CVS

PULSE
Pulse abnormality Description Causes

Relative bradycardia PR doesn’t increase in proportion to Typhoid,legionella,brucella,viral

(Faget sign) body temperature Drug induced,factitous,
fraudulent,pel Ebstein

Pulsus bigeminy Every alternate pulse is due to Digoxin

premature ventricular ectopic

Pulsus alternans Regular alteration in pulse amplitude LV (systolic) failure

Parvus et tardus Low amplitude late peak Aortic stenosis

Pulsus Bisferiens Two peaks in systole Aortic regurgitation

Pulsus paradoxus More inspiratory fall in pulse COPD,Asthma,Hypovolumia,SVC

amplitude and SBP obstruction,Pregnancy
Tamponade,CP,RCMP

JVP

Wave Mechanism Phase abnormalities

A Atrial contraction Late diastole Absent a= AF

Large a = TS
Cannon a = AV block, PSVT,
Junctional rhythm

C Tricuspid valve bulge into RA Isovolumetric contraction Large c = TR

X Tricuspid valve pulled downward Ejection phase Absent x= TR

by RV shortening
2 LIVE RAPID REVISION

V Venous filling of RA Late systole and isovolumetric Absent v= SVC obstruction

relaxation Large V = TR

Y RA blood moving passively into Passive filling phase Rapid Y = TR

RV Absent Y= tamponade

Kussmaul sign= JVP increases on inspiration

Causes- restrictive CMP, constrictive pericarditis

Heart Sounds

Heart sound Abnormality Causes

S1 Soft LVF, RVF, Bradycardia, AS, PS, AR, PR, MR, TR

Loud Tachycardia, MS, TS

Ejection click + AS, PS

Non ejection click + MVP

S2 Wide variable split Early A2- MR, VSD, WPW syndrome

Late P2- PS, RVF, RBBB

Reverse split Late A2- AS, LVF, LBBB

Wide fixed split ASD

Opening snap + MS, TS

Tumor plop + Atrial myxoma

Pericardial knock + Pericardial knock

S3 + High CO states
Ventricular systolic failure

S4 + Stiff ventricles
 CVS 3

Murmurs

Name Diagram Causes

Ejection systolic AS, PS

High CO

Pan systolic VSD

Chronic MR, TR

Early systolic Small muscular VSD

Acute MR, TR

Late systolic MVP

Early diastolic AR
PR

Mid diastolic MS
TS

Continuous AV fistula, PDA

Severe arterial stenosis

Factors affecting murmur intensity

If blood flow increases – all murmurs increase except MVP and HOCM(these will decrease)
If blood flow decreases- all murmurs decrease except MVP and HOCM(these will increase)

Maneuver Blood flow Murmur change

Inspiration Increases on right side of heart TS,TR,PS,PR increases

Decreases on left side of heart MS,MR,AS,AR decreases
MVP,HOCM increases

Expiration Increases on left side of heart MS,MR,AS,AR increases

MVP,HOCM decreases
Decreases on right side of heart TS,TR,PS,PR decreases

Valsalva maneuver Decreases overall to right followed by All murmur decreases

left side also MVP and HOCM increases
4 LIVE RAPID REVISION

Standing Decreases overall to both right and left All murmur decreases
side of heart MVP and HOCM increases

Squatting Immediate effect- increased blood All murmur increases

return into both side of heart MVP and HOCM decreases

Supine with passive leg raising Increased blood return into both side All murmur increases
of the heart MVP and HOCM decreases

Acute rheumatic fever (JONES criteria)

Major criteria Low prevalence area High prevalence area

Joint Polyarthritis Polyarthritis or monoarthritis or

MC major criteria polyarthralgia

Carditis(pan carditis) Mc valvular lesion- MR same

MCC death

Sydenham chorea Late manifestation same

SC nodules On extensor surface Same

Erythema marginatum On trunk and extremity Same

Minor criteria Low prevalence High prevalence

Arthralgia Polyarthralgia Monoarthralgia

Fever >38.5 C >38 C

ESR >60 >30

CRP High High

PR interval Prolonged prolonged

 CVS 5

Prophylaxis

Valvular Heart Disease

Valvular Cause Symptoms Murmur

lesion

MS RHD Dyspnea Mid diastolic at mitral area

Hemoptysis

TS RHD Swelling Mid diastolic at tricuspid area

MR RHD Palpitations Pansystolic at mitral area

TR RV dilatation Swelling Pansystolic at tricuspid area

MC CV lesion in carcinoid

AS Calcification Angina Ejection systolic at aortic area

Syncope

PS Congenital Swelling Ejection systolic at pulmonary area

AR Degeneration Palpitations Early diastolic at ERB’s area

PR Pulmonary Hypertension Swelling Early diastolic at pulmonary area

6 LIVE RAPID REVISION

Treatment-
Severe symptomatic (NYHA ≥ II) =

 Surgery

(Severe MS= Valve area < 1.5 cm2

Severe AS= Valve area < 1.0 cm2
Severe MR/AR= Regurgitant blood volume > 60 ml/beat)

