Cardiovascular diseases

IHD
1- Stable angina.
2- Unstable angina.
3- Prinzmetal's angina.
4- Myocardial Infarction.
5- Heart Failure.
MI
Acute complications:
1- Heart failure.
2- Arrhythmia.
3- Pericarditis.
4- Hypotension.
5- Valvular heart disease (papillary muscle, ventricular septum).
Chronic complications:
- Ventricular aneurysm:
 ST elevation > 6 weeks after MI:
Differential: 1- re infarction 2- developed ventricular aneurysm.
- Dressler's syndrome:
o muscle necrosis  antigen antibody reaction  autoimmune disease.
o shoulder joint pain , serositis.
o ttt: steroid.
Suspected ventricular aneurysm:
1- ECG > 6 weeks ST elevation.
2- Thromboembolism manifestation ( blood stagnant).
3- Recurrent HF not responding to medication.
History:
You should include in HPI:
* 1-DM.
2- HTN.
3- Hyperlipidemia.
4- Smoking.
5- Family history of IHD.
* Chest pain duration > 30 minutes.
Examination:
1- Vitals:
Blood Pressure: high Blood Pressure in HTN, MI may cause low BP.
Pulse: Arrhythmia.
Temp.: sometimes increase in MI.
2- Look for:
* Heart failure evidence:
Increase JVP, 3RD heart sound, basal lung crepitations, ascites,
hepatomegaly, lower limb edema.
* Valvular heart disease evidence: valve incompetence, VSD…etc.
* Pericardial rub on auscultation.
3- Look for underlying disease:
- DM complications.
- Atherosclerosis.
Investigations:
1-ECG:
*- type of MI: anterior, posterior, inferior …etc.
*- pericarditis.
*- arrhythmias: AF, ventricular ectopic, ventricular tachycardia, LBBB, RBBB,
2nd degree heart block, complete heart block.
*- evidence of previous ischemia  if pt. has previous MI, the new ECG
changes will NOT show  then do Cardiac Enzymes.
2- Cardiac enzymes: to be raised
time of each enzyme is important & common question in exams
 troponine  immediate 30 minutes- 1 hour (earliest to rise + more
sensitive).
 CPK  4 hours + CPK-MB ratio.
 LDH  72 hours.
3-chest x-ray  cardiomegaly, HF: pulmonary edema, pleural effusion.
4- Blood sugar.
5- Lipid profile.
6- PT, PTT (base line).
7- Urea & electrolytes: baseline ttt. or complication.
8- CBC: leukocytosis.
Treatment:
Typical history of retrosternal chest pain.
1- Chewable aspirin before investigation, will not kill pt. & will benefit + O2.
2- Relief pain: morphine & antiemetic.
3- & start tridine infusion to relief pain, vasodilation.
4- antithrombolytic therapy if no contraindication.
After stabilized:
Before discharge:
1- Echocardiogram for: (why do we do echo?)
* Valvular heart disease.
* Ejection fraction abnormality < 50  low.
It should be around 50  normal.
* Wall motion abnormality  hypokinesia:
Heart not contract at site of infarction, generalized in cardiomyopathy.
2- (Before not nowadays) submaximal stress ECG.
This is to do exercise for 10 minute= submaximal (maximal test is 30
minutes) to see if complications develop: 1- arrhythmia
2-hypotension
This was done before to decide if argent angiogram will done or delayed 4-5
weeks.
But now all patients i.e. MI. should have angiogram angioplasty dilation or
bypass surgery…. The earlier, the better the prognosis.
Role of thrombolytic therapy & angiogram:
If the time from ER door to angiogram more than 90 minutes, don't waste
time give thromolytic therapy.
If the time within 90 minutes immediately for angiogram.
Home medication:
2ry prevention of MI  4 medication
1- Aspirin
2- B-blocker.
3- ACE Inhibitors.
4- Statin.
+/- lasix.
