CHF Flashcards
Systolic Heart Failure
Ventricles cant generate enough SV- decreases CO, and Drop-in BP
CO = HR X SV,
SV inverse to Afterload- decrease Diastolic pressure
Decrease EF
Flappy, Dilated and Compliant myocardium
Decrease in Contractility in SHF
MI- Anterior/Lateral
Dilated CardioMyopathy - (Flappy Heart)
Increase in Preload with Decrease Contractility SHF
Mitral and Aortic Regurgitation
Other SHF conditions
Tachyarrythmias and Bradyarrythmias
Diastolic Heart Failure
EF maybe normal (preserved)- decreased filling/preload and increase in Afterload
Stiff, Fibrotic, Non-compliant myocardium
Decrease PReload DHF
MI,
Restrictive CM,
Constrictive Pericarditis
Increased Afterload
Hypertension,
Aortic stenosis,
Coarctation of Aorta (Narrowing of aorta)
Hypertrophic Constrictive Cardiomyopathy- Congenital (Thick myocardium)
What leads to RHF
LHF
Increase Afterload RHF
Pulmonary stenosis
Pulmonary hypertension
Pul. Embol
Cor. Pulmonale- COPD V/Q= <0.8
Increase in Preload RHF
Tricuspid and Pumonary Regurg (Not common)- common in IV drug users- Staph infection-infection of valves
Decrease in contractility
Inferior MI, Myocarditis
High Output HF is due to
underlying CVD
Symptoms of HOHF
Severe Anemia (hypoxia) Wet Beri-Beri (Thiamine deficiency- Alcoholics, CN6 palsy, Deficiency of PDH) Thyrotoxicosis Pregnancy (Volume overload) AV Fistula (hemodialysis complication)
Lactic acid accumulation in Myocardium
Vasodilation causes AV shunting (Fast shifting of blood from Atria to ventricle)
Receptors in Carotid sinus for BP
BAroreceptors
Detects low CO
receptors- LBP- Medulla- CArd. Acc Center- SNS- Increases Contractility (B1 receptors) inc. SV, HR
SNS effects
Sends fibers to Venous and arterial system- release epi. (a1 receptors)- Constricts Arterial Smooth muscle- Inc TPR= Increase BP
Constriction of V Smooth Muslce- Inc Venous return = Inc Preload = Inc SV=
Inc. CO = Inc- BP
a1 receptor in kidney = dec. GFR= inc Fluid retention= Inc Preload = Inc SV -= Inc CO = Inc BP
JG cells- b1 recep- inc. Renin= ACE in lungs (with angiotensinogen in Liver)= AT 2
Beta blockers helpful
Functions of AT2
Stim Post pituitary= ADH prod = Water retention= inc. BV = Inc Preload = Inc. SV= Inc Co= Inc BP
Vasoconstriction of arterioles= Inc TPR = Inc BP
Adrenal Gland (Zona G)- Secretes Aldosterone= Increase Na reabsorption in DCT and H20 Reabsorption= Inc BV = Inc Preload = Inc. SV= Inc Co= Inc BP
ACE inhibtors helpful
CHF symptoms
Pulmonary veins have a lot of blood- Inc pressure in Pulmonary veins= Leaking fluids- Pulmonary Edema (inc pressure in P. capillaries)= Hypoxemia
Symptoms of hypoxemia
Dyspnea
Cough (Dry)
Orthopnea (difficulty breathing when lying flat)
Paroxysmal Nocturnal Dyspnea- (Difficulty breathing)
Crackles in lungs (Rales) inspiration
Accumulating of Blood in Sup. Vena Cava
Inc Internal Jug Vein Pressure= Jug Vein Distention
Accumulation of blood into inf Vena Cava
inc Pressure due to pressure on liver, Decrease perfusion of Liver
Hepato-jug Reflex
> /= 3cm Inc in JVD
increased pressure in the liver and spleen due to accumulation causes
hepato-spleno-megaly and ascites
Accumulation of blood in GIT
Ascites- Nausea and abd. pain and
obstruction- dull precursive abdomen- Fluid wave test
Accumulation of blood in LE
Calf Edema- Pitting (Bilateral edema)
Decreased perfusion of extremities
Cold, Clammy, pale, Diaphoretic
Heart Sounds in CHF
Sys HF- S3
Dias. HF- S4
Diagnostic clues for HF
CXR
BNP >400pg
Echo
Cardiac Catheterization
Classes of NYHA CHF
1- Extreme exertion
2- Mod. ex
3- Mild
4- At rest (Emergency)
What should be treated first regardless of Class of HF
Underlying disease
Restrict Na+(<2g/day and H2O (<2L/day) intake
RAAS
Decrease perfusion of Kidneys = Stim. JG cells = Release Renin = Angiotensinogen to AT1 ACE converts to AT2
Problems with AT2
Vasoconstriction- Decrease lumen diameter- inc TPR (Afterload inc)- Inc BP
Ant Pitutary- ADH- Dec Urine output- Inc. Water reabsorp.= inc. Bp= inc. EDV = Inc. Preload
