patho II sec 4

what is collateral circulation

development of alternative vascular channels that perfuse myocardium distal to a stenosis

what comprises coronary artery disease

chronic coronary disease and acute coronary syndromes

what are the acute coronary syndromes

unstable angina, NSTEMI, STEMI

what causes chornic coronary diseases

a mismatch in myocardial oxygen supply and demand

what can alter oxygen supply

atherosclerosis, vasospasm, anemia, hypoxia

when does coronary perfusion occur and what condition impacts it

in diastole, with tachycardia there is less time for the coronary arteries to fill

what are the determinants of myocardial oxygen demand

HR, contractility, ventricular wall stress (preload, afterload)

how does angina usually present

transient chest pain

what features of chest pain are suggestive of ischemia

dull pain, worse with activity, broad area, lasts <20 mins, brought on by effort/emotion, relieved by rest/nitro

what features of chest pain are less suggestive of ischemia

sharp pain, no change with rest, pinpoint, lasts seconds to hours, brought on with food or a deep breath, improved with movement

what features of cardiac chest pain are suggestive of stable angina

exertional, predictable, lasts <20 mins, relieved with rest/nitro

what features of cardiac chest pain are concerning for ACS

new or worsening pain, occurs at rest, lasts >20 mins, not relieved by rest

what are risk factors of coronary artery disease

cigarette smoking, HTN, HLD, DM, men >45/women>55, FHx of premature CAD (male <55/female <65), obesity, physical activity

what are the key differences between the old pooled cohort equation for ASCVD risk score and the new PREVENT score

does not include rase, includes eGFR and BMI, broader model

what is coronary artery calcium and what is it reported as

calcium deposition within an atherosclerotic plaque

reported as an agaston score

what is clinical ASCVD

patients with one or more of the following:

CAD

stroke/TIA

peripheral artery disease

what causes prinzmetal angina

coronary vasospasm

what causes acute coronary syndrome

supply/demand mismatch, unstable plaque/plaque rupture, platelet aggregation, myocardial cell death

what is type 1 MI

spontaneous artery occlusion (plaque rupture)

what is type 2 MI

injury due to supply/demand mismatch (without acute occlusion)

what is type 3 MI

sudden cardiac death due to myocardial ischemia

what is type 4 MI

MI associated with percutaneous coronary intervention

what is type 5 MI

MI associated with CABG

what signs are used to evaluate MI

EKG and cardiac markers

what symptoms are used to evaluate MI

chest pain

how do you diagnose STEMI

chest pain+ ST elevation+elevated cardiac markers

how do you diagnose NSTEMI

chest pain+ non-ST elevation+ elevated cardiac markers

what causes ST elevation seen in STEMI

transmural injury (extends through the whole width of the myocardium)

what causes ST depression seen in NSTEMI

subendocardial injury (localized injury to the inner myocardium)

what cardiac marker is measured in STEMIs

high sensitivity troponin

what else is elevated post MI

AST

what scores on the TIMI indicate low, intermediate, and high risk

low: 0-2

intermediate: 3-4

high: 5-7

what scores on the grace ACS calculator is low, intermediate, and high risk for NSTEMI

low: 1-108

intermediate: 109-140

high: 141-372

what scores on the grace ACS calculator is low, intermediate, and high risk for STEMI

low: 49-125

intermediate: 126-154

high: 155-319

how does type 2 MI relate to type 1 MI

mortality is at least as high with type 2 as type 1

patients are usually older, female, and it presents with loewr peak troponin

what is heart failure

a complex clinical syndrome characterized by symptoms and/or signs resulting from structural or functional impairment of ventricular filling or ejection

what is HFrEF

LVEF ≤40%

what is HFimpEF

previous LVEF 40%

what is HFmrEF

LVEF 41-49%

what is HFpEF

LVEF >/=50%

what compensations are made for the decreased CO in HF

increased NE activation of SNS

increased activation of RAAS (more angII and aldo) leads to volume expansion and sodium retention

what labs are used to diagnose HF

BNP or NT-proBNP

what levels of BNP and NT-proBNP clue into HF diagnosis

BNP >/=35

NT-proBNP >125

when is BNP released

in response to ventricular stretch

when is BNP useful

in initial diagnosis and in determining prognosis

what are the signs of HF

peripheral edema, JVD, pulmonary rales, tachycardia, tachypnea, cardiomegaly, increased BNP

