Week 7 - Cardiovascular I (altered)

myocardial cells

nearly identical to muscle cells, but slight differences allow for specialized functions such as contraction and electrical conduction in the heart

preload

left ventricular end diastolic volume

afterload

load that the heart muscle must move after it starts to contract

S1

heard sound signalling beginning of systole where tricuspid/mitrial valves close; “LUB”

S2

heard sound that signifies the end of systole/beginning of diastole and the closure of aortic and pulmonary valves; "DUB"

cardiac output

volume of blood flowing through either the systemic or pulmonary circuit, measured in L/min

vessel endothelium

A single layer of specialized cells lining the blood vessels that plays a critical role in vascular function, including clotting cascade, permeability, and inflammatory response

Frank-Starling Law

the stroke volume of the heart increases in response to an increase in the volume of blood filling the ventricles

change vessel diameter, baroreceptors, chemoreceptors

what three things does the body have/do to control total peripheral resistance?

lymphatic system

special vascular system that picks up excess fluid and returns it to the bloodstream

primary hypertension (primary HTN)

caused by a dysregulation of mechanisms controlling vascular resistance and BV, resulting in consistently elevated blood pressure without any identifiable secondary cause

modifiable hypertension (modifiable HTN)

hypertension influenced by lifestyle factors such as diet, exercise, and stress management

<120/<80

normal BP value

secondary hypertension (secondary HTN)

hypertension caused by underlying conditions, such as kidney disease, hormonal disorders, or certain medications, leading to elevated blood pressure that can often be treated by addressing the specific cause.

endothelial injury and vascular remodelling

what are the main complications of HTN

malignant hypertension (malignant HTN)

a severe form of hypertension that progresses rapidly and can lead to organ damage, characterized by extremely high blood pressure, typically over 180/120 mmHg

heart failure (HF)

clinical syndrome resulting from structural and/or fxnal cardiac abnormalities that impair ventricular filling or ejection of blood

Heart failure with reduced EF (HFrEF)

predominantly systolic dysfunction causing impaired ventricular contraction and ejection, reducing stroke volume and CO

heart failure with preserved EF (HFpEF)

predominantly diastolic dysfunction causing impaired ventricular relaxation and filling

left heart failure

heart failure with manifestations being pulmonary congestion, and in some cases, decreased systemic perfusion; results from impaired left ventricular function.

right heart failure

most commonly occurs secondary to left-sided heart failure, causing increased right ventricular afterload. afterload, and is characterized by systemic venous congestion causing peripheral edema

high-output heart failure

heart failure where cardiac output is elevated but inadequate to meet increased systemic demands; can eventuallu lead to ventricular dilation and heart failure

alpha-1 receptor

receptor found on vascular smooth myo and when activated causes vasoconstriction and increased systemic vascular resistance/BP

alpha-2 receptor

receptor found in brain and periphery, when activated it decreases BP

beta-1 receptor

receptor located in heart that increases HR, contractility, and renin release

beta-2 receptor

receptor found in lungs that causes vasodilation and bronchodilation

alpha-1 antagonists (alpha blockers)

end in “-zosin”; treat hypertension by blocking alpha-1 adrenergic receptors, leading to vasodilation and reduced peripheral resistance

alpha-2 agonists (alpha agonists)

treat hypertension by activating alpha-2 adrenergic receptors to decrease resistance, HR, and BP; examples include clonidine, methyldopa, and guanfacine

beta blockers

end in “-olol”; act by blocking the effects of Epi and NE to reduce sympathetic (fight-or-flight) stimulation, make heart beat slower and with less force; watch for bradycardia/hypotension do not administer if HR <60 and dont abruptly discontinue

selective beta blockers

primarily block beta-1 in the heart; includes metoprolol, atenolol, and bisoprolol’ prefered when beta-blockade is necessary in pts with pulonary disease

nonselective beta blockers

block both beta-1/2 so can also cause bronchoconstriction, avoid use in pts with COPD

