A

>>TRIAD: upper body HTN, diminished lower extremity pulses, enlarged intercostal artery collaterals

>>stenosis is post-ductal (vs. infantile form, coarctation is preductal and fatal soon after birth sans surgical repair)

>>clincal a: can produce HTN in the upper aortic circulation and simultaneously low perfusion in the dital aorta supplying the legs

>>clinical b: HA and epistaxis may be caused by the HTN inthe arteries supplying head/neck

>>clinical c: lower extremity mu weakness orfatigue with exercsie may be caused by inadequate lower body perfuision

likelihood of adult type is greatly increased by the finding of enlarged, palpable intercostal cesse; these indicate the development of a collateral arterial circulation to the region of the aorta distal to the coarctation

>>radiographic exam: notching of the ribs as a result of enlarged tortuous intercostal arteries

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18
Q

Different cell types/dz assoc

A

>>Acanthocytes-cells with irregularly spaced surface projections that vary in length and width

spur cells=extreme form

typical of abetalipoproteinemia

>>Bite cells-from oxidant-induced damage (ex: G6PDH deficiency)

occur when spenic monocyte-macrophage system removes heinz bodies from erythrocytes

>>Spherocytes-small round erythrocytes without nml central pallor

common in hereditary spherocytosis also, autoimmune hemolytic anemia, burns, and non-fresh blood samples

>>Target cells-bulls eye morphology with central concentration of Hgb surround by colorless area

seen in: obstructive liver dz, thalassemia, iron deficiency anemia, and asplenia

>>Teardrop cells-myelofibrosis

when marrow is replaced with fibrosis (or metastatic cancer), RBC must squeeze through fibrous stranfs, later appearing in peripheral smear as teardrop cells

>>Shistocytes-DIC

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19
Q

What is PARAneoplastic syndrome of hypercoagulability?

A

>>can be seen in some pts with cancer, especially adenocarcinomas of the pancreas, colon, or lung

>>superficial VT can appear in one sit and resolved, only to recur in another site=Trousseau syndrome (migratory superficial thrombophlebitis); an indication of visceral cancer

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20
Q

LA enlargement

A

can sometimes cause left laryngeal nerve impingement; neurapraxia resulting in left vocal cord paresis and hoarseness may result

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21
Q

Congestive Heart Failure

  1. basic principles
  2. Left-sided
  3. R. sided
A
  1. pump failure, divided into L and R-sided
  2. Left-sided HF:
    causes: ischemia, HTN, dilated cardiomyopathy, MI, restrictive cardiomyopathy
    nonspecific: productive cough and exertional wheezing pr chest tightness

>>Clinical features due to decreased forward perfusion and pulmonary congestion.

I.pulmonary congestion leads to pulmonary edema: a. results in dyspnea, paroxysmal nocturnal dyspnea (due to increased venous return when lying flat), orthopnea=specific sign, and crackles

b. small, congested capillaries may burst, leading to intraalveolar hemorrhage; marked by hemosiderin-laden macrophages (HF cells)

II. decreased flow to kidneys leads to activation of RAA system and fluid retention exacerbates CHF

III. tx: ACE inhibitor

  1. R-sided HF

I. most commonly due o LSHF; other important causes: L-to-R shunt and chronic lung disease (cor pulmonale)

II. CP-due to congestions:

a. JVD
b. painful hepatosplenomegaly with characteristic nutmeg liver, ma lead to cardiac cirrhosis
c. dependent bilat lower extremity pitting edema (due to increased hydrostatic pressure)

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22
Q

AAA (Abdominal Aortic Aneurysm)

-RF

A
  • focal dilation of the abdominal aorta that most commonly occurs below the renal arteries (infrarenal AA)
  • RF: advanced age (>60), smoking, HTN, male sex
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23
Q

Coronary Arteries (Occclusion)

A

>>in 90% occlusion of the RIGHT coronary artery can result in trasmural ischemia of the inferior wall of the LV producing ST elevation in leads II, III, and avF and possible sinus node dysfunction

>>occlusion of proximal LAS results in anteroseptal transmural ischemia with ST elevations in leads V1-V4

>>occlusion of the LCX would produce transmural ischemia of the lateral wall of the LV with ST elevations in V5 and V6, and possibly I and aVL

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24
Q

Paroxysmal supraventricular tachycardia

A

definition: common dysrhythmia that frequently occurs in patients with no other heart disease.
cause: re-entrant circuit in the AV node
tx: adenosine (in the hospital) OR vagal manuevers (carotid sinus massage and Valsalva)

>>carotid sinus massage increases baroreceptor firing, and increases PS influence on the heart and vessels, will prolong the AV node refractory pd which stops AV re-entrant tachycardias

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25
Q

Which organ in the body has the largest oxygen extraction of any organ in the body?

