Internal medicine about heart diseases

1. By Hillary Vo (Vo Thao Duyen)
Definition Etiology/ risk factors/
Causes
Symptoms Treatment Diagnosis Dental significance
RF  Post-streptococcal
diseases
=> Lead to Acquired
valvular diseases
(young patient:
10-20yrs)
 Mainly left-sided
valves involved:
Aortic and mitral
valves
Anti-Streptolysin
antibodies:
Against Streptococci
give cross reaction
myocardium + soft
tissues of heart
(Pancarditis) + soft
tissues in big joints/
CNS
Cc. 2-3 weeks after
tonsilitis, pharyngitis:
=> Rheumatic fever
Arthritis
Carditis
Sydenham chordea:
Involuntary movement, CNS
problem!
*10-20 YEARS later, get the
symptoms for valvular
diseases
1. Antibiotics against
strepcoccus (penicillin) to treat
tonsilitis
2. Anti-inflammatory drugs :
- Steroid, prednisolone: more
specific for RF, to directly
againstanti-Streptolysin
- NSAIDs (aspirin,naproxen)
3. Anticoagulants:
- RF only affects myocardium;
no need
- RF affects myocardium +
valves (aortic and mitral valves
mainly involved):NEEDED:
INR 2-3
1. Lab test
Anti-streptolysin titre
(AST)
2. ECG
- Tachycardia
-Longer PQ
-ST segment,
-Arrthythmia
3. Echocardiography
Valvular destruction
Consider INR
level for those
taking
anticoagulants!
IE Severe inflammation of
the endothelium or
intracardiac artificial
surfaces caused by
MICROORGANISMS
-> Bacteria,fungi,
1. Rheumatic valvular
defects from RF
2. Mitral valveprolapse
3. Acquired valvular
diseases (AS, AR, MS,
1. Septic fever
2. Weakness
3. Weight loss
4. Heart murmur (AR/ MR)
due to regurgitation (valves
*We don’t wait for hemoculture
if many positivesymptoms
shown!!!
=>Full dosebactericid
antibioticsfor 4-6 weeks
usually IV.
1. Lab: (unspecific)
- ESR: anemia,
thrombocytopenia
- High WBC
Antibiotics
prophylaxis are
needed for dental
and high, medium
risk group

2. By Hillary Vo (Vo Thao Duyen)
mycoplasma…
Vegetation on the
valves,parietal
endocardium,chordae
or catheters,
pacemaker electrodes…
“Think of heart first,
then other organs
(microbes from heart
embolizes to other
places”
MR)
4. Hypertrophic
cardiomyopathy
5. Previous IE
6. Congenital valvular
diseases (cyanotic)
7. Prosthetic heart
valve (high risk)
8. Central venous
catheters
9. IV drug users
10. 50% has no risk
factors
11. Pacemaker
12. ASD, VSD (low risk)
Others are medium risk!
*Mortality
100% die with no
treatment
20-30% die with
antibiotics
can’t close)
5. Cardiac failure(rarely
pericarditis)
6. Abdomen: splenomegaly
due to bacteria activity
increasemakes spleen
enlarge (SEPSIS)
7. Microembolized from
vegetation to:
- kidney (focal GN):
hematuria
- Skin: petecchiae
- Brain: stroke, MI,
pulmonary embolism
(paradoxical embolismto
the brain due to ASD, VSD)
1. Antibiotics
A. Before hemoculture:
combined broaded spectrum:
- Cephalosporins
- Aminoglycosides
- Vancomycin (for staphy =>
Because staphy is resistant to
penicillin!)
B. After hemoculture: targetted
antibioticstherapy
2. Surgery (Done in caseof
antibioticsdoes not work):
prosthetic valvereplacement
(20% die)
3. If prosthetic valve undergo IE
early:100% reoperation
4. If prosthetic valve undergo IE
lately:30% reoperation
- high CRP
- Hematuria
- Bacteremia (due to
sepsis)
2. Hemoculture (specifc
diagnosis)
3x2 during 2x24 hours:
=> Culture minimum 3
times per day
- Never use 1 set of
culture, 2 sets of
cultureneeded
- Culture in 2 days
-Culture 24 hrs before
antibioticstreatment
(broad spectrum)
*Microbiology:
1/ Strepto: 50%
2/ Staphy: 20-25%
3/ Gram (-): 5-10%
Taken:
1. Prior to
intervention (1h)
2. Orally
3. Singlebig dose