Management of MI (briefly for 5th year):
1- Admit patient to the ICU & give O2  oxy-bed rest.
2- Prescribe painkillers.
3- Thrombolytic therapy  streptokinase  resolve the thrombus
4- angiogram & angioplasty (if possible, in good centers, & good
primary care units)
5- discharge on:
4 medications:
1- Aspirin.
2- B-blocker.
3- ACE Inhibtors.
4- Statin.
+/- Lasix.

Cardiovascular
diseases
IHD
1- Stable angina.
2- Unstable angina.
3- Prinzmetal's angina.
4- Myocardial Infarction.
5- Heart Failure.
MI
Acute complications:
1- Heart failure.
2- Arrhythmia.
3- Pericarditis.
4- Hypotension.
5- Valvular heart disease (papillary muscle, ventricular septum).
Chronic complications:
- Ventricular aneurysm:
 ST elevation > 6 weeks after MI:
Differential: 1- re infarction 2- developed ventricular aneurysm.
- Dressler's syndrome:
o muscle necrosis  antigen antibody reaction  autoimmune disease.
o shoulder joint pain , serositis.
o ttt: steroid.
Suspected ventricular aneurysm:
1- ECG > 6 weeks ST elevation.
2- Thromboembolism manifestation ( blood stagnant).
3- Recurrent HF not responding to medication.
History:
You should include in HPI:
* 1-DM.
2- HTN.
3- Hyperlipidemia.
4- Smoking.
5- Family history of IHD.
* Chest pain duration > 30 minutes.
Examination:
1- Vitals:
Blood Pressure: high Blood Pressure in HTN, MI may cause low BP.
Pulse: Arrhythmia.
Temp.: sometimes increase in MI.
2- Look for:
* Heart failure evidence:
Increase JVP, 3RD heart sound, basal lung crepitations, ascites,
hepatomegaly, lower limb edema.
* Valvular heart disease evidence: valve incompetence, VSD…etc.
* Pericardial rub on auscultation.
3- Look for underlying disease:
- DM complications.
- Atherosclerosis.
Investigations:
1-ECG:
*- type of MI: anterior, posterior, inferior …etc.
*- pericarditis.
*- arrhythmias: AF, ventricular ectopic, ventricular tachycardia, LBBB, RBBB,
2nd degree heart block, complete heart block.
*- evidence of previous ischemia  if pt. has previous MI, the new ECG
changes will NOT show  then do Cardiac Enzymes.
2- Cardiac enzymes: to be raised
time of each enzyme is important & common question in exams
 troponine  immediate 30 minutes- 1 hour (earliest to rise + more
sensitive).
 CPK  4 hours + CPK-MB ratio.
 LDH  72 hours.
3-chest x-ray  cardiomegaly, HF: pulmonary edema, pleural effusion.
4- Blood sugar.
5- Lipid profile.
6- PT, PTT (base line).
7- Urea & electrolytes: baseline ttt. or complication.
8- CBC: leukocytosis.
Treatment:
Typical history of retrosternal chest pain.
1- Chewable aspirin before investigation, will not kill pt. & will benefit + O2.
2- Relief pain: morphine & antiemetic.
3- & start tridine infusion to relief pain, vasodilation.
4- antithrombolytic therapy if no contraindication.
After stabilized:
Before discharge:
1- Echocardiogram for: (why do we do echo?)
* Valvular heart disease.
* Ejection fraction abnormality < 50  low.
It should be around 50  normal.
* Wall motion abnormality  hypokinesia:
Heart not contract at site of infarction, generalized in cardiomyopathy.
2- (Before not nowadays) submaximal stress ECG.
This is to do exercise for 10 minute= submaximal (maximal test is 30
minutes) to see if complications develop: 1- arrhythmia
2-hypotension
This was done before to decide if argent angiogram will done or delayed 4-5
weeks.
But now all patients i.e. MI. should have angiogram angioplasty dilation or
bypass surgery…. The earlier, the better the prognosis.
