CPR

HTN in pregnancy

“New Moms Love Hugs”

1. Nifedipine

2. Methyldopa

3. Labetalol

4. Hydralazine

Tids

• Native valve: viridans>enterococci>pyogenes

• Prosthetic:

  • Acute: epi> aureus/epi

  • Chronic: epi > aureus > viridans

• IV drug: aureus, Pseudomonas, viridans, candida

• A1 VC, A2 VD

• Shock:

  • PCWP low in hypovolemic, distributive, PE/pneumothorax

• MS -hi  PCWP > LVEDP, makes sense

• Regurgs make PV loop blobs

  • Inc SV in regurgs

  • Dec SV in stenoses, mitral decreases EDV while aortic increases ESV

• IV → RH IE → PE

• Gallolyticus → AR

Distributive shock

pressors (VC), epi, NE. Not for others bcuz hypoperfusion

Ezetimibe

Inhibit chol absorb @ brush border. NPC1L1 transporter

Bempedoic Acid

Inhibit ATP citrate lyase → ↓Chol synth (combo w/ statins)

Bile Acid Resins

Chol → bile acids in liver → ↓LDL (combo w/ statins)

• Cholestyramine

• Colestipol

• Colesevelam

PCSK9 Inhib

Monoclonal Ab prevent receptor degradation → ↑LDLR recycling → ↓LDL

• Alirocumab

• Inclisiran

• Evolocumab

Fibrates

LOWER TG. Activate PPAR-alpha → upregulate LPL, ↑Liver FA ox

“Gem is not a gem” - do NOT combine w/ statins

Niacin 

(B3, Nicotinic Acid)

Inhibit diacylglycerol acyltransferase 2.

Prostaglandins → flushing. Blunt w/ aspirin (inhibits prostagland).

Bile acid resins & statins overlap in what mech?

upregulate LDLR

VD (arterial)

Mech: ↓afterload → ↓BP

Adv: reflex tachy

- Hydralazine: lupus-like syndrome, fluid retention

- Minoxidil: opens K+ channels. Adv: hypertrichosis

Ca-Block Dihydropyridine

Mech: Greater effect on vessels. Coronary a VD = prevents vasospasm / ↓afterload → ↓O2 demand

Adv: edema, flushing, headache, constipation, gingival hyperplasia

Interactions: Inhibit action of simvastatin & digoxin

- Amlodipine

- Nifedipine: reflex tachy, hypotension, dizziness/transient headache, coronary steal

Ca-Block Non-Dihydropyridine

Mech: Greater effect on heart. 

Adv: edema, constipation, bradycardia, AV block, gingival hyperplasia

Interactions: B-block

Contra: HFrEF!

- Verapamil

- Diltiazem

ACEi

Mech: No Ang II → ↑bradykinin → VD → ↓aldosterone (inhibit RAAS) → fluid offload. Reduce myocardial remodeling.

Adv: hyperkalemia, dry cough (bradykinin), high creatinine, angioedema

Interaction: NSAIDS

Contra: renal a stenosis

• Lisinopril

• Enalapril

• Captopril

ARBs

Mech: Block Ang II → VD → ↓aldosterone → fluid offloading. No bradykinin impact = no cough.

Adv: hyperkalemia, mild creatinine

Contra: renal a stenosis

• Valsartan

• Losartan

Thiazide Diuretics

Mech: inhibit Na/Cl resorption in distal tubules → ↓venous return → ↓CO

Adv: “HyperGLUC” hyperGlycemia, dysLipidemia, gout (hyperUricemia), hyperCalcemia, hypokalemia (mm cramps, arrhythmia)

- Hydrochlorothiazide

- Chlorthalidone

Loops and thiazides both lead to gout, but…

Loops → hypocalcemia

Thiazide → hypercalcemia

Loop diuretics

Mech: Inhib Cl/Na/K symporter to offload Na/Cl → ↓CO, ↑TPR

Adv: hypokalemia, ototox, gout (hyperuricemia), alkalosis

• Furosemide (Lasix)

K+ sparing Diuretics

Mech: Na/H2O excretion, block K excretion

Adv: Hyperkalemia, GI upset, acidosis

1. Aldosterone Antag / Mineralocorticoid Receptor Antagonists:

   • Spironolactone - gynecomastia

   • Eplerenone

2. ENaC Inhib:

   • Directly block Na chann in collecting duct → Na offload

   • Adv: kidney stones

   • Amiloride

ACEs/ARBs

↓Afterload & Preload

Statin adverse effects

increased CK & myalgias, renal fail

How do B-blockers work?