Severe asymptomatic = Surgery if

 AF in MS
 AF or EF <60% in MR
 EF<50% in AS/AR

Infective Endocarditis
 CVS 7

IV drug abuse-
• MCC overall – staph aureus
• MCC on right side- Staph aureus
• MCC on left side- Enterococci

DUKE’s criteria
Major Minor

• evidence of micro-organism causing IE • predisposing factors

• Endocarditis evedence on ECHO or CT • Fever > 38 F
• Vegetations seen during surgery • Immune phenomena
• vascular events
• Culture/serology + but not satisfying major criteria
• FDG PET scan +
• Clinically: new regurgitant murmur

Definitive diagnosis = 2 major or 1 major + 3 minor or 5 minor

Treatment

Organism Drug(s)

Streptococcus Penicillin G + Gentamicin (6 weeks)

Enterococci Penicillin G + Gentamicin (4-6 weeks)

MS SA-Native valve Nafcillin, oxacillin or flucloxacillin (4-6 weeks)

MR SA- Native valve Vancomycin (4-6 weeks)

MS SA – prosthetic valve Nafcillin, oxacillin or flucloxacillin (6-8 weeks)+

Gentamicin (2 weeks) + rifampicin (6-8 weeks)

MR SA- prosthetic valve Vancomycin (6-8 weeks)+ Gentamicin (2 weeks)

+ rifampicin (6-8 weeks)

HAECK group Ceftriaxone (4 weeks)

Coxiella Burnetii Doxycycline + hydroxychloroquine (18 months for native

valve and 24 months for prosthetic valve)

Cardiomyopathy

Parameters Dilated Cardiomyopathy Restrictive Hypertrophic obstructive

cardiomyopathy CMP

Pathology Decreased systolic Decreased diastolic Increased systolic functions

functions functions

Symptoms Dyspnea Swelling Angina

MCC of sudden cardiac
death in adults
8 LIVE RAPID REVISION

Signs Pulsus alternans Pulsus paradoxus Bisferiens pulse

S3 S4 ESM at ERB’s area

ECHO(LVEF) <40% 60-70% >70%

Treatment ACE inhibitors Treat the cause Beta blockers

ICD

Etiology Titin mutation Amyloidosis Beta myosin mutation

Alcohol Hemochromatosis
Myocarditis Sarcoidosis

Heart failure

Nomenclature Mechanism EF Causes

Acute-MI
HFrEF Reduced contractility < 40% Chronic- DCMP,valvular
diseases

Ventricular stiffness with HOCM

HFpEF >50%
decreased blood filling RCMP

MC symptom- dyspnea
Most specific symptoms- PND
Most common sign- Tachycardia
Most specific pulse- Pulsus alternans
 CVS 9

First line agents=

• ACE inhibitors or Valsartan+sacubitril
• Beta blocker- Metoprolol,carvedilol, bisoprolol
• Anti-aldosterone- spironolactone
• SGLT inhibitors- empagliflozin,dapagliflozin
• If EF < 35% after first line- ICD

Pericardial diseases

Acute pericarditis Tamponade Constrictive pericarditis

Causes Idiopathic, viral Trauma, TB, Tumor Idiopathic, TB, radiation

Symptom Chest pain Dyspnea Swelling

Sign Pericardial rub Beck’s triad, absent Y Pericardial Knock

ECG

Electric alternans
PR segment depression and Low voltage ECG
ST segment elevation