3. By Hillary Vo (Vo Thao Duyen)
4/ Fungi: 1%
5/ Culture (-): 10%
3. Echocardiography
(specific)
-Transesophageal echo:
more detailed than
transthoracal.
- Vegetations are visible
after 2 weeks.
AS During systolic period,
obstruction to the
outflow of blood
Pressure gradient
appears between LV
and aorta.
=> LVH because the
heart try to pump
more! => LV dilated =>
LVF (irreversible)
1. RF
2. IE
3. Degenerative valve
destruction
(atherosclerosis)
1. No complaints for a long
period
2. Dyspnoe
3. Angina
4. Syncope
5. Lately LVF
6. Physical symptoms:
auscultation:ejection click,
mid-systolic murmur above
the aorta. =
Crescendo-Decresendo
murmur
=> Radiate to neck/carotid
In caseof SEVERE AS:
Do artificial/ prosthetic valve
implantation
1. Mechanical (Lifelong
anticoagulantswith coumarin)
Target INR: 3-4.5
2. Biological:
Target INR: 2-3 or no
anticoagulantsneeded
NB:
1. ECG: LVH
2. Chest X-ray:
cardiomegaly
3. Look at the sizeof
stenosis and pressure
gradient: normally low, if
gradient appear => AS
Normal value: 5cm2,
<5mmHg
Mild:>1.5cm2, <25
Moderate: 0.7-1.5,
25-50mmHg
Severe: <0.7, >50
Antibiotic
prophylaxis for IE
prevention.
Anticoagulant
therapy (heparin
and warfarin) due
to prosthetic valve
replacement

4. By Hillary Vo (Vo Thao Duyen)
arteries
7. BP: 100/80mmHg
8. Pulsus tardus et parvus
(slowand small)
Coumarin: Stops the growth of
thrombin
Heparin: Reduces the size of
thrombin
4. Angiography +
ventriculography before
surgery
AR Duringdiastolicperiod,
blood regurgitates from
the aorta into the LV
=> LVH in chronic AR
for long
accommodation period.
=> Angina pectoris
AS = AR 1. Auscultation:
Decrescendo diastolic
murmur above the aorta
but on the left sideof
intercostal space(ICS)
2. BP: 180/ 40mmHg
3. Pulsus celer et altus (fast
and high)
4. Complaints: Weakness,
dyspnoe
1. Mechanical prosthetic heart
valvereplacement
2. Pharmaco:
- ACE inhibitors:Captopril
- Nitrates:
=> Lower BP => VD: reduce
preload before surgery
1. ECG: LVH
2. Echocardiography:
Doppler echo for
regurgitation
3. CT Coronarography:
needed only in caseof
IHD
M
S
Duringdiastolicperiod,
obstruction to the BF
between LA and LV
BF back to lung/ pulmo
embolism-> pulmo
pressureincrease:
pulmonary
hypertension -> RVH =>
RF exclusively
=> cause commissural
fusion on mitral valves
=> MS
Physical signs:
1st sound is accentuated on
the apex.
- Mid-diastolic murmur on
the apex
- Opening snap (hardly
open)
Atrial fibrillation:
1. Moderate or severe form:
Catheter balloon dilation or
surgery (commissurotomy or
artificial replacement)
2. In case of atrial fibrillation:
lifelongoral anticoagulation
1. ECG: LAH, RVH
2. Echocardiography
3. Size and pressure
gradient:
Normal value: 4-6cm2,
<2 mmHg

5. By Hillary Vo (Vo Thao Duyen)
peripheral edema
LA can’t hypertrophy =>
become abnormal =>
atrial fibrillation
Tachy/ Brady/ Normocardia 3. In caseof Tachycardia:
beta blocker
4. Diuretics
Mild:>1.5, <5
Moderate: 1-1.5, 5-10
Severe: <1, >10
M
R
During systolic period,
Open of AV valve.
Volume loading to LV
then LA.
Heart try to pump
more => LVH => LV
dilation => no blood
supply to endocardium
=> Angina pectoris =>
LVF => Pulmonary
hypertension => Pulmo
congestion =>
pulmonary edema
1. RF
2. IE
3. Degenerative
disorders
4. Mitral valveprolapse
5. Cardiomegaly (Valves
are okay but increase
the space)
6. MI, or IHD =>Rupture
of papillary muscle
Physical signs:
Holosystolic murmur on the
apex.
Radiates to axilla!
In case of LVF => artificial valve
replacement
1. ECG: LAH, LVH
2. Echo: Doppler echo
3. Coronarography:
necessary in case of
surgery
Antibiotic
prophylaxis before
dental
intervention

