Cardiovascular overview Cardiac function and heart failure Valvular disease and endocarditis...

Cardiovascular overview

Cardiac function and heart failure Valvular disease and endocarditis Pericardial diseases Coronary artery disease Arrhythmias and syncope Congenital heart disease Coagulation

A

B

D

E

C100

50

0

Pressure(mm Hg)

Time

1. Which letter corresponds to the first heart sound?2. Which letter corresponds to the second heart sound?

Heart Failure: Definition

Problem with the heart which results in inability to eject an adequate amount of blood to meet the demands of the body

May be a problem with filling or with contraction

Determinants of heart function

Preload (LV end diastolic volume/pressure)

Afterload (peripheral vascular resistance) Contractility (force of contraction)

Anatomic classification of heart failure Pericardium

Constrictive pericarditis, tamponade

Coronary arteries Myocardial infarction

Myocardium Dilated, hypertrophic, restrictive cardiomyopathies

ValvesStenosis or regurgitation

Heart failure

Damage to LV results in dilatation and hypertrophy

Activation of renin-angiotensin-aldosterone, sympathetic nervous system, antidiuretic hormone: Short term gain for long term pain Fluid retention Vasoconstriction Cellular growth and premature death

Symptoms of heart failure

CongestionDyspneaPulmonary edemaPeripheral edema

Low outputFatigue

Signs of heart failure

Sinus tachycardia Elevated JVP Enlarged apical impulse S3 Mitral regurgitation Edema

Edema

Increased venous hydrostatic pressure Heart failure, deep vein thrombosis or varicose veins,

volume overload Obstructed lymphatics

Eg. Following mastectomy with axillary node dissection Decreased plasma oncotic pressure

Nephrotic syndrome, starvation “Leaky capillaries”

Bee sting

Cardiomyopathies Dilated: Myocardial damage leading to fibrosis and myocyte

loss. LV is dilated and hypokinetic with LVEF < 40% Apex is enlarged and a third heart sound may be present

Hypertrophic: Autosomal dominant condition with myocardial fiber disarray. Often disproportionate septal hypertrophy which can cause LV outflow tract obstruction because of systolic anterior motion of the mitral valve. Systolic murmur becomes louder when preload is decreased

Restrictive: Infiltrative disorders such as amyloid cause diastolic LV dysfunction

Heart Failure: Treatment

Diuretics as needed for fluid retention Angiotensin converting enzyme inhibitors (eg

enalapril): Decrease LV hypertrophy and dilatation. Prolong survival if LVEF < 40% Watch for hypotension with increasing dose

Beta-blockers: Blunt toxic effects of sympathetic nervous system. Prolong survival in heart failure

Spironolactone: Aldosterone inhibitor that also reduces myocardial collagen deposition and improves survival in severe heart failure

Digoxin: Improves functional capacity

An 80 year old man had a large anterior myocardial infarct 10years ago and now presents with shortness of breath with mildexertion such as walking one block at a slow pace. On physicalexamination, blood pressure is 104/88 mm Hg, heart rate is 110bpm. Jugular venous pressure is 10 cm above the sternal angle andthere is pitting leg edema. The apical impulse is enlarged and thereis a holosystolic mumur grade 2/6 at the apex. Which one of thefollowing statements is false?A. Left ventricular afterload is decreased.B. Left ventricular preload is increasedC. Left ventricular contractility is decreasedD. Circulating catecholamines are elevatedE. Angiotensin II levels are increased.

Therapy for this patient should include all of thefollowing except:A. FurosemideB. EnalaprilC. NifedipineD. DigoxinE. Spironolactone

StrokeVolume(mL)

LV diastolic pressure (mm Hg)

A

BCD

E

FG

10 20

70

30

1. CHF and diuretics2. CHF and ACE inhibitor3. CHF and NSAID with sodium retention

How does the patient shift on the Starling curve?

