Cardiac 03: Heart Failure , Pacers Flashcards
Definition of Heart Failure
The heart’s inability to adequately supply blood to meet the metabolic demands of the tissues. This results in inadequate tissue perfusion and volume overload
What’s different about Acute HF compared to HF?
It occurs suddenly, frequently w/o time for compensatory mechanisms to be activated. If severe/rapid enough, this can result in cardiogenic shock.
What is the demographic of HF?
It can be anyone, even a young person who got COVID->cardiogenic shock to postpartum cardiomyopathy.
What response does the heart have when the CO drops in cardiogenic shock? (4 steps)
- Drop in CO -> drop in EF
- Increased in End Diastolic Volume, leading to myocardial fiber stretch
- Increased contractility (augmented sensitivity to Ca++)
- Activation of the neurohormonal system
! What are 4 systems within the compensatory neurohormonal system?
All 4 occurs at the same time
- Adrenergic System
- Renin-Angiotensin-Aldosterone System
- Hypothalamic- Neurohypophyseal System
- Endothelium activated Mediators
Read and recall:
In adrenergic response..
Baroreceptors in aorta sense low bp/co. The SNS is activated by brain and norephinephrine and epinephrine is released. Leads to beta stimulation and increase in HR and contractility.
Alpha stimulation occurs -> vasoconstriction
Read and recall:
In Renin-Angiotension response
Low BP/CO leads to lower filturation rate/GFR -> Renin Release ->Angiotensin I->Angiotensin II -> vasoconstriction.
Aldosterone is released, leading to Na & water retention
Read and recall:
In Hypothalamic Neurohypophyseal System. Basically vasopressin effect
Low BP/CO leads to release of vasopressin (ADH) from Posterior Pituitary -> Vasoconstriction -> Sodium and Water retention.
UOP decreases
Delete
When low BP/CO occurs, it leads to endothelin-1 vasoconstriction.
Nitric oxide, endothelium-derived relaxin
What does the systems of the compensatory response do in CO? (4)
- Increased HR
- Increased Contractility
- Vasoconstriction
- Sodium & water retention
Compensatory responses for low CO are good in situ where patient is bleeding out, but not when the heart is failing, why?
Compensatory responses are great with a good working heart in a bleeding patient. But in a person with a bad heart, a positive feedback loop occurs where the afterload increases, and the compensatory normal response continues. It becomes progressive heart failure.
Read about during the progression of heart failure and what ANP and BNP does
Continued activation of sympathetic system causes an increase in afterload and the release of natriuretic peptides: ANP& BNP.
These peptides promotes diuresis, vasodilation and inhibition of RAAS. Atrial is produced by a stretch atria and BNP produced by ventricles.
What is TNF Alpha?
TNF-alpha: Tumor necrosis factor. Produces secondary to hypervolemia and triggers both systemic and cardiac inflammatory responses.
Releases cytokinesis during HF
What occurs to the heart anatomy in progressive HF?
It actually hypertrophies and remodels. Initially adaptive in nature, it leads to hypertrophy, ventricular dilation and increased O2 demands. But with increased demand, it leads to a decrease in CO and ischemia
Cardiac signs of HF: (9) List five or so
- Tachycardia, arrhythmia
- Weak pulses
- Low CO & BP
- Jugular venous distension
- S3 diastolic gallop
- Displaced PMI
- C xray cardiomegaly and vascular prominence
- Peripheral edema
9 Positive hepatojugular reflux
Pulmonary signs and symptoms of HF: (3)
- Dyspnea
- Rales
- Paroxysmal Nocturnal Dyspnea
All are from the heart volume backing up into the lungs
Neurological signs and symptoms of HF (3)
- Fatigue, weakness, dizziness
- LOC Change
- Sense of impending doom from decrease O2, increased CO2. Anxious , confusion etc.
TIA, strokes could occur from lack of perfusion.
If poor coronary perfusion is the primary cause of HF, what are some possible interventions?
- Thrombolytics
- PCI
- CABG
- Cardiac Transplant
- Treat the physiological cause, i.e CAD, HTN, dysrhythmia
Why are vasodilators helpful in the management of HF?
They decrease preload, decrease afterload and increase renal perfusion. So it improves symptoms of failure and and symptoms related to the compensatory response.
How do Angiotensin Converting Enzymes Inhibitors work? (ACE) 3
ACE is now main drug used in HF management.
1. Dilate arterioles -> decreases afterload, increase SV, inscrease CO, improve regional flow
2. Dilate veins -> Decrease preload -> decrease pulmonary congestion -> decrease cardiac dilation -> increase renal perfusion which then increases sodium and water excretion. This will also stop encouraging the positive feedback loop of the compensatory response.
3. Decrease aldosterone release -> Retention of K. Release of Na and water.
What hormone is aldosterone and how does it work?