A

Myocardial oxygen extraction>>any other tissue or organ in the body

>>high degrees of oxygen extraction causes increased myocardial oxygen demand (during exercise)-met by proportionate increase in coronary blood flow

>>heart muscles are perfused during diastole, subendocardium is more prone to ischemia

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26
Q

ANP (atrial natriuretic peptide) and its 3 main functions

A

>>secreted by atrial cardiomyocytes in response to atrial stretch induced by HTN or hypervolemia

>>causes peripheral vasodilation and increased urinary excretion of sodium and water

>>Neprisilyn inhibitors (SACUBITRIL) prevent its degradation, enhancing hemodynamic effects in HF pts

>>ANP function: binds to natriuretic peptide receptor on cell membranes, activating guanylate cyclase and forming cGMP; tissues and organs affected:

KIDNEY: ANP dilates afferent arterioles, increased GFR and urinary excretion of Na and water. ANP limits sodium reabsorption (in proximal tubule an dinner medullary collecting duct) and inhibits renin secretion

ADRENAL GLAND: ANP restricts aldosterone secretion leading to an increase in Na and water excretion by the kidenys

BLOOD VESSELS: ANP relaxes vascular smooth muscle in arteriole and venules, producing vasoDILATION. ANP also increases capillary permeability, leading to fluid extravasation into the interstitium and a decrease in circulating blood volume

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27
Q

A. What is carcinoid syndrome?

A

>>fibrous intimal thickening with endocardial plaques limited to the right heart

>>CP: episodes of skin flushing, diarrhea, bronchospasm, abdo cramping, N/V/D due to production of serotonin, kallikrein, bradykinin, hitamine, PG, and/or tachykinins by carcinoid tumors

>>level of endocardial fibrosis correlates with plasma levels of serotonin and urinary excretion of the serotonin metabolite 5-hydroxyindoleacetic acid

>>end up with: pulmonary stenosis and restrictive cardiomyopathy

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28
Q

What is an example of hereditary hepatic porphyrias?

A

Acute Intermitten porphyria

  • autosomal dominant
  • causes: porphobilinogen deamnase deficiency
  • CP: mostly asymptomatic, BUT, some acute attacks=abdominal pain, vomiting, peripheral neuropathy, neuropsych symptoms, reddish-brown urine
  • tx: iv glucose or heme preperation to down-regulate ALA synthase activity
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29
Q

A Fib

A
  • NO p waves
  • irregular irregular R-R intervals
  • narrow QRS complexes
  • loss of contraction reduces LV filling, causing hypotensions and pulmonary edema
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30
Q

Atherotic plaques

A
  • large ELASTIC arteries
    • aorta, carotid, iliac
  • large/med muscular arteries
    • coronary, popliteal
  • altogether, most involved:
    1. abdominal aorta
    2. coronary arteries
    3. popliteal
    4. internal carotid
    5. circle of Willis
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31
Q

Paroxysmal Nocturnal Hemoglobinuria (PNH)

A
  • TRIAD
    • hemolytic anemia + aplastic aemia
    • hypercoagulability and Budd-Chiari
    • pancytopenia
  • acquired mutation of PIGA gene
    • =absence of GPI anchor an associated deficiency of CD55 and CD5( complement inhibitor proteins=complemen-mediated hemolysis
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32
Q

Scleroderma (systemic sclerosis)

A
  • TRIAD:
    • autoimmunity
    • non-inflammatory vasculopathy
    • collagen deposition with fibrosis
  • commonly: skin, but also renal, pulm (most common cause of death), CV, GI
  • 75% female
  • diffuse scleroderma: widespread skin involvement, rapid progression, early visceral involvement.
    • assoc with anti-Scl-70 antibody (anti-DNA topoisomerase I Ab)
  • localized/limited variant of scleroderma: skin and face
  • caused by increased deposition of collagen in tissues
    • nti-centromere Ab
  • earliest damage: small arteioles and capillaries
  • C=calcinosis; calcium deposits
  • R=Raynaud syndrome (cold/stress-induced digital vasospasms)
  • E=esophageal dysmotility
  • S=sclerodactyly (taut skin)
  • T=telangiectasia
    *
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33
Q

Pulsus paradoxus

A
  • an exaggerated drop (>10mmHg) in systolic bp during inspiration
  • CP: patients with cardiac tamponade, severe asthma, COPD, hypovolemic shock, constrictive pericarditis
  • Echo: pericordial fluid accumulation with late diastolic collapse of RA
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34
Q

What are the characteristics of cardiac tamponade?

A

cardiac tamponade-BECK’s triad

  1. hypotension
  2. elevated JVP
  3. muffled heart sounds)
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35
Q

DIC (disseminated intravascular coagulation)

A
  • common complication of gram negative sepsis, acute pancreatitis, and burn injuries
  • with G-…step 1: activation of coagulation cascade by bacterial endotoxins
  • G- step 2: formation of micro-emboli
  • Peripheral smear: fragmented erythrocytes (schistocytes) and thrombocytopenia
  • Lab: decreased fibrinogen levels, prolonged prothrombin (INR) and prolonged partial thromboplatin times
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36
Q

Hemolytic anemia

A
  • CP: anemia, elevated LDH levels, indirect/unconjugated bilirubin
  • positive osmotic fragility test=diagnost test or spherocytes
  • complication: pigmented galstones
  • chronic hemolysisL bili from lysed RBCs precipitates as calcium bilirubinate and forms pigmented stone in the gallbladder
  • (mature pig stone: calcium salts, calcium bilirubinate, bilirubin polymers)
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37
Q

Hereditary Spherocytosis

A
  • autosomal dominant
  • cause: RBC cytoskeleton is abnormal
  • most common: spectrin and ankyrin
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38
Q

Iron deficiencies

A
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39
Q

What are th general characteristics of A fib on an EKG?

A
  • no P waves
  • irregular irregular R-R intervals
  • marrow QRS complexes
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40
Q

Supine hypOtension (aortacaval compression) syndrome:

A. pathophys

B. aggravating/alleviation factors

C. epidemiology

A

A. pathophys

  • compression of IVC
  • reduced venous return
  • reduced preload
  • decreased CO
  • hypotension (and syncope)
  • can lead to loss of consciousnes or fetal demise

B. resolve when sitting, standing, L. lateral decubitus position

C. women at >20 wk gestation-due to gravid uterus when it compresses/obstructs the IVC

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41
Q

Cystic Medial Degeneration

A
  • myxomatous changes with pooling of proteoglycans in the MEDIA layer of large arteries
  • pts with Marfan syndrome develop CMD of the aortic root at a young age=predisposed to ascending AAs and dissection
  • cystic medial necrosis:
    • loss of smooth mu, collagen, elastic tissue with formation of mucoid spaces in the aortic media
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42
Q

Heart Sounds-

S4

A
  • low frequency heart sound at the end of diastole, just before S1
  • cause: decreased LV compliance
  • associated with restrictive cardiomyopathy and LV hypertrophy
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43
Q

Jervell and Lange-Nielson syndrome (AR)

A
  • most common congenital long-QT syndromes
  • CP: congenital neurosensory deafness
  • Prog: QT-interval prolongation predisposes to syncopal episodes and possible cardiac death due to torsdes de pointes (ventricular tachy)
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44
Q

IV fluid infusions

A
  • increase intravascular volume by varying degress, depending on the composition of solute
  • resultant preload increase causes increased ventricular myocardial sarcomere length and thus, increase in SV and CO
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45
Q

IVC filter

A
  • prevents travel of DVT from legs to lung vasculatures
  • inhibits PE in pts who have ci to anticoagulations
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46
Q

Orthostatic hypotension

A
  • main causes:
      1. meds (alpha-1 adrenergic antagonists and diuretics)
      1. volume depletion
      1. autonomic dysfunction
  • CP: lightheadedness, syncope
  • Definition: on standing from supine…
    • decrease in systolic by greater than or equal to 20
    • –OR–
    • decrease in diastolic by greater than or equal to 10
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47
Q

Atrial myxoma

A
  • CP:
    • constitutional symptoms
    • mid-diastolic rumbling murmurs best heard at apex
    • positional CV symptoms (dyspnea and syncope)
    • embolic symptoms
    • large pedunculated mass in LA
  • tumor histo:
    • scattered cells within a mucopolysaccharide stroma
    • abnormal blood vessels
    • hemorrhaging
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48
Q

Atherosclerotic disease

A
  • CP: signs of embolism (blue toe, livedo reticularis with normla peripheral pulses) following an invasive vascular procedure (angiography, angiplasty, aortic sx)
  • cholesterol-containing debris gets dislodged from larger arteries, lodges in smaller vessels=ischemia days/wks later
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49
Q

Isolated systolic HTN (ISH)

A
  • age related decrease in compliance (increased stiffness) of the aorta and its proximal major branches
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50
Q

severe aortic stenosis

A
  • CP: SAD (exertional syncope, angina, dyspnea)
  • systolic ejection heard at R. second intercostal, may radiate to carotids
  • most common cause of AS: senile calcific aortic valve calcification at greater than or 70yo
  • AS associated with congenitally bicuspid aortic valves at greater than or 60yo
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51
Q

Chronic arteriovenous fistula

A
  • CP: increased CO and increase mean systemic pressure
    • decreased TPR
  • Acute: decreased TPR=increase CO=increase venous return
  • over time:
    • sympathetic nervous system and kidney compensate
      • increased cardiac contractility
      • increased vascular tone
      • increased circulating volume
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52
Q

DiGeorge syndrome

A
  • microdeletion of long arm of chromosome 22q11.2
    • detection via FISH (fluorescence in-situ hybridization)
  • congenital thymic and parathyroid aplasia
    • hypocalcemia
  • congenital CV anomalies
  • CP: facial and/or palatal malformation
    • velocardiofacial syndrome (cleft palate, cardiac anomalies, dysmorphic facies)
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53
Q

pulmonary arterial HTN

A
  • increased arteriolar smooth muscle thinckness (medial hypertrophy)
  • intimal fibrosis
  • significant luminal narrowing
  • with severe HTN lesions progress to form PLEXIFORM LESIONS
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54
Q

coronary dominance

A
  • which coronary artery supplies the posterior descnding artery (PDA)
    • 70% from the R. coronary artery (right dominant)
    • 20% from the RCA and L. circumflex artery (co-dominant)
    • 10% from the L. circumflex artery (left dominant)
    • PDA also upplies blood to th AV node (via AV nodal artery)
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55
Q

blunt aortic injury (traumatic aortic rupture)

A
  • cause: motor vehicle collisions
  • sudden deceleration causes extreme stretching and torsional forces
  • most common site of injury: aortic isthmus-tethered by ligamentum arteriosum
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56
Q

NITRATES

A
  • primary venodilators
  • increase peripheral venous capacitance
  • decrease cardiac preload
  • decrease LVEDV and pressure
  • SE: (throbbing) HA and cutaneous flushing + lightheadedness and hypo-TN d/t systemic vasoDILATION
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57
Q

cyanosis at birth

A
  • transposition and ToF are two main cardiovascular anomalies presenting with cyanosis at birth
  • transposition=most severe cyanotic condition
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58
Q

Right Ventricular Myocardial Infarction

A
  • CP: hypotension, elevated jugular venous pressure, clear lungs
  • occurs in setting of acute inferior wall MI
  • hemodynamic assessment: elevated RA and central venous pressures, reduced pulmonary capillary wedge pressure, and reduced CO
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59
Q

Retroperitoneal hemorrhage

A
  • riskis increased by an arterial puncture above the inguinal ligament which is directly over the retroperitoneal space
  • bleeding cant be controlled with manual compression and can lead to significant hemorrhage
  • CP: hemodynamic instability with significant hypotension, drop in hematocrit, and/or ipsi flank pain
  • most common cause of unexpected mortality after cardiac catheterization
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60
Q

Right Ventricle

A
  • composes the majority of the anterior surface of the heart
  • at risk in penetrating trauma at the left sternal border
  • pleura would be injured but the left lung itself would not be punctures as there is no middle lobe on the left side and the superior lobe of the left lung is displaced laterally by the cardiac impression
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61
Q

HTN

A
  • persistent systolic BP≥140 mmHg and/or diastolic BP ≥ 90 mmHg​​​
  • PATHOPHYSIOLOGY-RF: increased age, obesity, diabetes, physical inactivity, excess salt intake, excess alcohol intake, family history; black>white>asian. ​
    • 90%: primary (essential); related to increased CO or increased TPR​
    • 10%: secondary to renal/renovascular disease (fibromuscular dysplasia, usually found in younger women) and primary HYPERaldosteronism.​
  • CLINICAL PRESENTATION: ​
    • Hypertensive URGENCY=severe (≥180/≥120mmHg) HTN WITHOUT acute end-organ damage.​
    • Hypertensive EMERGENCY-severe HTN WITH evidence of acute-organ damage ​
  • DIAGNOSIS: predisposes to CAD, LVH, HF, a fib; aortic dissection, aortic aneurysm; stroke; CKD (hypertensive nephropathy); retinopathy​
  • TREATMENT: Loop diuretics, Thiazides, ACE-I, ARBs, Aliskiren​
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62
Q

Hyperlipidemia

A
  • PATHOPHYSIOLOGY​:​
    • Xanthomas-plaques​
  • CLINICAL PRESENTATION​
    • Xanthomas-plaques or nodules composed of lipid-laden histiocytes in skin, especially the eyelids (xanthelasma)​
    • tendinous xanthoma-lipid deposit in tendon (espeically Achilles)​
    • Corneal arcus-lipid deposit in cornea. common in elderly (arus senilis), but appears earlier in life in hypercholesterolemia​
63
Q

Arteriosclerosis

A
  • PATHOPHYSIOLOGY: hardening of ARTERIES, with arterial wall thickening and loss of elasticity ​
  • CLINICAL PRESENTATION:​
    • Arteriosclerosis-common. affects SMALL ARTERIES AND ARTERIOLES. 2 types​
    • HYALINE-thickening of vessel walls in essential HTN or DM​
    • HYPERPLASTIC-“ONION SKINNING” in severe HTN with proliferation to smooth muscle cells​
    • Monckeberg (medial calcific sclerosis)-UNcommon. affects MEDIUM-SIZED ARTERIES. calcification of elastic lamina of arteries–>vascular stiffening without obstruction. “PIPESTEM” appearance on x-ray. does NOT obstruct blood flow, intima NOT involved.
64
Q

Atherosclerosis

A
  • PATHOPHYSIOLOGY​:​ VERY common. disease of elastic arteries and LARGE AND MEDIUM-SIZD muscular arteries; a form of arteriosclerosis caused by buildup of cholesterol plaques. **Inflammation**, endothelial cell dysfunction–> macrophage and LDL accumulation –> foam cell formation –> fat streaks –> sooth muscle cell migration (involves PDGF and FGF), proliferation, and ECM deposition–> fibrous plaque –> complex atheromas​
  • CLINICAL PRESENTATION​: RF are modifiable and NON-modifiable.​​
    • Modifiable: smoking, HTN, hyperlipidemia, diabetes​
    • NON-modifiable: age, sex (increased in men and postmenopausal women), FHx.​
  • Symptoms: angina, claudication (cramping pain in leg induced by exercise), can also be asymptomatic​
  • DIAGNOSIS​: complications: aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli.​
65
Q

aortic aneurysm

A
  • PATHOPHYSIOLOGY​:​ ​localized pathologic dilatation of the aorta.​
  • CLINICAL PRESENTATION​: abdominal and/or back pain, which is a sign of leaking, dissection, or imminent rupture.​​​
  • DIAGNOSIS​:​
    • Abdominal aortic aneurysm: associated with atherosclerosis. RF: hx of tobacco use, increased age, male, Fhx. may present as palpable pulsatile abdominal mass​
    • Thoracic aortic aneurysm: associated with cystic medial degenration. RF: HTN, bicuspid aortic valve, connective tissue disease (Marfan’s synrome). **assoc. with 3° syphilis (obliterative endarteritis of the vasa vasorum)​
66
Q

Aortic Dissection

A
  • PATHOPHYSIOLOGY​: longitudinal intimal tear forming a false lumen. associated with HTN, bicuspid aortic valve, inherited connective tissue disorders (Marfan’s).​​
    • Stanford type A (proximal) [DeBakey 1&2], involves ascending aorta. may extend to aortic arch or descending aorta.​
    • ​Stanford type B (distal) [DeBakey 3], involves descending aorta and/or aortic arch. no ascending aorta involvement.​
  • CLINICAL PRESENTATION​: tearing chest pain, of sudden onset, radiating to back ± markedly unequal BP in arms.​ Can result in rupture, pericardial tamponade, death.​​
  • DIAGNOSIS​: CXR shows mediastinal widening​​​
  • TREATMENT:​
    • Stanford type A: surgery​
    • Stanford type B: medically with beta-blockers, then vasodilators
67
Q

Temporal arteritis (giant cell vasculitis)

A
  • inflamm condition, affects medium-sized and large arteries
  • light micro: granulomas in the media of the arteries, mononuclear infiltrates and multinucleated giant cells
  • segmental cange in arteries
  • affected segments cause narrowing of vessel with a decrease in blood supply to the perfused areas
  • median ag eonset: 65 yo
  • s/s:
    • HA, some scalp tenderness
    • craniofacial pain syndromes: jaw claudication
    • polymyalgia rheumatica in HALF the pts
      • neck, torso, shoulder, pelvic irlde pain and morning stiffness
      • fatigue, fever, weight loss
    • sudden vision loss!!
68
Q

Striated Muscle sarcomere

A
  • actin filaments are anchored into the Z-line of the sarcomere
  • Z-line lies in ctr of lucent region (I-band)
  • actin in the I band attaches at the Z-line
  • myosin in the H-band attaches at the M-line
  • all: an interesting zoo must have mammals
69
Q

Skeletal Muscle Contraction

A
  • SR=modified ER within skeletal muscle cells
  • network of tubules with terminal cisterns in contact with T-tubules so membrane depolarization signal can reach the SR
  • Ca-ATPase pump in SR membrane actively sequesters Ca to keep intracellular concentrations low
  • membrane depolarization causes ca release form SR into cytoplasm via SR ryanodine receptor
  • ca binds troponin C and allows binding of ctin to myosin
70
Q

Subclavian Steal syndrome

A
  • d/t severe stenosis of the proximal subclavian artery
  • leads to reversal in blood flow from the contralat vertebral artery to the ipsi vertebral artery
  • pts may hv symptoms related to arm ischemia in the affected extremity (exercise-induce fatigue, pain, paresthesias) –or– vertebrobasilar insufficiency (dizziness, vertigo)
71
Q

poor and rich countries-causes of IE

A
  • MVP (with or sans MR)=mc predisposing condition for native valve infective endocarditis in RICH
  • rheumatic heart dz=frequent cause of IE is POOR (because they got robbed form the rich to make the rich richer)
72
Q

precursor proteins or peptides responsible for localized amyloidosis (confined to single, specific organs)

A
  • cardiac atria-atrial natriuretic peptide (ANP)
  • thyroid gland-calcitonin
  • pancreatic islets-islet mayloid protein (amylin)
  • cerebrum/cerebral blood vessels-beta amyloid protein
  • pituitary gland-prolactin
  • (immune globulin LC cause multi-organ amyloid deposition in primary systemic amyloidosis
73
Q

first aortic arch

A

adult-pt of maxillary artery

CN5 trigeminal

74
Q

second aortic arch

A

adult:

  • hyoid artery
  • stapedial artery

CN7 facial

75
Q

third aortic arch

A

adult:

  • common carotid artery
  • proximal internal carotid artery

CN9 glossopharyngeal

76
Q

fourth aortic arch

A

adult:

  • on LEFT: (true) aortic arch
  • on RIGHT: proximal RIGHT sub-clavian artery

CN 10 (superior laryngeal branch)

…fifth arch is OBLITERATED

77
Q

sixth aortic arch

A

adults:

  • proximal pulmonary arteries
  • on LEFT: ductus arteriosus

CN 10 (recurrent laryngeal branch)

78
Q

antidote to NE extravasation

A
  • signs of NE extravasation and resulting vasoconstriction: blanching of a vein into which NE is being infused together iwth induration and pallor of tissues surrounding the IV site
  • tissue necrosis is best prevented by local injectio of an alpha-1 blocking drug (ex: PHENTOLAMINE)
79
Q

Which selective vasoDILATORS of coronary vessels can cause coronary steal

A

adenosine and dipyridamole

  • used in myocardial perfusion imaging studies to stimulare the generalized coronary vasodilation caused by exercise
  • get ischemia in areas of mycoardium that is perfused by OCCLUDED vessels
    • allows detection of ischemic areas that would otherwise NOT be seen in resting heart
80
Q

define coronary steal

A
  • blood flow in ischemic areas is reduced due to arteriolar vasodilation in nonischemic areas
  • can lead to hypoperfusion and worsening of existing ischemia
81
Q

what does venodilation do to ventricular volume

A

DEC ventricular colume thus allowing for a reduction in myocardial oxygen demand secondary to DEC ventricular wall tension

82
Q

systemic arterial vasodilation

A
  • DEC arterial pressure
  • allows for a redutio in myocardial oxygen demand by DEC afterload and thus ventricular wall tension
83
Q

what are possible triggers of variant (prinzmetal) angina?

A
  • cigarette smoking
  • cocaine/amphetamines
  • dihydro-ergotamine/triptans
  • tx: tobacco/drug cessation and vasodilator therapy (nitrates, CCB)
84
Q

Characterization of variant (prinzmetal) angina?