6. By Hillary Vo (Vo Thao Duyen)
Angina pectoris Stable Unstable
= NSTEMI
Prinzmetal/
Variant angina= STEMI
Silent ischemia Myocardial infarction
Definition:
Chest pain because of
episodic myocardial
ischemia
= Effort angina = warm
up angina
1. Pain after minor
exertion (short walk or
shaving)
2. Relieved at rest
3. Dangerous in the
morning
4. GERD-induced angina
5. Retrosternal pain
6. Lasts typically 2-5 min
7. If lasts longer than 20
mins
=> CHECK FOR ACS: Acute
coronary syndrome
= Crescendo pattern
1. Pain atrest/ or minor
exertion
2. Then increase
frequency of pain =>
plaquedisruption =>
acute obstruction in
coronary artery
3. Partof ACS
= Vasospasmic angina
1. Coronary artery spasm
due to smooth muscles
constrict => transmural
ischemia
2. Maybe due to VC
(TXA2…)
3. Happen anytime
Obstructive CAD, but
assymptomatic
Acute MI:
Result from acute
obstruction to a coronary
artery from sudden
disruption of atherosclerotic
plaque.
Risk factors:
1. Hypercholestemia
2. DM
3. Smoking
4. Hypertension
Range severity:
1. Unstableangina
2. NSTEMI
3. STEMI
4. SCD: sudden cardiac
death

7. By Hillary Vo (Vo Thao Duyen)
Morphology 1. Thick fibrous cap
2. Blocked by
atherosclerotic plaque
3. 70% stenosis
4. No thrombus
formation
1. Thin fibrous cap
2. Blocked by
atherosclerotic plaque+
thrombus
=> If plaquenot rupture,
keep unstableangina
=> if plaque ruptures,
become MI!
3. 75-80% blocked?
1. May or may not have
atherosclerosis
2. Transmural ischemia
Atherosclerotic present
in elder or in DM
patient
Complete obstruction of
LAD, circumflex artery
ST segment Depression Depression (more)
Or sloping=>
Non-persistent!
Elevation Changes duringactivity Elevation
Symptoms 1. Dyspnoe
2. Fatique, faint
3. Nausea, vomit
4. Sweating
5. Sense of impending
doom: cảm giác có điều
gì chẳng lành sắp xảy ra
6. Pain radiates to
Similar to angina

8. By Hillary Vo (Vo Thao Duyen)
shoulder, left arm, neck,
jaw, back
Physical signs:
1. 3rd and 4th heart sounds
2. Systolic murmur due to
MR (rupture of papillary
muscles)
3. Pulmonary congestion
Treatment 1. Beta blockers:
decrease BP and
contractility
2. Nitroglycerin (contains
nitrates/ isosorbide
dinitrate):Venous and
coronary vasodiation
3. CCB: Nifedipine,
amlodipine
4. Antiplatelet drugs:
clopidogrel: inhibitADP
receptors on platelet
1. Bed rest with ECG
monitoring
2. Same as stableangina
(Must have CCB)
3. PCI or CABG =
PERCUTANEOUS
CORONARY
INTERVENTION or
Coronary artery bypass
surgery/ graft
1. Nitroglycerine
2. CCB
1. Same as stable
angina
2. Lipid loweringstatins
1. Oxygen therapy
2. ECG monitoring
3. General treatment:
- Relieve stress
- Reverse ischemia if
possible(after 20-40 mins ->
irreversible)
4. Aspirin (home
treatment/ emergency): to
slow down the blood clot
to prevent secondary MI

9. By Hillary Vo (Vo Thao Duyen)
=> Best treatment for
angina:
Beta blockers +
nitroglycerins
Q. How to differentiate
between angina and MI?
Give nitroglycerine
sublingually in thefirst2
mins
=> If pain won’t be
relieved => MI
4. After stent, take
aspirin + clopidogrel for
at least1 year
5. Specific treatment
*If we can’t do PCI:
immediate fibrinolysis
(streptokinase) (preferably
<30 min after MI)
*PCI := angiography with
stent through femoral or
transradical access (goal
therapy): preferbly < 60
mins
6. If there are more than 1
blocked artery => do CABG!
Through internal thoracic
artery to coronary artery!