Role of thrombolytic therapy & angiogram:
If the time from ER door to angiogram more than 90 minutes, don't waste
time give thromolytic therapy.
If the time within 90 minutes immediately for angiogram.
Home medication:
2ry prevention of MI  4 medication
1- Aspirin
2- B-blocker.
3- ACE Inhibitors.
4- Statin.
+/- lasix.
Management of MI (briefly for 5th year):
1- Admit patient to the ICU & give O2  oxy-bed rest.
2- Prescribe painkillers.
3- Thrombolytic therapy  streptokinase  resolve the thrombus
4- angiogram & angioplasty (if possible, in good centers, & good
primary care units)
5- discharge on:
4 medications:
1- Aspirin.
2- B-blocker.
3- ACE Inhibtors.
4- Statin.
+/- Lasix.
Stable Angina
ER.
Same History, Examination, Investigation of MI.
If NO MI.
Sublingual nitroglycerin & 4 drugs:
1- Aspirin.
2- B-blocker.
3- ACE Inhibitors.
4- Statin.
 Send home
1- Typical angina: have 3 things :
a- Site.
b- Nature.
c- Increased by exertion and decreased by rest.
2- Atypical angina: have got two out three.
3- Non-Anginal chest pain: just one thing.
Unstable angina
- Same History, Examination, Investigation of MI.
- Heart enzymes not rise & evidence of ST segment depression ischemia on
ECG.
TREATMENT:
Tridile infusion & heparin infusion.
Start by:
1- Aspirin.
2- B-blocker.
3- ACE Inhibitors.
4- Statin.
If the pain does not improve  a cardiologist orders an urgent angiogram.
Angioplasty& pain control.
Prinzmetal's angina
Same History, Examination, Investigation of MI.
1- ST elevation.
2- Normal cardiac enzymes.
- No risk factors of MI, no DM, no HTN.
ttt: put on calcium channel blocker.
**BUT** IT SHOULD BE TRATED AS ANGINA unless proven otherwise.
ECG no change  Q wave  for 6 hrs  for 24 hrs, then every day.
Cardiac enzyme no rise, Q6 hrs.
Until angiogram shows normal coronary.
ECG differences:
[1] Angina:
ST depression
Cardiac Enzymes Normal
[2] Unstable angina:
T-wave changes
Cardiac Enzymes Normal
[3] Prinzmetal's angina:
ST elevation due to spasm
Cardiac Enzymes Normal
[4] MI:
ST elevation
Cardiac Enzymes elevated
MKSforum.net -14-
Heart Failure (HF)
Dr. Nabeel
Eight Causes are preferable to be Heard by any Students when Dr. Nabeel
Al-a3ma asks about the causes of HF?
1- Ischemic Heart disease (IHD) which is the commonest.
2- HTN or Hypertensive Heart disease with end Organ damage.
3- Valvular Heart disease…and the commonest cause is Rheumatic heart
disease.
4- Cardiomyopathy.
5- Congenital heart disease.
6- Core-pulmonale.
7- Constrictive pericarditis.
8- Heart failure with high cardiac Output... Like in Thyrotoxicosis,
anemia….
Also He loves to ask this Question:
Patient is known having HF... What are the causes that push him to a failure
and to the ER… i.e.: what are the precipitating factors for HF?
1- Infection (pneumonia).
2- P.embolism esp. if he's bedridden.
3- Ongoing Ischemic heart disease…MI.
4- No compliance with medications.
5- Arrhythmia.
6- Taking NSAID. Which cause salt and water retention.
7- Taking ca channel blocker…Negative inotropic agent.
8- High salt intake.
9- Uncontrolled HTN.
10- Hyperdynamic circulation.. Like in anemia... Thyrotoxicosis.
History in ER:
No History suggestive of IHD.
Known case of HF.
No History of palpitation.
Pt was compliant to his medications.
No change in diet.
That is important to mention in History,
لكن الكلام يصاغ حسب الحالة و المسبب
Examination:
Same of MI.