Treatment Aspirin+ Ibuprofen Pericardiocentesis pericardiectomy

Colchicine
Steroids

HYPERTENSION
Hypertension

Classification SBP DBP

Normal BP <130 and <85

Elevated BP 130-139 and/or 85-89

Grade I 140-159 and/or 90-99

Grade II ≥160 and/or ≥100

Resistant HT (with ≥3 drugs one of which is diuretic) ≥140 and/or ≥90

Malignant HT (with fibrinoid necrosis of vessels) ≥140 and/or ≥90

HT emergency (with end organ damage) ≥180 and/or ≥120

HT urgency (without end organ damage) ≥180 and/or ≥120

10 LIVE RAPID REVISION

Management

Associated diseases Preferred agent

Diabetes mellitus ACEi

CHF ACEi

Post MI ACEi

Unilateral renal artery stenosis ACEi

Angina Beta blocker

Hyperthyroidism Beta blocker

Pheochromocytoma Alpha blocker

BPH Alpha blocker

HT emergency Timeline to control BP Target BP Preferred drug

Encephalopathy Immediate Decrease MAP by 25% of Nicardipine or

presentation BP Labetalol

Acute coronary syndrome Immediate SBP<140 NTG or

labetalol

Aortic dissection Immediate SBP<120 esmolol

Pulmonary edema Immediate SBP < 140 NTG or nitroprusside

Hmg stroke Immediate SBP 130-180 Nicardipine or

(if SBP>180) labetalol

Ischemic stroke 1 hour Decrease MAP by 15% of Nicardipine or

(if BP>220/120) presentation BP labetalol
 CVS 11

Ischemic heart diseases

Treatment – Standard conservative

• Dual Antiplatelets (aspirin + Clopidogrel)
• Low Molecular weight heparin (Enoxaparin)
• Nitrates
• Beta blocker

PCI indications in unstable angina/NSTEMI

Immediate PCI (< 2hrs) Early PCI (< 24hrs) Delayed PCI (25-72 hrs)

Hemodynamic unstable New ST changes Diabetes

V. tachycardia Troponin increasing trend Prior CABG

S/S of heart failure Prior PCI < 6 months

12 LIVE RAPID REVISION

Treatment Prinzmetal angina –

• Nitrates
• CCB and/or alpha blockers

Contraindicated
• Beta blockers
• Aspirin
• Thrombolytic

ST elevation MI:
Site Artery ECG leads

Septum Left anterior descending V1, V2

Anterior wall Left anterior descending V3,V4

Lateral wall Left circumflex V5,V6,I,aVL

Inferior wall Right coronary II,III,aVF

Posterior wall Left circumflex V7,V8,V9 (reciprocal ST depression

in V1-V4)

RV free wall Right coronary Right sided V4

ST elevation in I and aVL = lateral wall MI

 CVS 13

ST elevation in II, III and aVF = inferior wall MI

ST elevation in I,aVL,V3-V6= anterolateral wall MI

Cardiac markers
-Best- Troponin I and troponin T
-Reinfarction (between 3-10 days)- CPK MB

Treatment
Initial = same as NSTEMI+ high dose statins+ ACE inhibitors
Definitive= Reperfusion (PCI better than thrombolytic)
14 LIVE RAPID REVISION

Absolute CI for thrombolytic

1. Haemorragic stroke (anytime)
2. Ischemic stroke < 3 months
3. BP> 180/110
4. Suspected aortic dissection
5. Active internal bleed

Placement of ECG leads

Limb leads –Bipolar

Lead I Lead II Lead III

Exploring Electrode LUL LLL LLL

Reference Electrode RUL RUL LUL

Unipolar limb leads

aVR = exploring electrode – RUL aVL= exploring electrode-LUL aVF = exploring electrode= LLL
reference electrode- LUL+LLL reference electrode- RUL+LLL reference electrode= RUL+LUL
 CVS 15

Chest leads

P wave
Normal P wave- In lead II width <2.5 mm, height < 2.5 mm.

Abnormalities-

LA enlargement
width of P wave in lead II > 2.5 mm = P mitrale
16 LIVE RAPID REVISION

RA enlargement
Height of P wave in Lead II > 2.5 mm= P pulmonale

PR interval
Normal- Duration is 0.12-0.20 sec = 3-5 mm

Abnormalities-
1. Prolonged PR interval:
1. Dyselectrolemia- hyperkalemia,hypokalemia
2. Drugs- beta blocker,calcium channel blocker(non DHP),digoxin,quinidine
3. Myocarditis- Rheumatic,viral,diphtheria
4. Infilterative disorders- amyloidosis,hemochromatosis

2. Short PR interval: If atrial impulse bypass AV node via accessory pathways

WPW syndrome
Lown Ganong Levine syndrome
(via Bundle of Kent)
(via James Pathway)
PR short+wide QRS and Delta wave
PR short + normal QRS
 CVS 17