1. ↓afterload → ↓BP, HR, contract → ↓O2 demand

2. B1 block in kidneys → ↓renin release → ↓BP

3. Over time ↑CO → allowing heart to recover from sympathetic activation

Adv for all: “FED” Fatigue (exercise intolerance), ED, Depression. Other: bronchospasm, reflex tachy from stopping abruptly, masking hypoglycemia symptoms like tachycardia & tremors, NOT sweating (muscarinic).

Non-selective unique adv: hyperlipidemia (↓HDL, ↑triglycerides)

Contra: AV block, COPD/asthma (especially non-select)

B-Block Breakdown

Non-selective (B1&2): Prop, Tim

• Adv: bronchospasm, hypotension, hyperlipidemia (↓HDL, ↑triglycerides)

Cardioselective (B1): Aten, Metop, Esm, Bisop

• Adv: brady, AV block, fatigue

Nonselective w/ A1 Block (B1,B2, A1): Carvedilol, Labetalol

• Partial VD effect from A1 antagonism

• Adv: orthostatic hypo

Partial Agonists (B1, B2): Pindolol, Acebutolol

• Less brady!

A1 Antag

Mech: VD smooth m → ↓Preload/Afterload → ↑CO

Adv: fainting

• Prazosin

• Terazosin

Direct Renin Inhib

Mech: ↓Ang I, II, aldosterone → ↓BP

• Alsikiren

“karen cares for her kidneys!”

Adverse effects of nifedipine

Dihydropyridine Ca Block: edema, flushing, headache, constipation, gingival hyperplasia

Nifedipine-specific:

• Reflex tachy

• hypotension

• dizziness/transient headache

• coronary steal

Class I antihypertensives have an adverse rxn w/ which class?

Chloroquines!

Effect:

Mortality benefit in HFrEF

1. RAA antag (ACE, ARB, Nep)

2. B-block

3. MRA

4. SGLT2

Maximal med therapy w/ EF <35% → cardioverter defibrillator to prevent vent arrhythmias

Side effects ACE/ARNI/ARB

• Angry (angioedema)

• Hyper (hyperkalemia)

• Hyppos (hypotension first dose)

• Guffaw (GFR) 

• Terribly (teratogenic)

Two high intensity statins…..

Atorvastatin

Rosuvastatin

Atropine

chronotropy

Amiodarone effects

Bluegray color, angioedema

Isolated HTN in African American

Thiazide

Propranolol

SVT hyperthyroidism

Angina w/o troponin

vasospastic. Ca block

Digoxin

vagal tone

AV conduction
(PR interval)

slows in B-block & Ca-block

Statins and fibrates contraindicated due to

myoglobinuria

Acute Rheumatic Fever —> RHD —> mitral regurg (early) → mitral stenosis (severe)

• Type II hypersensitivity rxn

• Ab to bacterial M proteins

• JONES

  • Joints (polyarthritis)

  • Carditis (valvulitis, myocarditis, pericarditis)

  • Nodules (subcu tendons/bones)

  • Erythema marginatum (rash on trunk)

  • Sydenham chorea (jerking)

A: hypovolemic shock

B: late-stage septic shock

C: cardiogenic shock

D: distributive shock

Most important risk factor for aortic dissection

HTN

PDGF

intimal migration of smooth m

• VD CHALK: CO2, H+, Adenosine, Lactate, K+

  • Prostacyclin

• VC: thromboxane, endothelin

CK-MB best for acute recent/recurring MI <48hr

Trop elev in nstemi & stemi. 4 hr, rises for days

WPW = Bundle of Kent

Tall V in MR Wiggers

A before P, IIa before III (&apoE!) - “extravasation of lipoproteins” = achilles

MI progression

• Coag necrose w/ dense neutrophilic infiltrate 1-3d - fibrinous pericarditis

• Hyperemic gran tissu w/ macros 3-10d 

• Rupture happens late, 3-5d

Homocystinuria

downward subluxation + learning disability. Marfan upward w/ normal learning.

