HEART FAILURE -

→
COP = INADEQUATE FOR
THE BODIES REQUIRMENTS

Structural IFunctional cactihe disaides that impair the of the ventricles to fill
ability or
eject blood
Most
commonly in the elderly
I I I
LEFT SIDED HE HE
CONGESTIVE RIGHT SIDED HF
* Reduction in Left ventricular output Both Sides * Reduction in right ventricular output
( I VC)
* Increased left aerial 4
pulmonaryvenous pressure ofthe fleet * Increased right aerial 4 systemic venous pressure

sudden MI T Left atrial pressure → * Most common causes chronic Lung disease
*
ey →
;
-
.

pulmonary edene pulmonary Embolism

-

* Grad net ey . Mitral stenosis → Reflex put .

-
Put
moneyvalue stenosis
vasoconstriction → No
put Edema
.
* Car pulmonate = RHF
Zryto chronicling disease
T Vascular resistance → Put HTN
bit →
put .

→
Right ventricular impairment
I I

Disease
affecting Both sides oftheMeet Lett heat Disease → chronic T left atrial pressure →

G . I HD ,
Cardiomyopathy put money HTN → Right HE

High Output (*
Us Low
Hypedynamic circulate )
-
Output
~

High Output → Normal I High amount of blood being pumped , but

body still isn't getting enough (T Need )

•
occurs in normal Heats , Earlier if diseased Heat

= Elevated COP ,
Low systemic vascular resistance ( Due to peripheral Vasodilation or AV Shunt )

•
causes ; Besi Beri , severe anemia , thyrotoxicosis ,
AV malformation , paget disease ,
pregnancy
(initial RUF her LVF )
y
LOW
~

Output →
Low COP , High systemic vascular resistance →

Low cop → Activation of sympathetic Nervous system } Resin Angiotensin Aldosterone system
I Atrial Dilation → Naturetic peptides →

* RA AS → Vasoconstriction { sodiumand water retention T GFR and treat Nat Resorption 's Relax smooth Muscles

compensate far salt retention at the begining)

* sms → T Myocardial contractility 's HR ( Arrhythmias)

( prolonged → Cardiac Food

Myocyte Apoptosis , cardiac
Hypertrophy , Myocardial Necrosis

P Ventricular Dilation

↳ ventricular
Hypertrophy → Diastolic Dysfunction
 pericardium

eoh=o
→

→
Myocardium
CAUSES → → endocardium

Rhythm Disturbance
→

Ventricular Dysfunction →
circulatory overload
→ us
at His #
Iffy Ma
I

Disease
Dysfunction;

! Df
,

→
Systolic =

Inability ofthe ventricles to contract ( Ejection fraction s 40%) ay to chronic was

Is putmoney HTN
Right Ver
Htfnuiifeet
Rvs .

disease
together Cardiomyopathy
,

often occur courses I HD MI Admit censer

; , ,

→ Diastolic =

Inability ofthe ventricles to relax Cstiff Incanpliant) C EF

↳ Asses ed by
> 50% → HF with preserved EF)

causes ; ventricular Hypertrophy , constrictive pericarditis , tamponade, restrictive cardiomyopathy , Obesity

# I
Hypertensive Elderly
→

V IU ht W Disease

* Impaired filling of ventricles ;

Mitral or tricuspid stenosis
infarction Segments ; thin 3 Dilated
oninfarct segments ; Hypertrophied

* obstructed
Ventricular Outflow ;

Awtic w
Pulmonary Stenosis
* Ventricular Overload;

Valvular Regurgitation

Side Note
; Pathophysiology
There are
physiologic charges that are compensatory and maintain copy peripheral perfusion ,
However as HE
progresses the mechanisms

overwhelmed and become

are
pathophysiological
I . Venous Return ( Preload ) →
Increased systemic Venous pressure → accumulation of Interstice y alveolar fluid ; Dyspnea ,

Hepatic enlargement, Ascites

, Edone

2 .
Outflow Resistance ( Afterload ) →
Decrees eel COP ,
Increased End diastolic volume → Ventricular Dilation

3 .

Myocardial Contractility ( Inotropic State) →

Increased Neuroharmand activation I Myocyte Apoptosis

4 . Neuro hormonal l Sympathetic system activation (salt I Fluid Retention) →

cardio toxicity ,
ventricular Dilation

5 .

Myocardial Remodelling →
Hallmarks =

Hypertrophy ,
loss of
myocytes ,
Interstice fibrosis
 CLINICAL PRESENTATION →
Symptoms ; paroxysmal noctwneldyspnoea fatigue
-

Exertions
Dyspnea , Orthoproea , ,

signs ; cardiomegaly 3rd 44th Heetsomds , Elevated JVP , Tachycardia ,

Hypotension Bi basal crackles , Pleural effusion , peripheral edema,
-

, ,

Ascites, Tender
hepatomegaly , Cyanosis , Narrow
pulse pressure pwlsus Attends, Displaced Apex ,
,
RV Heave ( Pulmonary HTN)

.me/. ,. .m. ,. . . . . . . . . . .
put . HTN Systemic HTN
Facial
Engorgement
} Epistaxis
-
I

Noctwia
Tender
2
cold peripheries
-

=3
weight-loss
Nausea / Anorexia
Dyspnoee , Orthoproeh,
PND Nocturne cough I
,
commonly in the
_÷,
most

µ.µ, .am * Increased lettalrial

LEFTSIDEDHF

{ pulmonaryvenous pressure
CONGESTIVE HF

oftretleet *
RIGHTS/ DEDHF

Increased right aerial } systemic venous preÑw%

/
Theft atrial pressure
YY¥%!
* sudden g. in → → * Most common causes
;

pulmonary edema

J µM
-

pwmaneyvaluesterois
vasoconstriction →
Nopal Edema *
www.e#-**onmiumsa-.eese
y
.

