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167 Cards in this Set

  • Front
  • Back

size of the heart

300-350 g....50 g less in females

sound upon closure of A-V valves

S1

Closure of Semilunar valve, Physiologic spitting on inspiration

S2

Physiologic heart sound in children and young adult, pathologic in those > 40 y/o

S3

Due to sudden rush of blood in overloaded ventricles

S3



Best heard at the apex in left lateral decubitus

S3

Coninsides with a wave, pathologic, due to concentric ventricular hypertrophy (noncompliant ventricle) and volume overloaded ventricle

S4

Failure of the heart to eject enough blood delivered to it by the venous system to meet the metabolic demands of the body

CHF

Most common admission diagnosis of elderly patient, in often preceeded by cardiac hypertrophy

CHF

Left sided heart failure may be due to

Systolic dysfunction


Diastolic Dysfunction

Decreased ventricular Conraction, low EF,


e.g. CAD, Post MI, Myocarditis, dilated cardiomyopathy

Systolic dysfunction

Non compliant ventricle, High or normal EF with S4, Concentric LVH due to HPN, restrictive cardiomyopathy, LV overload due to AR, MR

Diastolic dysfunction

Most common manifestation of LHF

Dysnea

Cxr findings in Left side heart failure

Congestion in Upper lobes (early finding)


Perihilar congestion (bat configuration) alveolar infiltrates

Right sided heart failure pahogenesis

Decreased contraction: RV infarct



Non-compliant right ventricle: RVH




Increased afterload (pulmonary circulation) : Left sided heart failure, Pulmo hpn




Increased preload: TV regurg, L-R Shunt





Most common symptom of Right sided heart failure

Ankle/Pedal and pretibial Edema

Chronic passive congestion of the liver can cause

Nutmeg liver, centrilobular necrosi or cardiac cirrhosis

Left sided heart failure in microscopy

Cardiac myocyte hypertrophy with enlarged peleiotropic nuclie




Lungs will show heart failure cells

Complications of LHF

Passive pulmonary congestion and Edema




Raas increased causing secondary


hyperaldosteronism




Cardiogenic shock

Most common cause of RVH

LVH

right sided heart failure caused by pulmonary hypertension from intrinsic lung disease

cor pulmonale

RVH presentation

JVD, Heposplenomegaly, dependent edema, ascites, weight gain, pleural and pericardial effusion

High output heart failure

Beri-beri (Vasodilation of arterioles


Anemia (decreased blood viscosity)


Hyperthyroidism (Increased SV)


Av Fistula: Increase venous return

Greatest risk factor of Congenital heart disease

Congenital heart disease in parent or preceding sibling

Top causes of CHD

VSD


ASD


PDA


TOF

MC genetic risk of CHD:

Down syndrome

Most common Cyanotic CHD

Tetralogy of follow

Tetralogy of follow is composed of

Pulmonic stenosis


RVH


Overriding the VSD by the aorta


VSD

Tetralogy of fallot in CXR

Boot shaped heart

Hypoxic spell which improves when squatting

TET spell

Ventriculo-arterial discordance, switching of the aorta and pulmonary arteries

Transposistion of the great arteries

Required shunt for TGA

VSD (35%) stable shunt


PDA (65%) Unstable shunt

CXR findings in TGA

Egg shaped cardiac silloutte

TGA is associated with

Offspring of diabetic mother

Closure of the ductus arteriosus occurs due to ____ and when?

increased O2 saturationi and decreased PGE2


Occurs during first 2 days

ductus arteriosus will become

ligamentum arteriosus

Single great artery associated with cyanosis with irreversible HPN


Assoc. Shunt

Truncus arteriosus




VSD

Complete occlusion of the tricuspid valve (failure of devopment)

Tricuspid atresia

Tricuspid atresia is associated with :

Hypopastic RV




ASD as shunt (right to left)




high mortality

connection between pulmonary veins and systemic veins wherein blood flow of the pulmo veins goes into the right atrium

TAPVC

MCC variant of TAPVC

Supracardiac (Drains to inominate/brachiocephalic vien)