what are the symptoms of HF

dyspnea, orthopnea, exercise intolerance, cough, mental status changes

what are symptoms of forward failure

fatigue, exercise intolerance, tachycardia, cool extremities

what is the patho behind forward failure

decreased CO decreases organ perfusion leading to SNS activation

what are the symptoms of backward failure

left sided: dyspnea, orthopnea, rales

right sided: JVD, peripheral edema, hepatic congestions

what is the patho of backward failure

RAAS activation leads to sodium and water retention causing volume expansion and congestion

what are risk failures for HF

HTN, ASCVD, DM, obesity, metabolic syndrome, FHx

what are the AHA/ACC stages of HF

stage A: at risk

stage B: structural disorder or abnormal biomarkers with no Sx

stage C: structural disease with current or prior symptoms

stage D: HF refractory to treatment

what are the NYHA classes

I: no activity limitation

II: ordinary physical activity causes Sx

III: less than ordinary activity causes symptoms

IV: symptoms at rest

what is the frank-starling curve

as ventricular EDV goes up, stroke volume goes up...until the sarcomere exceeds optimal length when it goes down

what is inotropy

ability of the heart to contract

what problem causes HFpEF

the heart cant fill properly, the pumping function is intact

why does decreased filling and normal EF cause HF symptoms

stiff LV leads to increased filling pressures and pulmonary congestion which lowers the end diastolic volume and decreases SV

what is a common symptom of right-sided HF

peripheral edema

what are common causes of right-sided HF

left sides HF, pulmonary HTN, cor pulmonale

what is a symptom of acute HF

flash pulmonary edema

what is the normal value for CO

4-6 L/min

what is the normal value for CI (cardiac index)

2.8-4.2 L/min/m2

what is the normal value for CVP (central venous pressure)

<5mmHg

what is the normal value for MAP

70-110mmHg

what is the normal value for PCWP (pulmonary capillary wedge pressure)

<12mmHg

what is the normal value for SVR (systemic vascular resistance)

900-1400 dyne.s/cm5

what are the compensatory mechanisms for shock to maintain MAP

increase NE/E, increase HR/contractility, increase angII/aldo, increased vasopressin > water retention

what is cardiogenic shock caused by

pump failure (MI)

what is hypovolemic shock caused by

massive fluid loss (blood loss, burns, dehydration, overdiuresis)

what is obstructive shock caused by

mechanical obstruction of blood flow (dissection aortic aneurysm, cardiac tamponade, pulmonary embolism)

what is distributive shock caused by

loss of vascular tone (enlarged vascular compartment)

what does high CO in distributive shock indicate

early septic shock

what are the 3 types of distributive shock

neurogenic, anaphylactiv, septic

what is HR/MAP/CI/SVR seen in distributive shock

high HR, low MAP, high CI, low SVR

what is HR/MAP/CI/SVR seen in cardiogenic shock

high HR, low MAP, low CI, high SVR

what is HR/MAP/CI/SVR seen in hypovolemic shock

high HR, low MAP, low CI, high SVR

what are signs of low perfusion

cool extremities, low urine output, altered mental status, azotemia

what are signs of congestion

JVD, peripheral edema, SOA, orthopnea, rales, weight gain

what is the hemodynamics of low perfusion and low congestion

dry and cold

what is the hemodynamics of high perfusion and low congestions

dry and warm

what is the hemodynamics of low perfusion and high congestion

wet and cold

what is the hemodynamics of high perfusion and high congestion

wet and warm

what are the complications of shock

death, ARDS, acute renal failure, mental status changes, hepatic failure

what is the pathway through the conduction system

SA node > AV noded > bundle of his > purkinje fibers

what cell is the pacemaker cell

SA node

what is phase 0 of an AP and what causes it

rapid depolarization caused by Na channels opening

what is phase 1 of an AP

early repolarization

what is phase 2 of an AP and what causes it

plateau caused by Ca channels opening

what is phase 3 of an AP and what causes it

rapid repolarization caused by K channels opening

what is an absolute refractory period

cell is insensitive to stimuli

what is a relative refractory period

more intense stimuli is required for a response

what is a supernormal excitatory period

weak stimuli can initiate a response

what is the P wave on an EKG

atrial depolarization

what is the QRS complex on an EKG

ventricular depolarization and (hidden) atrial repolarization

what is a T wave on an EKG

ventricular repolarization

how does sinus bradycardia present

normal P wave and PR interval

slow HR (<60 bpm)

how does sinus tachycardia present

normal P wave and PR interval

rapid HR (>100bpm)

how does sinus arrest present

SA node fails to discharge causing a "skipped beat"

what are the types of supraventricular arrhythmias

premature atrial contraction, supraventricular tachycardia, atrial flutter, atrial fibrillation