Look for evidence of – heart failure - arrhythmia - infection -underlying
cause.
Investigation: like MI
Same Q with Dr. Maimoona, but she only mentioned these:
This way, the pt got acute HF...
1- IHD.
2- Hyperdynamic circulation  anemia, Thyrotoxicosis.
3- Valvular heart disease.
4- HTN.
5- Arrhythmias.
6- Increased salt intake.
7- No compliance to drugs.
Management:
On admission:
1- Start loop diuretic fursemide 40 mg TID.
2- Start spironolactone 25 mg  take 3 days to work
in HF, nephrotic $, liver failure  low kidney perfusion  activate renineangiotensin
system.
Spironolactone will block it so no Na/H2O retention & not used as K sparing.
+ 4 drugs:
(1) Aspirin.
(2) B-blocker.
(3) ACEI.
(4) Statin.
Note: moderate/sever HF do not give B-blocker.
If echo show ejection fraction below 25% you have to give anticoagulant.
Restrictive Cardiomyopathy
Infiltration of myocardium: TB, hemochromatosis, amyloidosis.
ttt: treat underlying cause.
Hypertrophic Cardiomyopathy
ttt: B-blocker & - Amiodarone.
Dilated Cardiomyopathy
As heart failure.
- Diuretic
4 drugs:
1- Aspirin.
2- B-blocker.
3- ACEI.
4- Statin.
- anticoagulants
Causes:
1- Ischemic.
2- Alcoholic.
3- Thiamin deficiency.

Rheumatic Heart Disease
RHD
Session with Dr. Maimoona
2006
(1) Major:
- Carditis
- Arthritis
- Erythema marginatum
- Chorea
- Subcutaneous nodules
(2) minor:
 History of tonsillitis
 Fever
 Raised C-reactive protein
 Raised ESR
 Arthralgia
* ask about: rheumatism, recurrent tonsillitis, IV Penicillin monthly, long bed
rest …
[1] Carditis: if all 3 layers are involved  Heart Failure
 Tachycardia
[2] Chorea: Sydenham’s chorea (abnormal movement)
[3] Arthritis: fleeting arthritis: redness, hotness  improvement
But before cure  involvement of another joint
[4] Erythema marginatum: rash w/ very clear margins
Investigations:
- CBC  show leukocytosis
- Streptococcal antibody tests
- blood culture & throat culture looking for group A streptococcal
infection
- ESR & C-reactive protein  high
- ECG  PR interval prolongation
- Echocardiography  establishing cordites
- Synovial fluid analysis elevated white blood cell count with no crystals or
organisms
- X-ray  cardiomegaly or evidence of heart failure
- X-ray of joints only when there is mono joint involvement []
Complications of rheumatic fever:
1- Valvular Heart Disease: 
(1) Mitral  (2) Aortic  (3) Tricuspid  (4) Pulmonary
 Infective endocarditis  most important
Infective endocarditis  multisystem disease
Renal failure, heart failure, jaundice, brain involvement
(Multiorgan failure)
2- Heart failure
3- Arrhythmias
4- Thromboembolic manifestations
Treatment
- Bed rest
- High dose aspirin. The nonsteroidal anti-inflammatory drug (NSAID)
naproxen has also been studied. It is effective and may be easier to use than
aspirin.
- Penicillin  then long term to patient with persistent cardiac damage
- Heart failure may require digitalis
- Haloperidol may be helpful in controlling chorea.
