H+I 3 - Exam 1

Perfusion

Flow of blood through arteries / capillaries delivering O2 and nutrients to cells and removing waste.

Central perfusion

Blood flow generated by cardiac output (the pump + circulating volume)

Tissue / local perfusion

Volume of blood flowing through a specific target tissue/organ.

Ischemia

Blood supply is available but decreased - reversible if flow is restored.

Infarction

Death of tissue from prolonged uncorrected ischemia

Anoxia

Complete loss of oxygen supply

Cardiac out put

HR x SV - normal 4-8 L/min

Stroke volume (SV)

amount of blood ejected per beat; determined by preload, afterload, and contractility p

Preload

volume/stretch in the ventricle at end of diastole “how full the tank is before it squeezes”

Afterload

Resistance the ventricle must pump against to eject blood

Contractility

Force of ventricular contraction independent of preload/afterload

BP

CO x SVR

Ejection fraction (EF)

% of end diastolic ventricular volume ejected with systole; normal 55-65%

Autonomic Nervous System (ANS)

Sympathetic = increased HR, increased contractility, vasoconstriction

Parasympathetic = decreased HR

Baroreceptors

Detect BP changes and trigger ANS response

Chemoreceptors

Detect O2/CO2/pH changes and adjust HR and respiratory rate

RAAS (renin-angiotensin-aldosterone-system)

decreased renal perfusion → renin → angiotensin 1 → angiotensin 2 (potent vasoconstrictor) → aldosterone (Na+/water retention) → increases BP and preload

Atherosclerosis

Develops in the presence of endothelial damage and chronic inflammation

Stage 1 of Atherosclerosis

endothelial injury / inflammation - the initiating event

Stage 2 of Atherosclerosis

fatty streak - lipids accumulate in smooth muscle cells; earliest visible lesionv

Stage 3 of Atherosclerosis

fibrous plaque - arterial wall thickens as LDL/lipids build up and are covered by collagen

Stage 4 of Atherosclerosis

complicated lesion - plaque ruptures → thrombus forms → platelets aggregate (glycoprotein IIB/IIIA binds fibrinogen, recruiting more platelets) → vessel occlusion

Statins (atorvastatin, lovastatin, pravastatin)

inhibit cholesterol synthesis: decreasing LDL and increasing HDL

Statins nursing points

monitor LFTs and for myopathy / rhabdomyolysis, especially combined with niacin; take in evening

Niacin (vitamin b3)

decreases triglycerides and LDL, increases HDLN

Niacin nursing points

flushing and pruritus common; take with aspirin/NSAID to reduce flushing

Fibric acid derivatives (gemfibrozil)

decreases triglycerides and increases HDL

Fibric acid derivatives nursing points

gi upset, increased bleeding risk with warfarin

Chronic stable angina

transient, reversible myocardial ischemia from a fixed atherosclerotic obstruction - pain with exertion/stress, relieved by rest and/or nitroglycerin

Chronic stable angina therapy goal

reduce O2 demand and/or increase O2 supply

Chronic stable angina diagnostics

12 lead ekg, chest x-ray, echocardiogram, exercise stress test, labs (cardiac biomarkers, lipid profile, CRP)

Unstable angina cause

ruptured plaque, partial occlusion; ischemia at rest, new onset, or increasing pattern

Unstable angina ECG

ST depression and t wave inversion (no permanent change), no bio marker elevation

Unstable angina urgency

progressing to infarction if untreated

NSTEMI cause

partial coronary occlusion causing myocardial necrosis

NSTEMI ECG

ST depression/T wave inversion; NO ST elevation

NSTEMI biomarkers

elevated troponin

NSTEMI urgency

urgent - needs anticoagulation/antiplatelets possible PCI

STEMI cause

complete/total cornary occlusion S

STEMI ECG

ST elevation / new LBBB (left branch bundle block)

