Clin Med Cards 1

BP equation

Cardiac output (HR x stroke volume) times the Systemic Vascular Resistance

Stages of hypertension

Elevated: 120-129 / <80

Stage 1 HTN: 130-139 / 80-89

Stage 2 HTN: >140 / >90

default to the highest diagnosis (BP 115/90= stage 1 HTN)

Primary vs secondary HTN

Primary= unidentifiable cause (genetics, sodium, sympathetics, etc)

Secondary HTN= single identifiable cause (when onset, severity, or treatment response is abnormal)

Patho of primary HTN

Na+/volume

Ang II→ vasoconstriction, aldosterone→ water retention

Sympathetic tone: increases heart rate, contractility, and vasoconstriction

Vascular remodeling: persistent vasoconstriction increases systemic vascular resistance

Signs of injury from HTN

Creatinine/eGFR

Urine albumin:creatinine ratio

ECG

Heart, brain, retina, kidney, vasc ROS/exam

Signs of causes of HTN

Electrolytes+calcium

Glucose/A1c

TSH

Lipid profile

Red flags for secondary HTN

Abdominal bruit/creatinine rise after RAAS blockade

hypokalemia/endocrine sx

Episodic headaches+palpitations+diaphoresis

Sleep apnea

Drugs that can cause secondary HTN

NSAIDs, estrogen contraceptives, stimulants/sympathomimetics, cocaine/meth

Renal causes of secondary HTN

Renal parenchymal disease, renovasc disease (atherosclerotic RAS, fibromuscular dysplasia)

Endocrine causes of secondary HTN

Aldosteronism, Cushing, Pheochromocytoma, Thyroid, Hyperparathyroid

Random other causes of secondary HTN

Sleep apnea, coarcation of aorta, pregnancy, high ICP

difficulties when medicating HTN

Most patients need more than one medication to treat their HTN

When to initiate medication in someone with HTN

BP above 140/90 (unless they have a high risk condition)

Four first-line treatment classes

Thiazide-type diuretics

ACE inhibitors: lower angio II (watch for cough, avoid pregnancy) (-pril)

ARB: block AT1 receptor (avoid pregnancy)(-sartan)

DHP CCB: dilate arteries (watch for edema and headache) (-dipine)

What drug is not a first line treatment for HTN, and more reserved for HTN with comorbid heart disease?

Beta-blockers

treatment for stage 2 HTN

2 first-lines from different classes (but do NOT combine ACEi with ARB)

Treatment to consider for resistant stage 2 HTN

spironolactone

What are the two things that can define a hypertensive emergency

180/120 or higher, without organ damage (hypertensive urgency)

any severe BP elevation with organ damage (esp heart, brain, aorta, kidney, retina) (emergency)

Signs of HTN organ damage (for brain, heart, aorta, kidney, eye, pregnancy)

Brain: encephalopathy, ICH, stroke

Heart: ACS, pulmonary edema

Aorta: dissection

Kidney injury

Eye: retinopathy, papilledema

Pregnancy: pre/eclampsia

Malignant hypertension

Encephalopathy or nephropathy, accompanied by hypertensive retinopathy

Encephalopathy or nephropathy, accompanied by hypertensive retinopathy

Malignant HTN

regulations for treating HTN emergency with no compelling condition

Decrease MAP no more than 25% in the first hour

Common IV agents to treat HTN emergency

Nicardipine, labetalol, clevidipine, esmolol, nitroglycerin

Risk of lowering BP too fast

ischemia, especially kidney injury

Heart works harder because of reduced blood flow, leading to ischemia

Demand ischemia

What parts of the heart are often hypertophic with HTN

left ventricle

Left atrium (causing Afib)

chylomicrons

dietary triglycerides, from intestine→ tissues

VLDL

TG-rich, liver→tissues

LDL

Cholesterol-rich

delivers cholesterol, atherogenic

HDL

Reverse-transport (good lipoprotein, from the liver)

Key factor of atherosclerosis

apoB-containing particles (especially LDL and triglyceride-rich remnants)