Hypertension (HTN)
Session with Dr. Maimoona
1424 H
95%  essential HTN
5% 
R: Renal:
- Polycystic Kidney Disease
- CRF
- GlumeruloNephritis
- Renal Artery Stenosis
- Renal Cell Carcinoma
E: Endocrine:
- Cushing's
- Pheochromocytoma
- Acromegaly
- Thyrotoxicosis
- Conn's
- Carcinoid tumor
- Hyperparathyroidism
- Primary hypothyroidism
- Congenital adrenal hyperplasia
C:
- Corticosteroids
- Contraceptive pills
- Clonidine withdrawal
- Coarctation of aorta
A:
- Arteritis (eg. Takaiaso)
- Alcohol
P:
- Pregnancy
- Polycythemia rubra vera (PRV)
D: Drugs:
- NSAIDs
- Sympathomimitics
* Refractory "Resistant" HTN: 
3 anti-HTN medications with maximum dose. One of them is Diuretic for 3
months
Examination:
• Inspection:
- Acromegaly
- Cushing
- Thyroid
• Palpations:
- Renal "for polycystic"
- Radio femoral artery "Coarctation"
مھم
• auscultation:
Renal bruit for tumor, renal aneurysm
• Then look for an end organ damage
• Heart "apex beat"
• Eye for papilloedema
Investigations: in all patients with HTN
(1) U & E:
 К+
- Conn's
- Pheochromocytoma
- Cushing
 К+  CRF
(2) Blood glucose  hyperglycemia  DM
(3) Urinalysis (Active sediments):
- RBC cast
- Haematuria
- Proteinuria
(4) Lipid profile  atherosclerosis
(5) CXR
- Cardiomegaly
- Coarctation of aorta
(6) ECG  Left ventricular hypertrophy
(7) Echo  Left ventricular hypertrophy
------------------
Serum urea & Creatinine: RF
Serum uric acid before ttt with diuretics:
If the patient has hyperuricemia  diuretic therapy is contraindicated
Cushing:
Overnight suppression test
Or
24 hrs urine cortisone
If you're suspecting it's secondary to a Connective Tissue disease 
screening must be made.
Main diagnosis for renal artery stenosis:
(The most common cause of HTN in young patient)
1- Doppler US
2- INP = delayed uptake
3- Captopril renogram
4- Angiogram
Pheochromocytoma:  Investigation:
 Chatecholamines either in urine or blood
CT for the abdomen  localize the tumor
If not localized, do adrenal venous sampling to localize
GENE
RAL
Vasodilators
Β-blocker
diuretic
Treatment: step one management
- IHD: ACE inhibitor &/or B-Blocker
- DM: Diltiazam – verapamil
Never use Dihydro__?_____ in HTN & DM patient, because they worsen
proteinuria:
- Amlodipin
- Nifidipin
HTN Emergency:
HTN + Brain Hemorrhage  don't lower the Blood Pressure rapidly
HTN + HF  lower the Blood Pressure
 ناقص
 α-methyl dopa  poor or pregnant
ACE inhibitors
Β-blockers
Hydralazine
 Thiazide
Atrial fibrillation (AF)
Definition: It's totally chaotic atrial activity caused by simultaneous
discharge of multi atria foci.
Causes:
A- Cardiovascular :
1- HTN.
2- IHD (including acute MI).
3- Valvular heart disease esp. Rheumatic "Ms, MR, AS, AR".
4- VSD.
5- Cardiac surgery.
6- Inflammatory heart disease "pericarditis, myocarditis".
7- Cardiomyopathy.
8- Left atrial myxoma.
9- Sick sinus syndrome "tachy-Brady syndrome".
10- WPW syndrome (wolf Parkinson white).
B- Endocrinological causes:
1- Thyrotoxicosis.
2- Pheochromocytoma.
C- Pulmonary causes:
1- P.E.
2- Pneumonia.
3- COPD
4- Co poising.
5- Ca of the Bronchus.
D- Drugs:
1- Acute or chronic alcohol.
2- Theophylline toxicity.
E - Idiopathic:
Lone AF in which no cardiac cause can be identified, no DM, no HTN and no
CAD.
Symptoms of AF:
1- Asymptomatic.
2- Symptoms vary from Palpitation and SOB and aggravating of HF.
3- Embolization symptoms.
Investigation:
1- Thyroid function test.
