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