ACE inhibitors

drug names end in “-pril” block RAAS by inhibiting conversion of angiotensin I causing vasodilation and similar factors to treat HTN and heart failure; causes characteristic dry, persistent cough and possibly hyperkalemia

angiotensin II receptor blockers (ARBs)

block angiotensin II from binding to its receptors, inhibiting the RAAS system and causing vasodilation to treat HTN/HF; often used in place of ACE inhibitors and can also cause hyperkalemia

calcium channel blockers (CCBs)

block calcium from entering cells which reduces heqart’s workload and oxygen demand; when acting on the heart (nondihydropyridines) it decreases HR/contractility, for vessels (dihydropyridines) it causes vasodilation; may cause gingival hyperplasia

dihydropyridines

type of CCB, ending in “-dipine” that acts on blood vessels to cause vasodilation; can cause peripheral edema

nondihydropyridines

type of CCB that acts on the heart to decrease HR and conduction; no useful ending but includes diltiazem and verapamil; can cause bradycardia and constipation

renin inhibitors

bind to renin to prevent activation of RAAS, only drug in class is Aliskiren and use can cause hypotension and hyperkalemia; do not combine with ACE inhibitors or ARBs

diuretics

decreases sodium reabsorption in nephron to decrease BP and treat hypertension; many different types; main issue is electrolyte imbalance, especially hypokalemia, and dehydration so daily weights and I&O monitoring

thiazide diuretics

act in DCT to decrease sodium reabsorption and therefore BV and BP; first-line treatment of HTN and also treats edema; main one is hydrochlorothiazide (HCTZ)

loop diuretics

drugs end in “-nide/-mide” (includes furosemide/Lasix) and act in ascending loop of Henle and prevent Na+ reabsorption, causing decreased BV and BP; most potent of the diuretics and commonly used to treat heart failure and edema; potentially oto/neuro/nephrotoxic

potassium sparing diuretics

diuretics that either block sodium channels or aldosterone to decrease BP while retaining K+; examples include amiloride or spironolactone respectively; be cautious of hyperkalemia

direct vasodilators

drugs (hydralazine and minoxidil) that relax vascular smooth muscle causing vessels to dilate and decrease systemic vascular resistance; generally not first-line but is used for severe/resistant HTN; often given with beta blocker to control reflex tachycardia

sodium nitroprusside

very potent, fast-acting IV vasodilator used for hypertensive emergencies and requires continuous BP monitoring; risk for toxicity with prolonged use

angiotensin receptor-neprilysin inhibitors (ARNIs)

combination drug of sacubitril and valsartan used to treat HFrEF by decreasing preload, afterload, and cardiac workload; cannot be given with ACE inhibitors

sodium glucose cotransporter 2 inhibitors (SGLT-2 inhibitors)

drugs, ending in “-flozin”, that were originally developed for type II DM but are now used for heart failure by causing a mild diuretic effect that decreases BV and cardiac workload

positive inotropic agens

drugs that increase the strength and contractility of the heart in order to increase cardiac output, includes digoxin, dobutamine, and milrinone

cardiac glycosides

Digoxin is the main one; changes electrical conduction of heart to increase myocardial contractility and increase SV/diastole filling time and decrease HR; treats HF and Afib

digoxin

cardiac glycoside and positive inotrope that has a narrow therapeutic window and should not be used if pt has hypokalemia

Digoxin Immune Fab (DigiFab)

an antidote used to treat severe or life-threatening digoxin toxicity

pulmonary hypertension

a condition characterized by elevated blood pressure in the pulmonary circulation, leading to symptoms like shortness of breath, fatigue, and chest pain. It can cause right heart failure if left untreated

pulmonary arterial hypertension (PAH)

type of pulmonary hypertension that is caused by abnormalities of the small pulmonary arteries that cause vasoconstriction and vascular remodeling

endothelin receptor agonists

drugs ending in “-entan” that treat pulmonary arterial hypertension by blocking endothelin and causing vasodilation; teratogenic

PDE-5 inhibitors

drugs ending in “-afil” that treat PAH by increasing cGMP to cause vasodilation and decrease vascular resistance, do NOT combine with nitrates

prostacyclin pathway drugs

meds containing “-prost-” that treat PAH by causing potent vasodilation and inhibiting platelet aggregation

orthostatic hypotension

drop in BP within 3 mins of standing by >20 mmHg systolic or >10 mmHg diastolic; results from an inadequate compensatory response leading to dizziness, lightheadedness, or fainting.