2- ECG  absence P wave + Irregular R-R interval more than 100.
3- U and E  if hypo K  don’t give digoxin because it will lead also to
arrhythmias.
4- PT and PTT.
5- Cardiac enzymes.
6- CXR  p. edema.
7- Echo  so in here we're doing:
A- Assess etiology and recurrence of:
1- Cardiac chamber size and function  i.e.: left atrium.
2- Valvular function.
3- The pericardium.
4- The myocardium.
B- Identification of patient at high risk of thromboembolism
complication of AF.
Management of AF:
1- Treat the cause.
2- How to Control Ventricular rate ( VR)?
3- How to convert to sinus rhythm?
4- How to maintain sinus rhythm?
5- When and How to use anticoagulant and antiplatlets?
Types of AF:
1- Isolated one “single".
2- Paroxysmal  don't give digoxin.
3- Sustained one  chronic.
So the Management:
If the Patient is not stable  Do DC cardioversion.
If stable follow that previously mentioned points.
So,
1- Treat the cause.
2- Control Ventricular rate By A-V node blocking Drugs:
A- Digoxin:
- Loading dose: 0.25 - 0.5 mg/30mints IV.
- Maintenance: 0.125 - 0.25 mg/6h.
- Contraindication of Digoxin:
1- HOCM.
2- WPW so in here use procainamide.
3- Narrow QRS  atrial tachycardia.
- Digoxin dose: in Normal Patient: 0.25 mg, and in renal disease: 0.06 -
0.125 mg.
B- B-Blocker:
Usually given with Ca channel blocker  because more rapid control. But
digoxin is more preferable in the setting of LVF or HF.
So, propranolol 0.5 mg IV  followed by IV bolus 1 mg every 5 mints till
…???
The contraindication of B-blocker is:
Asthma, Dm and HF.
C- Ca Channel blocker:
Verampil 5 – 10 mg bolus / 10 mints.
If you want to give verampil + digoxin  decrease digoxin dose.
3- Convert to Sinus Rhythm:
Indicated when VR is more than 140 B/m.
The drugs used in here:
- Class 1a: Quinidine - procainamide.
- Class 1c: Flecainide - propafenone
- Class 3: Amiodarone
So the preparation:
1- Start Quinidine at least 24 h before to help maintain NSR once it's
achieved.
2- Hold Digoxin and check its serum level.
3- Anticoagulant  3 weeks before and after if there's thrombus shown
in echo.
Indications for anticoagulation: Clinically and ECG:
Clinically:
1- Previous MI or Stroke.
2- HTM +/- Dm.
3- Previous MI.
4- Thyrotoxicosis  in here, decrease the Warfarin dose because of
increased clearance of vitamin K in Hyperthyroidism.
EchoCardioGraphically:
1- Large Left atrium or Left atrium dysfunction.
2- Large Left Ventricle.
3- Left Ventricle aneurysm.
4- Intracardiac Thrombus.
Complications of cardioversion:
1- Ventricular fibrillation.
2- Thromboembolism.
3- MI damage due to the Current.
4- Erythema on the chest wall.
Risk of Systemic Embolization with AF is divided to:
- High: when Mitral valve disease seen: previous Mi or stroke.
- Intermediate: age more than 65 or RF.
- Low risk: age less than 65.
4- Maintenance of sinus rhythm is better with:
1- Left atrium less than 60 mm.
2- Absence of mitral valve dis.
3- Short AF.
4- Conversion with drug only.
Please see the classes of anti-arrhythmic drugs.

Respiratory
diseases
Management of asthma in ER
HISTORY:  mainly history of the etiology of the disease.
