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



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
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)

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?
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

>20mmHg drop in systolic pressure between supine and sitting &/or standing measur­ements
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
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

Charac­terized by insuff­icient oxygen supply to cardiac muscle
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
Lifestyle changes, NO, nitrates, B-bloc­kers, CCB, Ranola­zine, ASA/Cl­opi­digrel, revasc­ula­riz­ation


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)
1) Thiazide or Loop diuretic + ACEi. 2) CCB (amlod­ipine). 3) Antico­agu­lants or antiar­rhy­thmics 4) Pacers­/di­fib­ril­lators 5) Coronary revasc­ula­riz­ati­on/­tra­nsplant

EKG Locations

V1, V2
V1, V2
V1, V2, V3
V4, V5, V6


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
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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