Abdominal aorta common site of endothel strain →

atherosclerotic plaques

Loops ↓CO, ↑TPR

Restrictive CM findings Congo, biatrial enlarge

Endothel cell dysfunc → LDL oxidation → foam cell (fatty streak)

subacute endocarditis: fibrin clot formation

ANP released from atria → cGMP → inhibit RAAS

BNP released from ventricles → cGMP → inhibit RAAS

Driving pressure for pulmonary circulation

diff btwn PA  & LA (start to finish). MPAP - LAP

What part of myocyte AP does T wave (repolarization) occur?

phase 3 (rapid repolarization toward membrane pot)

PVR high in fetus

Low BP physiology effect

Low V → ↓ Kid perfusion (renin release) → Angiotensin I → Angiotensin II → VC

Atropine

blocks parasympathetics

Cardiac myocyte chng after blockage

cardiomyocyte will have increased excitability & expanded QRS complex (ischemia → less O2 → less ATP → less Na increase, shorter plateau

Look @ slope of phase 0 for conduction velocity. Fast = steeper slope.

Nodal cell phase 0 depolarization mainly triggered by opening of L-type Ca. Phase 4 gradual depolarization by funny chann

DADs provoked by

digitalis glycosides, ischemia, hypokalemia, catecholamine

Exercise pv loop: ↑ contractility = ↓ESV. ↑ venous return = ↑EDV. ↑ afterload = ↑Systolic P

Pressure increased upon birth

LAP

What part of the nodal AP does sympathetics and para alter?

Phase 4 funny channel slope to cause faster or slower depolarization

Non-infective endocarditis

procoagulant release

lymphocytes indicate a viral infection

neutrophils indicate a bacterial infection

• A-hemolysis: green, partial RBC lysis

• B-hemolysis: clear zone, complete lysis

• Y-hemolysis: no lysis

Aortic regurg

Mitral stenosis

Mitral regurg

Aortic stenosis

AV delay: 1st degree, Wenckebach, 3rd degree possible

His delay: Mobitz 2, 3rd degree possible

LV compliance decrease

RHC - vv

LHC - aa

HIS bundle = AV block

BBBs are just one side, not AV!

AV Blocks

Lyme disease, Borrelia burgdorferi can cause any of the following:

• First Degree: PR > 0.2 (one large box)

  • Group beating diff from 3rd degree.

• Second Degree: 

  • Mobitz 1: “Long long PR drop, then you have a Wenckebach”

  • Mobitz 2: PR constant, random QRS drop

• Third Degree (complete): P and QRS uncoordinated

  • Atria and vents beating rhythmically @ own paces

Side note:

• First degree: R is far from P

• Second degree: Some R’s don’t get through

• Third degree (complete): The P’s and Q’s don’t agree

Extravasation of lipoproteins means

Achilles xanthomas

R dom: PDA off RCA

L dom: PDA off circumflex

Fenestrated cap in renal glomerulus

Sinusoidal cap in liver, spleen, marrow, lymph

DCM: TTN mutation. Balloon/banana appearing.

• Cause: viral myocard

HCM:

• ADom b-myosin

Restrictive CM:

• “No restrictions in the Congo”

• Bi-atrial enlarge & improper vent filling

• dyspnea, edema, ascites, elev JVD

Takotsubo CM: Broken heart

• stunned

Acute pericarditis: Fibrinous (triphasic friction rub), Hemorrhagic, Purulent (neutrophil bacterial or lymphocyte viral)

Chronic pericarditis: constrictive. Kussmaul, knock, PParadox on inspiration. Rapid y descent (Friedreich)

Subendocardial ischemia: non-totals

Hibernating: LV systolic dysfunc. Reversibly w/ revascularization.

Stunned: short-term ischemia.

Ischemic preconditioning: Brief episodes of ischemia prepare for prolonged episodes of ischemia.

Vent remod: weeks

Dressler syndrome

Type III.