StrokeVolume(mL)

LV diastolic pressure (mm Hg)

A

BCD

E

FG

10 20

70

30

NSAIDACE-I

Diuretic

A 74 year old woman presents with peripheral edema. Which oneof the following signs is most specific for a cardiac cause ofedema?A. Apical systolic murmurB. Elevated jugular venous pressureC. Varicose veinsD. Decreased volume of posterior tibial pulsesE. Fourth heart sound

Valvular disease

Mitral regurgitation: Mitral valve does not close completely in systole and there is flow from LV to LA Systolic murmur at apex, third heart sound Increased left atrial pressure and LV diastolic pressure can be problem with LV, papillary muscles, chordae, leaflets.

Mitral stenosis: Mitral valve doesn’t open completely in diastole Diastolic murmur at apex Increased LA pressure and normal LV diastolic pressure Usually a problem with commissural fusion secondary to rheumatic

fever

Valvular disease

Aortic regurgitation: Aortic valve doesn’t close completely in diastole Bicuspid aortic valve or dilated aortic root that

stretches the leaflets apart Aortic stenosis: Aortic valve doesn’t open

completely in systole Bicuspid aortic valve or degenerative valve disease LV systolic pressure is higher than aortic systolic

pressure

Endocarditis

Infection of the valves usually secondary to staphylococcus or streptococcus

Predisposing conditions are valve disease and intravenous drug use

Presents with fever, heart murmur and positive blood cultures

Can lead to valve destruction and severe regurgitation with heart failure

Treatment is iv antibiotics and valve replacement if heart failure develops

Pericardial diseases

Pericarditis: Inflammation of the pericardium. Pericardial friction rub may be present. Treated with NSAIDs.

Pericardial tamponade: Fluid under pressure in the pericardial space. Heart can’t fill. Dyspnea and presyncope. Pulsus paradoxus and elevated JVP. Treatment is removal of fluid.

Pericardial constriction: Fibrous encasement of the heart. Leads to heart failure because the heart can’t expand and fill. Elevated JVP and peripheral edema. Treatment is surgical pericardiectomy

D i a g n o s t i c a l g o r i t h m

A n g inaU n sta b le A ng ina

M yo card ia l in fa rc t ion

Isch e m ic

P e rica rd it isA o rtic D isse c tion

N o n isch e m ic

C a rd iac

G E R DS p a sm

P e p tic U lce r

G I

P n eu m o tho raxP u lm on a ry e m b o lism

C h e s t w a llP a n ic a tta ck

N o n G I

N o n ca rd iac

C hest pa in

When taking a history of chest pain askProvoking and alleviating factors: When does it

come on? What makes it better? Worse?

Quality: What does it feel like?

Region: Where is it? Does it go anywhere?

Severity: Does it stop you from continuing what you’re doing?

Timing: How does it start and how long does it last?

CAD

Angina: Atherosclerotic narrowing of coronary arteries results in myocardial ischemia when demand exceeds the supply Chest pain with exertion and relieved by rest or

nitroglycerine

Acute coronary syndrome

Myocardial infarction: Necrosis which results from thrombotic occlusion of a coronary arteryECG: ST elevation followed by Q waves (total

occlusion of coronary artery) or ST depression/T inversion (subtotal occlusion)

Cardiac enzymes: Troponin, CPK MB are elevated

Ischemia

Increased myocardial oxygen demand

Increased heart rate Increased afterload Increased contractility

Decreased myocardial oxygen supply

CAD Anemia Hypoxemia

CAD: Treatment

Stable angina: ASA and statins to prevent myocardial infarction. ACE inhibitors

also improve survival if significant CAD. Beta-blockers, nitrates, calcium channel blockers to improve

symptoms

Myocardial infarction: ASA and thrombolytics (streptokinase, rtPA) or primary

angioplasty to dissolve intra-coronary clot (ST elevation MI) Heparin, glycoprotein IIB/IIIA inhibitors in unstable angina or non

ST elevation MI ASA, statins, beta-blockers and ACE-I to improve survival following

MI

Acute coronary syndrome (nonST elevation MI): ulcerated plaque with subocclusive thrombus

What is the cause of chest pain in these patients?

A 70 year old man with hypertension develops sudden onset of severe retrosternal pain. He is diaphoretic and a murmur of aortic regurgitationis present.

A 20 year old man has severe,sharp precordial chest pain which is made worse by inspiration and relieved by sitting up. A rubbing sound is heard over the precordium.

A 30 year old woman has sharp left chest pain which is reproduced by palpation of the fourth sternochondral joint.

A 67 year old woman with diabetes has retrosternalchest discomfort with exertion that is relieved by rest.

A 50 year old man has severe central chest heaviness for the past two hours. He is nauseated and diaphoretic.What is the most likely problem?

Current management of ST elevation myocardial infarction includes all ofthe following except:A. Acetylsalicylic acidB. tPA or emergency percutaneous coronary interventionC. Beta-blockerD. Calcium channel blocker

Schematic Diagram OfCardiac Conduction Pathways

Na in

Ca in

K outNa outK in

AbsoluteRefractoryPeriod

Components Of The ECG

A

B

C

D

E

1. Which letter represents ventricular depolarization?2. Which letter represents potassium efflux from myocardial cells?3. Which letter represents atrial depolarization?

Mechanisms of arrhythmias

Increased automaticity Re-entry

Propagation of electrical impulse

Reentry results in a self perpetuating fast rhythmAtria Atrial fibrillation or flutterAV node AV nodal re-entrant tachycardiaVentricles Ventricular tachycardia

Unidirectional block

Slowed retrograde conduction

Palpitations

Subjective sensation of abnormal heart beat

Ask: Describe what you feel.Have you ever passed out or felt close to

passing out?

What is the cause of palpitations in this

25 year old athlete?

What is the cause of palpitations in these patients?

A 75 year old man comes to the ER because of chest pain. What is the appropriate treatment?

While you are thinking about what to do he becomes unresponsive.

Management of arrhythmias

Slow AV node conduction: in SVT, atrial fibrillation/flutter Use Calcium channel blocker , beta blocker, digoxin

Slow ventricular depolarization or repolarization to terminate ventricular tachycardia Use amiodarone, xylocaine, procainamide

Prevent clot in left atrium: in atrial fibrillation Use warfarin

Syncope

Transient loss of consciousness Cardiac

ArrhythmiaObstruction

VascularNeurocardiogenic: Most commonOrthostatic hypotension

Neurocardiogenic syncope

•Young person•Response to fear or injury•Predisposing factors:

• prolonged standing, venipuncture, heat, dental surgery, eye surgery•Pallor, nausea, sweating are associated•Reflex

•Decrease preload and increased contractility •Stimulation of baroreceptors in LV•Afferent vagal fibers to medulla•Efferent outflow results in

•increased vagal tone (bradycardia)•withdrawal of peripheral sympathetic tone (vasodilatation)

•Resolves with lying down

Which of these patients is most likely to have syncope?

Congenital heart disease: Acyanotic Atrial septal defect: Communication between atria

with LA to RA shunt. RA and RV dilated. Ventricular septal defect: Shunt from LV to RV

with LA and LV dilatation. Patent ductus arteriosus: Shunt from descending

aorta to pulmonary artery. LA and LV dilated. Congenital aortic stenosis: Presents with heart

failure Coarctation of the aorta: Narrowing of the

descending aorta at the site of ductus arteriosus. Heart failure and hypertension.

Congenital heart disease: Cyanotic

Tetralogy of Fallot: VSD and RV outflow tract or pulmonic valve stenosis with RV to LV shunt

Transposition of the great arteries: Aorta arises from RV and PA from LV.Need PDA or ASD/VSD to survive.

Eisenmenger’s syndrome: Severe irreversible pulmonary hypertension secondary to chronic volume overload with reversal of left to right intracardiac shunt

Central cyanosis occurs commonly in patientswho have which one of these congenital heartproblems?A. Tetralogy of Fallot (pulmonic stenosis and

ventricular septal defect)B. Bicuspid aortic valveC. Ventricular septal defectD. Atrial septal defectE. Patent ductus arteriosus

Coagulation: What’s the diagnostic test? Warfarin therapy Disseminated

intravascular coagulation Heparin therapy Thrombotic

thrombocytopenic purpura

von Willebrand’s disease

Bleeding time PTT PT INR Fibrinogen Platelet count

Coagulation: What’s the diagnostic test? Warfarin therapy Disseminated

intravascular coagulation Heparin therapy Thrombotic

thrombocytopenic purpura

von Willebrand’s disease

PT INR Fibrinogen

PTT Platelet count

Bleeding time

Good luck!