CHF, shock

cardiac diseases

congestive heart failure, shock

congestive heart failure

heart's inability to pump sufficiently to meet metabolic needs of body causing decreased tissue perfusion due to decreased cardiac output

acute congestive heart failure

pulmonary edema, cardiogenic shock

chronic congestive heart failure

left-sided heart failure, right-sided heart failure

congestive heart failure pathophysiology

damage to the pump leads to decreased cardiac output and decreased tissue perfusion

congestive heart failure causes

any condition that damages or overworks the heart muscle; coronary artery disease, high blood pressure, diabetes, cardiomyopathy, heart valve disease, arrhythmias, congenital heart defects

systolic dysfunction

decreased contractility; ventricle experiences damage and doesn't contract effectively; stroke volume decreases with increased preload; ventricle becomes distended with decreased cardiac output

diastolic dysfunction

restriction in ventricular filling; decreased ability of heart to comply; decreased ventricular filling (preload); decreased stroke volume with hypotension

compensation: Frank-Starling mechanism

force of contraction determined by amount of stretch; greater the stretch, greater the contraction; increased force leads to increased cardiac output; BUT increased myocardial demand

sympathetic nervous system compensation

decreased CO stimulates sympathetic nervous system and catecholamine release; increased heart rate, vasoconstriction, and contractility, increased vascular resistance, increased venous return; BUT decreased filling with tachycardia, increased vascular res

renin-angiotensin system compensation

decreased CO results in decreased renal perfusion that stimulates renin angiotensin system; vasoconstriction and increased BP; BUT increased myocardial work

aldosterone compensation

angiotensin stimulates aldosterone release from adrenal cortex; salt and water retention by kidneys with increased vascular volume and BP; BUT increased preload and afterload; pulmonary congestion

antidiuretic hormone compensation

antidiuretic hormone is released from posterior pituitary; water retention by kidneys, increased vascular volume, vasoconstriction; BUT increased preload and afterload with pulmonary congestion

atrial natriuretic compensation

atrial natriuretic factor is released (stimulated by stretched heart muscle); increased sodium excretion with diuresis; good results

blood flow redistribution compensation

blood flow is redistributed to vital organs (heart and brain); decreased perfusion of other organs, skin, and muscles; BUT renal failure and anaerobic metabolism and lactic acidosis

compensation: ventricular hypertrophy

increased cardiac workload causes myocardial muscle to hypertrophy with ventricles dilated; increased force of contraction to maintain CO; BUT increased myocardial demand, cells enlarge and stiffen with decreased force of contraction

left-sided heart failure

affected more than right side; results in lung congestion (back-up of fluids); increased pulmonary vascular pressure; fluids shift to lungs; pulmonary edema

left-side heart failure s/s

fatigue, dizziness, dyspnea, shortness of breath, cough, orthopnea, crackles, S3 heart sound

right-sided heart failure

caused by pulmonary hypertension; increased pressure that right ventricle must pump against; hypertrophy and dilation; blood accumulates in systemic veins (backs up)

right-sided heart failure

lower extremity edema, sacral or scrotal edema, hepatomegaly with RUQ pain, GI congestion (anorexia, nausea), jugular venous distension

biventricular heart failure

both ventricles fail, paroxysmal nocturnal dyspnea, dyspnea at rest, dysrhythmias, cardiogenic shock

congestive heart failure diagnosis

echocardiogram, EKG changes (ischemia or infarction), increased ANP and BNP levels, CXR

brain atrial natriuretic

a hormone, produced by cells in the wall of the ventricle of the heart, that promotes the excretion of sodium ions in the urine

below 100 pg/mL indicates

no heart failure

100-300 suggest

heart failure is present

above 300 pg/mL indicates

mild heart failure

above 600 pg/mL indicates

moderate heart failure

above 900 pg/mL indicates

severe heart failure


the cardiovascular system fails to perfuse the tissues adequately resulting in widespread impairment of cellular metabolism; a syndrome associated with many diseases or injuries; usually a major insult to the body

types of shock

hypovolemic, cardiogenic, obstructer, distributive (anaphylactic and septic)

shock differences?

the reactions and symptoms will generally follow the same course no matter the type of shock; first identify that shock is occurring rather than the type

shock pathophysiology

body attempts to achieve homeostasis after an insult resulting in problems with perfusion and oxygenation

4 stages of shock

initial stage, compensatory stage, progressive stage, refractory stage

initial stage

the body experiences a reduced cardiac output; body switches from aerobic to anaerobic metabolism; elevated lactic acid level (normal 1-2.5 mmol/L); subtle changes in clinical signs

compensatory stage

body's attempt to regain homeostasis and improve tissue perfusion; sympathetic nervous system stimulated (increased catecholamine release, cardiac contractility); neurohormonal response (vasoconstriction and blood shunted to vital organs); aldosterone rel

progressive stage

the body has lost its compensatory mechanisms; electrolyte imbalance; metabolic acidosis (increased lactate levels); respiratory alkalosis (increased respiratory rate); peripheral edema; irregular tachyarrhythmia; hypotension; pallor (decreased perfusion

refractory stage

shock becomes unresponsive to treatment; irreversible cellular and organ damage; impending death

hypovolemic shock

inadequate intravascular volume; loss of blood or body fluid; tachycardia, systemic vasoconstriction; decreased urinary output; nausea; cold periphery; poor skin turgor; thready pulse

hypovolemic shock causes

hemorrhage, burns, diarrhea, vomiting, fluid shifts

cardiogenic shock

cardiac pump failure; decreased cardiac output; tachycardia, systemic vasoconstriction; left ventricular failure; right sided heart failure; oliguria; cold periphery

cardiogenic shock causes

MI, dysrhythmias, chronic left-sided failure

septic shock

overwhelming infection in bloodstream; vasodilation (feels warm); hypotension refractory to adequate volume resuscitation; inadequate tissue perfusion; tachycardia, tachypnea, fever; presume or confirmed infectious process; WBC > 12,000

septic shock causes

systemic infection, immunosuppression, prolonged hospital stay

sepsis steps


obstructive shock

inability of cardiac ventricles to fill or empty appropriately due to obstruction of blood flow from heart; increased pressure on right side of heart with inadequate blood return (pulmonary embolism, cardiac tamponade)

obstructive shock diagnosis

metabolic acidosis; urinalysis (increased specific gravity and osmolality, more concentrated); blood urea nitrogen (increases with renal damage)

obstructive shock treatment

maintain life support measures (ABC's: airway, breathing, circulation); continuous cardiac monitoring; sympathomimetic medications

multiple organ dysfunction

failure of two or more organ systems in a critically ill patient because of a complex and interrelated series of events