Adremal gland= Aldosterone= inc NA and Water reabsorption= Inc BV= Inc EDV = Inc Preload
Class 1 drugs
ACE inhibitors- Inhibit ACE which decreases AT2 and reduces stress
Captopril
Enalapril
Lisinopril
Benazepril
What if the patient cannot tolerate ACE inhibitors- Dry cough and angioedema Class 1
ARBs (AT2 Receptor blockers)-
Lazartan
Valsartan
Candesartan
Class 3 Drugs
Aldosterone antagonist-
Spirnolactone
Eplerenone
Dec Remodelling, K+ sparing
Class 3 drug that can be used if normal fail
Entresto
MOA of Entresto
HF= Inc BNP = Blocks AT2 actions decrease afterload
Problems- Neprilysin- Breaks down BNP
Neprilysin Inhib to prevent breakdown
Neprilysin Inhibitors to inc BNP and increase action
Sacubatril + ARB (Valsartan) = Entresto
SNS effects
b1 receptors Dec CO= inc. SNS= inc. HR (b1 receptors on SA node and Myocardium = Inc BP= inc Contractility= inc CO = inc BP= inc O2 demand
a1 on renal arterioles= inc. renin and vasoconstriction= inc TPR= Inc BP and in Afterload
Class 1 SNS drugs
ACE inhib and ARb cant tolerate, give b-blockers
Metoprolol- b1 only selective
Carvedilol- both a1 and b1 activity
negative chronotropic (dec HR) and neg Ionotropic (dec Contractility) negative renin release
Where are BEta blockers contraindicated
Decompensated HF
Class 4 SNS drugs for contractility (last-ditch effort to save patient)
Digoxin (+ve inotrope, -ve Chronotropic)
Dobutamine class 4
Decomp. HF
Cardiogenic shock
Class 2 (Diuretics) for edema
Loop- Furosemide (Lasix)
Thiazide- Hydrochlorothiazide & metolazone)
Metolazone
significant edema start at 2mg Furosemide sometimes add Metolazone to pull out more water and not inc. Furosemide Dosage
loop diuretics MOA-
Act on Loop- inhibit Na+/K+ cotransporter
Increase buildup of Na, k and H2O= Increase urination (25%) Decreases EDV= Dec Preload
Thiazide MOA
Inhib Na/Cl transporter- dec. reabsorption (10-15% GFR) inc. Urine output= Dec.BV= Dec. EDV= Dec Preload= Dec Stress
Class 3 Drugs
Hydralazine
Isosorbide Dinitrate
Only use when ACE1 and ARBS fail
MOA of Hydralazine
Hydralazine= well-tolerated in African American patients, safe for pregnancy
Acts on art. SM= Inc NO= inc Guanylyl Cyclase- GTP to cGMP- with Protein kinase- Promotes inhibits Ca entry and relax smooth muscle
MOA of ISD
Acts on art. SM= Inc NO= inc Guanylyl Cyclase- GTP to cGMP- with Protein kinase- Promotes inhibits Ca entry and relax smooth muscle
The difference in ISD and Hydralazine
Arterial relaxation= dec. TPR, Dec. Afterload in Hydralazine
ISD- relaxation of venous system= Dec. right Venous return, Dec EDV = Dec. Preload= Dec. Stress
Decomp. HF
L- lasix- Edema M- Morphine N- Nitrates (hydralazine, ISD- dec. AL and Chest pain) O- OXygenation- BIPAP, CPAP P- position- Decrease fluid by gravity
Ivabradine
HCn channel Blocker
used in patients on b blockers or contraindicated on b blocker
Inc. SV= Slow Heartrate
6hr half-life 2 times a day
side eff- bradycardia no eff. on rate control in a-fib luminous phenomena in eye Contraindicated in pregnancy, adv. Heart blocks and 3A4 inhibtors
Adverse effects of ACE inhibitors
Postural hypertension Renal insuffeciency Hyperkalemia- monitor K+ while using simultaneously with Spirnolactone Creatinine increase Teratogen
Adverse effects of ARBs
similar to ACE inhibtor
hoewever, lo effects on Cough and angioedema
Thiazide Diuretics Adv. Effects
Hypokalemia Hyponatremia Hypomagnesemia Hyperuricemia Hypovolemia Hypercalcemia Hyperglycemia
Loop Diuretics Adv. effects
Acute Hypovolemia\ hypokalemia Hypomagnesemia Ototoxicity- hearing loss Hyperuricemia
K+ Sparing Diruretics Adv. Eff
Hyperkalemia
Gynecomastia
Adv Effects of Neprilysin inhib
Same as ARB and ACE
Adv. Effects of Digoxin
narrow TI Anorexia Nausea Emesis Blurred vision Arrhythmias due to Na+/K+ ATPase inhibition Hypokalemia inhibitors of P-gp Clarithromycin, Verapamil, and Amiodarone can cause worse side effects to digoxin as they act on P-gp