QRS complex
Normal width- 2-3 mm
Wide QRS- causes:
[Link] depolarisation of RV= RBBB
[Link] depolarisation of LV= LBBB
[Link] depolarisation of LV= WPW syndrome
[Link] below BOH= ventricular ectopic, complete AV block
[Link]= Hyperkalemia

Abnormality of QRS morphology-

1. LBBB – M pattern in V5 or V6 leads

2. RBBB- rSr’ or ‘rabbit ear pattern’ in V1

J point = Abnormality Diagram Causes

[Link] wave Hypothermia

Hypothyroidism
Hypercalcemia
SAH

[Link] wave Arrhythmogenic RV dysplasia

18 LIVE RAPID REVISION

ST segment ST elevation ST depression

Cardiac (ischemic) Acute MI (transmural) Subendocardial MI

Transmural ischemia Classical angina
(Prinzmetal’s angina,Tako tsubo CMP)

Cardiac (non ischemic) Acute pericarditis Constrictive pericarditis

Acute myocarditis
Brugada syndrome

Non cardiac Hypercalcemia, hyperkalemia Hypokalemia

Hypothermia Digoxin

Abnormal morphology of ST segment

Abnormality Diagram Causes

Grave Stone ST elevation Acute MI

Smiling face ST elevation(concave Acute pericarditis

upward)

Brugada pattern Brugada syndrome

(coved ST elevation)

Hockey stick or inverted tick ST digoxin

depression
 CVS 19

T wave

T wave abnormality Diagram Causes

Eiffel tower T wave(peaked and hyperkaemia

narrow base tall T)

Broad base and rounded Tall T wave Hyperacute MI

QT interval

Normal – 10 mm

Corrected QT = QT/

(Bazett’s formula)

Causes of prolonged QT interval

1. Dyselectrolemia-hypocalcemia, hypomagnesemia, Hypermagnesemia, hypokalemia(rare)
2. Drugs-
• Antiarrhythmic drugs Class IA: Quinidine， disopyramide， procainamide
• Class III: Sotalol， amiodarone, ibutilide， dofetilide， almokalant
• Antibiotics Macrolides: Erythromycin， clarithromycin， azithromycin
• Fluoroquinolones: Levofloxacin，
• chloroquine
• Antifungals: Ketoconazole， itraconazole
• Antipsychotics
• Tricyclic and tetracyclic antidepressants
3. Intracranial disorders- SAH
4. Congenital- AR(Jervell Lange Nielsen syndrome associated with deafness), AD (Romano
Ward syndrome not associated with deafness)
20 LIVE RAPID REVISION

Causes of short QT interval-

1. Dyselectrolemia- hypercalcemia
2. Drug effect – digitalis
3. Hyperthermia

Arrythmia=

Bradyarrythmias-

SA node origin ECG

Sinus bradycardia

Each P followed by QRS+ HR < 60/min

Sinus arrest

P wave absent+ HR 40-60/min

AV node origin
1o AV block

Each P wave followed by QRS+ PR interval prolonged

2o AV block

Each P not followed by QRS and PR interval is variable

=Mobitz type I

Each P not followed by QRS and PR interval is fixed

=Mobitz type II
3o AV block

QRS is wide and no relation between P and QRS

 CVS 21

Supraventricular tachyarrhythmia

Arrythmia ECG Treatment

Sinus Treat the cause

Tachycardia

each P followed QRS + HR > 100/min

Atria Treat hypoxia

tachycardia

Abnormal P wave and if more than 3 different P waves=

multifocal atrial tachycardia

Atria flutter Unstable – DC shock

Stable- betablocker

Saw tooth P wave appearance

Atria Unstable- DC shock

fibrillation Stable- Rate control= betablocker
Rhythm control = amiodarone

P wave absent with irregular heart rate

PSVT Unstable – DC shock

Stable- carotid massage,
adenosine

P wave absent with regular heart rate

22 LIVE RAPID REVISION

Ventricular tachyarrhythmias

Name ECG Treatment

Ventricular tachycardia Unstable-DC shock

Stable- amiodarone

Wide QRS and HR -100- 250/min

Ventricular flutter DC shock

Wide QRS and HR > 250/min

Ventricular fibrillation DC shock

No definitive QRS

Torsades de pointes DC shock

Polymorphic QRS with increasing and decreasing QRS amplitude

 GIT
H PYLORI
Clinical-
• Increased risk= Gastritis,peptic ulcer,stomach ca,MALT
• Decreased risk= GERD,Barrett’s esophagus,Esophageal ca