MC adult CHD- Asymptomatic untill 30 y/o

ASD



Cardiac auscultion finding in ASD

Fixed widely split S2 with mild systolic murmer of upper sternal border

3 types of ASD

Primum


Secundum (90 %)


Sinus Venosus

Adjcent to AV vavle and usually assoc with cleft anterior mitral, assoc with Downs

Primum ASD

Due to deficient/ Fenestrated oval fossal

Secundum ASD

Near the entrance; commonly accompanied by TAPVC

Sinus venusos ASD

Most common CHD overlall

VSD

Frequently assoc with other structural defects (e.g. Cri du chat, Fetal alcohol syndrome)

VSD

Multiple VSD is called

Swiss cheese septum

Types of VSD

Membranous (90 %)


Infundibular- hole is below pulmonary valve


Ventricular septum- Muscular septum

PDA is most commonly associated with what type of infection

Congenital rubella

It is the direct communication between the aorta and the pulmonary artery

PDA

Auscultation sound in PDA

Continuous machinery murmur

two forms of Atrioventricular septal defect

Partial- Primary ASD and cleft anterior mitral leaflet causing mitral insufficiency




Complete- hole in the center of the heart: 1 /3 have down syndrome

segmental narrowing of the Aorta

Coarctation of the aorta

associated wit turner's syndrome and causes severe narrowing of aorta proximal to the ductus arteriorusus

Preductal (infantile) Coarctation

Causes narrowing distal to the ductus arteriosus

postductal (adult) Coarctation

Symptoms associated with infantile coarctation

Lower body cyanosis

Symptoms associated with adult coarctation

Upper extremity HPN


Rib notching on CXR


Possible rupture of berry aneurysm


Collateral circulation

what CHDs are associated with

Congenital rubella syndrome- PDA


Turner's syndrome- Coarctation (infantile)


Down's- ASD primum


Marfan's syndrome- MVP, aortic dissection


Offspring of diabetic mom- Transposition of the great Arteries

infantile Coartation will be associated with what ventricular defect to survive

PDA


RVH

What is the cause of rib noching

Remodeling as a consequence to increased blood flow though the intercostal arteries

Complications of adult coarctation could be

CHF, intracerebral hemorrhage, dissectic aortic aneuryms

Coronary vessels supplying the


-anterior wall of LV


- Anterior ventricular septum


- Apex



LAD

MC affected in MI


- V1-V4 anterior wall MI

LAD

Coronary vessels supplying the


- Inferior/Posterior LV and RV, posterior ventricular septum

RCA

Coranary vessel supplying the lateral wall of LV except apex

LCX

(II, III, AVF, right side chest leads)

Inferior wall exchemia

I, AVL, V5-V6

lateral wall ischemia

The most common type of ischemia, caused by coronary atherosclerosis with narrowing/stenosis of coronary vessels > 70 %

Stable angina

Chest pain is relieve by rest and nitrates

Stable

Chest pain is relieve by nitrates

Prinzmetal



Chest pain occurs during exertion, excercise due to increase cardiac demand

Stable

Angina pectoris with ST- segment depression ( sub- endochondral ischemia)

Stable anginga

Pre infarction angina

Unstable/Cresendo angina

angina caused by vasospasm due to thromboxane or endothelin

Prinzmetal angina

angina characterised by increasing frequency, intensity, and duration associated with nonocclusive thrombus in an area of atherosclerosis

Stable/cresendo

Death with i hour after onset of SsX secondary to arrhythmia

Sudden cardiac death

SCD associated with what syndromes

Romano-Ward syndrome ( long QT syndrome -V Fib)




Brugada syndrome (RBBB)

types of myocardial infarction

Transmural/Full thickness


- ST-elevation, Q wave


- Increased early mortality rate


-Occured if > 50 % of myocardial wall


-associated with regional occlusion by thrombus

Types of MI

Subendocardial


- Partial thickness


- ST depression


- Inner third of myocardium


- < 50 % wall involved


- Associated with hypoperfusion

Changes in MI (gross)

6- 12 hours- MI usually grossly inapparent


18-24- Pale to cyanotic


1 week- Yellow and softend


7-10 days- Hyperemic granulation at infarct edge


1-2 mos- fibrous scar

Irreversible cell injury in MI within how many minutes

20-40 mins

wavy fibers of myocardium

within 4 hours

Early coagulative necrosis

4-12 hours

Pnemonics in MI 1313

1 - 3 days Neutrophils (acute inflammation)