10. By Hillary Vo (Vo Thao Duyen)
7. Morphine
8. Others are sameas stable
+ ACE inhibitors:
antithrombotic (rtPA...)
9. Thrombolytic drugs:
Fibrin specific: tPA
Fibrin non-specific:
streptokinase
*Indication:ST elevation,
LBBB
*Absolute contraindication:

11. By Hillary Vo (Vo Thao Duyen)
Aortic dissection,
intracranial tumor,
pericarditis,previous stroke
Diagnosis 1. ECG (ST)
2. Stress ECG to
distinguish between
stableand unstable
-Negative stress test:
target HR reached
without ECG alteration.
3. Angiography is done
after positivestress test is
confirmed
4. Nuclear cardiology
*Differential diagnosis
1. GI: GERD
2. Other cardiac
disorders:
Pericarditis,mitral valve
prolapse,ventricular
tachycardia
1. ECG
2. Stress ECG:
-Positivestress test: ST
depressed
3. Cardiac markers
Troponin, CK-MB:
negative
(wolf in the sheep’s cloth)
4. Angiography
ECG 1. ECG
-ST elevation to
* 1mm in two or more limb
leads
* >2mm in two or more
precordial leads
- LBBB
- Muscle nerosis: Q wave
enlargement
2. Cardiac markers
-CK-MB peak 24h, decline
2-3 days
- Troponin T,I, LDH: peak
24-48hrs, decline in 7-10
days
- myoglobulin: not specific
for MI

12. By Hillary Vo (Vo Thao Duyen)
No echocardiogram for
ischemia and MI!
3. Coronary catherization
and angiography (invasive
cardiac imaging)
Complication of MI:
Cardiac failure:
 Failureof systolic or diastolicfunctions
 can be in rightor left or both,
 happens duringmajor, minor exerciseor even in rest

13. By Hillary Vo (Vo Thao Duyen)
 Symptoms depends on onset (acute, chronic),causes,localization (left,right)
Etiology Symptoms Treatment Diagnosis
LVF
(Acute LVF = cardiac
asthma)
*Blood/fluid go back
to lung
1. IHD
2. Valvular disorders
3. Primary cardiomyopathies:dilative,
hypertrophic or restrictive
4. Secondary cardiomyopathies:
Hypertension, alcoholic,myocarditis
5. Congenital cardiac disease
6. Cor pulmonale
Main causes of Acute LVF:
1. MI
1. Hypertensive crisis (exceed 150mmHg)
or 180/110mmHg
2 forms: LVF and acute LVF
*LVF:
1. Congestion in the lung(still okay)
2. Shortness of breath
3. Dyspnoe after exercise, even in rest
4. Orthopnoe (feel worse while in
supine position, but feel better when
stand up)
5. Paroxysmal nocturnal dyspnoe
*Acute LVF = Cardiac asthma
Cardiac asthma: is not a type of asthma,
it’s a type of coughing and wheezing that
occurs with left heart failure
1. Pulmonary edema (acute form) due
to severe and acute pulmonary
congestion (Pulmonary hypertension)
1. Non-drug therapy
Salt and water restriction:
to decreaseBP
2. Drug therapy
-Diuretics: decrease fluild buid up
*Furosemide: specific for heart failure
treatment (For hypertension,use thiazidemore)
*Spironolacton:(aldosteroneantagonist)
*triamteren
-Beta blocker: Slower HR and lower BP
-ACE inhibitors:(Captopril) improve
coronary circulation by decreasingBP
and plasma volume
-Nitrates: VD
- Digitalis: stronger, longer muscle
contraction
1. Physical
examination
(according to
the
symptoms)
2. Chest x-ray
3. Echocardio
graphy
4. ECG
5. Lab data
Differential
diagnosis:
1. Pulmo
diseases
2. Obesity
3. Renal or
liver failure
4. Circulatory

14. By Hillary Vo (Vo Thao Duyen)
=> excess fluid in bronchial tree
=> Pink foam from the mouth,
Crackles over the lung
=> V/Q mismatch
=> Hypoxia, cyanosis
“Pinky nằm ngủ”
3. Invasive,surgical interventions
- Artificial heartvalve
- Pacemaker
- Coronary bypass (CABG)
- Cardiac transplant
failure of both
legs
(If just 1 leg
=> not
cardiac
failure!!!
RVF
*Blood/ fluid go back
to body
1. Primarily: from
- chronic lungdisorders (Cor pulmonale)
- MS
- ASD, VSD, pulmonary stenosis
2. Secondary: followed by LVF
1. Peripheral edema: edema of lower
limbs or in sacral region
2. Abdomen: Splenomegaly,
hepatomegaly
3. Ascites (fluid in peritoneal space)
4. Pleural effusion???
5. Kidney: Nocturnal urination
6. Dilated jugular vein
*Usually appear all together*
Same

15. By Hillary Vo (Vo Thao Duyen)
3. If the cause come from pulmonary
embolism(PE)-->
From (PE) => ACUTE RIGHT
VENTRICULAR FAILURE
- Hypotension (Due to decreased SV
=> decreased CO => decreased BP)
- Hypoxia
- Cyanosis
- Tachycardia
- Severe chest pain
- In acute cor pulmonale:COPD --> RVF
--> eventually lead to LVF
From PE: