- Directly inhibits Na-K-ATPase in myocardial cells - Causes v in Na efflux => ^ intracellular Na levels => reduces Na-Ca exchanger => ^ intracellular Ca => improved myocyte contractility and left ventricular systolic function

- Absence of P waves - Irregularly irregular rhythm with varying R-R intervals

Ergot alkaloid - Stimulates alpha-adrenergic and serotonergic recetpors - In pts w/ pinzmetal's angina, low doses can induce coronary spasm, chest pain, and ST elevation

- Peripheral neuropathy of distal L/UEs - Sensory/motor impairments

- Dry beriberi plus cardiac involvement - Cardiomyopathy, high-output CHF, peripheral edema, tachy

Subfascial space in upper thigh: - Inguinal ligament (superior) - Adductor longus (medial) - Sartorius (lateral)

CV 1 Flashcards by Eooooo m

Mitral valve regurgitation

Holosystolic murmur

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Myocarditis due to acute rheumatic fever

Develops after untreated strep
Aschoff bodies on microscopy (interstitial myocardial granulomas)
Aschoff bodies contain plump macros w/ abundant cytoplasm and central, slender ribbons of chromatin

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Supine hypotension syndrom in preggers

=> Supine/right lateral decubitus position
=> Compression of IVC
=> reduced venous return
=> reduced preload
=> decreased CO
=> hypotension

Sx resolve when standing or sitting

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Digoxin MOA

Directly inhibits Na-K-ATPase in myocardial cells
Causes v in Na efflux => ^ intracellular Na levels => reduces Na-Ca exchanger => ^ intracellular Ca => improved myocyte contractility and left ventricular systolic function

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Go review blood vessel anatomy around the heart

NOW

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V1-V2 ST elevation. Which coronary artery?

Left anterior descending

Anteroseptal infarct

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V3-V4 ST elevation. Which coronary artery?

LAD distal

Anteroapical

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V5-V6 ST elevation. Which coronary artery?

LAD or LCX

Anterolateral

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I, aVL ST elevation. Which coronary artery?

LCX

Lateral

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II, III, aVF

RCA

Inferior

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Afib presentation

Palpitations
Tachycardia
Irregularly irregular rhythm

Precipitated by acute systemic illness, increased sympathetic tone, excessive alcohol consumption (holiday heart syndrome)

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ECG of Afib

Absence of P waves

- Irregularly irregular rhythm with varying R-R intervals

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Ergonovine

Ergot alkaloid

Stimulates alpha-adrenergic and serotonergic recetpors
In pts w/ pinzmetal’s angina, low doses can induce coronary spasm, chest pain, and ST elevation

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IV drug users and heart issues

Tricuspid (right sided) endocarditis
S. aureus (1) and P. aeruginosa (2)
Can develop multiple septic emboli in lungs
Pulm infarcts are almost always hemorrhagic

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Turner syndrome cardiac anomalies

Aortic coarctation

- Bicuspid aortic valve

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Aortic coarctation presentation

Infancy:

Cyanosis of LE
Severe form

Adolescent/youth

Decreased femoral pulses
Pain/cramping in legs during exercise
More common w/ Turner syndrome

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Which part of the heart makes up the anterior surface?

Right Ventricle

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Penetrating injury to RV occurs where?

Left sternal border

Fourth intercostal space

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Which layers would a penetrating injury to RV go through?

1) Skin/subcutis 2) Pectoralis major m.
3) External intercostal membrane
4) Internal intercostal m
5) Internal thoracic a. & v.
6) Transversus thoracis m
7) Parietal pleura
8) Pericardium
9) R. ventricular myocardium

Pleura of lungs is injured but not the actual lungs (no middle lobe on left side)

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Dry beriberi

Peripheral neuropathy of distal L/UEs

- Sensory/motor impairments

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Wet beriberi

Dry beriberi plus cardiac involvement

- Cardiomyopathy, high-output CHF, peripheral edema, tachy

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Femoral triangle

Subfascial space in upper thigh:

Inguinal ligament (superior)
Adductor longus (medial)
Sartorius (lateral)

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Path of LAD

arises off l. main a.

- courses along anterior aspect in the anterior interventricular groove toward apex of the heart

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Pathogenesis of atherosclerotic plaques

Study These Flashcards

Release of PDGF from locally adherent plts, endo cells, and macros
Promotes migration of SMCs into intima

Which part of the body has the highest O2 extraction?

The heart!!! Drains into coronary sinus

Nitroglycerin affects which vessels?