CM/ NU WGh/
"
→
Right ventricular impairment
#

Disease
affecting Botnsidesoftretieetlettheetdiseere-ohrnictletta.tn'd pressure →

G. IHD ,
cardiomyopathy pulmonary HTN → Right HF

*
f) W/ JW A /tf@N)
→ Lvtaiiwe

* Gallop Rhythm

* Basal crackles

ACUTE -
CHRONIC -

=
Cardiogenic Put Edema
.

congestion is but arterial pressure is well

-

•
Venous cannon
=
Newansetw decompensation of chronic HF ,

maintained until very late

characterized
by;pÉÉMeddmr with or without signs
ofpipEypwfm.se Relapsing } Remitting course

symptoms of tcop ; fatigue , cold peripheries how Bp

It

Bp= SNS activation , but maybe normal alow if poor renal

usually high because of
, ,

in cardiogenic shock perfusion → oliguria uremia ,

symptoms of pulmonary Edema

Notimefw ventricular dilation displaced ;
•
:
Apex not

Acute an chronic ? signs ofChronicleFaswellasaeule Left-side → Dyspnea, Inspiratory crepitations over

1mg bases

Right-side → Raised JUP , Hepatic congestion, peripheral Edema

• * www..ca.⇐ .
 COMPLICATIONS ;

I . Renal Failure →
poor rera perfusion Cd cop) ,
worsened by therapy
2 .

Hypokalemia → Kt
loosing diuretics , Hypealdosterone
'sm

3 .

Hyperkalemia → Drugs esp . combination of ACE i , -

ARB s ,
Mineralocorticoid receptor antagonists , Amplified if Resat dysfunction
4 .

Hyponatremia → Feature
of severe HE
; poor prognostic sign

5. Impaired Liver function → Hepatic Venous congestion 's Pow arterial perfusion

G. Thromboembolism → systemic thrombi → A -

fib ,
Intracardiac → Mitral stenosis , MI , Left ventricular Aneurysm

7
Arrhythmias → Electrolyte disturbance, cordial disease , sympathetic activation Ivest fib poor prognosis ,
.
-
-
A Fib 20% )
- =

8. Sudden Death → Ventricular fibrillation

DIAGNOSIS →
I .
Chini cel pt comes with signs 4 symptoms

2 . Cardiac Disease ? went Peptides C Normal

ECG , CXR, Nati = a 100
pglml )
→
If harmed HF =

Unlikely
B type Natiivetic peptide released by the Right Atrium Differentiates between HE 3 Pulmonary Disease
,

3 ECHO
Keyinvestigation
=
.

4 Others . CBC I Renal profile , Endo

myocardial Biopsy

T Uric
BNP
Acid
I Ia BNP -

high ve
-

predictive Value

Resp ve
IWdiv
-

the
MANAGEMENT →
ACUTE CHRONIC

i. cardiac Bed
Lifestyle Modifications ; stop smoking , stop drinking alcohol , Eat less salt ,

2.
oxygen Exercise , optimize weight 7 Nutrition , vaccination ,
Education

Treat cause 4 Exacerbating factors I Monitoring

Drug management ;

I . Diuretics ; loop diuretics eg furosemide → SE

; Renal impairment
3 Iv Opiates used
→
sparingly as they
.

7 Hypotension C to Kt → Kt thiazide diuretics )

maycause respiratory sporing ,
Refractory Edema →

depression

4. N
loop diuretics 2 . ACE i ; -

esp → LVSD , cough ? → ARB ,

SE ; T Kt 4 Hypotension

contraindications ; Renal
5- IV Nitrates esp if Bp is High
.
Artery stenosis , pregnancy , previous angioedema
I
Sublingual

B blockers ; with Caution ,

3 . use 32 weeks between doses , d Mortality

4 . Mineralocorticoid receptor Antagonist ; spironolactone , I mortality

pts that we still symptomatic , post Ml , LV SD SE ; Hype Kt lesp with ACEi)

.

5 .
Digoxin ; monitor Kt between 4- 5mmol IL as 4kt risks digoxin toxicity I v.v
(I . 91 2. visual ; YellowGreer 3 .
Arrhythmia)
improves morbidity but not mortality i.
Stop z . let correction 3 . Anti Fcb

G Vasodilators Black pts I pts intolerant to ACEi laRBs → combination

;
.

of Hydraarise C SE; Drug induced Lupus)4 Nitrates ( Iso sorbide di nitrate )

Non pharmacologic treatments ; implantable defibrillators Resynchronization ,

devices,
coronary revascularization , cardiac transplantation ,
VAD

(only chronic ; Low Dose I Gradually T )

* B blowers contraindicated

Drugs t Mortality } Morbidity ; I

B Blockers 2 Spironolactone 3 ACE i 4 Nitrates
Hydraoilnet
-
. . . .

Drugs t
Morbidity only ; I .

Digoxin 2 .
Furosemide 3 Hydra arise
.

only