Cardiology and Nephrology

182 Pages·98.716 MB·English

by  Mahmoud Sewilam

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Malhsuismdl Ss^aiaaii
Kasr Al-Ainy School of Medicine
Cairo University
مﻠﻌﻟا رﺷﻧ ﺔﯾﻧﺑ ﮫﺛﯾدﺣﺗ مﻋداو بﺎﺗﻛﻟا كﻌﻔﻧ اذإ كﺗﺧﺳﻧ يرﺗﺷا
مﻠﻌﻟا رﺷﻧ ﺔﯾﻧﺑ ﮫﺛﯾدﺣﺗ مﻋداو بﺎﺗﻛﻟا كﻌﻔﻧ اذإ كﺗﺧﺳﻧ يرﺗﺷا
By
Mahmoud Sewilam
Kasr Al-Ainy School of Medicine
Cairo University
First Edition
مﻠﻌﻟا رﺷﻧ ﺔﯾﻧﺑ ﮫﺛﯾدﺣﺗ مﻋداو بﺎﺗﻛﻟا كﻌﻔﻧ اذإ كﺗﺧﺳﻧ يرﺗﺷا
مﻠﻌﻟا رﺷﻧ ﺔﯾﻧﺑ ﮫﺛﯾدﺣﺗ مﻋداو بﺎﺗﻛﻟا كﻌﻔﻧ اذإ كﺗﺧﺳﻧ يرﺗﺷا
Cardiology
Topic Page
o Cardiac cycle 1
o Neck veins 4
o Symptomatology 5
o Heart Failure 15
o Acute Pulmonary Edema 31
o Diseases Of Pericardium 33
o Diseases Of Myocardium: Myocarditis & Cardiomyopathy 39
o Rheumatic Fever 44
o Infective Endocarditis 48
o Coronary Artery Disease : Angina pectoris & Myocardial 55
infarction
o Dyslipidemia 65
o Pulmonary Hypertension 67
o Pulmonary Embolism 69
o Systemic Hypertension 72
o Valvular heart diseases 80
o Congenital heart diseases 95
o Arrhythmias 104
o Sudden cardiac death 118
o Diseases of aorta: Aortic Aneurysm & Dissecting Aortic 120
Aneurysm
o Peripheral arterial diseases 125
o Shock 127
o Heart Transplantation 131
مﻠﻌﻟا رﺷﻧ ﺔﯾﻧﺑ ﮫﺛﯾدﺣﺗ مﻋداو بﺎﺗﻛﻟا كﻌﻔﻧ اذإ كﺗﺧﺳﻧ يرﺗﺷا
مﻠﻌﻟا رﺷﻧ ﺔﯾﻧﺑ ﮫﺛﯾدﺣﺗ مﻋداو بﺎﺗﻛﻟا كﻌﻔﻧ اذإ كﺗﺧﺳﻧ يرﺗﺷا
Cardiac cycle
n n
SI S2 SI
Systole Diastole Systole
I. Systole: II. Diastole:
1. First heart sound : 4. Second heart sound:
• After evacuation of blood, the ventricles relax, so the
The cardiac cycle start by contraction of
pressure in the aorta and pulmonary artery will exceed the
ventricles resulting in closure of mitral &
pressure in the ventricles resulting in closure of aortic &
tricuspid valves producing the first heart
pulmonary valves producing the second heart sound (82)
sound (SI)
2. Isometric contraction phase: 5. Isometric relaxation phase:
• T he ventricles continue to contract while the
The ventricles continue to relax while four valves of the
four valves of the heart are closed, so the heart are closed, so pressure inside the ventricles falls
pressure inside the ventricles rises rapidly
rapidly without change in the volume.
without change in the volume
3. Ejection phase: 6. Ventricular filling phase:
When the pressure in the ventricles becomes lower than the
When the pressure in the ventricles exceeds the
pressure in the atria, blood flows to the ventricles passively,
pressure in the aorta & pulmonary artery, the
First rapidly : maximum filling phase
aortic & pulmonary valves will open (normally
Then slowly :r educed filling phase
with no sound)
7. Atrial systole:
Then the blood rushes from the ventricles to
• T he last amount of blood in the atria is pushed actively by
the aorta and pulmonary artery,
atrial contraction in the late diastole.
First rapidly: maximum ejection phase
Then slowly: reduced ejection phase
8. Ventricular contraction: occurs again & the cycle is repeated.
N.B.: any change in heart rate , is a change in diastole, systole is constant:
Tachycardia shortens diastole while bradycardia lengthens diastole.
