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Cardio I: Shock, CHF, HTN, ACS Cheat Sheet by

Cardiology
medical     medicine     pathophysiology     shock     cardiology     heart

Shock

Defi­nit­ion
Severe cardio­vas­cular failure caused by poor blood flow or inadequate distri­bution of flow
1) Hypovo­lemic Shock
Hemorr­hage, fluid loss, loss of plasma or electr­olytes. All result in decreased intrav­ascular volume. Caused by obvious loss or subtle third-­space seques­tra­tion.
2) Cardio­genic Shock
MI, dysrhy­thmias, heart failure, valve/­septal failure, HTN, myocar­ditis, cardiac contusion, septum rupture, myocar­dio­pathies
3) Obstru­ctive Shock
Tension PTX, perica­rdial tamponade, obstru­ctive valvular disorder, pulmonary embolism
4) Distri­butive Shock (poorly regulated distri­bution of blood volume)
Septic shock, SIRS (signs of systemic inflam­mation w/out end-organ damage), anaphy­laxis, neurogenic shock
Clinical features
Hypote­nsion + Tachyc­ardia (also AMS, orthos­tatic changes, metabolic acidosis, insulin resist­ance, oligur­ia/­anuria, peripheral hypope­rfu­sion)
Sign of end-organ hypope­rfu­sion
Cool or mottle extrem­ities, and weak ("th­rea­dy") or absent peripheral pulses
Trea­tment
1) ABCs. 2) Treat the underlying cause. 3) T-Burg maximizes brain perfusion 4) O2 + IV fluids 5) Urine output at least 0.5 mL/kg/hr 6) Cardiac monitoring and central venous pressure 7) Pressors (Dopamine, etc.) will increase GFR, contra­cti­lity, HR

ACS (Acute Coronary Syndromes)

Defi­nit­ion
Spectrum of problems ranging from unstable angina to MI
Clas­sified into 2 types
ST-ele­vated and Non-ST­-el­evated events
Most common etiology of MI
Preexi­sting athero­scl­erotic plaque­-->­thr­ombus format­ion­-->­pro­longed myocardial ischem­ia-­->MI
What is a common cause of death in MI patients before they can get to hospit­al?
V-fib
Clinical features
**Chest pain (most common), sweating, anxiety, weakness, dyspnea, light-­hea­ded­ness, syncope, N/V, fever
EKG changes
Acute MI: progre­ssion from peaked T-wave­s--­>ST­-de­gment elevat­ion­/de­pre­ssi­on-­->Q­-wa­ve-­->T­-wave inversions (hours­-days)
**One of the most sensitive tests to quantify extent of infarction
MRI w/ gadolinium
Trea­tme­nt--all patients
IV fluids + O2 + NO + pain management +/- benzo + anti platel­et/­ant­ico­agu­lation + B-blockers +/- CCBs
Trea­tme­nt--ACS + STEMI
Reperf­usion intere­ntion: aspirin + clopid­ogrel, coronary angiog­raphy w/in 90 min, thromb­olytic therapy, statin therapy
 

Orthos­tas­is/­Pos­tural Hypote­nsion

Defi­nit­ion
>20mmHg drop in systolic pressure between supine and sitting &/or standing measur­ements
Etio­logy
May be related to reduced cardiac output, paroxysmal cardiac dysrhy­thmias, low blood volume, medica­tions, and various metabolic and endocrine disorders
A reversible cause of syncope and major cause of falls in this popula­tion
Elderly
If the cause is depleted blood volume
then there will also be a rise in pulse of more than 15 bpm when testing orthos­tatics
If there is no change in pulse accomp­anying the change in BP
then consider CNS disease or peripheral neurop­athies
Labs and Treatm­ent
Directed at the specific cause