Investigations-
• Most sensitive= biopsy urease test
• Most specific= culture
• Best non-invasive= breath urea test
• Best for treatment follow up= breath urea test

Treatment- OBMT for 2 weeks

Malabsorption

Test Description Causes

72 hour stool fat estimation Stool fat > 7 % after defined oral fat is given Proximal SI disease-celiac sprue
Distal SI disease-tropical sprue, Whipple
disease

D xylose test Urine D xylose excretion of Pyloric stenosis

< 4.5 g after 25g oral D xylose is given Proximal SI disease

Schilling test Urine excretion of < 10 % after oral B12 Pernicious anemia
given Distal SI disease

Malabsorption causes

Features Celiac sprue Tropical sprue Whipple disease

Cause Hypersensitivity to gliadin Bacterial toxins/corona Tropheryma Whipelii

protein present in gluten virus+ folic acid deficiency
impairing epithelial cell
healing

Extraintestinal features Dermatitis herpetiformis Not associated with extra Joint-Migratory arthritis
Autoimmune hepatitis intestinal features CVS- Pancarditis
Primary biliary cirrhosis CNS-MC is dementia
Auto splenectomy Specific-Oculo-
IgA deficiency masticatory-myorhythmia
Eyes-Uveitis
LN,Polyserositis
24 LIVE RAPID REVISION

Investigations-biopsy absence or a reduced height Same changes as celiac PAS positive macrophages
of villi sprue but will not reverse containing bacilli
crypt hyperplasia after gluten free diet

Serology Most specific ab-Anti -- --

endomysial ab
Most sensitive ab- Anti tTG
(MC done ab)

Treatment Gluten free diet Doxycycline + folic acid IV ceftriaxone for initial 2
Steroid indications for 6 months weeks then cotrimoxazole
[Link] sprue (no for 1 year
response in 6-12 months)
[Link] shock
[Link] lymphoma
[Link] hepatitis

Diarrhea
Acute < 2 weeks

Persistent 2-4 weeks

Chronic > 4 weeks

 GIT 25

Inflammatory/Invasive infectious diarrhea

Clinical Diagnosis Preferred antibiotic

Source: raw eggs, Faget sign Salmonella Cephalosporins

MC infectious cause of GBS Campylobacter jejuni Macrolide

Causes HUS, Ekiri syndrome Shigella Ciprofloxacin

Pseudoappendicitis Yersenia Macrolide

Liver abscess E. Histolytica Metronidazole

Inflammatory bowel disease

Ulcerative colitis Crohn’s disease

MC site Recto-sigmoid Ileum

Tenesmus + --

Fistula -- +

Stricture -- +

Toxic megacolon + Uncommon

Creeping fat -- +

Ab p-ANCA ASCA

Non caseating granuloma -- +

Drug for mild-moderate P/R mesalamine(distal disease) Ileal release budesonide(ileum)

Oral sulfasalazine(Pancolitis) Oral prednisone(SI+LI)

DOC for severe IV methylprednisolone IV methylprednisolone

Irritable Bowel Syndrome:

IBS is defined by ROME IV criteria-

Abdominal pain for at least 1day/week for > 3months associated with 2 or more features-
1. Pain associated with defecation.
2. Onset associated with change in stool frequency.
3. Onset associated with change in stool consistency.
(total symptom duration > 6 months)
26 LIVE RAPID REVISION

Treatment- It depends on type of IBS:

SYMPTOM DRUG

Diarrhea Loperamide

Cholestyramine resin

Alosetron*

Constipation Psyllium husk

Methylcellulose

Calcium polycarbophil

Lactulose syrup

70% sorbitol

Polyethylene glycol 3350

Lubiprostone (Amitiza)

Magnesium hydroxide

Linaclotide

Abdominal pain Smooth-muscle relaxant

Tricyclic antidepressants

Selective serotonin
Reuptake inhibitors

Gas and bloating Low FODMAP diet

Probiotics

Rifaximin

Jaundice
Type of bilirubin elevated Urine bilirubin Liver enzyme

Prehepatic
Hemolysis
Unconjugated Absent Normal
Gilbert’s syndrome
Crigler Najar Syndrome