Steps of atherosclerosis

endothelial dysfunction

lipoprotein entry (into intima)

inflammation (monocytes→macrophages→foam cells)

Fibrous plaque (smooth muscle and matrix form a cap over the lipid)

Ruptured plaque (with platelet activation)

difference in clinical pattern of stable vs ruptured plaque

stable: chronic ischema or stable angina, or PAD claudication

ruptured: acute coronary syndrome or ischema

High LDL-C vs high triglycerides vs mixed lab results

LDL-C: hypercholesteremia (above 190=severe)

Triglycerides: above 150= high, above 500= pancreatitis concern

Mixed: common with diabetes, obesity, CDK, etc. Other secondary causes

Secondary causes of Dyslipidemia

Diabetes, hypothyroidism, CKD, alcohol, medications, diet

When to treat a patient with dyslipidemia and CKD or HIV

give a statin at age 40-75 regardless of LDL-C

Signs of dyslipidemia

Xanthelasma, tendon xanthoma (fat on tendons), eruptive xanthomas (papules), lipoma retinalis (creamy-colored retinal veins),

metabolic dysfunction-associated liver disease

pancreatitis

Clinical ASCVD

ACS, prior MI, angina, coronary or arterial revascularization, stroke or TIA, peripheral arterial disease

Diagnostic workup for ASCVD

HDL-C, triglycerides, calculated LDL-C

add Lp(a) once in adulthood

Selective apoB if triglycerides are elevated or diabetic

Screening guidelines for adults and children with no ASCVD risk

adults at age 19, and every 5 years. Lp(a) at least once

children once from 9-11

LDL-C goals

100> for low-risk

70> for high-risk

55> for very high-risk

Moderate vs high-intensity statin impacts

Moderate: 30% lower LDL-C

High: 50% lower LDL-C

Risks of high-intensity statins

Myopathy, rhabdomyolysis (muscle components building up in blood)

Nonstatins

Ezetimibe, Bempedoic acid

PCSK9 mAb, Inclisiran (the two strongest)

What to treat hypertriglyceridemia in a high-risk patient

icosapent ethyl

What to treat SEVERE hypertriglycerinemia

Fibrate ± Omega-3

Difference between ischemia and infarction

Ischemia CAUSES infarction. Infarction is cell death, and can be seen on MRI

Stable vs unstable angina

Stable=fixed plaque

unstable=platelet aggregation

Type 1 vs type 2 NSTEMI

1= atherosclerosis

2= supply vs demand; sepsis, hypoxia, tachycardia (heart is overworked, and normal O2 supply is insufficient)

why is aspirin given in CAD

to prevent platelet activation

classic cause of widened mediastinum

aortic dissection

Normal ST elevation in females vs males (V2 and V3 specifically)

>1.5mm on females, >2mm on males
(all other leads is >1mm)

What leads localize to which area?

II, III, aVF = Inferior

V1-V4 = Anterior/septal

I, aVL, V5, V6 = Lateral

VERY IMPORTANT TO KNOW THESE star this card

what do you need to classify a STEMI on an ECG

ST elevation in 2 or more contiguous leads

STEMI in V1-V4

LAD (left interventricular)

STEMI in II, III and aVF

RCA

STEMI in I, aVL, V5-V6

Left Circumflex Artery, Diagonal Artery

What is a goal heart rate for stress test?

85% of predicted (predicted is 220-age)

What is a CAC?

Coronary artery calcium test

100-400=med risk (do more diagnostics)

Elderly, exertional chest pain, relieved with rest or nitro, resolves in under 5min

Stable angina

Diagnosis of stable angina

Atherosclerosis with Stable plaque

Supply vs Demand Mismatch

Dx’d when NSTEMI/STEMI ruled out

hx of illicit drug use (especially cocaine), reynauds, or migraines, japanese descent. Chest pain (usually at rest, and at night) and elevated troponin, but clean coronaries

Vasospasm

Relieved by nitro,

Cocaine treated with Benzos,

migraine/japanese/reynauds treated with CCBs

HEART score

History, ECG, Age, Risk factors, Troponin

go home w f/u <4<moderate; observation/next day eval <6< admit for cardio eval

chest pain at rest, not relieved by anything

Unstable angina

Normal troponin

<20

(above =STEMI or NSTEMI)

Diffuse ST depression with ST elevation in AVR

Left Coronary Artery occlusion

Unstable angina treatment

Aspirin, nitro, plavix, heparin (bolus+drip),

How fast to get an EKG?

less than 10 min

Door to balloon time for stemi?