A
  • episodic, transient attacks of coronary vasospasm (at rest and at night)
    • produces temporary myocardial ischemia with ST-segment elevation
85
Q

What are the effects of stimulated beta-1 adrenergic receptors

A

get INC production of cAMPT in target cells and causes the following effects:

  • positive inotropic effect
  • positive chronotropic effect
    • combo with INC HR=INC MVO2..can trigger/exacerbate MI
  • mild vasoDILATION
86
Q

nml morphological changes inthe aging heart

A
  • DEC in LV chamber apex-to-base dimension
  • development of a sigmoid-shaped ventricular septum
  • myocardial atrophy with INC collagen deposition
  • accumulation of cytoplasmic LIPOFUSCIN pigment with cardiomyocytes
87
Q

Why does dilated cardiomyopathy have an INC r/o mural thrombi

A

DCM causes an INC in the LV chamber size, and there is INC r/o mural thrombi d/t contractile dysfxn

88
Q

which changes are responsible for maintaining CO in the setting of AR

A
  • regurgitant blood flow from the aorta into the LV in chronic AR leads to an INC in LVEDV (preload) and wall stress with resultant ECCENTRIC hypertrophy
  • gradual INC in LV chamber size INC total SV and helps maintain CO
89
Q

acute AR

A
  • eccentric hypertrophy does NOT have time to develop and potential INC in LV SV is limited
  • resulting DEC in CO triggers a reflexive INC in HR
90
Q

Statins

A
  • HMG-CoA reductase inhibitors
  • most effective lipid lowering drugs for preventing CV events
  • indicated for secondary prevention in all pts with known atherosclerotic CV dz REGARDLESS of baseline lipid levels
  • atorva, rosuva, simva
  • DEC LDL
91
Q

Fibrates

A
  • Fenofibrate and Gemfibrozil
  • DEC serum TG
92
Q

Lets talk about HDL-whats its job

A
  • reverse cholesterol transport
  • helps remove cholesterol form peripheral tissues and transports it to the liver for metabolism
  • two different pathways: indirect and direct
93
Q

What are the two pathways used by HDL

A
  • DIRECT:
    • HDL delivers cholesterol esters directly to the liver via a scavenger receptor (SCARB1) on the hepatocyte cell membrane
  • INDIRECT:
    • cholesterol in HDL is transferred to a LDL and VLDL by the cholesteryl ester transfer protein
94
Q

Bile acid sequestrants/cationic exchange resins/CHOLESTYRAMINE

A
  • MOA: DEC LDL, INC sTG
  • interfere with enterohepatic circulation of bile acids
  • **can significantly INC TG levels in pts with pre-existing HYPER-TG
  • (exercise and weight loss DEC sTG)
95
Q

Paradoxical embolism

A
  • PP: thrombus form venous system crosses into the arterial circulation via an abnml connection between the right and left cardiac chambers
    • patent foramen ovale, ASD, VSD
  • atrial R-to-L shints cause wide and fixed splitting of S2, can facilitate paradoxical embolism d/t periods of transient shunt reversal (d/t straining or coughing)
96
Q

define paradoxical embolism

A
  • cerebrovascular event (TIA, stroke) in the setting of known venous thromboembolic dz
97
Q

What are the three HOLO-systolic murmurs

A
  • MR
  • TR
  • VSD
98
Q

during inspiration what are the two things that happen when the INTRA-THORACIC pressure drops

A
  • allows more blood to return to the RIGHT heart
    • RV SV rises d/t INC venous return
  • INC pulm vessel capacity
    • transient DEC in LV venous return
99
Q

diastolic heart sounds (FOUR)

A
  • AR/PR
  • MS/TS
100
Q

OWR (Osler-Weber-Rendu syndrome)

A
  • hereditary hemorrhagic telangiectasia
  • AD, marked by presence of telangiectasias inthe skin and mucous membranes of the lips oronasophaync respiratory tract, GI tract, and urinary tract
  • rupture can cause:
    • epistaxis
    • GI bleeding
    • hematuria
101
Q

pulm HTN d/t LEFT heart dz

A
  • INC diastolic filling pressure-needed to maintain SV and CO
    • d/t concentric LVH an DEC LV diastolic compliance
    • INC in pressure transmitted backward to LA and pulm veins
  • INC LAP and subsequent R-sided HF
    • JVD, prominent peripheral edema
  • pulm venous congestion
  • INC pulm arterial pressure
    • =endothelial damage, capillary leakage of serum proteins into interstitium: DEC NO, INC endothelin production
  • vasoconstriction
  • intimal thickening and fibrosis (collagen and elastase deposition) and medial hypertrophy (smooth mu cell proliferation)
102
Q

What is the major determinent of whether or not a coronary artery plaque will cause ischemic myocardial injury

A

rate at which it occludes the involved artery

  • slowly developing occlusion
    • formation of colaterals that could prevent myocardial necrosis
  • fast coronary occlusion
    • thin fibrous cap, rich lipid core, active inflamm in the atheroma would decrease plaque stability…occlusion via suprimposed thrombosis
103
Q

What are the target organs of beta-1 adrenergic blockade

A

heart, kidney

104
Q

What are the target organs of beta-2 adrenergic blockade

A
  • muscular vasculature
  • LUNGS
  • liver
  • most tissues (SE: HYPER-kalemia)
105
Q

How can beta blockers be used in acute MI

A
  • reduce HR, CO, MVO2
  • non-cardioselective can trigger bronchospasm in pts with underlying astham or COPD
    • cardioselective with predom beta-1 action are preferred in these pts
106
Q

organ susceptibility to infarction after occlusion of a feeding artery is ranked from greatest to least as follows:

A
  • CNS (weaksauce-super susceptible to infarction)
  • myocardium
  • kidney
  • spleen
  • liver
    • dual and/or collat blood supply (Ex: liver has hepatic artery and portal vein)=organ can tolerate arterial occlusion better than those with end-arterial circulations
107
Q

What is the mc c/o RHF??

A

LHF!!!