[1] Drugs
1. B-blockers
o Propranolol
o Atenolol
o metoprolol
2. NSAID
o ASPIRIN (acetylsalicylic acid)
o VOLTARINNE (DICLOFENAc)
[2] CHEST INFECTION
[3] Irritants  animals + dust + fumes + house dust mite
[4] Newly changed furniture + painting
[5] Exercise
[6] Occupation
EXAMINATION:
1- Vital signs
a- Pulse  tachycardia, arrhythmias
b- Blood pressure, palsus paradoxes
c- Tachypnea
d- Temperature  increase  infection
2- General examination
a- Tremor
b- Cyanosis
c- Accessory muscles
3- Signs of Pneumothorax  You fail if you don't mention
them!!
4- Severity of asthma
(1) Signs of infection
(2) Signs of status asthmaticus
1- Silent chest
2- Drowsiness
3- Cyanosis
4- Tachycardia > 120
5- Pulsus paradoxus
INVESTIGATIONS: {FOR ALL ASTHMATICS}
1- CBC  LEUCKOCYTOSIS + EOSONEPHILIA
2- ABG
3- U+E
a- Hyperventilation  dehydration
b- β2-agonist
c- Theophyllin
d- Sputum + steroid
4-CXR  INFECTION, PNEUMOTHOARX
5-ECG  ARRHYTHMIA + hypertrophy
6-Pulmonary function test
7-Peak flow meter  drop inonter base ……
8-Sputum culture
9-Positive skin
Note:
Mg, Ca, and Ph are not part of U-E
MANAGEMENT:
1- Bed rest
2- Oxygen according to blood gases 
(1) DecreaseO2+decrease CO2
(2) DecreaseO2+normal CO2
(3) DecreaseO2+IncreaseCO2
3- I.V FLUID
4- KCL  DECREASE K
5- Pharmacological medications
(1) Bronchodilator
a- B2 agonist
b- Nabulizar
c- Salbutamol - terbutaline  SlE: TACHYCARDIA
FOR 24hours / hourly
d- Anti-cholenergic drugs
Ventolin/atrovent
Ibratropum promide
Decrease mucus secretion
f- I.V Theophyllin "narrow therapeutic index"  bronchodilator
increases contractility and diaphragm
{A} IF PATIENT RECEIVES ORAL THIOPHYLIN AT HOME
MANTINANCE DOSE SHOULD BE STARTED IMMEDIATILY
{B} IF PATIENT DOES NOT TAKE THIOPHYLIN AT HOME
BOLUES 5-6 Mg/kg/30 min
Maintenance 0.2-0.6 mg/kg/hour
IF AFTER 4 HOURS THE PATIENT DOES NOT IMPROVE 
MECHANICAL VENTILATION
(2) +/- Antibiotics:
If there are sought of infection mainly  H.influenza + streptococci
We USE AMPICILLIN  G (positive) OR G (negative)
(3) Anti inflammatory
Hydrocortisone  100-200mg/4hours for 24 hours (IV)
Then prednisone  60mg/orally daily for 2 weeks
Discharge on B-agonist in halor +steroid inhalor
Present to the CLINIC History: exercise tolerance decrease and change
color of sputum
Investigation  PEAK Flow meter
COPD
The management of COPD is the same as that of bronchial asthma
EXCEPT the concentration of O2 to be delivered to the patient.
In patient with COPD  chronic hypercapnia  chronic stimulation of
respiratory center, so, when you admit the patient you must increase
the conc. Of O2
YOU should wash out the remnant of hypoxemia which stimulates the
drive for ventilation  worsening hypercapnia
Note:
A PATIENT WITH HYPERCAPNIA CHRONIC  COPD SHULD RECEIVE LOW
CONCENTRATION OF O2 (24-28%) THEN ADJUST ACCORDING TO "ABG"
ASTHMA  NO CHRONIC HYPERCAPNIA  SAFE TO GIVE INCREASE
CONCONCENTRATION OF O2 (60%)
SIGNS OF SEVERE ASTHMA "STATUES ASTHMATUCUS"
1- Patients are unable to speak (cannot give history), inability to complete
sentences
2- Silent chest
3- Pulses paradoxus
4- Tachycardia
5- Pulse>120
6- Use of accessory muscles of respiratory
7- R.R >33
8- Drowsiness - exhaustion
9- Cyanosis
COMPLICATION:
1- DEHYDRATION
2- EXHAUSTION
3- PNUMOTHORAX
4- RESPIRATORY FAILUER
Respiratory failure
** Influence on respiratory center
Hypercapnia = P CO2 > 6 kPa = > ~ 5 mmHg
Stimulation Depression
(1) Voluntary → over breathing.