مﻠﻌﻟا رﺷﻧ ﺔﯾﻧﺑ ﮫﺛﯾدﺣﺗ مﻋداو بﺎﺗﻛﻟا كﻌﻔﻧ اذإ كﺗﺧﺳﻧ يرﺗﺷا
Pulmonary valve
Heart Sounds and their relation to cardiac cycle: Aortic valve
Right coronary a.
1. Heart sounds (S1,S2,S3,S4)
II. Additional heart sounds (Systolic clicks & opening snap) coronary a
III. Murmurs
Heart sounds Tricuspid
n:
Mitr^
valve
Coronary sinus Posterior inlenrentricuiar
branch of right coronary a
a
o
••C
u
V
w"
SI S2 S3 S4 SI
Systole Diastole Systole
1. l irst heart sound, SI 2. Second heart sound, S2
1 v Time: I
1 n Beginning of systole n B eginning of diastole |
v Caused by : 1
n Valvular: closure of atrioventricular (mitral & n Valvular: Closure of semilunar (aortic & pulmonary)
tricuspid) valves valves:
n Muscular: early ventricular contraction (vibrations o Over aortic area : S2 is single( A2 only heard)
of chordae tendineae & papillary muscles) o Over pulmonary area : S2 is split( A2 followed by P2)
v Site of maximum intensity : I
n At the apex of the heart n O ver base of the heart
v Intensity: I
®" Causes of Accentuated SI: ®" Causes of Accentuated 82:
1. MS-TS
2. Systemic hypertension 1. t A2 in systemic hypertension
2. t P2 in pulmonary hypertension
®" Causes of Weak (muffled) SI: Causes of Weak (muffled) 82:
1. MR-TR 1. iA2inA8«&AR
2. Calcified MS 2. iP2inP8&PR
3. Third heart sounds, S3 4. Fourth heart sound, 84
¤¤¤ Time:
n E arly diastole sound heard shortly after S2 best n L ate diastole (presystolic) sound heard just before
heard by the cone in left lateral position. 81 best heard by the cone in left lateral position.
"> Mechanism:
n E xcess ventricular vibrations (blood gush in n F orcible atrial contraction against high ventricular
ventricle after opening of atrioventricular valve) end diastolic pressure
1 C auses of the sound: I
1. Normal in children & young adult 1. Normal in elderly person
2. Volume overload in: 2. Pressure overload in :
o LV; MR, AR, VSD o LV: systemic hypertension, AS
o RV:TR,PR, ASD o RV: pulmonary hypertension, PS
o Hyperkinetic circulation
3. Flabby myocardium in: 3. Reduced compliance of ventricles in:
o LVF (apical gallop) o Myocardial infarction
o RVF (tricuspid gallop) o Restrictive & Hypertrophic cardiomyopathy
o Dilated cardiomyopathy
v N.B.: Callop rhythm (triple rhythm): (S3 or S4 or Both)+ tachycardia
A. Protodiastohc (ventricular) gallop = S3 + tachycardia B. Presystolic (atrial) gallop = S4 + tachycardia
C. Summation gallop = S3 + S4 + tachycardia e.g. hypertensive heart failure
مﻠﻌﻟا رﺷﻧ ﺔﯾﻧﺑ ﮫﺛﯾدﺣﺗ مﻋداو بﺎﺗﻛﻟا كﻌﻔﻧ اذإ كﺗﺧﺳﻧ يرﺗﺷا
Expiration Inspiration
Jl Ir
Normal
S2 S2
Normally : left ventricle ejection period is shorter than that of right ventricle ,s o the pressure closing aortic valve is
higher than that closing pulmonary valve so aortic valve closes before pulmonary valve I.e. A2 precedes P2
Relation of splitting to respiration:
S Splitting Is Only Detected Over Pulmonary Area :
Pulmonary component is weak & heard over pulmonary area only while aortic component is loud heard at both A &
P areas.
During inspiration :
t Venous return will increase RV Load, with delayed closure of pulmonary valve.
Meanwhile the lung is expanded & retains more blood in its vessels with decrease in LV load, and so earlier
closure of aortic valve.
So during inspiration —* wide splitting of S2
During expiration: the reverse occurs —> narrow splitting or fusion (single S2)
Causes of:
<* Wide splitting Of S2: delay of pulmonary closure. *1* Reversed (paradoxical) splitting: delay of
aortic closure.