Venous anything Decreases preload => decreases ventricular wall stress => decreasing CO demand Large veins are most susceptible

What does the pulm cap wedge pressure measure?

L. atrial end diastolic pressure (LAEDP) LAEDP = LVEDP in normal conditions

Go review the LV pressure-volume relationship

NOW

DiGeorge - lack of development of which embryologic structure

- Third & Fourth branchial/pharyngeal pouch Deletion of chr 22 Absent thymic shadow, hypocalcemia, cleft palate, mandibular deformity, low-set ears, aortic arch abnormalities

VSD

presents in neonate period after pulm vascular resistance has declined (so not at birth) HOLOsystolic murmur

Prussian blue stains what?

Intracellular IRON

Gold cytoplasmic granules in macros that turn blue with Prussian blue staining?

hemosiderin laden macrophases (siderophages)

What is the significance of hemosiderin laden macros?

- Indicates chronic elevation of pulm cap hydrostatic pressures - Most commonly due to left-sided HF

Bicuspid aortic valve?

Common cause of aortic stenosis Class auditory: - harsh, cres-descres systolic ejection murmur - heard best at R. 2nd intercostal space`

adenosine and dipyridamole

Selective vasodilators of coronary vessels

What is coronary steal?

- Blood flow to ischemic areas (after an MI) is reduced - Because of arteriolar vasodilation in nonischemic areas - Can lead to hypoperfusion and worsening existing ischemia

Right heart failure => ^ed CVP What happens after that?

- Increased cap hydrostatic pressure - Increased net plasma filtration - Increased interstitial fluid pressure => increased lymphatic drainage (prevents peripheral edema development)

Cardiac AP (speed of conduction) slowest to fastest

AV node

Blood flow radius and resistance

BF: - Directly proportional to vessel radius^4 Resistance: - BF is innersely proportional to radius^4

Where do K sparing diuretics act on the kidney?

collecting duct Blocks absorption of Na Blocks excretion of K, H

Where do loop diuretics act?

Thick ascending limb of loop of Henle Blocks absorption of Na, Cl, K

Where do thiazide diuretics act?

Distal convoluted tubule Blocks absorption of Na, Cl

Beta blocker MOA

- Inhibits renin release from renal juxtaglomerular cells through antagonizing beta-1 receptors - Prevents activation of RAAS pathway => decreased vasoconstriction & renal Na &H20 retention

Dobutamine

- Beta- adrenergic agonist - Predominantly B1 receptors - Increases HR, contractility => increase myocardial O2 consumption

Nitrates MOA

Vasodilation - ^ NO in VSMCs => ^ in cGMP and SM relaxation - Dilates veins >>> arteries - Decrease preload

Nitrates SEs

- Reflex tachy - Hypotension - Flushing - HA - "Monday disease"

Where is the MI with a ST elevation of II, III, aVF?

Inferior RCA occlusion Think RVMI Presentation: hypotension, distended jugular veins, clear lungs

Hemodynamic assessment of RVMI

- Elevated RA and CVP - Reduced PCWP - Reduced CO

Chlorthalidone MOA

Thiazide - Inhibits NaCl resorption in early DCT - Decreased Ca excretion

Chlorthalidone SEs

- Hypokalemic metabolic alkalosis - HYPOnateremia - HYPERglycemia/lipidemia/uricemia/calcemia Sulfa allergy

Coadmin of ACEIs and diuretics

Significant first-dose hypertension ACEIs must be initiated at low doses to decrease the reaction

Pros of using mineralcorticoid receptor antagonists (e.g. spironolactone, eplerenone) in pts with HF?

- Improve survival - Regression of myocardial fibrosis & improvement of ventricular remodeling Used in pts w/ decreased LVEF

In transient ischemia, why do myocytes increase in size?

No O2 = No ATP - Can't stimulate Na(going out)/K (going in) pump - Can't maintain Na (going in)/Ca (going out) exchange

MOA of statins

HMG-CoA reductase inhibitors Lower total cholesterol and LDL Most effective for prevention of CV events REGARDLESS of baseline lipid levels

Anatomical findings in tetralogy of Fallot

PROV 1) Pulm infundibular stenosis 2) R. ventricular hypertrophy 3) Overriding aorta 4) VSD

Cause of TOF

Anterosuperior displacement of infundibular septum

Clinical Presentation of TOF

Early childhood cyanosis Squatting: ^ SVR, v R-to-L shunt, improves cyanosis Harsh systolic murmur (pulm stenosis)

Hibernating myocardium

- Presence of LV systolic dysfunction - Because of reduced coronary blood flow - Completely reversible by coronary revascularization

CV 1 Flashcards

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