Other MI comp:

• Fibrinous pericard: 1-3w

Carcinoid HD: intestinal tumors secrete serotonin. Elev 24-urinary-5-hydroxyindoleacetic acid. RHF

Carcinoid syndrome: flushing, diarrhea, wheezing, intestinal tumors.

Atherosclerosis:

• Causes AAA

• Transmural inflamm w/ foam cells in tunica intima

Dissection:

• HTN → intimal tear.

• Cocaine, Marfan

• Complication: tamponade

• Myxomatous chng

• Marfan-related Aortic Root Disease:

  • Cystic Medial Degeneration: mucopolysaccharide.

“Crescendo-decrescendo mid-systolic murmur” means….

Ejection. AS, PS, HOCM

R-sided valves: PT

• R murmurs get louder on inspiration

• Except: HCM (L-sided but louder w/ insp)

L-sided valves: AM

• L murmurs get louder on exhalation

• Except: HCM (L-sided but louder on inspiration)

AV valves: TM

• Close, beginning systole (S1)

• Start of isovolumetric contraction

• Aortic P lowest during this time

Semilunar valves: AP

• Close @ end of systole (S2)

• Start of isovolumetric relaxation

Systolic murmurs “AM PT”: aortic sten, mit regurg, pulm sten, tri regurg

• Happen during ventricular contraction

• Between S1 & S2

Diastolic murmurs “AM PT”: aortic regurg, mit sten, pulm regurg, tri sten

• Happen during atrial contraction

• Between S2 & S1

Ejection murmurs:

AS, PS, HOCM.

“Crescendo-decrescendo” mid-systolic.

 ↑afterload after & ↑EDP before affected valve due to valve obstruction during ejection

Holosystolic murmurs:

MR, TR, VSD.

Stenotic murmurs

↑P gradient across the valve to get blood across obstruction. ↑P before valve, ↓P after.

Mitral stenosis has opening snap… while mitral prolapse has

systolic click.

Mitral prolapse → regurg

HCM, endocarditis, RHD, congenital (Downs/cushion defect) → mitral regurg

Crescendo-decrescendo mid-systolic ejection.

AS, PS.

Early peaking murmur indicates early stenosis, late = severe

Ortner syndrome

Mitral stenosis → hoarseness from impingement of recurrent laryngeal n by enlarged LA → dysphagia

Kussmaul’s sign

increased JVP w/ inspiration

• seen in constrictive pericarditis along w/ pericardial knock, PParadoxus (>10mmhg drop in systolic w/ insp), calcification

Tamponade

• Beck triad: muffled sounds, hypotension, JVD

• PParadox (>10mmHg systolic drop w/ insp)

• Pulsus alternans (beat-to-beat variation in pulse amplitude (systolic BP)

• Electric alternans: EKG conduction voltage R wave changes in R wave from sloshing

• Equalization of pressures (four chambers become one)

• Accentuated x descent (rapid drop in RAP)

Digoxin

• Inhibits Na/K ATPase → indirectly limits Na/Ca exchange → contractility/+inotrope

• Last resort refractory

• Low K increases toxicity but it can lead to hyperkalemia

• Do not use in AV block, brady, sick sinus, PVCs, WPW w/ Afib

What drug combo reduces mortality in African-American pts?

Hydralazine & Isosorbide dinitrate

PeRsistent/ “wide” S2 split:

• Present throughout insp/exp, but wider during insp & narrower during exp

• R-sided delay

• Pulm HTN (“loud P2”), RBBB

Fixed S2 split:

• ASD

• Present throughout insp/exp

ParadoxicaL S2 split:

• Only split in exp, normal insp

• L-sided delay

• LBBB

• Pulmonic closes first

• AS

*Cause of all splits is increased venous return*

Murmur grading

RUSB: AS

LUSB: Pulm, PDA

LSB (Erb’s): AR, HCM

LLSB: Tricusp

Apex: Mitral

PMI lateral shift = enlarged L heart

PMI epigastric/subxiphoid = enlarged R heart

AS & HOCM sound similar, both being ejection murmurs & all…

AS gets quieter w/ Valsalva while HOCM gets louder!

DeMusset’s sign

head bobbing. Seen in AR