108
Q

what is the difference between systolic and diastolic dysfunction

A
  • systolic:
    • CHF d/t progressive DEC in myocardial contractility
  • diastolic:
    • inability of heart to relax sufficienty to accomodate incoming blood in diastole
109
Q

what are some of the compensatory mechanisms triggered by DEC CO

A
  • RAA activation and INC sympathetic output raise arterial resistance (afterload) and exacerbate HF by making it more difficult for the failing heart to pump blood to the tissues
110
Q

MAO inhibiters <tranylcypromine></tranylcypromine>

A
  • MAO is a mitochondrial enzyme that degrades xs monoamine NT in pre-synaptic nerve terminals
  • detoxifies dietary tyramine in the GI tract
  • tyramine hypertensive crisis can occur in pts taking MAOi following the consumption of foods containing high amounts of tyramine (aged cheeses, cured meats, draft beer)
111
Q

Fick principle

A
  • applied to calculate CO using the rate of oxygen consumption and the arteriovenous oxygen content difference:
  • CO=rate of O2 consumption/arteriovenous O2 content difference
  • arterial oxygen content is measured from arterial blood (directly)
  • mixed venous oxygen content is measured from pulmonary arterial blood
112
Q

What is the mc c/o AS in RICH

A
  • calcific degeneration of the tri-leaflet aortic valve
  • AS:
    • characterized by progressive aortic valve leaflet thickening and calcification
    • leads to restricted leaflet excursion and mobility
    • harsh ejection-type systolic murmur
    • best heard: base of heart in the “aortic area” (2nd right intercostal space) with radiation to the carotid arteries
113
Q

What causes an INC ventricular preload (larger than nml LVEDV)?

A
  • any state of fluid overload
    • renal failure
    • CHF
    • after infusion of IV fluids (ex: nml saline infusion)
114
Q

Lymphangiosarcoma

A
  • persistent lymphedema (with chronic dilatation of lymphatic channels) predisposed to the development of lymphangiosarcoma
  • rare malignant neoplasm of the endothelial lining of lymphatic channels
  • ca may arise approx 10 yrs after radical mastectomy with axillary LN dissection for breast cancer
115
Q

What is the most life-threatening complication assoc with Marfan syndrome?

A
  • cardiovascular lesions
    • early-onset cystic medial degeneration of the aorta predisposes to aortic dissection (mc cod in these pts)
116
Q

splinter hemorrhages and IE

A
  • (Janeway lesions) microemboli from the valvular vegetations of bacterial endocarditis are the mc c/o sub-ungual splinter hemorrhages
  • do a careful cardiac auscultation to detect a possible new-onset regurgitant murmur
117
Q

What is the tx for PDA

A
  • common in pre-term infants
  • CP: continuous murmur, widened pulse pressures, signs of CV strain
  • Tx: Indomethacin or Ibuprofen
    • can inhibit PGE2 synthesis and accelerate closure
118
Q

AAA pathogenesis

A
  • trasmural aortic wall inflammation
  • abnml collagen remodeling and cross-linking
  • loss of elastin and SMC.
  • leads to weakening and progressive expansion of the aortic wall
  • end result: aneurysm formation
  • >>focal intimal tear in aortic wall=primary event involved in the pathophys of aortic dissection
119
Q

what is the primary event involved in the pathophys of aortic dissection

A

intimal tear in the aortic wall

120
Q

what is pathognomonic for a large PDA complicated by Eisenmenger syndrome (reversal of shunt from L-t-R tooo R-t-L

A

differential clubbing and cyanosis (most pronounced in the lower extremities) without bp or pulse discrepancy

121
Q

what causes whole body cyanosis

A

R-to-L shunting in pts with large septal defects and tetralogy of Fallot

122
Q

dystrophic calcification

A
  • occurs in damaged or necrotic tissue
  • setting: nml ca levels
  • metastatic calcification occurs in nml tissue in the setting of HYPER-calcemia
123
Q

intracellular hemosiderin accumulation

A

common in pts who have hemolytic anemia or who undergo frequent blood transfusions

124
Q

CILOSTAZOL and intermitten claudication

A
  • (along with graded exercise) used as symptomatic management of peripheral artery dz (PAD)
  • MOA: phospho-diesterase inhibitor that inhibits platelet aggregation and acts as a direct arterial vasodilator
  • pts with PAD should also receive an anti-platelet agent (aspirin or clopidogrel) for secondary prevention of coronary heart disease and stroke (they do NOT improve PAD symptoms)
125
Q

Buerger’s Disease (Thromboangiitis obliterans)

A
  • epi: heavy cigarette smokers,
  • Assoc w/: HSR to intradermal injections of tobacco extracts
  • PP: segmental thrombosing vasculitis often extends into contiguous veins and nerves encasing them in fibrous tissue
  • general: vasculitis of medium and small-sized arteries (*tibial and radial arteries)
126
Q

What are the (FIVE) most important steps for prevention of central venous catheter infections?

A
  1. proper hand hygiene
  2. full barrier precautions during insertion
  3. Chlorhexidine skin disinfection
  4. avoidance of the femoral insertion site
  5. prompt removal of the catheter when it is no longer needed
127
Q

during bacteremia (from any cause) what do microorganisms colonize?