Hepatitis Conjugated Present SGLT,SGOT elevated

Obstructive Conjugated Present ALP,GGT elevated

 GIT 27

Acute viral hepatitis

Hepatitis A Hepatitis E

Mode of transmission

MC Feco-oral Feco-oral

Clinical

Epidemiology MCC of AVH in children MCC of AVH in adults/pregnancy

Unique feature Relapsing hepatitis Cholestatic hepatitis

Serology Anti- HAV Anti- HEV

IgM Acute hepatitis A infection Acute hepatitis E infection

IgG Past infection/post vaccination Past infection

Treatment Supportive Supportive

Hepatitis B Hepatitis C

Mode of transmission

Common MC (endemic/overall)- vertical MC overall- percutaneous

MC (non endemic)- percutaneous

Clinical

Epidemiology MC viral cause of chronic hepatitis MC viral cause of cirrhosis

MCC of carrier state Max risk of chronicity
MCC of HCC

Unique feature Causes serum sickness like illness Causes insulin resistance
(HbsAg+anti Hbs)= joint pain,skin
rash

Serology HbsAg+ IgM anti HBc= HCV RNA+ IgM anti HCV=
acute infection acute infection

HbsAg+ IgG anti HBc= HCV RNA+ IgG anti HCV=

chronic infection chronic infection

HBV DNA high+ HbeAg negative=

precore mutant
28 LIVE RAPID REVISION

Treatment
Acute infection Supportive Dual antiviral

Chronic infection HBV DNA < 2000 iu/ml= observation Dual antiviral

HBV DNA > 2000 iu/ml and liver Sofosbuvir+velpatasvir

biopsy- normal/mild inflammation=
Observation

HBV DNA > 2000 iu/ml 12 weeks

and liver biopsy- moderate-
severe inflammation= anti
viral(monotherapy)

Tenofovir > 1 year

Post exposure prophyalxis for hepatitis B

Unvaccinated – Ig(asap) + first dose vaccine

Vaccinated- if anti HBs < 10 miu/ml= Ig (asap) + booster dose

If anti HBs > 10 miu/ml= nothing to be done

Hepatitis D

Mode of transmission MC in endemic= close contact

MC in non endemic = percutaneous

Clinical

Epidemiology Max risk of fulminant hepatitis

Unique feature Always associated with hepatitis B

Serology Coinfection= acute hep D + acute hep B = IgM antiHDV+IgM anti HBc
Superinfection=acute hep D + chronic hep B = IgM anti HDV+IgG anti HBc

Treatment Alpha interferon

Chronic hepatitis Cause Clinical Investigations Treatment

Alcoholic liver Ethanol inhibits beta Neuropathy SGOT/SGPT > 2 Steroids if Maddrey
disease oxidation (pyridoxine discriminant function
deficiency) > 32

Metabolic syndrome Insulin resistance Obesity,type 2 SGOT/SGPT < 1 Vitamin E

associated fatty liver diabetes
disease Acanthosis nigricans

Wilson disease ATP 7 B mutation Neuropsychiatry S. ceruloplasmin low Zinc + penicillamine

features,KF rings Liver cu high
 GIT 29

1° hemochromatosis HFE mutation Bronze skin % transferrin Phlebetomy

Bronze diabetes saturation high
Pseudogout Genetic studies

Autoimmune Ab mediated damage Recurrent hepatitis ANA/anti LKM1 Steroids+

hepatitis Plasma cells in liver azathioprine
biopsy

Primary biliary Intrahepatic bile duct Pruritis AMA Ursodeoxycholic acid

cholangitis autoimmune damage I/H bile duct
inflammation on Bx
30 LIVE RAPID REVISION

Complications of Liver Failure

Encephalopathy Portal Spontaneous Hepato-renal Hepato-

hypertension bacterial syndrome pulmonary
peritonitis syndrome

Clinical Asterixis Hematemesis Fever, abdomen Decrease urine Platypnea

Earliest sym- splenomegaly distension output
altered sleep cycle
Earliest sign-
dysgraphia

Investigations EEG- triphasic Endoscopy- Ascites fluid- Serum creatinine Orthodeoxia

waves esophageal neutrophils> 250 > 1.5 mg/dl
varices

Treatment Rifaximin Doc-octreotide Cefotaxime Terlipressin Liver transplant

Lactulose Liver transplant
Zinc Rx of choice-
Band ligation

Ascites-
 GIT 31

Treatment of cirrhosis induced ascites-