(2) Upper brainstem lesion.
(3) Input from receptors (pain,
muscles, and joints,
pulmonary).
(4) Pyrexia.
(5) ↑ PaCO2
(6) ↓ Pa O2
(7) ↑ Arterial H+ concentration.
(1) Voluntary → hold breathing
(2) Brainstem lesion.
(3) Hyperthermia
(4) Sedative Drugs
opiates Benzodiazepin
(1) Hypoventilation = Depression in Respiratory center in medulla
(2) Ventilation- perfusion mismatching = COPD
Acute
Chronic
PaO2 ↓
Pa CO2 ↑
HCO3 ↔
PaO2 ↓
PaCO2 ↑
HCO3 ↑
** Respiratory Failure: A disorder of the lungs where the lungs don’t
function accordingly to match the metabolic requirements.
Type 1 (hypoxia & hypo or normal CO2)
Type 2 (hypoxia & hypercapnia)
***Asthma (severe) **Emphysema
PE Lung fibrosis
P. edema R → L shunt
ARDS Anemia
Pneumothorax
Pneumonia
Acute Chronic
Pa O2 ↓↓
Pa CO2 ↓ or ↔
HCO3 ↔
Pa O2 ↓
Pa CO2 ↔
HCO3 ↔
 Severe acute asthma (life threatening) * COPD
 Respiratory muscle paralysis * Chest wall ds
(Kyphoscoliosis) + fractured rib + intercostals ms tear.
 Brainstem lesion = CNS depression * Ankylosing Spondylitis
(Narcotic drugs)
Other Causes of Type 1 Failure:
 Extrinsic allergic alveolitis.
 Interstitial fibrosing alveolitis.
Other Causes of Type 2 Failure:
 Neuromuscular disease ( gullain barre syndrome )
 Pulmonary Embolism
 Inhaled foreign body
 Pneumothorax
 Retention of secretion
☺ Refer to the Oxford hand book of Medicine
Complication of type 2 Respiratory Failure:
 Cardiac Arrythmias.
 GIT hemorrhage
 Pneumothorax
 Bronchial Obstruction.
 LVF
 Pulmonary Embolism
 Convulsion.
Management of Type 1 Respiratory Failure:
 High flow O2
 Maintain adequate O2 and O2 Saturation > 90 %
 Mechanical ventilation
 Avoid O2 toxicity PO2 > 55 mmHg
 Control underlying problem (pneumonia, infection, sepsis, pancreatitis)
☻YOU should know the indication for CAOT
(chronic ambulatory oxygen therapy)
Management of Type 2 Respiratory Failure:
(1) Oxygen supply ( venture mask )
Start with 1 liter/min = 24%
2 liter/min = 28%
3 liter/min = 35%
4 liter/min = 40%
5 liter/min = 50%
** then titrate the requirement according to ABG
** Provide O2 to keep the O2 saturation >90% but < 93% without
inducing marked hypercapnia
*****************
(2) Treat underlying causes:
*Antibiotic in case of infection/pneumonia
*Bronchodilator in case of COPD/ Asthma
*Anticholenergic in case of COPD/Asthma
*Corticosteroid in case of severe bronchospasm
*****************
(3) Theophyllin ( improve muscle contraction
* Diuretics LVF
* Chest physiotherapy
* Hydration & mucolytic (Danse)
******************
(4) Mechanical Ventilation
• Failure to provide adequate oxygenation without marked hypercapnia.
• Decrease level of conconcentaration
• Failure of Respiratory stimulant.