STEMI biomarkers

elevated troponin

STEMI urgency

EMERGENT - reperfusion within 90 min (PCI) or fibrinolytics

ACS manifestations

chest pain unrelieved by rest or nitroglycerin lasting >15-20 mins, dyspnea, diaphoresis, cool/clammy skin, pallor, nausea/vomiting, epigastric discomfort, anxiety, sense of impending doom, atypical presentation in women, older adults, and diabetics: fatigue, indigestion like discomfort, back/jaw pain, dyspnea without chest pain

Myoglobin

Earliest to rise but NOT cardiac specific (can be associated with skeletal muscle damage/rhabdomyolysis)

CK-MB

Cardiac specific isoenzyme, useful for detecting reinfarction

Troponin

Most sensitive/definitive marker for myocardial injury

THROMBINS2

T - theinopryidines (clopidogrel/plavix)

H - heparin / enoxaparin

R - RAAS blockers (ACE inhibitors)

O - oxygen

M - morphine

B - beta morphine

I - intervention (PCI)

N - nitroglycerin (SL)

S2 - Statin (80mg) / salicylate (aspirin 162-325mg)

PCI (percutaneous coronary intervention)

first line for STEMI - door to balloon goal less than 90 mins at a PCI capable hospital

Fibrinolytic / thrombolytic therapy

used when PCI is not available within 120 mins; door to needle goal less than 30 mins

Intra aortic balloon pump (IABP)

Inflates during diastole ( increased coronary perfusion), deflates just before systole (decrease afterload) - a bridge therapy for cardiogenic shock / severe HF

Impella (ventricular assist device)

percutaneous device that directly unloads the ventricle and augments cardiac output

Complications of ACS/MI

post mi chest pain, cardiac tamponade, dysrhythmias, ventricular remodeling, cardiogenic shock

Cardiogenic shock

HR high (compensatory), BP is normal then low as it progresses, CO/CI low (core problem), CVP/PAWP high (backup of volume behind the failing pump), SVR high (compensatory vasoconstriction), SVO2 low (tissue extracting more O2 due to poor delivery)

Cardiogenic shock physical assessment

dyspnea/pulmonary congestion, pallor, cool/clammy skin, decrease cap refill, anxiety, confusion, agitation, decreased UO

Cardiogenic shock goal

restore balance between myocardial O2 supply and demand / restore adequate CO

Cardiogenic shock medications

nitrates, positive inotropes, vasopressors, diuretics, beta blockers

Cardiogenic shock procedures

emergent PCI/revascularization, IABP, impella, possible CABG

Hypovolemic shock

not enough volume in the tank

Cardiogenic shock

The pump has failed

Obstructive shock

something blocks flow to/from the pump

Distributive shock

Pipes too big - massive vasodilation

Systole

Ventricular contraction / ejection

Diastole

ventricular relaxation / filling

Left sided HF cause

LV fails to empty (systole) or fill (diastole) adequately

Left sided HF blood backs up into

pulmonary circulation → lungs

Left sided HF signs and symptoms

dyspnea, orthopnea, paroxysmal nocturnal, dyspnea, crackles/rales, cough (frothy pink sputum if pulmonary edema), s3 heart sounds, fatigue, activity intolerance

Right sided HF cause

most common cause is left sided HF; also cor pulmonale, PE

Right sided HF blood backs up into

systemic venous circulation → body

Right sided HF signs and symptoms

peripheral/dependent edema, JVD, hepatomegaly, abdominal ascites, weight gain, gi bloating/anorexia

HFrEF problem

ventricle cannot contact / eject normally

HFrEF EF

<40% ( can be as low as 5%)

HFrEF primary cause

closely associated with CAD/MI (damaged muscle cant contract)

HFrEF CO variable

contractility decreased → decreased SV

HFrEF therapy

ACE/ARB/ARNI, beta blockers, aldosterone antagonist, SGLT2i

HFpEF problem

venticle cannot relax/fill normally (diastolic failure)

HFpEF EF

Normal but CO is still inadequate because SV is low

HFpEF cause

primary cause is hypertension

HFpEF CO variable

preload/filling decreased → decreased SV despite normal EF%

HFpEF therapies

focus is symptom control + treating underlying HTN/conditions