A

the sterile fibrin-platelet nidus on the endothelial surface with subsequent microbial growth leading to further activation of the coag system

128
Q

Chest Anatomy-reach of the LV

A
  • LV forms the apex of the heart
    • can reach as far as the 5th intercostal space at the left midclavicular line
129
Q

Ca and Cytomegaly

A
  • ion pump failure d/t ATP deficiency d/r cardiac ischemia causes intracellular accumulation of Na+ and Ca+
  • INC intracellular solute concentration draws free water into the cell=cellular and mitochondrial swelling (seen on histo)
130
Q

NITRATE hemodynamics

A
  • primarily veno-DILATORS
  • INC peripheral venous capacitance
  • …reduce cardiac preload (less shit rushing into the heart, it can just sit there a chill in the extra space)
  • ..reduce LVEDV and P..wont fill up as much, b/c slowly moving in
  • also: modest effect on arteriolar dilation
  • (@higher doses) cause DEC in systemic vascular resistance and cardiac afterload
131
Q

what are common features of constrictive pericarditis

A
  • calcification and thickening of the pericardium seen on CT
  • clinical findings:
    • slowly progressive dyspnea
    • peripheral edema
    • ascites
132
Q

coagulopathies vs. platelet defects

A
  • coagulopathies: deep-tissue bleeding into joint muscles and subQ tissue
  • platelet defects: mucoQ bleeding (ex: epistaxis, petechiae)
133
Q

Factor 7 v. Factor 8 deficiency

A
  • 7: prlonged PT
  • 8: prolonged aPTT
134
Q

a. nml bleeding time=?
b. nml aPTT=?
c. nml PT=?

A
  • a. nml bleeding time=adequate platelet function
  • b. nml aPTT=intact IN-trinsic (left side, big numbers)
  • c. nml PT=intact EX-trinsice coag pathway (r. side)
135
Q

hemophilia A vs. C

A
  • hemophilia A:
    • classic X-linked
    • factor 8 deficiency
    • nml bleeding time, nml PT, prolonged aPTT
  • hemophilia C:
    • rare AR
    • factor 11 deficiency
    • at INC r/o bleeding following sx or trauma
    • nml PT, prolonged aPTT
136
Q

Which ventricle composes most of the heart’s anterior surface?

A

RIGHT VENTRICLE

-will be punctured by a penetrating injury at the L. sternal border in the 4th intercostal space

137
Q

What is the drug of choice for sustained arrhythmias

A

AMIODARONE

138
Q

Which group of anti-arrhythmics are highly efficacious in inhibiting ischemia-induced ventricular arrhythmias?

A
  • class 1B
139
Q

which medications can cause HYPER-kalemia?

A
  • non-selective beta-adrenergic blockers
  • ACEi
  • ARBs
  • K-sparing
  • cardiac glycosides (Digoxin)
  • NSAIDs
140
Q

Which vascular beds have the highest atherosclerotic burden?

A

lower abdominal aorta and coronary arteries

141
Q

LV wall rupture

A
  • 5-14 days after initial MI
  • CP: sudden onset of CP, profound shock, rapid progression to death
  • morphologically: slit-ike tear in the infarcted myocardium
  • (preference for the LV d/t higher systolic pressures)
142
Q

What is one pre-req to maintain vlood flow through the body?

A

blood flow in the pulm circulation must closely match the blood flow in the systemic circulation

(same d/r exercise and at rest b/c circulatory system is a continuous circuit)

143
Q

pulsus paradoxus

A
  • exaggerated drop (>10mm Hg) in systolic bp d/r inspiration
  • mc: pts with cardiac tamponade
    • also: severe asthma, COPD, hypovolemic shock, constrictive pericarditis
144
Q

what is the most serious complication of DIGOXIN

A

life-threatening ventricular arrhythmias

145
Q

Kawasaki

A
  • vasculitis of med-sized arteries
  • CP:
    • persistent fever for >5d
    • bilat conjunctivitis
    • cervical lymphadenoapthy
    • mucoQ involvement
  • serious complication: coronary artery aneurysms
146
Q

jugular venous tracing

A
  • a: RA contraction (absent in pts with a fib)
  • b: bulging of tricuspid valve d/r RV contraction
  • x: RA relaxation
  • v: continued inflow of venous blood
  • y: passive emptying of RA after tricuspid valve opening
147
Q

IVC filters

A
  • placed in pts w/ DVT or PE who have contraindication sto anticoagulation
148
Q

BNP (brain natriuretic peptide)

A
  • elevated in pts with HF and often used as a lab test to determine if a pt is suffering CHF exacerbation
  • released by the ventricles when they are stretched
  • act with ANP t cause vasodilation (DEC preload) and diuresis
  • BOTH AN and BNP activate guanylate cyclase–>induces an INC of intracellular cGMP
149
Q

hepatic angiosarcoma

A
  • assoc w/ exposure to carcinogens:
    • arsenic
    • thorotrast
    • polyvinyl chloride (plastic f/m industry)
  • tumor cells express CD31
    • PECAM1 platelet endothelial cell adhesion molecule
    • PECAM1 functions in leukocyte migration through the endothelium
  • rare malig vascular enfothelial cell neoplasm
150
Q

Cool stuff via ACh and Adenosine

A
  • reduce the rate of spontaneous depolarization in cardiac pacemaker cells by prolonging phase 4
151
Q

alpha-1 blockers

A
  • who: Doxazosin, Prazosin, Terazosin
  • Ci: BPH and HTN
  • MOA: block alpha 1 adrenergic=relaxation of smooth muscle in arterial and venous wals leading to a DEC in peripheral vascular resistance
  • NO EFFECT on chronotropy or inotropy
152
Q

Neprilysin

A
  • an enzyme that metabolizes endogenous natriuretic peptides
  • NP promote vasodilation and natriuresis and provide beneficial counter-regulatory mechs in pts with HF
  • inhibition of NEPRILYSIN improves outcomes in pts with chronic systolic HF
153
Q

LA enlargment and neighbors

A
  • CV dysphagia can result from external compression of the esophagus by a dilated and posteriorly displace LA in ts with rheumatic heart dz and MS/MR

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