HF

Determinants of COP
1- Preload
2- Afterload
3- Contractility
Types of HF
1- ACUTE and CHRONIC
2- LOW COP and HIGH COP
If preload is markedly increased u will have a congestive manifestation like leg
edema in right sided hf and hemoptysis, dyspnea, cough and pulmonary edema in
cases of left sided HF
If the afterload is markedly increased u will have a COP manifestation like
dyspnea secondary to pulmonary oligemia in cases of right sided hf and dizziness,
fatigue, cold in case of left sided one.
AIM of TTT
Decrease preload and afterload and increase the contractility.
-Decreasing preload by:
1- Diuretics like loop diuretics
2- Venodilators (or mixed vasodilators like ACEI, ARBs and Na nitroprusside)
3- Salt restriction
-Decreasing Afterload by:
1- Arteriodilators (or mixed vasodilators like ACEI, ARBS and Na nitroprusside)
2- Physical and mental rest
-Increasing contractility by:
+ve inotropics like digoxin, dopamine or dobutamine
-Improve the exhausted cardiac status by B-blockers like bisoprolol, metoprolol or
carvedilol.
-Decrease mortality by B-Blockers, ACEI, ARBS, Hydralazine/Nitrates Mixture,
Aldosterone antagonists like spironolactone
-Order of TTT in CHF
1-Loop Diuretics
2.ACEI
3.BB
4.Digoxin
5.ARBs
-Vasodilators used in TTT of HF
For the veins it is Nitrates
For the Arteries it is hydralazine
Mixed like Na nitroprusside and ACEI.
ACEI: prevent Angiotensin I into Angiotensin II and u know the mechanism.
But it increases bradykinin which stimulate cough.
Inhibit aldosterone and cardiac remodeling.
Members: captopril, ramipril, enalapril and lisinopril.
Uses: CHF, AMI, Hypertension, and diabetic and non-diabetic nephropathy.
Adverse effects: 1st dose hypotension, Rash, Dry cough, angioedema,
hyperkalemia and fetotoxicity.
ARBS: block A2 receptors
Pros: don’t increase bradykinin so no cough
Inhibit A2 from renin and non renin pathways and activate A2 receptors which VD
Na Nitroprusside: release NO from smooth muscles which lead to VD in arteries
and veins so increase the COP and decrease systemic and pulmonary congestion
Uses: by IV infusion: HF and hypertensive encephalopathy
Precautions: avoid light, freshly prepared and monitor the ABP
Adverse effects: Hypotension and cyanide toxicity
Digitalis glycosides:
PK: it is 2 parts glycon part and aglycon part (effective one)
Cardiac effect: +ve inotropic and inhibits membrane bound ATPase lead to
increase intracellular Na and extracellular potassium and intracellular ca+
increased because of exchange with sodium
Calcium entry lead to CICR from sarcoplasmic reticulum
Significance of increasing inotropy:
1- Decrease sympathetic over activity.
2- It acts as a diuretic as it increases the renal blood flow.
3- Decrease venous pressure because of increasing COP.
Effects on electrophysiological properties:
It is extracardiac vagomimetic.
It decrease SAN rate and AVN conduction.
By increasing vagal activity and decrease sympathetic activity
It leads to a DAD (delayed after depolarization)
Significance of SAN inhibition:
It is an indicator for optimal digitalization.
Digitalis is contraindicated in cases of hypertensive carotid sinus syndrome or SAN
dysfunction.
It produces SAN depression In cases of toxicity
It is contraindicated in bradycardia and can be treated by atropine.
Significance of AVN conduction inhibition:
It is contraindicated in heart block but can be treated by atropine.
It can be used for decreasing conduction in patients with AF or Af.
Therapeutic uses: Systolic Heart Failure or AF or Af or Both conditions and this is
the best indication for Digitalis.

Verapamil and Diltiazem is contraindicated in cases of Systolic HF.

Effect on ECG
Digitalis toxicity correct by k+ in general by atropine in case of ↗️ vagal activity
All Contraindications

And thank u <3.