3 - 7 days Macrophages


1 week- granulation tissue


3 weeks- scar

Coagulation necrosis with strong neutrophil infiltrates

> 12 hours

ATP reduced to 50 % of normal

10 minutes

Loss of contractility

2 minutes

Microvascular injury

> 1 hour

Reversible phase of MI

Glycogen depletion, Mitochondrial swelling, relaxation of myofibrils

Irreversible phase

Sarcolemmal disruption, mitochondrial amourphous densities

result of calcium overload and hypertetanic contraction after reperfusion of injured myosyte

Contraction band necrosis

Myocardial rupture will most like occur within what days post MI

3- 7 days


-rupture causing tamponade

Common 2-3 days post MI

Dressler syndrome (fibrinous pericarditis)

% mortality in cardiogenic shock

70 %

Hypertrophy and dilatation of non-infarted myocardium is called, which can become substrate of aneurysm, secondary arrhytmia

Cardiac remodelling


- prevented by ACE i

Preferred biomarkers in MI

trop I


- occurs 2-4 hours


- peak at 2 days


- disappears at 7 days

can diagnose reinfarction

CKMB


- 2-4 hours


- peak 24 hours


- disappears after 72 hours

ECG changes in MI

Inverted T waves


- Correlates with infarct periphery




Elevated ST segment- Injured myocardial cells sorrounding necrosis




New Q waves- Coagulation of necrosis

TReatment of MI

Antiplatelet (ASA, Clopidogrel)

NItrates, B-blockers, ACE


Pain Medications (morphine)


- morphine is not used in inferior wall MI


Reperfusion therapy

Opening snap, loud s1, diastolic rumble, Atrial fib

MS

Due to MVP


Pansystolic murmur

Mitral regurgitation

Midsystolic clicks

MVP

Most common cause of congenital aortic stenosis

Bicuspid valve

Widened pulse pressure, austin flint murmur

Aortic regurgitaion

Graham steel murmur

pulmonary regurgitation

IE in drug abusers, carcinoid heart, JVP, pulsating liver,

tricuspid regurgitation

Carcinoid heart disease

Pulmonary stenosis


Tricuspid valve plaques

Bounding pulse

Corrigan water hammer

De musst sign

head nodding with diastole

quincke's pulse

pulsating nail bed

Mueller's sign

systolic pulsation of uvula

durosiers

femoral retrograde bruit

traubes sign

pistol shot femorals

hill's sign

BP LE> BP UE

acute, immune mediated, multisystemic inflammatory disease due to pharyngitis from GABHS ( M proteins)

Rheumatic fever

Clinical features

MAJOR:


Joints (migratory Polyarthritis)


OH my heart (Carditis)


Nodules (subcutaneous)


Erythema marginatum


Syndenham chorea

Diagnosis of RF

Upon onset of SSx, pharyngeal culture are negative


but ASO and Anti-DNAse titers will be positive

Pathognomonic of RF and RHD found in all layers of the heart

Aschoff bodies




Anitschow cells

Foci of swollen eosinophilic collagen surrounded by T cells, plasma cells

Aschoff bodies

Macrophages containing abundant cytoplasm, round nuclei with slender wavy ribbon of chromatin and aschoff giant cells

Anitschkow

Morphology of RF and RHF

Bread and butter pericarditis


Macculum plaques


fibrinoid necrosis


Mitral stenosis


Fish mouth/ buttonhole stenosis

Locations, etiologic agent, valve, prognosis of Infective endocarditis

Acute IE- Previously normal valve, Tricuspid, Staph aureus, Worse prog, Rapid onset, associated with IV drug use




Subacute- Previously abnormal valve, Mitral valve, Strep viridans, Better prog, insiduous onset less destruction, more granulation, RHD

Friable, bulky, destructive vegetation with fibrin, inflamatory cells and other organisms in the heart

infective endocarditis

Most common symptom

Fever

Microemboli in IE

Subungual hemorrhage, jane way, osler's nodes

Red linear flame shaped streak on nail beds

Subungual hemorrhage

Red hemorrhage painless lesions on palms and soles

Jane way

subcutaneous nodules in the pulp of digits

osler's node

sterile, non destructive vegetations that may cause emboli along the line of closure of valve leaflets