It’s a corticosteroid. More of it retains water and sodium and excretes potassium in the urine.
How does ARBs work? Stands for…
Angiotensin II Receptor Blockers.
it blocks the action of Angiotensin II. Same effects as ACE inhibitors but without adverse effects of cough, hyperkalemia & angioedema. May not be used with ACE inhibitors.
What are some adverse effects of ACE? (3)
1.Angioedema
2. Cough
3. hypErKalEmia
5 types of vasodilators to manage HF
- ACE
- ARB
- Hydralazine
- Nitroglycerin
- Calcium Channel Blockers
C
AHA
N
What kind of dilator is Hydralazine?
Selective arteriole dilator
What kind of vasodilator is Isosorbide Dinitrate?
It’s a nitrate that is a selective VENOUS dilator. Used with hydralazine to create a similar effect as ACE inhibiting agents
How does nitroglycerin work as a vasodilator?
Works directly on the vascular smooth muscle, casing venodilation and minimal arteriole dilation
How does diuretics work for HF management?
It decreases preload and afterload. The goal is to decrease the work of failing heart muscle.
How does aldosterone blockers work?
Retains K. Loses Na and water.
Weak diuretic used with K+ losing diuretics.
Aldosterone Antagonist Properties
How does thiazide diuretics work?
Weak diuretic that increases sodium excretion.
Effective as long as CO and renal perfusion are adequate.
Major side effect is HYPOKALEMIA.
How does loop diuretics work?
i.e Furosemide
inhibits Na & Cl- reabsorption from the loop of Henle. Poten diuretics, increases sodium excretion 20-25%.
Side effect of hypotension and hypokalemia.
How does digoxin work? (inotrope)
Promotes Ca++ accumulation int he cardiac cell and contractility by inhibiting Na/K Atpase.
Decreases HR by slowing conduction through AV node.
Increases CO, and filling time. Decrease renin release and sympathetic tone.
How does Dobutamine work? (inotrope)
Syntethetic catecholamine with selective beta-adrenergic agonist properties. Increases myocardial contractility -> stroke volume -> incr CO.
Mild vasodilator.
Increases AV conduction and HR
How does amrinone and milrinone work? (inotrope )
Non catecholamine agents that increases contractility. Block sympathetic vasoconstriction.
- increase contractility and incr CO
- vasodilation decreases after load which increases CO
- no effect on HR or myocardial oxygen demands
How does beta blockers work in HF pts?
- Decrease effects of chronic sympathetic activation
- alleviates tachycardia
- Increase EF and improve resting cardiac function
- less HF and symptoms and increased exercise tolerance
Why are calcium channel blockers bad for management of HF?
It has negative inotropic properties. It worsens CO.
What 3 devices could be used to decrease demands on the heart?
- IABP
- Impella
- VAD
How does an IABP work?
Improves coronary perfusion and decreases afterload.
How does an impella work?
Increase CO by moving blood out of ventricle with mini motor
How are VADs typically used?
- bridge to transplantation
- recovery/rest therapy
About half the deaths from HF are from what?
dysrhythmia
Pacers, id what each DDDR
- Paced
- Sense
- Response what was sensed, to inhibit or trigger response.
- Rate
What does failure to capture mean?
Spike is not followed by complex. Pacer followed, but didn’t cause depolarization of the heart.
What does failure to sense mean?
Fails to sense native cardiac activity. Over pacing may occur accidentally.
Lower the sensitivity number, the more sensitive. Think of sensitivity as height of fence. Higher means less likely to see and sense.
What are notable differences between systolic HF and diastolic HF?
sHF: low EF, weak muscle, large volume held.
dHF: normal EF, stiff ventricles, small volumes
Which heart blocks have constant PR intervals?
1st AVB, 2nd AVB Type II wenckebach (QRS just drops, P waves paced out)
Which 2 heart blocks have variable PR intervals?
2nd HB type II, gone going. Pr elongates till QRS drops.
3 degree HB PR and QRS doesn’t match
What meds are used in hypertrophic cardiomyopathy?
It should be meds to reduce outflow tract obstruction.
beta blockers/ calcium channel blocker would decrease contractility.
Positive inotropes should be avoided, e.g digoxin, dobutamine, milrinone.
Read signs of R ventricular failure and what type of MI most likely causes it?
elevated RAP
R sided S3
JVD
Most likely caused by inferior MI
R sided leads V4-6
Pacemaker code. What does each initial stand for? Think PSR
- Pacing: where does pacer pace, atria, vents or both?
- Sensing: Where does it sense intrinsic cardiac activity? A, V or D?
- Response: Does it inhibit or trigger a response? Initials, Inhibit, Dual (inhibit and triggers) or O (no response)
Why does BNP get released during acute HF?
It’s released by the ventricle when the ventricle is under wall stress in attempts to dilate and decrease ventricular pressure.