Ischemic Heart Disease

Defi­nit­ion
Charac­terized by insuff­icient oxygen supply to cardiac muscle
Etio­logy
1) **Athe­ros­cle­rotic narrowing (most common). 2) Constr­iction of coronary arteries. 3) (Rare) congen­ital, emboli, arteritis, dissection
Risk Factors
Metabolic syndrome, male, older age, smoking, FmHx, HTN, DM, low-es­trogen state, abdominal obesity, inacti­vity, dyslip­idemia, EtOH, low fruits­/ve­ggies (cocai­ne-­->MI)
Meta­bolic Syndrome is 3 or more of:
abdominal obesity, Tri>150, HDL<40­men­<50­women, fasting sugar>110, HTN
Clinical Features
Angina pectoris (chest squeez­ing­/pr­essure, can radiate, <3m­in.), three types:
1) Stable Angina
Exacer­bated by physical activity, relieved by rest
2) Prinzm­etal's (Variant) Angina
Caused by vasospasm at rest, exercise capacity preserved
3) Unstable Angina
Increasing pattern of pain in previously stable patients. Occurs at rest or with exertion.
Levine's Sign
Clenched fist over sternums and clenched teeth
How to relieve angina
Sublingual nitrog­lycerin
EKG Findings
Horizontal or downsl­oping ST-segment depression
Trea­tment
Lifestyle changes, NO, nitrates, B-bloc­kers, CCB, Ranola­zine, ASA/Cl­opi­digrel, revasc­ula­riz­ation
 

CHF

Defi­nit­ion
Clinical syndrome: dyspnea + water/­sodium retention
Results from changes in 1+ of the follow­ing
Contra­ctile ability of heart muscle, preload and after load of the ventricle, and heart rate
Etio­logies of these changes
MI, perica­rdial disorders, valvular disorders, congenital abnorm­ali­ties, and non cardiac causes (high-­output heart failure from thyrot­oxi­cosis or severe anemia)
CHF adversely affects
Left atrial pressure + cardiac output
Clinical features of LEFT-sided failure
Exertional dyspnea, non-pr­odu­ctive cough, fatigue, orthopnea, PND, basilar rales, gallops, exercise intole­rance
Clinical features of RIGHT-­sided failure
Distended neck veins, hepatic conges­tion, nausea, dependent pitting edema, *edema + hepato­megaly, (R-sided failure often caused by L-sided failure)
Other symptoms of CHF
Nocturia, cold/c­lammy skin, hypote­nsion, narrow pulse pressure, S3 gallop
CXR signs
Kerley B lines (aka inters­titial edema)
Trea­tment
1) Thiazide or Loop diuretic + ACEi. 2) CCB (amlod­ipine). 3) Antico­agu­lants or antiar­rhy­thmics 4) Pacers­/di­fib­ril­lators 5) Coronary revasc­ula­riz­ati­on/­tra­nsplant

EKG Locations

Inferior
II, III, aVF
Posterior
V1, V2
Antero­septal
V1, V2
Anterior
V1, V2, V3
Antero­lateral
V4, V5, V6

Hypert­ension

Primary HTN
Causes 95% of cases of HTN; multif­act­orial pathog­enesis (genetics, salt, obesity, RAAS, NSAIDs, smoking, lack of exercise, metabolic syndrome)
Seco­ndary HTN
coarc. of aorta, RAS, chronic steroids, Cushings syndrome, pregnancy, thyroid and parath­yroid disease, primary hypera­ldo­ste­ronism, parenc­hymal renal dz)
Esse­ntial HTN is exacer­bated in this popula­tion
Males, blacks, sedentary people, smokers
Hype­rte­nsive urgency def.
Must bring down BP within hours
Hype­rte­nsive emergency def.
Must bring down BP within 1 hour to prevent end-organ damage­/death
Mali­gnant hypert­ension def.
Elevated BP + papill­edema + enceph­alo­pat­hy/­nep­hro­pathy. In untrea­ted­-->­pro­gre­ssive renal failure.
Comp­lic­ations of untreated HTN
Cardio­vas­cular dz, cerebr­ova­scular dz, dementia, renal dz, aortic dissec­tion, and athero­scl­erotic compli­cations
Diag­nostic criter­ia-­-es­sential HTN
Systolic >140 OR Diastolic >90 on 3 diff. occasions
Diag­nostic criter­ia-­-hy­per­tensive urgency
Systolic >220 OR Diastolic >125
Diag­nostic criter­ia-­-hy­per­tensive emerge­ncy
Diastolic >130 + papill­edema
Comp­lic­ations of hypert­ensive emerge­ncy
Hypert­ensive enceph­alo­pathy, nephro­pathy, intrac­ranial bleeding, aortic dissec­tion, preecl­amp­sia­/ec­lam­psia, pulmonary edema, unstable angina, MI
Trea­tme­nt-­-HTN
1) DASH diet/l­ife­styles change­s/s­moking cessation. 2) Diuretics (*HCTZ). 3) Beta blockers 4) ACEi 5) ARB 6) CCB
Trea­tme­nt--HTN urgenc­y/e­mer­gency
Parenteral agents, but don't lower BP too fast. Use NO, B-bloc­kers, hydrazine, loops, clonidine, nifedipine

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