Positive chronotrope increases HR ie. Atropine Baroreceptors increase or decrease HR in response to pressure changes, ie: hypotension Torsades de Pointes Ventricular Tachycardia in the setting of prolonged QT interval. Can cause VF. Causes include electrolytes and medications Troponin only in heart muscle, elevates 3-6 hrs after injury, peaks at 12-48 hrs, returns to baseline 1-2 weeks after SA node the natural pacemaker of the heart HR 60-100 Complete Heart Block atria beat independently of ventricles. 20-40 BPM, Low CO, requires pacemaker Sinus Tachycardia causes include stimulants, pain, fever, shock, hemorrhage Preload volume of blood in LV at end of diastole. Affected by venous return to heart, total blood volume, atrial kick and stiffness and thickness of heart. Cardiac Output (CO) the volume of blood ejected by the heart in 1 min. 4-6L at rest, HR x SV Positive inotrope increases heart pumping/ contraction ie. Digoxin Ventricular Tachycardia (VT) wide and bizarre complexes, treat with synchronized cardioversion and meds, pulseless requires ACLS and code Sinus Bradycardia causes include vagal responses, ICP, MI, BB, digoxin Ejection Fraction (EF) percent of blood ejected by left ventricle. SV/EDV > 50% is normal Stroke Volume (SV) volume of blood ejected by the heart with each beat Supraventricular Tachycardia (SVT) dysrhythmias that start above AV node, treat with carotid massage, Valsalva, adenosine AV node intrinsic HR 40- 60 Contractility ability of heart to pump, inotropy Creatinine kinase (CK) found in heart, brain and skeletal muscle Starling’s Law the more the LV is stretched the more forceful the contraction. Can only stretch so much and for so long. Afterload resistance LV must overcome to circulate blood. ↑aortic stenosis, septal hypertrophy, vasoconstriction ↓sepsis, vasodilation Natriuretic peptides cause vasodilation, increase natriuresis and inhibit SNS and RAAS End Diastolic Volume (EDV) amount of blood in ventricles at end of diastole before contraction Negative inotrope decreases the heart pumping/contraction ie. BB CK- MB specific to heart, elevates 3-12 hrs after injury, peaks at 24 hr returns to baseline 2-3 days after Negative chronotrope decreases HR ie. BB Compliance ability of ventricles to distend or expand Chemoreceptors sense changes in PaO2 or PaCO2, triggers SNS Positive chronotrope increases HR ie. Atropine Baroreceptors increase or decrease HR in response to pressure changes, ie: hypotension Torsades de Pointes Ventricular Tachycardia in the setting of prolonged QT interval. Can cause VF. Causes include electrolytes and medications Troponin only in heart muscle, elevates 3-6 hrs after injury, peaks at 12-48 hrs, returns to baseline 1-2 weeks after SA node the natural pacemaker of the heart HR 60-100 Complete Heart Block atria beat independently of ventricles. 20-40 BPM, Low CO, requires pacemaker Sinus Tachycardia causes include stimulants, pain, fever, shock, hemorrhage Preload volume of blood in LV at end of diastole. Affected by venous return to heart, total blood volume, atrial kick and stiffness and thickness of heart. Cardiac Output (CO) the volume of blood ejected by the heart in 1 min. 4-6L at rest, HR x SV Positive inotrope increases heart pumping/ contraction ie. Digoxin Ventricular Tachycardia (VT) wide and bizarre complexes, treat with synchronized cardioversion and meds, pulseless requires ACLS and code Sinus Bradycardia causes include vagal responses, ICP, MI, BB, digoxin Ejection Fraction (EF) percent of blood ejected by left ventricle. SV/EDV > 50% is normal Stroke Volume (SV) volume of blood ejected by the heart with each beat Supraventricular Tachycardia (SVT) dysrhythmias that start above AV node, treat with carotid massage, Valsalva, adenosine AV node intrinsic HR 40- 60 Contractility ability of heart to pump, inotropy Creatinine kinase (CK) found in heart, brain and skeletal muscle Starling’s Law the more the LV is stretched the more forceful the contraction. Can only stretch so much and for so long. Afterload resistance LV must overcome to circulate blood. ↑aortic stenosis, septal hypertrophy, vasoconstriction ↓sepsis, vasodilation Natriuretic peptides cause vasodilation, increase natriuresis and inhibit SNS and RAAS End Diastolic Volume (EDV) amount of blood in ventricles at end of diastole before contraction Negative inotrope decreases the heart pumping/contraction ie. BB CK- MB specific to heart, elevates 3-12 hrs after injury, peaks at 24 hr returns to baseline 2-3 days after Negative chronotrope decreases HR ie. BB Compliance ability of ventricles to distend or expand Chemoreceptors sense changes in PaO2 or PaCO2, triggers SNS
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increases HR ie. Atropine
increase or decrease HR in response to pressure changes, ie: hypotension
Ventricular Tachycardia in the setting of prolonged QT interval. Can cause VF. Causes include electrolytes and medications
only in heart muscle, elevates 3-6 hrs after injury, peaks at 12-48 hrs, returns to baseline 1-2 weeks after
the natural pacemaker of the heart HR 60-100
atria beat independently of ventricles. 20-40 BPM, Low CO, requires pacemaker
causes include stimulants, pain, fever, shock, hemorrhage
volume of blood in LV at end of diastole. Affected by venous return to heart, total blood volume, atrial kick and stiffness and thickness of heart.
the volume of blood ejected by the heart in 1 min. 4-6L at rest, HR x SV
increases heart pumping/ contraction ie. Digoxin
wide and bizarre complexes, treat with synchronized cardioversion and meds, pulseless requires ACLS and code
causes include vagal responses, ICP, MI, BB, digoxin
percent of blood ejected by left ventricle. SV/EDV > 50% is normal
volume of blood ejected by the heart with each beat
dysrhythmias that start above AV node, treat with carotid massage, Valsalva, adenosine
intrinsic HR 40-60
ability of heart to pump, inotropy
found in heart, brain and skeletal muscle
the more the LV is stretched the more forceful the contraction. Can only stretch so much and for so long.
resistance LV must overcome to circulate blood. ↑aortic stenosis, septal hypertrophy, vasoconstriction ↓sepsis, vasodilation
cause vasodilation, increase natriuresis and inhibit SNS and RAAS
amount of blood in ventricles at end of diastole before contraction
decreases the heart pumping/contraction ie. BB
specific to heart, elevates 3-12 hrs after injury, peaks at 24 hr returns to baseline 2-3 days after
decreases HR ie. BB
ability of ventricles to distend or expand
sense changes in PaO2 or PaCO2, triggers SNS
