Download cardio review

Cardiovascular overview







Cardiac function and heart failure
Valvular disease and endocarditis
Pericardial diseases
Coronary artery disease
Arrhythmias and syncope
Congenital heart disease
Coagulation
C
100
D
Pressure
(mm Hg)
B
1. Which letter corresponds to the first heart
sound?
2. Which letter corresponds to the second heart
sound?
50
A
E
0
Time
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

Coronary arteries
 Myocardial

infarction
Myocardium
 Dilated,

pericarditis, tamponade
hypertrophic, restrictive cardiomyopathies
Valves
 Stenosis
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

Congestion
 Dyspnea
 Pulmonary
edema
 Peripheral edema

Low output
 Fatigue
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 10
years ago and now presents with shortness of breath with mild
exertion such as walking one block at a slow pace. On physical
examination, blood pressure is 104/88 mm Hg, heart rate is 110
bpm. Jugular venous pressure is 10 cm above the sternal angle and
there is pitting leg edema. The apical impulse is enlarged and there
is a holosystolic mumur grade 2/6 at the apex. Which one of the
following statements is false?
A. Left ventricular afterload is decreased.
B. Left ventricular preload is increased
C. Left ventricular contractility is decreased
D. Circulating catecholamines are elevated
E. Angiotensin II levels are increased.
Therapy for this patient should include all of the
following except:
A. Furosemide
B. Enalapril
C. Nifedipine
D. Digoxin
E. Spironolactone
1. CHF and diuretics
2. CHF and ACE inhibitor
3. CHF and NSAID with sodium retention
Stroke 70
Volume
(mL)
30
A
F
D
C
B
G
E
20
10
LV diastolic pressure (mm Hg)
How does the patient shift on the Starling curve?
Stroke 70
Volume
(mL)
30
A
F
D
ACE-I
B
C
NSAID
G
Diuretic
E
20
10
LV diastolic pressure (mm Hg)
A 74 year old woman presents with peripheral edema. Which one
of the following signs is most specific for a cardiac cause of
edema?
A. Apical systolic murmur
B. Elevated jugular venous pressure
C. Varicose veins
D. Decreased volume of posterior tibial pulses
E. 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
Diagnostic algorithm
Chest pain
Cardiac
Non cardiac
Ischemic
Nonischemic
GI
Non GI
Angina
Unstable Angina
Myocardial infarction
Pericarditis
Aortic Dissection
GERD
Spasm
Peptic Ulcer
Pneumothorax
Pulmonary embolism
Chest wall
Panic attack
When taking a history of chest
pain ask
 Provoking 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 artery
 ECG: 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 regurgitation
is 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 retrosternal
chest 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 of
the following except:
A. Acetylsalicylic acid
B. tPA or emergency percutaneous coronary intervention
C. Beta-blocker
D. Calcium channel blocker
Schematic Diagram Of
Cardiac Conduction Pathways
Ca in
K out
Na in
Absolute
Refractory
Period
Na out
K in
Components Of The ECG
B
C
A
E
D
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
Unidirectional block
Slowed retrograde
conduction
Reentry results in a self perpetuating fast rhythm
Atria
Atrial fibrillation or flutter
AV node
AV nodal re-entrant tachycardia
Ventricles
Ventricular tachycardia
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

Slow ventricular depolarization or repolarization
to terminate ventricular tachycardia
 Use

Calcium channel blocker , beta blocker, digoxin
amiodarone, xylocaine, procainamide
Prevent clot in left atrium: in atrial fibrillation
 Use
warfarin
Syncope
Transient loss of consciousness
 Cardiac

 Arrhythmia
 Obstruction

Vascular
 Neurocardiogenic:
Most common
 Orthostatic 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 patients
who have which one of these congenital heart
problems?
A. Tetralogy of Fallot (pulmonic stenosis and
ventricular septal defect)
B. Bicuspid aortic valve
C. Ventricular septal defect
D. Atrial septal defect
E. 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!