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

A Home & Health › Medical cheat sheet in English by ksellybelly

Cardiology

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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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