90 min

Complications of a STEMI

Cardiac death, arrhythmias, cardiogenic shock, pericarditis

chest pain, fever, pericardial effusion

Pericarditis

modifiable risk factors for MIs

smoking, dyslipidemia, HTN, diabetes, obesity, psychosocial, diet, alcohol, sedentary

What is a sedentary lifestyle defined as?

less than 20 minutes of activity less than 3x per week

What is involved in a preoperative eval

Focused history and physical

Cardio, pulm, and anesthesia risk assessment

if indicated, labs/ecg/imaging

perioperative med management

prior DVT or leg injury, edema, brawny hyperpigmentation, venous ulcers, telangiectasias

chronic venous insufficiency

Age presentations of CVI in women vs men

Women- age 40

Men- age 70

timeline of chronic venous disease worsening

telangiectasias,

edema,

pigmentation,

ulcer

(c4-c6 is most severe stages of the disease)

Conservative treatments of chronic venous insufficiency

compression, elevation, exercise (esp calves), weight loss

Check the ABI (BP at the ankle) before prescribing compression, because peripheral artery disease often coexists

what veins most commonly become varicose?

Great and small saphenous

Management of varicose veins

Compression stockings,

sclerotherapy

Endovenous thermal ablation

virschow’s triad

Hypercoagulability, vascular damage, circulatory statis

indicates risk for DVT

Homan’s sign

Pain with dorsiflexion of the foot

Usually indicates a DVT (not super specific, though)

phlegmasia cerulea dolens (swelling, blue, pain), dyspnea, pleuritic chest pain, syncope
red flags for:

DVT
Phlegmasia Cerulea Dolens=urgent thrombus removal

DVT diagnostic steps

Wells score under 1=unlikely (d-dimer), above 2=likely (ultrasound)
d-dimer positive=ultrasound

general treatment for DVT

DOACs (-xaban) for at least 3 mo

Red, painful induration along a superficial vein, often at the site of an IV

Superficial venous thrombosis

Treatment of Superficial Venous Thrombosis

If less than 3cm from the femoral vein, treat like DVT

If more than 5cm long, fondaparinux for a month

if less than 5cm long, NSAIDS

(in general, Long or Close to deep system, anticoagulants. Short and distal, supportive)

Exertional calf pain, relieved with rest within 10 min.
weak pulses, bruit, delayed cap refill, hair loss, wounds, pallor on elevation

Peripheral artery disease

Diagnosis of PAD

Ankle Brachial index, then treadmill ABI

Breakdown of ABI

less than 0.9 is PAD, above 1 is normal

Toe brachial index indication, and what’s the abnormal result?

ABI above 1.4→do TBI

less than 0.7 indicates PAD

treatment for PAD

Walking, low dose antithrombolytics

persistent claudication: cilostazol

maybe revascularize

pain while resting, nonhealing ulcer/wound, worsens at night

Limb-threating chronic ischemia

Limb-threating chronic ischemia treatments

revascularize whenever possible

Acute limb ischemia diag requirements

hypoperfusion for less than 2wks

pain, pallor, pulselessness, poikilothermia, parasthesia, paralysis

acute limb ischemia treatment

Immediate heparin, immediate revascularization

Nicotine user with distal arterial ischemia, with or without migratory superficial thrombosis. Atherosclerosis ruled out

Thromboangiitis obliterans

Why is popliteal artery aneurysm dangerous?

It thromboses and embolizes (it doesn’t usually rupture)

What drug treats claudication, and what is a contraindication for it?

cilostazol- contra in heart disease

S3 (increased atrial pressure), crackles, displaced apical impulse

dyspnea on exertion, orthopnea, fatigue, edema

Left ventricular HF