• Widening of splitting which will be heard without deep • With deep inspiration, splitting closes or
mspiration disappears.
• Delayed P2 in PS A2| A2| • Delayed A2 in AS "l\" - ll
• RBBB • L BBB
S2 S2 S2 S2
• VSD • P DA
• ASD; wide fixed splitting: unaffected by respiration v Reversed splitting due to:
• Delay of A2 to come after P2 -+ reversal of
"Ir "Ir
relation to respiration i.e. splitting closes
S2 S2 during inspiration & widens during expiration.
v Murmurs
1
PDA
MR,T R, VSD AR,PR
AS,P S
MS,I S
MVP,H OCM
SI S2 SI
Diastole | Systole
Systole
Definition : musical sounds produced by turbulent blood flow
Types of murmur:
1. Organic murmur 2. Functional = relative = flow murmur
Caused by structure anatomical abnormality *> Caused by functional (physiological) abnormality due to :
in heart or vessel e.g. A. Increases the blood flow through a structurally normal heart
A. Valvular affection e.g. MS e.g. hyperdynamic circulation
B. Abnormal opening (shunts) e.g. VSD B. Flow into dilated chamber e.g.
• Ventricular dilatation in HP
• Aortic or pulmonary dilatation in systemic or P.HTN
o May propagate to other areas o Localized
o Associated with thrill + symptoms & signs o No thrill - no symptoms nor signs
مﻠﻌﻟا رﺷﻧ ﺔﯾﻧﺑ ﮫﺛﯾدﺣﺗ مﻋداو بﺎﺗﻛﻟا كﻌﻔﻧ اذإ كﺗﺧﺳﻧ يرﺗﺷا
Neck veins
Introduction :
Internal jugular vein is valveless i.e. has no venous valves: so it's direct continuous with the right atrium which
acts as manometer which reflects exactly the changes in right atrium
Right IJV is preferred as left sided ones may be present falsely prominent( high) as the left innominate vein
(Brachio-cephalic) may be compressed by the arch of aorta.
Normal neck veins: pulsating not
Physiology of the waves:
congested, empty with inspiration
o Normal Jugular venous pressure (JVP)= 0-5 cmH20
with systolic collapse
o Since right atrium is 5 cm below the sternal angle. ■■Hyb
o So Central Venous Pressure (GYP) = JVP + 5 cm = ... cmH20 {Normal CVP = 7-12 cmH20 }
o Consists of 3 positive (A,C & V) & 2 negatives (X & Y)
IVENTRICU
ayeioiB
istss
SYSTOLE DIASTO
ATRIAL
syntote diasloie
•I
a wave X descent V wave y descent
C wave
Wave v Represents Timing
n a wave o Right atrial contraction (atrial systole) • Diastolic
(Presystolic) wave
n c wave o Upward bulge of tricuspid valve into right atrium at start of • Systolic wave
ventricular contraction or transmitted from adjacent carotids
at the onset of ventricular systole
n X descent o Right atrial relaxation (normal systolic collapse) • Systolic wave
n V wave o Right atrial filling from the venous blood • Systolic wave
n y descent o Right atrial emptying to right ventricle (diastolic collapse) • Diastolic wave
• Possibilities after measurement:
a) Normally the JVP is visible 2-4 cm above the sternal angle i.e. not congested
b) Abnormally: the upper border of the IJV pulsation > 4 cm i.e. congested; comment on the following :
1. Congested Pulsating neck vein cm above angle of Lewis
2. Relation to respiration:
o Either empty with inspiration or inspiratory filling.
3. Hepato-jugular reflux or abdomino-jugular reflux or one minute abdominal compression test: -i-ve or -ve
o Compression of right hypochondrium for 1 minute -+ engorged neck veins( |J VP > 3 cm for 30 seconds) due to
painful reflex contraction of abdominal wall.
4. Timing: e ither systolic collapse or systolic expansion
• R adial pulsation is preferred for timing of the venous pulsation
• All causes are systolic collapse except { AF, TR & cannon a waves ^ Systolic expansion }
مﻠﻌﻟا رﺷﻧ ﺔﯾﻧﺑ ﮫﺛﯾدﺣﺗ مﻋداو بﺎﺗﻛﻟا كﻌﻔﻧ اذإ كﺗﺧﺳﻧ يرﺗﺷا