Marantic endocarditis

Marantic endocarditis commonly occurs in

Cancer ( mucinous AdenoCA of pancreas and other adenoca




Debilitating illness (e.g. renal failure, chronic illness) with DIC




Hypercoagulable states

Small sterile vegetations on both sides of the leaftlets, with hematoxylin bodies, associated with SLE

Libman Sakcs disease


-resembles fibrosis and may require surgery

Small, warty vegetations along the lines of closures of the valve leaflets

RHD

Small bland vegetations, usually attatched at the line of closure

NBTE

Large, irregular masses on the valve cusps that can extend onto the chordae

IE

small or medium sized vegetations on either or both sides of valve leaflets

LSE

Heart disease due to primary abnormality of the myocardium, diagnosed with a bioptome

Cardiomyopathy

Pattern of Cardiomyopathy

Dilated


Hypertrophic


Restrictive

Characteristic auscultation finding in pericarditis

Friction rub

Type II reaction where necrotic heart muscle induces immune sytem to generate autoantibodies to cardiac self antigen

Dressler syndrome

Most common form of cardiomyopathy, due to enlargement of with dialtation of all four chambers, resulting in progressive CHF

Dilated cardiomyopathy

Some causes of DIlated cardiomyopathy

IDIOPATHIC


Alcohol


pregnancy


Beri beri


Chagas


Doxurobucin


Cocoine


Solvents


Chronic anemia

LV-EF in the different forms of Cardiomyopathy

Dilated < 40 %


Restrictive >45 - 90 %


Hypertrophic > 50 - 80 %

Wall description of Cardiomyopathies

Dilated- thin walls, dilated lumen


Hypertrophic- Thick walls, constricted lumen


Restrictive- Normal wall and lumen but stiff

The only effective therapy for dilated cardiomyopathy is

Heart transplant

also called assymetrical septal hypertrophy, idiopathic hypertrophic subaortic stenosis

Hypertrophic cardiomyopathy

Common cause of deeath in young atlethes due to extensive myocyte hypertrophy with myofiber disarray

hypertrophic cardiomyopathy

Common cause of hypertrophic cardiomyopathy

Genetic, friedrich ataxia, storage disease, infants with DM mothers

Etiologies of restrictive cardiomyopathy

amyloidosis, sarcoidosis, fibrosis after surgery, loeffler endomyocarditis

Right sided endocardial and valvular fibrosis secondary to serotonin, Diagnosis via demonstration of 5 HIAAA

Carcinoid heart disease

Etiology of myocarditis

Microbes (coxsackie, t. cruzi, B. burgodorferi)


RF


Toxins (diphteria, co)


Drugs ( Coxurobucin, Cocaine


SLE, SS, Sarcoidosis

Morphology of myocarditis

Instertitial inflammatory infiltrate with focal myocyte necrosis

Clinical findings in pericardial effusion

Muffled heart sounds


NVE


Hypotension with pulsus paradoxus



ECG finding in Pericardial effusion




CXR

Electrical alterans




Water bottle configuration



Follow suppurative or caseaous pericarditis, previous surgery, or irradiation to the mediatinum

Adhesive mediastinopericarditis

Heart sorrounded by fibrous tissue resembling plaster mold usually due to TB or open heart surgery

Constrictive pericarditis

Precordial chest pain, tachycardia, fever, pericardial friction rub

Pericarditis

ECG changes in pericarditis

Diffuse ST elevation


PR Depression

Most common Primary tumor of the heart associated with wrecking ball effect on valve, ball-valve obstruction

Myxoma

Heart tumor associated with Tuberous sclerosis

Cardiac rhabdomyosarcoma

Autosomal dominant mutation in TSC1 (hamartin) and TSC2 (tuberin) which are tumor supressor gene

Tuberous sclerosis

MC common heart tumor

metastasis

Most common primary tumor in children

Rhabdomyosarcoma



MC site of metastisis

pericardium

thanks

thanks